Carrel name: keyword-ros-cord Creating study carrel named keyword-ros-cord Initializing database file: cache/cord-001769-2sdg5ll7.json key: cord-001769-2sdg5ll7 authors: Guo, Sheng; Yang, Chengying; Diao, Bo; Huang, Xiaoyong; Jin, Meihua; Chen, Lili; Yan, Weiming; Ning, Qin; Zheng, Lixin; Wu, Yuzhang; Chen, Yongwen title: The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis date: 2015-09-14 journal: PLoS Pathog DOI: 10.1371/journal.ppat.1005155 sha: doc_id: 1769 cord_uid: 2sdg5ll7 file: cache/cord-000799-s70onyix.json key: cord-000799-s70onyix authors: Wang, Ting; Wang, Lichun; Moreno-Vinasco, Liliana; Lang, Gabriel D; Siegler, Jessica H; Mathew, Biji; Usatyuk, Peter V; Samet, Jonathan M; Geyh, Alison S; Breysse, Patrick N; Natarajan, Viswanathan; Garcia, Joe G N title: Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation date: 2012-08-29 journal: Part Fibre Toxicol DOI: 10.1186/1743-8977-9-35 sha: doc_id: 799 cord_uid: s70onyix file: cache/cord-004508-ok3px98z.json key: cord-004508-ok3px98z authors: Armando, Federico; Gambini, Matteo; Corradi, Attilio; Giudice, Chiara; Pfankuche, Vanessa Maria; Brogden, Graham; Attig, Friederike; von Köckritz-Blickwede, Maren; Baumgärtner, Wolfgang; Puff, Christina title: Oxidative Stress in Canine Histiocytic Sarcoma Cells Induced by an Infection with Canine Distemper Virus Led to a Dysregulation of HIF-1α Downstream Pathway Resulting in a Reduced Expression of VEGF-B In Vitro date: 2020-02-11 journal: Viruses DOI: 10.3390/v12020200 sha: doc_id: 4508 cord_uid: ok3px98z file: cache/cord-001347-ssrs0cwf.json key: cord-001347-ssrs0cwf authors: Michaelis, Martin; Sithisarn, Patchima; Cinatl Jr, Jindrich title: Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A date: 2014-06-23 journal: BMC Res Notes DOI: 10.1186/1756-0500-7-384 sha: doc_id: 1347 cord_uid: ssrs0cwf file: cache/cord-014661-mrh2pbi6.json key: cord-014661-mrh2pbi6 authors: Dumitrascu, Georgiana R.; Bucur, Octavian title: Critical physiological and pathological functions of Forkhead Box O tumor suppressors date: 2013-12-31 journal: nan DOI: 10.15190/d.2013.5 sha: doc_id: 14661 cord_uid: mrh2pbi6 file: cache/cord-005280-a23oy0sz.json key: cord-005280-a23oy0sz authors: Yang, Shenshu; Lian, Gaojian title: ROS and diseases: role in metabolism and energy supply date: 2019-12-07 journal: Mol Cell Biochem DOI: 10.1007/s11010-019-03667-9 sha: doc_id: 5280 cord_uid: a23oy0sz file: cache/cord-013415-110b95cg.json key: cord-013415-110b95cg authors: Aquino-Martinez, Ruben; Khosla, Sundeep; Farr, Joshua N.; Monroe, David G. title: Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? date: 2020-10-09 journal: Int J Mol Sci DOI: 10.3390/ijms21207441 sha: doc_id: 13415 cord_uid: 110b95cg file: cache/cord-102808-c7ajfvt5.json key: cord-102808-c7ajfvt5 authors: Sundqvist, Martina; Holdfeldt, André; Wright, Shane C.; Møller, Thor C.; Siaw, Esther; Jennbacken, Karin; Franzyk, Henrik; Bouvier, Michel; Dahlgren, Claes; Forsman, Huamei title: Barbadin selectively modulates FPR2-mediated neutrophil functions independent of receptor endocytosis date: 2020-05-01 journal: bioRxiv DOI: 10.1101/2020.04.30.070011 sha: doc_id: 102808 cord_uid: c7ajfvt5 file: cache/cord-048478-ftlb5b95.json key: cord-048478-ftlb5b95 authors: Mroczek, Seweryn; Kufel, Joanna title: Apoptotic signals induce specific degradation of ribosomal RNA in yeast date: 2008-04-01 journal: Nucleic Acids Res DOI: 10.1093/nar/gkm1100 sha: doc_id: 48478 cord_uid: ftlb5b95 file: cache/cord-289034-yl3emjef.json key: cord-289034-yl3emjef authors: Moro, Loredana title: Mitochondria at the Crossroads of Physiology and Pathology date: 2020-06-24 journal: J Clin Med DOI: 10.3390/jcm9061971 sha: doc_id: 289034 cord_uid: yl3emjef file: cache/cord-012495-r6nkdeaw.json key: cord-012495-r6nkdeaw authors: Bonora, Massimo; Patergnani, Simone; Ramaccini, Daniela; Morciano, Giampaolo; Pedriali, Gaia; Kahsay, Asrat Endrias; Bouhamida, Esmaa; Giorgi, Carlotta; Wieckowski, Mariusz R.; Pinton, Paolo title: Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology date: 2020-07-04 journal: Biomolecules DOI: 10.3390/biom10070998 sha: doc_id: 12495 cord_uid: r6nkdeaw file: cache/cord-273992-xddikzxs.json key: cord-273992-xddikzxs authors: Wiseman, A. title: Avoidance of oxidative‐stress perturbation in yeast bioprocesses by proteomic and genomic biostrategies? date: 2004-11-10 journal: Lett Appl Microbiol DOI: 10.1111/j.1472-765x.2004.01624.x sha: doc_id: 273992 cord_uid: xddikzxs file: cache/cord-034321-ohjik0pf.json key: cord-034321-ohjik0pf authors: Vorobjeva, N. V.; Chernyak, B. V. title: NETosis: Molecular Mechanisms, Role in Physiology and Pathology date: 2020-10-27 journal: Biochemistry (Mosc) DOI: 10.1134/s0006297920100065 sha: doc_id: 34321 cord_uid: ohjik0pf file: cache/cord-020646-s7eopu9y.json key: cord-020646-s7eopu9y authors: nan title: Die Pathophysiologie der Entzündung date: 2005 journal: Die Akute Entzündung DOI: 10.1007/3-211-29899-1_2 sha: doc_id: 20646 cord_uid: s7eopu9y file: cache/cord-003841-7uaj9hmx.json key: cord-003841-7uaj9hmx authors: Desmonts de Lamache, D.; Moges, R.; Siddiq, A.; Allain, T.; Feener, T. D.; Muench, G. P.; McKenna, N.; Yates, R. M.; Buret, A. G. title: Immuno-modulating properties of Tulathromycin in porcine monocyte-derived macrophages infected with porcine reproductive and respiratory syndrome virus date: 2019-08-23 journal: PLoS One DOI: 10.1371/journal.pone.0221560 sha: doc_id: 3841 cord_uid: 7uaj9hmx file: cache/cord-035015-slgywe0c.json key: cord-035015-slgywe0c authors: Nunn, Alistair V. W.; Guy, Geoffrey W.; Brysch, Wolfgang; Botchway, Stanley W.; Frasch, Wayne; Calabrese, Edward J.; Bell, Jimmy D. title: SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing date: 2020-11-09 journal: Immun Ageing DOI: 10.1186/s12979-020-00204-x sha: doc_id: 35015 cord_uid: slgywe0c file: cache/cord-262759-ec2c25q3.json key: cord-262759-ec2c25q3 authors: Hsieh, Yi-Ting; Lin, Mei-Hui; Ho, Hung-Yao; Chen, Lei-Chin; Chen, Chien-Cheng; Shu, Jwu-Ching title: Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Epithelial Cells Are Less Tolerant to Infection by Staphylococcus aureus date: 2013-11-04 journal: PLoS One DOI: 10.1371/journal.pone.0079566 sha: doc_id: 262759 cord_uid: ec2c25q3 file: cache/cord-034294-ti1cc24m.json key: cord-034294-ti1cc24m authors: Wang, Cuixue; Zhou, Jiedong; Wang, Jinquan; Li, Shujing; Fukunaga, Atsushi; Yodoi, Junji; Tian, Hai title: Progress in the mechanism and targeted drug therapy for COPD date: 2020-10-27 journal: Signal Transduct Target Ther DOI: 10.1038/s41392-020-00345-x sha: doc_id: 34294 cord_uid: ti1cc24m file: cache/cord-293319-oo0w6faj.json key: cord-293319-oo0w6faj authors: Seo, Youngsik; Park, Keunchun; Hong, Yonggun; Lee, Eun Sik; Kim, Sang-Soon; Jung, Yong-Tae; Park, Heonyong; Kwon, Chian; Cho, Young-Sik; Huh, Young-Duk title: Reactive-oxygen-species-mediated mechanism for photoinduced antibacterial and antiviral activities of Ag(3)PO(4) date: 2020-06-11 journal: J Anal Sci Technol DOI: 10.1186/s40543-020-00220-y sha: doc_id: 293319 cord_uid: oo0w6faj file: cache/cord-017817-ztp7w9yh.json key: cord-017817-ztp7w9yh authors: Land, Walter Gottlieb title: Cell-Autonomous (Cell-Intrinsic) Stress Responses date: 2018-03-28 journal: Damage-Associated Molecular Patterns in Human Diseases DOI: 10.1007/978-3-319-78655-1_18 sha: doc_id: 17817 cord_uid: ztp7w9yh file: cache/cord-278846-nqj7ctk3.json key: cord-278846-nqj7ctk3 authors: Ogger, Patricia P.; Byrne, Adam J. title: Macrophage metabolic reprogramming during chronic lung disease date: 2020-11-12 journal: Mucosal Immunol DOI: 10.1038/s41385-020-00356-5 sha: doc_id: 278846 cord_uid: nqj7ctk3 file: cache/cord-257514-gw9xnb4x.json key: cord-257514-gw9xnb4x authors: Yang, Mengling; Dong, Yinmiao; He, Qingnan; Zhu, Ping; Zhuang, Quan; Shen, Jie; Zhang, Xueyan; Zhao, Mingyi title: Hydrogen: A Novel Option in Human Disease Treatment date: 2020-09-05 journal: Oxid Med Cell Longev DOI: 10.1155/2020/8384742 sha: doc_id: 257514 cord_uid: gw9xnb4x file: cache/cord-319614-4qi59pbz.json key: cord-319614-4qi59pbz authors: Benej, Martin; Danchenko, Maksym; Oveckova, Ingrid; Cervenak, Filip; Tomaska, Lubomir; Grossmannova, Katarina; Polcicova, Katarina; Golias, Tereza; Tomaskova, Jana title: Quantitative Proteomics Reveal Peroxiredoxin Perturbation Upon Persistent Lymphocytic Choriomeningitis Virus Infection in Human Cells date: 2019-10-25 journal: Front Microbiol DOI: 10.3389/fmicb.2019.02438 sha: doc_id: 319614 cord_uid: 4qi59pbz file: cache/cord-273093-u79r80ip.json key: cord-273093-u79r80ip authors: Laforge, Mireille; Elbim, Carole; Frère, Corinne; Hémadi, Miryana; Massaad, Charbel; Nuss, Philippe; Benoliel, Jean-Jacques; Becker, Chrystel title: Tissue damage from neutrophil-induced oxidative stress in COVID-19 date: 2020-07-29 journal: Nat Rev Immunol DOI: 10.1038/s41577-020-0407-1 sha: doc_id: 273093 cord_uid: u79r80ip file: cache/cord-291190-f6km3c7z.json key: cord-291190-f6km3c7z authors: Nasi, Aikaterini; McArdle, Stephanie; Gaudernack, Gustav; Westman, Gabriel; Melief, Cornelis; Kouretas, Demetrios; Arens, Ramon; Sjölin, Jan; Mangsbo, Sara title: Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention date: 2020-06-18 journal: Toxicol Rep DOI: 10.1016/j.toxrep.2020.06.003 sha: doc_id: 291190 cord_uid: f6km3c7z file: cache/cord-313825-bbjxd86y.json key: cord-313825-bbjxd86y authors: Xia, Tian; Zhu, Yifang; Mu, Lina; Zhang, Zuo-Feng; Liu, Sijin title: Pulmonary diseases induced by ambient ultrafine and engineered nanoparticles in twenty-first century date: 2016-10-08 journal: Natl Sci Rev DOI: 10.1093/nsr/nww064 sha: doc_id: 313825 cord_uid: bbjxd86y file: cache/cord-271939-m1ko4yal.json key: cord-271939-m1ko4yal authors: Rouco, Lara; González-Noya, Ana M.; Pedrido, Rosa; Maneiro, Marcelino title: Pursuing the Elixir of Life: In Vivo Antioxidative Effects of Manganosalen Complexes date: 2020-08-10 journal: Antioxidants (Basel) DOI: 10.3390/antiox9080727 sha: doc_id: 271939 cord_uid: m1ko4yal file: cache/cord-291559-h6czy5bh.json key: cord-291559-h6czy5bh authors: Koirala, Prashamsa; Jung, Hyun Ah; Choi, Jae Sue title: Recent advances in pharmacological research on Ecklonia species: a review date: 2017-08-24 journal: Arch Pharm Res DOI: 10.1007/s12272-017-0948-4 sha: doc_id: 291559 cord_uid: h6czy5bh file: cache/cord-288238-36hiiw91.json key: cord-288238-36hiiw91 authors: Keshavarz, Mohsen; Solaymani-Mohammadi, Farid; Namdari, Haideh; Arjeini, Yaser; Mousavi, Mohammad Javad; Rezaei, Farhad title: Metabolic host response and therapeutic approaches to influenza infection date: 2020-03-05 journal: Cell Mol Biol Lett DOI: 10.1186/s11658-020-00211-2 sha: doc_id: 288238 cord_uid: 36hiiw91 file: cache/cord-260348-83ftjqev.json key: cord-260348-83ftjqev authors: Xu, Yinlan; Zheng, Jiangang; Sun, Panpan; Guo, Jianhua; Zheng, Xiaozhong; Sun, Yaogui; Fan, Kuohai; Yin, Wei; Li, Hongquan; Sun, Na title: Cepharanthine and Curcumin inhibited mitochondrial apoptosis induced by PCV2 date: 2020-09-18 journal: BMC Vet Res DOI: 10.1186/s12917-020-02568-0 sha: doc_id: 260348 cord_uid: 83ftjqev file: cache/cord-295459-ffi1043k.json key: cord-295459-ffi1043k authors: Khan, Naseem Ahmed; Singla, Mohit; Samal, Sweety; Lodha, Rakesh; Medigeshi, Guruprasad R. title: Respiratory Syncytial Virus-Induced Oxidative Stress Leads to an Increase in Labile Zinc Pools in Lung Epithelial Cells date: 2020-05-27 journal: mSphere DOI: 10.1128/msphere.00447-20 sha: doc_id: 295459 cord_uid: ffi1043k file: cache/cord-320591-re99v1qt.json key: cord-320591-re99v1qt authors: Le, Thanh Ninh; Chiu, Chiu-Hsia; Hsieh, Pao-Chuan title: Bioactive Compounds and Bioactivities of Brassica oleracea L. var. Italica Sprouts and Microgreens: An Updated Overview from a Nutraceutical Perspective date: 2020-07-27 journal: Plants (Basel) DOI: 10.3390/plants9080946 sha: doc_id: 320591 cord_uid: re99v1qt file: cache/cord-331673-xv1tcugl.json key: cord-331673-xv1tcugl authors: Reina, Giacomo; Peng, Shiyuan; Jacquemin, Lucas; Andrade, Andrés Felipe; Bianco, Alberto title: Hard Nanomaterials in Time of Viral Pandemics date: 2020-07-15 journal: ACS Nano DOI: 10.1021/acsnano.0c04117 sha: doc_id: 331673 cord_uid: xv1tcugl file: cache/cord-316244-s5ua0re3.json key: cord-316244-s5ua0re3 authors: Park, Mi Hee; Jo, MiRan; Kim, Yu Ri; Lee, Chong-Kil; Hong, Jin Tae title: Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases date: 2016-04-26 journal: Pharmacol Ther DOI: 10.1016/j.pharmthera.2016.03.018 sha: doc_id: 316244 cord_uid: s5ua0re3 file: cache/cord-335676-7ak53hto.json key: cord-335676-7ak53hto authors: Meftahi, Gholam Hossein; Jangravi, Zohreh; Sahraei, Hedayat; Bahari, Zahra title: The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of “inflame-aging” date: 2020-06-11 journal: Inflamm Res DOI: 10.1007/s00011-020-01372-8 sha: doc_id: 335676 cord_uid: 7ak53hto file: cache/cord-268527-wbfnhedy.json key: cord-268527-wbfnhedy authors: Smith, Sylvia B.; St Jules, Robert S.; O'Brien, Paul J. title: Transient hyperglycosylation of rhodopsin with galactose date: 1991-10-31 journal: Experimental Eye Research DOI: 10.1016/0014-4835(91)90170-j sha: doc_id: 268527 cord_uid: wbfnhedy file: cache/cord-336201-fl606l3b.json key: cord-336201-fl606l3b authors: Daryabor, Gholamreza; Atashzar, Mohamad Reza; Kabelitz, Dieter; Meri, Seppo; Kalantar, Kurosh title: The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System date: 2020-07-22 journal: Front Immunol DOI: 10.3389/fimmu.2020.01582 sha: doc_id: 336201 cord_uid: fl606l3b file: cache/cord-298265-elbnzgx6.json key: cord-298265-elbnzgx6 authors: Mutua, Victoria; Gershwin, Laurel J. title: A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics date: 2020-08-01 journal: Clin Rev Allergy Immunol DOI: 10.1007/s12016-020-08804-7 sha: doc_id: 298265 cord_uid: elbnzgx6 file: cache/cord-310723-ogo9mvi5.json key: cord-310723-ogo9mvi5 authors: Belinskaia, Daria A.; Voronina, Polina A.; Shmurak, Vladimir I.; Vovk, Mikhail A.; Batalova, Anastasia A.; Jenkins, Richard O.; Goncharov, Nikolay V. title: The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin date: 2020-10-09 journal: Antioxidants (Basel) DOI: 10.3390/antiox9100966 sha: doc_id: 310723 cord_uid: ogo9mvi5 file: cache/cord-323730-5iawbnua.json key: cord-323730-5iawbnua authors: Ohl, Kim; Tenbrock, Klaus; Kipp, Markus title: Oxidative stress in multiple sclerosis: Central and peripheral mode of action date: 2016-03-31 journal: Experimental Neurology DOI: 10.1016/j.expneurol.2015.11.010 sha: doc_id: 323730 cord_uid: 5iawbnua file: cache/cord-297469-26d8o1xk.json key: cord-297469-26d8o1xk authors: Choi, Won Hyung; Lee, In Ah title: The Mechanism of Action of Ursolic Acid as a Potential Anti-Toxoplasmosis Agent, and Its Immunomodulatory Effects date: 2019-05-09 journal: Pathogens DOI: 10.3390/pathogens8020061 sha: doc_id: 297469 cord_uid: 26d8o1xk file: cache/cord-313918-uv9xdp5f.json key: cord-313918-uv9xdp5f authors: Marí, Montserrat; de Gregorio, Estefanía; de Dios, Cristina; Roca-Agujetas, Vicente; Cucarull, Blanca; Tutusaus, Anna; Morales, Albert; Colell, Anna title: Mitochondrial Glutathione: Recent Insights and Role in Disease date: 2020-09-24 journal: Antioxidants (Basel) DOI: 10.3390/antiox9100909 sha: doc_id: 313918 cord_uid: uv9xdp5f file: cache/cord-268122-74nj66vb.json key: cord-268122-74nj66vb authors: Xie, Na; Zhang, Lu; Gao, Wei; Huang, Canhua; Huber, Peter Ernst; Zhou, Xiaobo; Li, Changlong; Shen, Guobo; Zou, Bingwen title: NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential date: 2020-10-07 journal: Signal Transduct Target Ther DOI: 10.1038/s41392-020-00311-7 sha: doc_id: 268122 cord_uid: 74nj66vb file: cache/cord-307148-k1uo3fxm.json key: cord-307148-k1uo3fxm authors: Bradshaw, Patrick C.; Seeds, William A.; Miller, Alexandra C.; Mahajan, Vikrant R.; Curtis, William M. title: COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm date: 2020-09-09 journal: Oxid Med Cell Longev DOI: 10.1155/2020/6401341 sha: doc_id: 307148 cord_uid: k1uo3fxm file: cache/cord-032561-x3qbqy69.json key: cord-032561-x3qbqy69 authors: Liu, Gengqi; Lovell, Jonathan F.; Zhang, Lei; Zhang, Yumiao title: Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment date: 2020-09-02 journal: Int J Mol Sci DOI: 10.3390/ijms21176380 sha: doc_id: 32561 cord_uid: x3qbqy69 file: cache/cord-006230-xta38e7j.json key: cord-006230-xta38e7j authors: nan title: Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie e.V. date: 2012-02-22 journal: Naunyn Schmiedebergs Arch Pharmacol DOI: 10.1007/s00210-012-0736-0 sha: doc_id: 6230 cord_uid: xta38e7j file: cache/cord-022940-atbjwpo5.json key: cord-022940-atbjwpo5 authors: nan title: Poster Sessions date: 2016-09-07 journal: FEBS J DOI: 10.1111/febs.13808 sha: doc_id: 22940 cord_uid: atbjwpo5 Reading metadata file and updating bibliogrpahics === updating bibliographic database Building study carrel named keyword-ros-cord === file2bib.sh === id: cord-273093-u79r80ip author: Laforge, Mireille title: Tissue damage from neutrophil-induced oxidative stress in COVID-19 date: 2020-07-29 pages: extension: .txt txt: ./txt/cord-273093-u79r80ip.txt cache: ./cache/cord-273093-u79r80ip.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 6 resourceName b'cord-273093-u79r80ip.txt' === file2bib.sh === id: cord-262759-ec2c25q3 author: Hsieh, Yi-Ting title: Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Epithelial Cells Are Less Tolerant to Infection by Staphylococcus aureus date: 2013-11-04 pages: extension: .txt txt: ./txt/cord-262759-ec2c25q3.txt cache: ./cache/cord-262759-ec2c25q3.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-262759-ec2c25q3.txt' === file2bib.sh === id: cord-001347-ssrs0cwf author: Michaelis, Martin title: Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A date: 2014-06-23 pages: extension: .txt txt: ./txt/cord-001347-ssrs0cwf.txt cache: ./cache/cord-001347-ssrs0cwf.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 2 resourceName b'cord-001347-ssrs0cwf.txt' === file2bib.sh === id: cord-000799-s70onyix author: Wang, Ting title: Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation date: 2012-08-29 pages: extension: .txt txt: ./txt/cord-000799-s70onyix.txt cache: ./cache/cord-000799-s70onyix.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-000799-s70onyix.txt' === file2bib.sh === id: cord-102808-c7ajfvt5 author: Sundqvist, Martina title: Barbadin selectively modulates FPR2-mediated neutrophil functions independent of receptor endocytosis date: 2020-05-01 pages: extension: .txt txt: ./txt/cord-102808-c7ajfvt5.txt cache: ./cache/cord-102808-c7ajfvt5.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-102808-c7ajfvt5.txt' === file2bib.sh === id: cord-273992-xddikzxs author: Wiseman, A. title: Avoidance of oxidative‐stress perturbation in yeast bioprocesses by proteomic and genomic biostrategies? date: 2004-11-10 pages: extension: .txt txt: ./txt/cord-273992-xddikzxs.txt cache: ./cache/cord-273992-xddikzxs.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-273992-xddikzxs.txt' === file2bib.sh === id: cord-289034-yl3emjef author: Moro, Loredana title: Mitochondria at the Crossroads of Physiology and Pathology date: 2020-06-24 pages: extension: .txt txt: ./txt/cord-289034-yl3emjef.txt cache: ./cache/cord-289034-yl3emjef.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-289034-yl3emjef.txt' === file2bib.sh === id: cord-291190-f6km3c7z author: Nasi, Aikaterini title: Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention date: 2020-06-18 pages: extension: .txt txt: ./txt/cord-291190-f6km3c7z.txt cache: ./cache/cord-291190-f6km3c7z.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 6 resourceName b'cord-291190-f6km3c7z.txt' === file2bib.sh === id: cord-260348-83ftjqev author: Xu, Yinlan title: Cepharanthine and Curcumin inhibited mitochondrial apoptosis induced by PCV2 date: 2020-09-18 pages: extension: .txt txt: ./txt/cord-260348-83ftjqev.txt cache: ./cache/cord-260348-83ftjqev.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-260348-83ftjqev.txt' === file2bib.sh === id: cord-001769-2sdg5ll7 author: Guo, Sheng title: The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis date: 2015-09-14 pages: extension: .txt txt: ./txt/cord-001769-2sdg5ll7.txt cache: ./cache/cord-001769-2sdg5ll7.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-001769-2sdg5ll7.txt' === file2bib.sh === id: cord-293319-oo0w6faj author: Seo, Youngsik title: Reactive-oxygen-species-mediated mechanism for photoinduced antibacterial and antiviral activities of Ag(3)PO(4) date: 2020-06-11 pages: extension: .txt txt: ./txt/cord-293319-oo0w6faj.txt cache: ./cache/cord-293319-oo0w6faj.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-293319-oo0w6faj.txt' === file2bib.sh === id: cord-268527-wbfnhedy author: Smith, Sylvia B. title: Transient hyperglycosylation of rhodopsin with galactose date: 1991-10-31 pages: extension: .txt txt: ./txt/cord-268527-wbfnhedy.txt cache: ./cache/cord-268527-wbfnhedy.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-268527-wbfnhedy.txt' === file2bib.sh === id: cord-005280-a23oy0sz author: Yang, Shenshu title: ROS and diseases: role in metabolism and energy supply date: 2019-12-07 pages: extension: .txt txt: ./txt/cord-005280-a23oy0sz.txt cache: ./cache/cord-005280-a23oy0sz.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-005280-a23oy0sz.txt' === file2bib.sh === id: cord-313825-bbjxd86y author: Xia, Tian title: Pulmonary diseases induced by ambient ultrafine and engineered nanoparticles in twenty-first century date: 2016-10-08 pages: extension: .txt txt: ./txt/cord-313825-bbjxd86y.txt cache: ./cache/cord-313825-bbjxd86y.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 6 resourceName b'cord-313825-bbjxd86y.txt' === file2bib.sh === id: cord-034321-ohjik0pf author: Vorobjeva, N. V. title: NETosis: Molecular Mechanisms, Role in Physiology and Pathology date: 2020-10-27 pages: extension: .txt txt: ./txt/cord-034321-ohjik0pf.txt cache: ./cache/cord-034321-ohjik0pf.txt Content-Encoding ISO-8859-1 Content-Type text/plain; charset=ISO-8859-1 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-034321-ohjik0pf.txt' === file2bib.sh === id: cord-297469-26d8o1xk author: Choi, Won Hyung title: The Mechanism of Action of Ursolic Acid as a Potential Anti-Toxoplasmosis Agent, and Its Immunomodulatory Effects date: 2019-05-09 pages: extension: .txt txt: ./txt/cord-297469-26d8o1xk.txt cache: ./cache/cord-297469-26d8o1xk.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-297469-26d8o1xk.txt' === file2bib.sh === id: cord-295459-ffi1043k author: Khan, Naseem Ahmed title: Respiratory Syncytial Virus-Induced Oxidative Stress Leads to an Increase in Labile Zinc Pools in Lung Epithelial Cells date: 2020-05-27 pages: extension: .txt txt: ./txt/cord-295459-ffi1043k.txt cache: ./cache/cord-295459-ffi1043k.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-295459-ffi1043k.txt' === file2bib.sh === id: cord-048478-ftlb5b95 author: Mroczek, Seweryn title: Apoptotic signals induce specific degradation of ribosomal RNA in yeast date: 2008-04-01 pages: extension: .txt txt: ./txt/cord-048478-ftlb5b95.txt cache: ./cache/cord-048478-ftlb5b95.txt Content-Encoding ISO-8859-1 Content-Type text/plain; charset=ISO-8859-1 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-048478-ftlb5b95.txt' === file2bib.sh === id: cord-004508-ok3px98z author: Armando, Federico title: Oxidative Stress in Canine Histiocytic Sarcoma Cells Induced by an Infection with Canine Distemper Virus Led to a Dysregulation of HIF-1α Downstream Pathway Resulting in a Reduced Expression of VEGF-B In Vitro date: 2020-02-11 pages: extension: .txt txt: ./txt/cord-004508-ok3px98z.txt cache: ./cache/cord-004508-ok3px98z.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-004508-ok3px98z.txt' === file2bib.sh === id: cord-003841-7uaj9hmx author: Desmonts de Lamache, D. title: Immuno-modulating properties of Tulathromycin in porcine monocyte-derived macrophages infected with porcine reproductive and respiratory syndrome virus date: 2019-08-23 pages: extension: .txt txt: ./txt/cord-003841-7uaj9hmx.txt cache: ./cache/cord-003841-7uaj9hmx.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-003841-7uaj9hmx.txt' === file2bib.sh === id: cord-320591-re99v1qt author: Le, Thanh Ninh title: Bioactive Compounds and Bioactivities of Brassica oleracea L. var. Italica Sprouts and Microgreens: An Updated Overview from a Nutraceutical Perspective date: 2020-07-27 pages: extension: .txt txt: ./txt/cord-320591-re99v1qt.txt cache: ./cache/cord-320591-re99v1qt.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 6 resourceName b'cord-320591-re99v1qt.txt' === file2bib.sh === id: cord-288238-36hiiw91 author: Keshavarz, Mohsen title: Metabolic host response and therapeutic approaches to influenza infection date: 2020-03-05 pages: extension: .txt txt: ./txt/cord-288238-36hiiw91.txt cache: ./cache/cord-288238-36hiiw91.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 7 resourceName b'cord-288238-36hiiw91.txt' === file2bib.sh === id: cord-014661-mrh2pbi6 author: Dumitrascu, Georgiana R. title: Critical physiological and pathological functions of Forkhead Box O tumor suppressors date: 2013-12-31 pages: extension: .txt txt: ./txt/cord-014661-mrh2pbi6.txt cache: ./cache/cord-014661-mrh2pbi6.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-014661-mrh2pbi6.txt' === file2bib.sh === id: cord-335676-7ak53hto author: Meftahi, Gholam Hossein title: The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of “inflame-aging” date: 2020-06-11 pages: extension: .txt txt: ./txt/cord-335676-7ak53hto.txt cache: ./cache/cord-335676-7ak53hto.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 7 resourceName b'cord-335676-7ak53hto.txt' === file2bib.sh === id: cord-319614-4qi59pbz author: Benej, Martin title: Quantitative Proteomics Reveal Peroxiredoxin Perturbation Upon Persistent Lymphocytic Choriomeningitis Virus Infection in Human Cells date: 2019-10-25 pages: extension: .txt txt: ./txt/cord-319614-4qi59pbz.txt cache: ./cache/cord-319614-4qi59pbz.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-319614-4qi59pbz.txt' === file2bib.sh === id: cord-271939-m1ko4yal author: Rouco, Lara title: Pursuing the Elixir of Life: In Vivo Antioxidative Effects of Manganosalen Complexes date: 2020-08-10 pages: extension: .txt txt: ./txt/cord-271939-m1ko4yal.txt cache: ./cache/cord-271939-m1ko4yal.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 2 resourceName b'cord-271939-m1ko4yal.txt' === file2bib.sh === id: cord-012495-r6nkdeaw author: Bonora, Massimo title: Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology date: 2020-07-04 pages: extension: .txt txt: ./txt/cord-012495-r6nkdeaw.txt cache: ./cache/cord-012495-r6nkdeaw.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-012495-r6nkdeaw.txt' === file2bib.sh === id: cord-013415-110b95cg author: Aquino-Martinez, Ruben title: Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? date: 2020-10-09 pages: extension: .txt txt: ./txt/cord-013415-110b95cg.txt cache: ./cache/cord-013415-110b95cg.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-013415-110b95cg.txt' === file2bib.sh === id: cord-257514-gw9xnb4x author: Yang, Mengling title: Hydrogen: A Novel Option in Human Disease Treatment date: 2020-09-05 pages: extension: .txt txt: ./txt/cord-257514-gw9xnb4x.txt cache: ./cache/cord-257514-gw9xnb4x.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-257514-gw9xnb4x.txt' === file2bib.sh === id: cord-278846-nqj7ctk3 author: Ogger, Patricia P. title: Macrophage metabolic reprogramming during chronic lung disease date: 2020-11-12 pages: extension: .txt txt: ./txt/cord-278846-nqj7ctk3.txt cache: ./cache/cord-278846-nqj7ctk3.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 2 resourceName b'cord-278846-nqj7ctk3.txt' === file2bib.sh === id: cord-323730-5iawbnua author: Ohl, Kim title: Oxidative stress in multiple sclerosis: Central and peripheral mode of action date: 2016-03-31 pages: extension: .txt txt: ./txt/cord-323730-5iawbnua.txt cache: ./cache/cord-323730-5iawbnua.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 2 resourceName b'cord-323730-5iawbnua.txt' === file2bib.sh === id: cord-298265-elbnzgx6 author: Mutua, Victoria title: A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics date: 2020-08-01 pages: extension: .txt txt: ./txt/cord-298265-elbnzgx6.txt cache: ./cache/cord-298265-elbnzgx6.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-298265-elbnzgx6.txt' === file2bib.sh === id: cord-313918-uv9xdp5f author: Marí, Montserrat title: Mitochondrial Glutathione: Recent Insights and Role in Disease date: 2020-09-24 pages: extension: .txt txt: ./txt/cord-313918-uv9xdp5f.txt cache: ./cache/cord-313918-uv9xdp5f.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-313918-uv9xdp5f.txt' === file2bib.sh === id: cord-291559-h6czy5bh author: Koirala, Prashamsa title: Recent advances in pharmacological research on Ecklonia species: a review date: 2017-08-24 pages: extension: .txt txt: ./txt/cord-291559-h6czy5bh.txt cache: ./cache/cord-291559-h6czy5bh.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-291559-h6czy5bh.txt' === file2bib.sh === id: cord-336201-fl606l3b author: Daryabor, Gholamreza title: The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System date: 2020-07-22 pages: extension: .txt txt: ./txt/cord-336201-fl606l3b.txt cache: ./cache/cord-336201-fl606l3b.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-336201-fl606l3b.txt' === file2bib.sh === id: cord-035015-slgywe0c author: Nunn, Alistair V. W. title: SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing date: 2020-11-09 pages: extension: .txt txt: ./txt/cord-035015-slgywe0c.txt cache: ./cache/cord-035015-slgywe0c.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-035015-slgywe0c.txt' === file2bib.sh === id: cord-310723-ogo9mvi5 author: Belinskaia, Daria A. title: The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin date: 2020-10-09 pages: extension: .txt txt: ./txt/cord-310723-ogo9mvi5.txt cache: ./cache/cord-310723-ogo9mvi5.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-310723-ogo9mvi5.txt' === file2bib.sh === id: cord-331673-xv1tcugl author: Reina, Giacomo title: Hard Nanomaterials in Time of Viral Pandemics date: 2020-07-15 pages: extension: .txt txt: ./txt/cord-331673-xv1tcugl.txt cache: ./cache/cord-331673-xv1tcugl.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-331673-xv1tcugl.txt' === file2bib.sh === id: cord-017817-ztp7w9yh author: Land, Walter Gottlieb title: Cell-Autonomous (Cell-Intrinsic) Stress Responses date: 2018-03-28 pages: extension: .txt txt: ./txt/cord-017817-ztp7w9yh.txt cache: ./cache/cord-017817-ztp7w9yh.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 3 resourceName b'cord-017817-ztp7w9yh.txt' === file2bib.sh === id: cord-034294-ti1cc24m author: Wang, Cuixue title: Progress in the mechanism and targeted drug therapy for COPD date: 2020-10-27 pages: extension: .txt txt: ./txt/cord-034294-ti1cc24m.txt cache: ./cache/cord-034294-ti1cc24m.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-034294-ti1cc24m.txt' === file2bib.sh === id: cord-316244-s5ua0re3 author: Park, Mi Hee title: Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases date: 2016-04-26 pages: extension: .txt txt: ./txt/cord-316244-s5ua0re3.txt cache: ./cache/cord-316244-s5ua0re3.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-316244-s5ua0re3.txt' === file2bib.sh === id: cord-307148-k1uo3fxm author: Bradshaw, Patrick C. title: COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm date: 2020-09-09 pages: extension: .txt txt: ./txt/cord-307148-k1uo3fxm.txt cache: ./cache/cord-307148-k1uo3fxm.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 4 resourceName b'cord-307148-k1uo3fxm.txt' === file2bib.sh === id: cord-032561-x3qbqy69 author: Liu, Gengqi title: Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment date: 2020-09-02 pages: extension: .txt txt: ./txt/cord-032561-x3qbqy69.txt cache: ./cache/cord-032561-x3qbqy69.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-032561-x3qbqy69.txt' === file2bib.sh === id: cord-268122-74nj66vb author: Xie, Na title: NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential date: 2020-10-07 pages: extension: .txt txt: ./txt/cord-268122-74nj66vb.txt cache: ./cache/cord-268122-74nj66vb.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 5 resourceName b'cord-268122-74nj66vb.txt' === file2bib.sh === id: cord-020646-s7eopu9y author: nan title: Die Pathophysiologie der Entzündung date: 2005 pages: extension: .txt txt: ./txt/cord-020646-s7eopu9y.txt cache: ./cache/cord-020646-s7eopu9y.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 6 resourceName b'cord-020646-s7eopu9y.txt' === file2bib.sh === id: cord-006230-xta38e7j author: nan title: Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie e.V. date: 2012-02-22 pages: extension: .txt txt: ./txt/cord-006230-xta38e7j.txt cache: ./cache/cord-006230-xta38e7j.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 12 resourceName b'cord-006230-xta38e7j.txt' === file2bib.sh === id: cord-022940-atbjwpo5 author: nan title: Poster Sessions date: 2016-09-07 pages: extension: .txt txt: ./txt/cord-022940-atbjwpo5.txt cache: ./cache/cord-022940-atbjwpo5.txt Content-Encoding UTF-8 Content-Type text/plain; charset=UTF-8 X-Parsed-By ['org.apache.tika.parser.DefaultParser', 'org.apache.tika.parser.csv.TextAndCSVParser'] X-TIKA:content_handler ToTextContentHandler X-TIKA:embedded_depth 0 X-TIKA:parse_time_millis 35 resourceName b'cord-022940-atbjwpo5.txt' Que is empty; done keyword-ros-cord === reduce.pl bib === id = cord-001769-2sdg5ll7 author = Guo, Sheng title = The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis date = 2015-09-14 pages = extension = .txt mime = text/plain words = 6529 sentences = 330 flesch = 41 summary = We show that wild-type mice infected with murine hepatitis virus strain-3 (MHV-3), a model for viral FH, manifest with severe disease and high mortality in association with a significant elevation in IL-1β expression in the serum and liver. Further experiments show that mice deficient of p47 (phox), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit that controls acute ROS production, present with reductions in NLRP3 inflammasome activation and subsequent IL-1β secretion during viral infection, which appears to be responsible for acquiring resilience to viral FH. The hallmarks of MHV-3-induced FH in susceptible BALB/cJ and C57BL/6 mice include the appearance of liver sinusoidal thrombosis and hepatocellular necrosis, resulting from over expression of a virus-induced, monocyte/macrophage-specific procoagulant, fibrinogen-like protein-2 (FGL2). cache = ./cache/cord-001769-2sdg5ll7.txt txt = ./txt/cord-001769-2sdg5ll7.txt === reduce.pl bib === id = cord-001347-ssrs0cwf author = Michaelis, Martin title = Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A date = 2014-06-23 pages = extension = .txt mime = text/plain words = 1995 sentences = 125 flesch = 43 summary = title: Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Next, we investigated whether the reduction of baicalein-or biochanin A-induced enhanced ROS levels in H5N1-infected A549 cells by NAC influences the antiviral effects of these flavonoids. Notably, NAC also inhibited baicalein-and biochanin A-induced oxidative stress in H5N1-infected primary human monocytederived macrophages but did not affect H5N1 replication in this cell type (Figure 3 ). These findings emphasise that flavonoids, a class of natural compounds known to exert anti-influenza effects [16] [17] [18] [19] 28] , induce a complex range of pharmacological actions by which they modify influenza A virus replication including highly pathogenic avian H5N1 strains. Differential antiviral and anti-inflammatory mechanisms of the flavonoids biochanin A and baicalein in H5N1 influenza A virus-infected cells cache = ./cache/cord-001347-ssrs0cwf.txt txt = ./txt/cord-001347-ssrs0cwf.txt === reduce.pl bib === id = cord-004508-ok3px98z author = Armando, Federico title = Oxidative Stress in Canine Histiocytic Sarcoma Cells Induced by an Infection with Canine Distemper Virus Led to a Dysregulation of HIF-1α Downstream Pathway Resulting in a Reduced Expression of VEGF-B In Vitro date = 2020-02-11 pages = extension = .txt mime = text/plain words = 8265 sentences = 382 flesch = 38 summary = Based on these findings, the aim of the present study was to investigate the impact of a persistent CDV-infection on oxidative stress mediated changes in the expression of hypoxia-inducible factor (HIF)-1α and its angiogenic downstream pathway in DH82 cells in vitro. In summary, these results suggest a reduced activation of the HIF-1α angiogenic downstream pathway in DH82Ond pi cells in vitro, most likely due to an excessive, unusually localized, and non-functional expression of HIF-1α triggered by a CDV-induced increased oxidative stress. In a hypothesis-driven approach, an online available microarray data set of quadruplicates of non-infected DH82 and DH82Ond pi cells (ArrayExpress; http://www.ebi.ac.uk/arrayexpress; accession number E-MTAB-3942 [11, 44] ) was investigated for differentially expressed genes related to ROS production and scavenging, ER-stress and HIF-1α pathway, with a special focus on the angiogenic downstream targets of the latter. cache = ./cache/cord-004508-ok3px98z.txt txt = ./txt/cord-004508-ok3px98z.txt === reduce.pl bib === id = cord-000799-s70onyix author = Wang, Ting title = Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation date = 2012-08-29 pages = extension = .txt mime = text/plain words = 5884 sentences = 363 flesch = 46 summary = title: Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation OBJECTIVES: We explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction. We investigated the role of ROS and calpain in PM-induced pulmonary inflammation by examining protein leakage, white blood cell infiltration (inflammatory leukocytes), and the release of proinflammatory cytokines into BAL fluids ( Figure 5 ). These data represent the first evidence that calpain signaling, via calcium leakage from activated TRPM2 by ROS, plays a critical role in modulating endothelial cell barrier function, resulting in tight junction protein ZO-1 degradation (Additional file 1 Figure S7 ). Particulate matter induces endothelial cell intracellular oxidative stress, which leads to the activation of calpain, one of the major cytoskeletal regulators. cache = ./cache/cord-000799-s70onyix.txt txt = ./txt/cord-000799-s70onyix.txt === reduce.pl bib === id = cord-014661-mrh2pbi6 author = Dumitrascu, Georgiana R. title = Critical physiological and pathological functions of Forkhead Box O tumor suppressors date = 2013-12-31 pages = extension = .txt mime = text/plain words = 9235 sentences = 419 flesch = 38 summary = FOXO proteins are considered unique cellular targets, regulating a wide variety of critical cellular processes, such as: apoptosis, oxidative stress, DNA damage repair, cell cycle, stem cell proliferation and maintenance, metabolism, angiogenesis, vascular tone, cardiovascular development, fertility, immune response and neuronal survival 4, 20 . Hence, the FOXO transcription factors control the expression of a wide spectrum of genes that regulate essential physiological cellular processes, such as cell death/cell survival, cell cycle, cell proliferation, cell differentiation/development, angiogenesis, cell metabolism, stress response and stem cell maintenance 33,34,35,36,37,38 (Figure 2) . Moreover, the consensus FOXO recognition element (FRE) -(G/C)(T/A)AA(C/T)AA -which differs from that of other forkhead proteins, seems to have a very important role in both apoptotic pathways, since matching functional FRE sites have been identified in the promoters of FOXO target genes encoding Fas ligand (FasL), insulin like growth factorbinding protein 1 (IGFBP1), the apoptotic regulator Bcl-2 interacting mediator of cell death (Bim) and others 30 . cache = ./cache/cord-014661-mrh2pbi6.txt txt = ./txt/cord-014661-mrh2pbi6.txt === reduce.pl bib === id = cord-005280-a23oy0sz author = Yang, Shenshu title = ROS and diseases: role in metabolism and energy supply date = 2019-12-07 pages = extension = .txt mime = text/plain words = 5898 sentences = 379 flesch = 38 summary = Although ROS play an important role in pathogen resistance and cellular signalling, they are also broadly recognized as harmful reactive particles to cell as they damage intracellular proteins, lipids and nucleic acids. The homeostasis of ROS plays an important role in reducing oxidative damage and fulfil energy demand. Relatively high levels of ROS may cause oxidative damage or induce apoptosis during immunological defences or pathological conditions. However, ROS themselves could activate extracellular signal-regulated kinase (ERK) by targeting proteins Gαi and Gα0 and protect cardiac cell from oxidative damage [18] . Apart from oxidative damage, ROS also serve as signalling molecules and play an important role in homeostasis, metabolism, growth and differentiation [3] . PGC-1α could protect neural cells from oxidative damage by reducing ROS level via antioxidative enzymes GPx1 and SOD2 [15] . ROS regulate vascular cell proliferation and apoptosis with their fundamental role in metabolism. cache = ./cache/cord-005280-a23oy0sz.txt txt = ./txt/cord-005280-a23oy0sz.txt === reduce.pl bib === id = cord-013415-110b95cg author = Aquino-Martinez, Ruben title = Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? date = 2020-10-09 pages = extension = .txt mime = text/plain words = 10333 sentences = 522 flesch = 27 summary = Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. In contrast to transient DNA damage, persistent genomic lesions promote constitutive DNA damage signaling and cellular senescence, which is correlated with increased secretion of inflammatory signals [26, 30] In agreement with this observation, several studies have reported that premature senescence can also be induced by exposing human cells to subtoxic H 2 O 2 concentrations [31, 32] . As a consequence of chronological aging, the burden of senescent cells increases in different tissues in humans, mice, and other species, where they contribute to the development of chronic pathologies including arthritis, osteoporosis, Alzheimer's disease, atherosclerosis, cancer, and diabetes [58, 59] Similar to other agerelated pathologies, the etiology of diabetes may be the result of the impact of different aging mechanism, including stem cell exhaustion, chronic low-grade inflammation, macromolecular damage, and cellular senescence. cache = ./cache/cord-013415-110b95cg.txt txt = ./txt/cord-013415-110b95cg.txt === reduce.pl bib === id = cord-102808-c7ajfvt5 author = Sundqvist, Martina title = Barbadin selectively modulates FPR2-mediated neutrophil functions independent of receptor endocytosis date = 2020-05-01 pages = extension = .txt mime = text/plain words = 5708 sentences = 236 flesch = 34 summary = The formyl peptide receptor 2 (FPR2), belonging to the family of G protein-coupled receptors (GPCRs), regulates directional neutrophil migration (chemotaxis), granule secretion (degranulation), formation of F-actin filaments (through polymerization of G-actin), and activation of the reactive oxygen species (ROS) producing NADPH-oxidase [3, 5, 6] . The fact that F2Pal10 and Cmp 14 cannot induce -arrestin recruitment at these concentrations ([9-11], Fig 2A) , strongly suggests that the priming effect of Barbadin on FPR2-mediated ROS production is independent of the ability of the activating agonist to recruit -arrestin. Collectively, these results suggest that Barbadin primes neutrophils in their response to FPR2 agonists, and the increased NADPH-oxidase activation is regulated independently of FPR2 internalization and FPR2-induced -arrestin recruitment. Barbadin was added to WKYMVM-activated neutrophils at a time point when ROS production had returned to a background level; interestingly, these FPR2-desensitized cells could be resensitized to produce ROS also by Barbadin, similar to the effect of latrunculin A ( Fig 5A) . cache = ./cache/cord-102808-c7ajfvt5.txt txt = ./txt/cord-102808-c7ajfvt5.txt === reduce.pl bib === id = cord-289034-yl3emjef author = Moro, Loredana title = Mitochondria at the Crossroads of Physiology and Pathology date = 2020-06-24 pages = extension = .txt mime = text/plain words = 3790 sentences = 197 flesch = 27 summary = Two mitochondria quality control mechanisms are in place to meet the functional needs of any given cell under different physiological and pathological conditions: (a) mitochondrial biogenesis, fusion and fission [4] [5] [6] ; (b) mitophagy [7, 8] . The second mechanism, mitophagy, is a specific form of autophagy that removes damaged mitochondria and reduces the mitochondrial mass upon microenvironmental stresses, such as hypoxia and nutrient starvation, promoting cell survival [11] . In this context, mutations in three TCA cycle enzymes, namely succinate dehydrogenase, fumarate hydratase and isocitrate dehydrogenase, have been shown to play a causal role in carcinogenesis [54, 55] , thus providing compelling evidence for the involvement of mitochondrial metabolic alterations as cancer drivers. Mitochondrial dysfunction is implicated in several pathological conditions, ranging from neurodegenerative and cardiovascular diseases, to aging, cancer and inflammation. cache = ./cache/cord-289034-yl3emjef.txt txt = ./txt/cord-289034-yl3emjef.txt === reduce.pl bib === id = cord-048478-ftlb5b95 author = Mroczek, Seweryn title = Apoptotic signals induce specific degradation of ribosomal RNA in yeast date = 2008-04-01 pages = extension = .txt mime = text/plain words = 9796 sentences = 418 flesch = 45 summary = One striking characteristic, which accompanies apoptosis in both vertebrates and yeast, is a fragmentation of cellular DNA and mammalian apoptosis is often associated with degradation of different RNAs. We show that in yeast exposed to stimuli known to induce apoptosis, such as hydrogen peroxide, acetic acid, hyperosmotic stress and ageing, two large subunit ribosomal RNAs, 25S and 5.8S, became extensively degraded with accumulation of specific intermediates that differ slightly depending on cell death conditions. For example, in metazoans the programmed cell death (PCD) called apoptosis, in addition to irreversible DNA damage, which is considered an apoptotic hallmark (3) , also involves specific cleavage of several RNA species, including 28S rRNA, U1 snRNA or Ro RNP-associated Y RNAs (4) . Together, this strongly suggests that rRNA degradation observed in apoptotic and oxidative stress conditions is not simply a result of cell death but is produced in the process that requires enzymatic activity and functional cellular machinery. cache = ./cache/cord-048478-ftlb5b95.txt txt = ./txt/cord-048478-ftlb5b95.txt === reduce.pl bib === id = cord-012495-r6nkdeaw author = Bonora, Massimo title = Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology date = 2020-07-04 pages = extension = .txt mime = text/plain words = 11954 sentences = 657 flesch = 34 summary = Mitochondrial calcium overload and ROS levels can trigger either the activation of intrinsic apoptotic pathway (left side) through the recruitment of Bcl-2 family proteins at the mitochondria, or permeability transition pore complex (PTPC) formation which could lead to mitochondrial outer membrane permeabilization (MOMP), energetic imbalance, and subsequent release of proapoptotic cofactors from the inter membrane space, such as SMAC/DIABLO, CytC, and ENDOG (right side). MPT is associated with the opening of the mitochondrial permeability transition pore complex (PTPC), a voltage-dependent, high-conductance Mitochondrial calcium overload and ROS levels can trigger either the activation of intrinsic apoptotic pathway (left side) through the recruitment of Bcl-2 family proteins at the mitochondria, or permeability transition pore complex (PTPC) formation which could lead to mitochondrial outer membrane permeabilization (MOMP), energetic imbalance, and subsequent release of proapoptotic cofactors from the inter membrane space, such as SMAC/DIABLO, CytC, and ENDOG (right side). cache = ./cache/cord-012495-r6nkdeaw.txt txt = ./txt/cord-012495-r6nkdeaw.txt === reduce.pl bib === id = cord-273992-xddikzxs author = Wiseman, A. title = Avoidance of oxidative‐stress perturbation in yeast bioprocesses by proteomic and genomic biostrategies? date = 2004-11-10 pages = extension = .txt mime = text/plain words = 2658 sentences = 122 flesch = 35 summary = The main impact of the study is that the utilization of genetically modified (GM) yeast produced by recombinant DNA technology genomic strategies could circumvent the bioprocessing problems that otherwise result from the bioprocess perturbations: this is as a result of oxidative stress caused by ROS, which is avoidable by deployment of appropriate antioxidants such as vitamins E, C and D (and antioxidant proteins and enzymes often of microbial origin via recombinant DNA technology). Catalases ( Table 3 ) in yeasts and other micro-organisms (Antioxidants such as vitamins E and C chain terminate the formation of membrane-degrading ROS) relates to more than just structural damage that is sometimes obvious and predictable: functional damage may also follow. Avoidance biostrategies against ROS and RSS in many oxidatively stressed bioprocesses that utilise yeasts (and other micro-organisms) are essential where human therapeutic proteins are expected to be produced in high yield. cache = ./cache/cord-273992-xddikzxs.txt txt = ./txt/cord-273992-xddikzxs.txt === reduce.pl bib === id = cord-034321-ohjik0pf author = Vorobjeva, N. V. title = NETosis: Molecular Mechanisms, Role in Physiology and Pathology date = 2020-10-27 pages = extension = .txt mime = text/plain words = 7605 sentences = 432 flesch = 43 summary = NETosis is a program for formation of neutrophil extracellular traps (NETs), which consist of modified chromatin decorated with bactericidal proteins from granules and cytoplasm. NETosis includes release of the granule components into the cytosol, modification of histones leading to chromatin decondensation, destruction of the nuclear envelope, as well as formation of pores in the plasma membrane. 1178 Abbreviations: ARDS, acute respiratory distress syndrome; CGD, chronic granulomatous disease; COPD, chronic obstructive pulmonary disease; GSDMD, gasdermin D; LPS, lipopolysaccharide of the bacterial wall; MPO, myeloper oxidase; mPTP, nonselective mitochondrial permeability tran sition pore; NE, neutrophil elastase; NETs, Neutrophil Extra cellular Traps; PCD, programmed cell death; PKC, protein kinase C; PMA, phorbol 12 myristate 13 acetate; ROS, reac tive oxygen species. At the same time, we also showed that in neutrophils isolated from the blood of patients with X linked CGD formation of NETs in response to A23187 depended on the enhanced gener ation of mtROS without participation of NADPH oxi dase [16] . cache = ./cache/cord-034321-ohjik0pf.txt txt = ./txt/cord-034321-ohjik0pf.txt === reduce.pl bib === id = cord-020646-s7eopu9y author = nan title = Die Pathophysiologie der Entzündung date = 2005 pages = extension = .txt mime = text/plain words = 30141 sentences = 4154 flesch = 55 summary = Die Wirkung des Histamins auf Zielzellen erfolgt über spezifi sche Rezeptoren, von denen zwei Arten bekannt und gut studiert sind. Bei plötzlicher Aufhebung der Rezeptorblockade nach Ende einer Therapie sind die betroffenen Zellen mit einer hohen Rezeptorzahl bestückt und reagieren folglich auf Histamin verstärkt, was zum massiven Wiederauftreten der Krankheitssymptomatik führen kann (sog. Disponierte Personen, die als "Atopiker" bezeichnet werden, reagieren auf gewisse Antigene (AG) mit der Bildung spezifi scher Antikörper (AK) vom IgE-Typ. Die atopische Veranlagung ist angeboren, tritt oft familiär auf und zeigt eine Konvergenz mit gewissen MHC I Typen. Dem PAF wird heute eine wesentliche Rolle beim Pathomechanismus des Asthma bronchiale und der COPD zugeschrieben, wobei die Wirkung auch indirekt, nämlich über eine Potenzierung anderer Mediatoren wie LT, PG, Histamin zu laufen scheint. Diese Bindung ist der Mechanismus, über den die Zelle ein Partikel erkennt und von Material unterscheidet, das nicht phagozytiert werden soll, und der den Phagozytosereiz auslöst. cache = ./cache/cord-020646-s7eopu9y.txt txt = ./txt/cord-020646-s7eopu9y.txt === reduce.pl bib === id = cord-003841-7uaj9hmx author = Desmonts de Lamache, D. title = Immuno-modulating properties of Tulathromycin in porcine monocyte-derived macrophages infected with porcine reproductive and respiratory syndrome virus date = 2019-08-23 pages = extension = .txt mime = text/plain words = 7978 sentences = 414 flesch = 37 summary = The findings indicate that tulathromycin, in the absence of a direct anti-viral effect, is able to restore the phagocytic function and to attenuate the pro-inflammatory phenotype of PRRSV-infected monocyte-derived porcine macrophages. However, Immuno-modulating properties of Tulathromycin in PRRSV-infected porcine monocyte-derived macrophages PRRSV-induced IL-10 inhibition was abolished when the cells were pre-treated with tulathromycin at 2 and 12 hours post infection (Fig 6) . Another set of experiments assessed the effects of PRRSV, and of tulathromycin, on the nonopsonized and opsonized phagocytic functions of MDMs. PRRSV infection significantly Immuno-modulating properties of Tulathromycin in PRRSV-infected porcine monocyte-derived macrophages inhibited both phagocytic functions of the cells (Figs 10 and 11 ). The findings indicate that TUL inhibits PRRSV-induced inflammatory responses in porcine monocyte-derived macrophages and protects against the phagocytic impairment caused by the virus, in the absence of any direct anti-viral effects. cache = ./cache/cord-003841-7uaj9hmx.txt txt = ./txt/cord-003841-7uaj9hmx.txt === reduce.pl bib === id = cord-035015-slgywe0c author = Nunn, Alistair V. W. title = SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing date = 2020-11-09 pages = extension = .txt mime = text/plain words = 14660 sentences = 715 flesch = 36 summary = Data is now showing that COVID-19 patients do have populations of T-cells displaying mitochondrial dysfunction, as well as altered mitochondrial markers in monocyteshinting that immune-metabolic phenotyping could be used to understand disease pathogenesis and possible treatments; this could include targeting mitochondria [32] . The underlying aetiology for "inflammaging" has long thought to be associated with mitochondrial dysfunction as suggested by Nick Lane in 2003 in his "double agent" theory [5] , and is now receiving renewed interest, for instance, in how decreasing mitochondrial function can reduce T-cell function and enhance immune senescence, as mitochondria are pivotal in metabolic reprogramming towards the Warburg effect [40] . Furthermore, as evidence indicates that many viruses, which most likely include SARs-CoV-2, modulate bioenergetics and redox in both the immune system and other cells they infect to enhance their own replication, they could potentially induce excessive stress in these systems if their mitochondria are already sub-optimally functional. cache = ./cache/cord-035015-slgywe0c.txt txt = ./txt/cord-035015-slgywe0c.txt === reduce.pl bib === id = cord-262759-ec2c25q3 author = Hsieh, Yi-Ting title = Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Epithelial Cells Are Less Tolerant to Infection by Staphylococcus aureus date = 2013-11-04 pages = extension = .txt mime = text/plain words = 4838 sentences = 223 flesch = 40 summary = The impairment of ROS removal is predicted to enhance apoptotic activity in G6PD-deficient cells, and this enhanced apoptosis was observed by annexin V/PI staining under a confocal fluorescence microscope and quantified by flow cytometry. We hypothesized that G6PD-deficient cells are less tolerant to oxidative stress upon bacterial infection, leading to the accumulation of more intracellular ROS when compared to the control scramble cells. To determine whether the reduced ROS accumulation and apoptotic activity, particularly in G6PD-deficient cells, was due to deceased αhemolysin expression upon VRSA infection in the presence of vancomycin, the production of intracellular ROS and cell apoptosis when the α-hemolysin inhibitor Oroxylin A was added to the media was quantified by flow cytometry. Our results presented here indicate that expression of active caspase-9, as well as the downstream caspase-3, was much higher in G6PD-deficient cells than in control scramble cells upon VRSA infection, suggesting that mitochondrial dysfunction may be the major cause of the increase in cell apoptosis (Figure 4) . cache = ./cache/cord-262759-ec2c25q3.txt txt = ./txt/cord-262759-ec2c25q3.txt === reduce.pl bib === id = cord-034294-ti1cc24m author = Wang, Cuixue title = Progress in the mechanism and targeted drug therapy for COPD date = 2020-10-27 pages = extension = .txt mime = text/plain words = 16476 sentences = 989 flesch = 37 summary = Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. EPAC and PKA inhibit the human airway smooth muscle induced by a cigarette smoke extract (CSE) by blocking the activation of the NF-κB and ERK, respectively, and by releasing neutrophil chemokine IL-8, which together exert anti-inflammatory effects. 101 In COPD, increases in cAMP levels, activation of PKA and enhanced protein phosphorylation have the potential to reduce inflammation and immunomodulation, relax airway smooth muscle, inhibit chemotaxis and abnormal release of inflammatory and cytotoxic mediators, and reduce proliferation and migration of inflammatory cells. 135 The PI3K/Akt signalling pathway plays an important role in COPD by regulating inflammatory cell activation, inflammatory mediator release and airway remodelling. cache = ./cache/cord-034294-ti1cc24m.txt txt = ./txt/cord-034294-ti1cc24m.txt === reduce.pl bib === id = cord-017817-ztp7w9yh author = Land, Walter Gottlieb title = Cell-Autonomous (Cell-Intrinsic) Stress Responses date = 2018-03-28 pages = extension = .txt mime = text/plain words = 17727 sentences = 855 flesch = 40 summary = Autophagy is an evolutionarily highly conserved self-digestive process in response to environmental stress to eukaryotic cells, by which cytoplasmic components such as defective/damaged or redundant organelles or protein aggregates are delivered to the lysosome for recycling and degradation. More recent studies then revealed that these transcription factors, notably Nrf2, are activated by Keap1 as the primary negative regulator of Nrf2, that is, a molecule that simultaneously operates as a sensor protein able to perceive dyshomeostatic Subclass IIC-4 DAMPs, for example, in terms of redox changes reflecting electrophilic stress. Strikingly, a complex relationship reportedly exists between autophagy and DAMPs in cellular adaption to stress and injury and cell death characterized by a crosstalk between autophagy induction and secretion or release of DAMPs. In fact, growing evidence indicates that autophagic mechanisms are involved in regulating release and degradation of DAMPs including CALR, HMGB1, ATP, and DNA in several cell types [37, 148, 175] . cache = ./cache/cord-017817-ztp7w9yh.txt txt = ./txt/cord-017817-ztp7w9yh.txt === reduce.pl bib === id = cord-293319-oo0w6faj author = Seo, Youngsik title = Reactive-oxygen-species-mediated mechanism for photoinduced antibacterial and antiviral activities of Ag(3)PO(4) date = 2020-06-11 pages = extension = .txt mime = text/plain words = 2918 sentences = 148 flesch = 54 summary = The antibacterial activities against Escherichia coli, Listeria innocua, and Pseudomonas syringae DC3000 in both the absence and presence of Ag(3)PO(4) under dark conditions and in the presence of Ag(3)PO(4) under red-light (625 nm) and blue-light (460 nm) irradiation were examined. The photoinduced enhancement of the Ag(3)PO(4) antibacterial activity under blue-light irradiation is explained by the formation of ROS during the antibacterial action of the Ag(3)PO(4). Moreover, the antiviral activity of Ag(3)PO(4) against amphotropic 10A1 murine leukemia virus enhanced under blue-light irradiation via ROS production. coli in the absence and presence of Ag 3 PO 4 under dark conditions and in the presence of Ag 3 PO 4 under red-light (625 nm) and blue-light (460 nm) irradiation. These data indicate that the antibacterial activity of Ag 3 PO 4 under blue-light irradiation corresponds to the amount of ROS in E. The photoinduced enhancement of the antibacterial and antiviral activities of Ag 3 PO 4 under blue-light irradiation was observed. cache = ./cache/cord-293319-oo0w6faj.txt txt = ./txt/cord-293319-oo0w6faj.txt === reduce.pl bib === id = cord-278846-nqj7ctk3 author = Ogger, Patricia P. title = Macrophage metabolic reprogramming during chronic lung disease date = 2020-11-12 pages = extension = .txt mime = text/plain words = 10123 sentences = 516 flesch = 31 summary = While these initial observations were made during steady state or using in vitro polarised macrophages, recent studies have indicated that during many chronic lung diseases (CLDs), AMs adapt their metabolic profile to fit their local niche. By generating reactive oxygen species (ROS) for pathogen defence, utilising aerobic glycolysis to rapidly generate cytokines, and employing mitochondrial respiration to fuel inflammatory responses, AMs utilise metabolic reprogramming for host defence, although these changes may also support chronic pathology. Indeed, many recent studies have indicated that in chronic lung diseases (CLDs), such as asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF), and during infection such as with Mycobacterium Tuberculosis (Mtb), there are significant alterations in AM metabolic processes and that targeting these pathways could represent an exciting therapeutic approach 6, 7 . Iron metabolism is therefore likely a key pathway in IPF-AMs and targeting it would be a viable option to decrease ROS, oxidative stress and macrophage activation. cache = ./cache/cord-278846-nqj7ctk3.txt txt = ./txt/cord-278846-nqj7ctk3.txt === reduce.pl bib === id = cord-319614-4qi59pbz author = Benej, Martin title = Quantitative Proteomics Reveal Peroxiredoxin Perturbation Upon Persistent Lymphocytic Choriomeningitis Virus Infection in Human Cells date = 2019-10-25 pages = extension = .txt mime = text/plain words = 8900 sentences = 479 flesch = 45 summary = Experimental data indicate that during persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate regulatory cellular processes and alter cellular functions that are not critical for survival, but are essential for cell homeostasis. Increased levels of ROS were accompanied by changes in the pattern of telomere restriction fragments (TRFs) in infected cells and mediated activation of hypoxia-inducible transcription factor-1 (HIF-1) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways. These data suggest that LCMV maintains its replication in persistently infected cells by regulating redox signaling through modulation of local levels of H 2 O 2 and subsequent activation of cellular processes that it uses for its own benefit. Notably, the treatment with antioxidants also resulted in reduced levels of viral NP in HeLa, as well as in A549 LCMV-infected cells, suggesting a link between ROS-dependent signaling and virus replication (Figures 7B,D and Supplementary Figure S2B ). cache = ./cache/cord-319614-4qi59pbz.txt txt = ./txt/cord-319614-4qi59pbz.txt === reduce.pl bib === id = cord-257514-gw9xnb4x author = Yang, Mengling title = Hydrogen: A Novel Option in Human Disease Treatment date = 2020-09-05 pages = extension = .txt mime = text/plain words = 10425 sentences = 526 flesch = 33 summary = H(2) gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. found that HW inhibited cardiomyocyte apoptosis by activating the PI3K/AKT and JAK2-STAT3 signaling pathways and can also reduce the level of oxidative stress in myocardial tissue by upregulating the expression of the nuclear erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway, which alleviated I/R injury in isolated rat hearts [39, 40, 91] . Effects of hydrogen-rich water on the PI3K/AKT signaling pathway in rats with myocardial 12 Oxidative Medicine and Cellular Longevity ischemia-reperfusion injury Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation cache = ./cache/cord-257514-gw9xnb4x.txt txt = ./txt/cord-257514-gw9xnb4x.txt === reduce.pl bib === id = cord-273093-u79r80ip author = Laforge, Mireille title = Tissue damage from neutrophil-induced oxidative stress in COVID-19 date = 2020-07-29 pages = extension = .txt mime = text/plain words = 1348 sentences = 71 flesch = 35 summary = The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. By producing excessive ROS, deregulated neutrophils can spread a local inflammatory response so that it becomes systemic, which explains why they have been involved The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. In conclusion, the presence of oxidative stress markers (for example, lipid peroxidation, rTEM and a high neutrophil to lymphocyte ratio) in patients with COVID-19 may help to identify high-risk individuals early in the course of the disease and prevent their sudden deterioration. cache = ./cache/cord-273093-u79r80ip.txt txt = ./txt/cord-273093-u79r80ip.txt === reduce.pl bib === id = cord-291190-f6km3c7z author = Nasi, Aikaterini title = Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention date = 2020-06-18 pages = extension = .txt mime = text/plain words = 2999 sentences = 155 flesch = 42 summary =  SARS-CoV has been reported to modulate PARP function and thereby NAD+ biosynthesis  Cellular homeostasis and redox imbalances by SARS-CoV2 can cause stress responses  Antioxidants such as NAC could limit ROS mediated tissue damage during COVID-19 Hereby, based on literature review from the current pandemic and previous outbreaks with corona viruses we analyze the impact of the virus infection on cell stress responses and redox balance. PLA2G2D expression was shown to be increased in the lungs of middle aged mice, resulting in decreased survival and impaired T cell responses upon infection with SARS-CoV1 [20] . Interestingly, NAC administration to aged mice, diminished PLAG2D expression in both lung cells and CD11c+ DCs. In addition, increased levels of oxidized phospholipidsare a common feature associated with acute respiratory distress syndrome (ARDS) caused by viruses including SARS and H5N1. cache = ./cache/cord-291190-f6km3c7z.txt txt = ./txt/cord-291190-f6km3c7z.txt === reduce.pl bib === id = cord-313825-bbjxd86y author = Xia, Tian title = Pulmonary diseases induced by ambient ultrafine and engineered nanoparticles in twenty-first century date = 2016-10-08 pages = extension = .txt mime = text/plain words = 8765 sentences = 389 flesch = 43 summary = The lung is the first target organ for air pollution and PM exposure is associated with reduced lung function, increased lung inflammation, asthma, respiratory infections, lung cancer and exacerbation of COPD, which lead to systemic inflammation and oxidative stress affecting blood, vasculature, heart and brain, ultimately contribute to the premature mortality ( Fig. 2) [3, 8, 14, 16] . These specific features of UFPs can significantly contribute to the adverse effects through ROS over-production by the redox-active organic chemicals and metals on particle surface, resulting in cellular oxidative stress [18, 19, 21, 44, 48] . These include: (i) carbon core of PM and UFPs could induce ROS generation and oxidative stress; (ii) catalytic conversion of PAHs to quinones by cytochrome P450 in the endoplasmic reticulum; (iii) quinone redox cycling by NADPH-dependent P450 reductase in microsomes; (iv) mitochondrial perturbation leading to electron leakage in the inner membrane; and (v) NADPH oxidase activity in the macrophage surface membrane and associated phagosomes. cache = ./cache/cord-313825-bbjxd86y.txt txt = ./txt/cord-313825-bbjxd86y.txt === reduce.pl bib === id = cord-271939-m1ko4yal author = Rouco, Lara title = Pursuing the Elixir of Life: In Vivo Antioxidative Effects of Manganosalen Complexes date = 2020-08-10 pages = extension = .txt mime = text/plain words = 10266 sentences = 584 flesch = 37 summary = Thus, manganosalen complexes have been shown to exhibit superoxide dismutase, catalase, and glutathione peroxidase activities, and they could potentially facilitate the scavenging of excess reactive oxygen species (ROS), thereby restoring the redox balance in damaged cells and organs. Manganosalen complexes exhibit high SOD, catalase, and peroxidase activities, which has led to their development as catalytic antioxidants [6] [7] [8] [9] [10] 13, [18] [19] [20] [21] 23] , a term used for all cases in which one single molecule of catalyst induces the detoxification of numerous ROS molecules. This manganese complex and the cyclic analogue EUK-207 were used in a study with C57BL/6N Sim middle-age mice [105] , which usually exhibit a dramatic decrease in learning and memory function between 8 and 11 months of age, associated with oxidative protein damage in the brain [106] . Salen-manganese complexes for controlling ROS damage: Neuroprotective effects, antioxidant activity and kinetic studies cache = ./cache/cord-271939-m1ko4yal.txt txt = ./txt/cord-271939-m1ko4yal.txt === reduce.pl bib === id = cord-291559-h6czy5bh author = Koirala, Prashamsa title = Recent advances in pharmacological research on Ecklonia species: a review date = 2017-08-24 pages = extension = .txt mime = text/plain words = 12240 sentences = 567 flesch = 34 summary = A study investigated the protective effect of ES in alcoholic fatty liver and found that ES treatment suppressed adipogenesis and increased the expression of fatty acid oxidation-related genes, e.g., peroxisome proliferator-activated receptor (PPAR)-a and CPT-1, but decreased the expression of sterol regulatory element-binding protein (SREBP)-1, a triglyceride (TG) synthesis-related gene, suggesting that ES extract could be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver (Bang et al. Fucoidan extracted from EC exhibited prominent effects on peroxyl radical scavenging activity and 2, 2 0 -azobisdihydrochloride-induced oxidative stress in Vero cells and reduced ROS generation, lipid peroxidation, and cell death in a zebrafish model, proving its antioxidant capacities in vitro and in vivo despite being neither a polyphenol nor a flavonoid. Dieckol, isolated from the edible brown algae Ecklonia cava, induces apoptosis of ovarian cancer cells and inhibits tumor xenograft growth cache = ./cache/cord-291559-h6czy5bh.txt txt = ./txt/cord-291559-h6czy5bh.txt === reduce.pl bib === id = cord-288238-36hiiw91 author = Keshavarz, Mohsen title = Metabolic host response and therapeutic approaches to influenza infection date = 2020-03-05 pages = extension = .txt mime = text/plain words = 8134 sentences = 425 flesch = 32 summary = It is also reported that influenza infection significantly increases ROS production by inducing Nox4, and the proliferation of this virus in lung epithelial cells is dependent on redox-sensitive pathways activated by Nox4-derived ROS [16] . IFN can also exert its function on metabolic changes by producing several mediators including indoleamine-2,3-dioxygenase (IDO) and nitric oxide (NO), both of which appear to have either an inducible or an inhibitory role in viral replication [33] . In addition, increased temperature of cells during infection (which could be the result of virus replication and fever) causes heat stress which in turn can considerably downregulate carnitine palmitoyltransferase II (CPT II) activity and reduce the β-oxidation and ATP levels in fibroblasts of influenza-associated encephalopathy patients and healthy volunteers [110] . Through enhancing the activity of the mTORC1 complex, the influenza virus strengthens several metabolic pathways, including glycolysis, glutaminolysis, pentose phosphate, and fatty acid synthesis, to provide more ATP and structural materials for viral replication. cache = ./cache/cord-288238-36hiiw91.txt txt = ./txt/cord-288238-36hiiw91.txt === reduce.pl bib === id = cord-260348-83ftjqev author = Xu, Yinlan title = Cepharanthine and Curcumin inhibited mitochondrial apoptosis induced by PCV2 date = 2020-09-18 pages = extension = .txt mime = text/plain words = 3752 sentences = 220 flesch = 48 summary = The results of qPCR and Western blot showed that, compared with the PCV2 infected group, the expression of Cap in Paeonol (0.4 mg/mL and 0.2 mg/mL), Cepharanthine (0.003 mg/mL, 0.0015 mg/mL and 0.00075 mg/mL) and Curcumin (0.02 mg/mL, 0.001 mg/mL and 0.005 mg/mL) treated groups were significantly lowered in a dose-dependent manner. The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. The results showed that Compared to the PCV2-infected group, the cell apoptosis rates were significantly decreased in the group treated with Cepharanthine, Curcumin or Ribavirin, demonstrating a dose-dependent response except the group of 0.005 mg/mL Paeonol (P < 0.05) ( Fig. 3a and b). cache = ./cache/cord-260348-83ftjqev.txt txt = ./txt/cord-260348-83ftjqev.txt === reduce.pl bib === id = cord-320591-re99v1qt author = Le, Thanh Ninh title = Bioactive Compounds and Bioactivities of Brassica oleracea L. var. Italica Sprouts and Microgreens: An Updated Overview from a Nutraceutical Perspective date = 2020-07-27 pages = extension = .txt mime = text/plain words = 8182 sentences = 395 flesch = 34 summary = Particularly, these studies mostly focused on the antioxidant and anticancer activities of broccoli sprouts and microgreens owing to the functions of glucosinolates and phenolic compounds (Tables 4 and 5 ). Particularly, these studies mostly focused on the antioxidant and anticancer activities of broccoli sprouts and microgreens owing to the functions of glucosinolates and phenolic compounds (Tables 4 and 5 ). In summary, previous studies showed that broccoli sprout extracts rich in vitamins, carotenoids, and phenolic compounds showed very high antioxidant activity in both in vitro and in vivo tests (Table 4) . Moreover, the previous studies have focused on several biological activities of broccoli seedlings, such as antioxidant, anticancer, antimicrobial, and anti-inflammatory, as well as the potentially beneficial effects for patients with cancers, diabetes, and obesity. cache = ./cache/cord-320591-re99v1qt.txt txt = ./txt/cord-320591-re99v1qt.txt === reduce.pl bib === id = cord-295459-ffi1043k author = Khan, Naseem Ahmed title = Respiratory Syncytial Virus-Induced Oxidative Stress Leads to an Increase in Labile Zinc Pools in Lung Epithelial Cells date = 2020-05-27 pages = extension = .txt mime = text/plain words = 6785 sentences = 345 flesch = 54 summary = Small interfering RNA (siRNA)-mediated knockdown of the ubiquitous zinc uptake transporter ZIP1 suggests that labile zinc levels are increased due to the increased uptake by RSV-infected cells as an antiviral response. Our results suggest that zinc homeostasis plays a critical role in the host response to RSV infection by regulating oxidative stress and inhibiting virus replication. As with A549 cells, we observed a time-dependent increase in labile zinc levels in SAECs infected with RSV without any effect on cell viability ( Fig. 2A and B) . To further confirm the role of oxidative stress in RSV infection, cells infected with RSV were treated with 300 M H 2 O 2 (one of the ROS) and virus titers were measured at 24 h p.i. As observed in the case of zinc chelation, addition of H 2 O 2 led to a modest but significant increase in RSV titers at 24 h p.i. cache = ./cache/cord-295459-ffi1043k.txt txt = ./txt/cord-295459-ffi1043k.txt === reduce.pl bib === id = cord-331673-xv1tcugl author = Reina, Giacomo title = Hard Nanomaterials in Time of Viral Pandemics date = 2020-07-15 pages = extension = .txt mime = text/plain words = 15712 sentences = 976 flesch = 44 summary = For instance, in the case of Herpesviridae and Paramyxoviridae viruses (both enveloped viruses with embedded viral-encoded glycoproteins), AgNPs can effectively reduce their infectivity, by blocking the interaction between the viral particles and the host cells with an antiviral activity strictly dependent on the size and ζ potential of the AgNPs. As a general observation, it was reported that smaller nanoparticles have better antiviral effect. cAgNPs could reduce cytopathic effects induced by RSV and showed efficient antiviral activity against infection by directly inactivating the virus prior to entry into the host cells. have reported that porous AuNPs are able to inhibit influenza A infection more efficiently than nonporous AuNPs. 39 This effect has been associated with the higher surface area of the porous material that favors their interaction with capsids and thus increases their antiviral activity ( Figure 4 ). cache = ./cache/cord-331673-xv1tcugl.txt txt = ./txt/cord-331673-xv1tcugl.txt === reduce.pl bib === id = cord-316244-s5ua0re3 author = Park, Mi Hee title = Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases date = 2016-04-26 pages = extension = .txt mime = text/plain words = 19183 sentences = 1015 flesch = 41 summary = PRDX6 is an oxidative stress inducible protein regulated by Nrf2 and activation of the gene expression was observed in mouse lungs by hyperoxia and in cultured lung epithelial cells following treatment with H 2 O 2 or paraquat . One previous study reported that hypoxia increases AR activity in prostate cancer cells, and that PRDX1, which is upregulated by hypoxia, interacts with AR to enhance the expression of androgen-regulated genes (Chhipa, Lee, Onate, Wu, & Ip, 2009; Park et al., 2006) . PRDX2 is overexpressed in colorectal carcinoma tissues compared with the matched non-cancer colorectal mucosa tissues and that expression is positively associated with tumor metastasis and the TNM stage by regulation of oxidation induced apoptosis (Lu et al., 2014a) . Other researchers also demonstrated that PRDX2 knockdown using a lentiviral vector-mediated specific shRNA inhibited cell growth, stimulated apoptosis, and augmented the production of endogenous ROS that led to an altered expression of proteins associated with the Wnt signaling pathway (Lu et al., 2014b) . cache = ./cache/cord-316244-s5ua0re3.txt txt = ./txt/cord-316244-s5ua0re3.txt === reduce.pl bib === id = cord-335676-7ak53hto author = Meftahi, Gholam Hossein title = The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of “inflame-aging” date = 2020-06-11 pages = extension = .txt mime = text/plain words = 8208 sentences = 435 flesch = 43 summary = It seems that "cytokine storm" phenomenon in elderly patients with severe COVID-19 infection, is associated with many age-related pathophysiologic processes, including alteration of angiotensin-converting enzyme 2 (ACE2) receptor expression [9] , excess ROS production [10] , alteration of autophagy [11] , the inflammatory phenotype of senescent cell activity, particularly adipose tissue [12] , and immune-senescence [13] , as well as lack of vitamin D content [14] . As shown in Fig. 2 , several factors, including alteration of ACE2 receptor expression, excess reactive oxygen species (ROS) production, senescent adipocytes activity, alteration of autophagy and mitophagy, immune-senescent, as well as vitamin D (VD) deficiency, may associate "inflame-aging" to cytokine storm in elderly patients of COVID-19. Furthermore, the lack of VD in aged subjects is associated with the pro-inflammatory phenotype of immune cells, leading to likely increasing the risk of elderly adults with chronic mild inflammation condition [122] . cache = ./cache/cord-335676-7ak53hto.txt txt = ./txt/cord-335676-7ak53hto.txt === reduce.pl bib === id = cord-336201-fl606l3b author = Daryabor, Gholamreza title = The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System date = 2020-07-22 pages = extension = .txt mime = text/plain words = 13863 sentences = 715 flesch = 38 summary = Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. T2DM, the most common form of diabetes (∼90%), is characterized by a systemic inflammatory disease accompanied by insulin resistance (IR) or decreased metabolic response to insulin in several tissues, including the adipose tissue, liver, and skeletal muscle, as well as by reduced insulin synthesis by pancreatic beta cells (4, 5) . During the progression of diabetes, hyperglycemia promotes mitochondrial dysfunction and induces the formation of reactive oxygen species (ROS) that cause oxidative stress in several tissues such as blood vessels and pancreatic beta cells (7) (8) (9) . In addition, the attachment of AGEs to their receptors [e.g., CD36, galectin-3, scavenger receptors types I (SR-A1), and II (SR-A2)] on the surfaces of immune cells in the circulation and tissues activates the expression of pro-inflammatory cytokines and increases free radical generation (18) . cache = ./cache/cord-336201-fl606l3b.txt txt = ./txt/cord-336201-fl606l3b.txt === reduce.pl bib === id = cord-268527-wbfnhedy author = Smith, Sylvia B. title = Transient hyperglycosylation of rhodopsin with galactose date = 1991-10-31 pages = extension = .txt mime = text/plain words = 8560 sentences = 468 flesch = 58 summary = Following subcellular fractionation of retinas, ConA purified rhodopsin from ROS was applied to one of two additional lectin columns: Ricinus communis agglutinin (RCA) or Griffonia simplicifolia I (GSA). To radiolabel existing galactose moieties on rhodopsin, bovine ROS purified by a discontinuous sucrose density gradient procedure, were subjected to enzymatic treatment with galactose oxidase followed by a reduction with tritium labeled sodium borohydride. In this method, ConA purified rhodopsin or in some cases the clarified extract of ROS from six rat retinas labeled with [35S]methionine was applied to columns of either Ricinus communis agglutinin I (RCA) or GrifSonia simplicijolia I (GSA), specific for P-linked or a-linked galactose residues, respectively. Rats injected intravitreally with [35S]methionine were maintained in darkness for 2 hr at which time 12 retinas were collected for subcellular fractionation and rhodopsin purification by ConA sepharose chromatography. cache = ./cache/cord-268527-wbfnhedy.txt txt = ./txt/cord-268527-wbfnhedy.txt === reduce.pl bib === id = cord-298265-elbnzgx6 author = Mutua, Victoria title = A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics date = 2020-08-01 pages = extension = .txt mime = text/plain words = 10404 sentences = 565 flesch = 35 summary = Studies have demonstrated that circulating neutrophils of RA patients are more easily stimulated to NETosis than those from healthy subjects [73, 74] , and as in other autoimmune conditions, NETs act as a source of extracellular autoantigens leading to excessive innate and adaptive immune responses in the joints and subsequent tissue injury [73, 75] . Inhibits ROS production, prevents thrombus formation [190] [191] [192] [193] [194] [195] Nucleases Recombinant human DNase DNA matrixes Reduces neutrophil infiltration, cleaves DNA matrixes [196] [197] [198] [199] [200] [201] [202] [203] [204] [205] [206] [207] Staphylokinase Plasminogen, alpha-defensins Converting NETs to deoxyadenosine mediating death of immune cells [208] [209] [210] [211] Notable compounds Probiotics PKC pathway run a study to evaluate the effect of inhibition of PAD4 in NETosis using an antagomiR-155, a pleiotropic microRNA important in the regulation of immune responses, demonstrating a decreased induction of PAD4 mRNA and subsequent reduced NETs in response to PMA challenge [13] . cache = ./cache/cord-298265-elbnzgx6.txt txt = ./txt/cord-298265-elbnzgx6.txt === reduce.pl bib === id = cord-310723-ogo9mvi5 author = Belinskaia, Daria A. title = The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin date = 2020-10-09 pages = extension = .txt mime = text/plain words = 13775 sentences = 724 flesch = 46 summary = Therefore, the correct extrapolation of in vivo results obtained in rats to a human organism requires the identification of amino acids involved in protein-ligand interaction, determination of all structural and conformational features of the binding sites and comparison of the obtained characteristics in HSA vs. Therefore, the correct extrapolation of in vivo results obtained in rats to a human organism requires the identification of amino acids involved in protein-ligand interaction, determination of all structural and conformational features of the binding sites and comparison of the obtained characteristics in HSA vs. It was demonstrated by the method of electron paramagnetic resonance (EPR) that oxidation of albumin of the healthy subjects with hydrogen peroxide and tert-butyl hydroperoxide led to conformational changes in the microenvironment of the binding sites of maleimide and iodoacetamide spin labels, which interact predominantly with the thiol group of Cys34. cache = ./cache/cord-310723-ogo9mvi5.txt txt = ./txt/cord-310723-ogo9mvi5.txt === reduce.pl bib === id = cord-323730-5iawbnua author = Ohl, Kim title = Oxidative stress in multiple sclerosis: Central and peripheral mode of action date = 2016-03-31 pages = extension = .txt mime = text/plain words = 9168 sentences = 438 flesch = 39 summary = Whatever the trigger factors for lesion Experimental Neurology 277 (2016) [58] [59] [60] [61] [62] [63] [64] [65] [66] [67] Abbreviations: APCs, antigen-presenting cells; ARE, antioxidant response element; DMF, dimethyl fumarate; FAEs, fumaric acid esters; GSH, glutathione; HO, heme oxygenase; IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; Keap1, Kelch ECH associating protein 1; MDSC, myeloid-derived suppressor cells; MMF, monomethyl fumarate; NQO1, NAD(P)H: quinone oxidoreductase 1; Nrf2, nuclear factor (erythroid-derived 2)-like 2; RNS, reactive nitrogen species; ROS, reactive oxygen species; S1P, sphingosine 1-phosphate; TGF, transforming growth factor; T h , T helper cell; T reg , regulatory T cell; Trx, thioredoxin. Furthermore, redox stress is important for the functional outcome during experimentally-induced adaptive-immunity responses; e.g. in a graft-versus-host disease mouse model, free radical scavenger therapy with NecroX-7 attenuates disease severity, probably via the induction of T reg cells (Im et al., 2015) and oxidative damage regulates antigen-specific T cell responses in agerelated macular degeneration (Cruz-Guilloty et al., 2014) . cache = ./cache/cord-323730-5iawbnua.txt txt = ./txt/cord-323730-5iawbnua.txt === reduce.pl bib === id = cord-297469-26d8o1xk author = Choi, Won Hyung title = The Mechanism of Action of Ursolic Acid as a Potential Anti-Toxoplasmosis Agent, and Its Immunomodulatory Effects date = 2019-05-09 pages = extension = .txt mime = text/plain words = 6997 sentences = 266 flesch = 43 summary = gondii effects of ursolic acid, and analyzed the production of nitric oxide (NO), reactive oxygen species (ROS), and cytokines through co-cultured immune cells, as well as the expression of intracellular organelles of T. Furthermore, ursolic acid effectively increased the production of NO, ROS, interleukin (IL)-10, IL-12, granulocyte macrophage colony stimulating factor (GM-CSF), and interferon-β, while reducing the expression of IL-1β, IL-6, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1 (TGF-β1) in T. gondii-infected cells were treated with different concentrations (12.5-200 µg/mL) of ursolic acid (UA) and sulfadiazine (SF) at 37 • C for 24 h, respectively; their survival rates were inhibited a dose-dependent manner. We evaluated the effect of ROS and NO production induced by ursolic acid in immune cells infected with T. We evaluated the effect of ROS and NO production induced by ursolic acid in immune cells infected with T. cache = ./cache/cord-297469-26d8o1xk.txt txt = ./txt/cord-297469-26d8o1xk.txt === reduce.pl bib === id = cord-313918-uv9xdp5f author = Marí, Montserrat title = Mitochondrial Glutathione: Recent Insights and Role in Disease date = 2020-09-24 pages = extension = .txt mime = text/plain words = 10385 sentences = 524 flesch = 31 summary = Abbreviations 2-oxoglutarate carrier (OGC; SLC25A11); adenine nucleotide translocator (ANT); alcoholic liver disease (ALD); alcoholic steatohepatitis (ASH); Alzheimer's disease (AD); amyloid beta peptides (Aβ); amyloid precursor protein/presenilin 1 (APP/PS1); amyotrophic lateral sclerosis (ALS); Cu/Zn-superoxide dismutase (SOD1); diabetic nephropathy (DN); electron transport chain (ETC); endoplasmic reticulum (ER); free cholesterol (FC); glyoxalase II (GLO2); Glutathione (GSH); glutathione disulfide (GSSG); glutathione reductase (GR); glutathione S-transferase (GST); GSH ethyl ester (GEE); GSH peroxidases (GPx); hepatic steatosis (HS); metabolic associated fatty liver disease (MAFLD); mitochondrial dicarboxylate carrier (DIC; SLC25A10); mitochondrial glutathione (mGSH); mitochondrial NADP+-dependent isocitrate dehydrogenase (IDPm); mitochondrial permeability transition (MPT); non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); Parkinson's disease (PD); peroxiredoxins (Prx); protein disulfide isomerase (PDI); reactive oxygen species (ROS); S-adenosyl-l-methionine (SAM); S-d-lactoylglutathione (SLG); sterol regulatory element binding protein 2 (SREBP-2); thioredoxin 2/thioredoxin reductase 2 (Trx2/TrxR2); tumor necrosis factor (TNF). cache = ./cache/cord-313918-uv9xdp5f.txt txt = ./txt/cord-313918-uv9xdp5f.txt === reduce.pl bib === id = cord-268122-74nj66vb author = Xie, Na title = NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential date = 2020-10-07 pages = extension = .txt mime = text/plain words = 32037 sentences = 1955 flesch = 39 summary = The NAD + decline during normal aging results in oxidative damage, metabolic disorder, circadian rhythm abnormalities, and mitochondrial dysfunction through regulating signaling pathways, such as p53, NF-κB, PGC-1α and HIF-1α, by sirtuins and PARPs. NAD + and its metabolites function as crucial regulators to maintain cellular redox homeostasis through replenishing the reducing power or modulating the activity of NAD + -consuming enzymes including sirtuins and PARPs. However, disequilibrium of NAD + metabolism could disturb physiological processes, including mitochondria function, circadian rhythm, inflammation, DNA repair and metabolism, leading to aging-associated dysfunction and cancer. c The deduced NAD + levels in kidney are attributed to the decreased expression of enzymes in NAD + de novo synthesis and increased consumption by DNA damage activated PARPs. NAD + depletion inhibits the SIRT1/PGC1α mediated mitochondrial quality control, ATP production and NAD + de novo biosynthesis. cache = ./cache/cord-268122-74nj66vb.txt txt = ./txt/cord-268122-74nj66vb.txt === reduce.pl bib === id = cord-307148-k1uo3fxm author = Bradshaw, Patrick C. title = COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm date = 2020-09-09 pages = extension = .txt mime = text/plain words = 20788 sentences = 1093 flesch = 40 summary = R-BHB activates anti-inflammatory GPR109A signaling and inhibits the NLRP3 inflammasome and histone deacetylases, while a ketogenic diet has been shown to protect mice from influenza virus infection through a protective γδ T cell response and by increasing electron transport chain gene expression to restore energy metabolism. Others have also suggested that increasing systemic ketone levels may aid host defenses against respiratory viral infection, in part, by decreasing inflammation [1, 2] , including a recent comprehensive review [3] , while a clinical trial of the effects of a ketogenic diet on intubated SARS-CoV-2 patients has recently been registered (NCT04358835). Coronaviruses have been shown to increase the oxidation of phospholipids, which stimulate toll-like receptor 4 (TLR4) signaling on macrophages, leading to cytokine production and acute lung injury [163] , so HDAC inhibition with R-BHB appears to be a viable treatment to decrease cytokine levels and inflammation. cache = ./cache/cord-307148-k1uo3fxm.txt txt = ./txt/cord-307148-k1uo3fxm.txt === reduce.pl bib === id = cord-032561-x3qbqy69 author = Liu, Gengqi title = Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment date = 2020-09-02 pages = extension = .txt mime = text/plain words = 25208 sentences = 1664 flesch = 46 summary = demonstrated that nanodrug carriers with diselenides could release more drugs using poly (ester carbamate) triblock copolymers (PAUR-Se-Se) with Se-Se bonds compared with poly (ester carbamate) triblock copolymers (PAUR-S-S) [54, 55] Thioether Selenium Tellurium Besides the development of drug delivery systems, pH-responsive systems can also be used for tumor detection and image-guided surgery [46] . demonstrated that nanodrug carriers with diselenides could release more drugs using poly (ester carbamate) triblock copolymers (PAUR-Se-Se) with Se-Se bonds compared with poly (ester carbamate) triblock copolymers (PAUR-S-S) [65] PBA/PBE Besides the development of drug delivery systems, pH-responsive systems can also be used for tumor detection and image-guided surgery [46] . Therefore, pH responsive system can be combined with other stimulus conditions such as light, redox, enzymes and others with the aim of improved selectivity for drug release in diseased tissues [47, 48] . In addition to photothermal therapy and PDT, light-responsive strategies have also been applied in the design of prodrug systems and drug delivery carriers. cache = ./cache/cord-032561-x3qbqy69.txt txt = ./txt/cord-032561-x3qbqy69.txt === reduce.pl bib === id = cord-006230-xta38e7j author = nan title = Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie e.V. date = 2012-02-22 pages = extension = .txt mime = text/plain words = 135419 sentences = 7042 flesch = 43 summary = Here, we will present our analysis of Ca 2+ signaling following stimulation of the FcεRI receptor and application of secretagogues that are supposed to affect Ca 2+ -dependent mast cell activation such as adenosine, endothelin-1, substance P and compound 48/80 in BMMCs and PMCs derived from mouse lines with inactivation of TRPC1, TRPC3, TRPC4, TRPC5 or TRPC6 since specific antagonists are still lacking for these TRP channels. These data indicate that increased PP2A activity is associated with modified gene expression in TG hearts possibly affecting stress response and regulation of cell signalling. As demonstrated by qPCR and Western blot experiments, mesangial cells showed a marked time-and dose-dependent upregulation of CSE mRNA and protein levels after treatment with platelet-derived growth factor (PDGF-BB). The transcription factor cAMP response element (CRE)-binding protein (CREB) plays a critical role in regulating gene expression in response to activation of the cAMPdependent signaling pathway, which is implicated in the pathophysiology of heart failure. cache = ./cache/cord-006230-xta38e7j.txt txt = ./txt/cord-006230-xta38e7j.txt === reduce.pl bib === id = cord-022940-atbjwpo5 author = nan title = Poster Sessions date = 2016-09-07 pages = extension = .txt mime = text/plain words = 241182 sentences = 12746 flesch = 47 summary = We have studied the effect of inhibition of IRE1 (inositol requiring enzyme 1), which is a central mediator of endoplasmic reticulum stress and controls cell proliferation and tumor growth, on hypoxic regulation of the expression of different proliferation related genes in U87 glioma cells. Transient inhibition of Akt and mTOR protein kinase activation in tumor cells followed by reactivation of signaling pathway did not result in a time-dependent difference on EGFR, HER2 and HER3 expression levels. In our study we aimed to determine cytotoxic effect of RES in K562 human CML cell line and to evaluate the expressions of miRNAs that are associated with genetics of leukemia after treatment with RES; to investigate target genes of miRNAs which show significant expression alterations and molecular mechanisms of RES treatment. cache = ./cache/cord-022940-atbjwpo5.txt txt = ./txt/cord-022940-atbjwpo5.txt ===== Reducing email addresses cord-331673-xv1tcugl Creating transaction Updating adr table ===== Reducing keywords cord-001769-2sdg5ll7 cord-000799-s70onyix cord-001347-ssrs0cwf cord-004508-ok3px98z cord-014661-mrh2pbi6 cord-005280-a23oy0sz cord-013415-110b95cg cord-102808-c7ajfvt5 cord-289034-yl3emjef cord-048478-ftlb5b95 cord-012495-r6nkdeaw cord-273992-xddikzxs cord-034321-ohjik0pf cord-020646-s7eopu9y cord-003841-7uaj9hmx cord-034294-ti1cc24m cord-035015-slgywe0c cord-262759-ec2c25q3 cord-017817-ztp7w9yh cord-278846-nqj7ctk3 cord-319614-4qi59pbz cord-293319-oo0w6faj cord-257514-gw9xnb4x cord-291190-f6km3c7z cord-273093-u79r80ip cord-313825-bbjxd86y cord-271939-m1ko4yal cord-291559-h6czy5bh cord-288238-36hiiw91 cord-260348-83ftjqev cord-320591-re99v1qt cord-295459-ffi1043k cord-331673-xv1tcugl cord-316244-s5ua0re3 cord-335676-7ak53hto cord-336201-fl606l3b cord-268527-wbfnhedy cord-298265-elbnzgx6 cord-310723-ogo9mvi5 cord-323730-5iawbnua cord-297469-26d8o1xk cord-313918-uv9xdp5f cord-268122-74nj66vb cord-307148-k1uo3fxm cord-032561-x3qbqy69 cord-006230-xta38e7j cord-022940-atbjwpo5 Creating transaction Updating wrd table ===== Reducing urls cord-004508-ok3px98z cord-048478-ftlb5b95 cord-034321-ohjik0pf cord-034294-ti1cc24m cord-035015-slgywe0c cord-319614-4qi59pbz cord-260348-83ftjqev cord-331673-xv1tcugl cord-336201-fl606l3b cord-268122-74nj66vb cord-006230-xta38e7j cord-022940-atbjwpo5 Creating transaction Updating url table ===== Reducing named entities cord-000799-s70onyix cord-001769-2sdg5ll7 cord-014661-mrh2pbi6 cord-001347-ssrs0cwf cord-004508-ok3px98z cord-005280-a23oy0sz cord-013415-110b95cg cord-102808-c7ajfvt5 cord-289034-yl3emjef cord-048478-ftlb5b95 cord-273992-xddikzxs cord-034321-ohjik0pf cord-012495-r6nkdeaw cord-020646-s7eopu9y cord-003841-7uaj9hmx cord-035015-slgywe0c cord-034294-ti1cc24m cord-262759-ec2c25q3 cord-017817-ztp7w9yh cord-293319-oo0w6faj cord-257514-gw9xnb4x cord-278846-nqj7ctk3 cord-319614-4qi59pbz cord-291190-f6km3c7z cord-273093-u79r80ip cord-313825-bbjxd86y cord-271939-m1ko4yal cord-288238-36hiiw91 cord-291559-h6czy5bh cord-260348-83ftjqev cord-320591-re99v1qt cord-295459-ffi1043k cord-331673-xv1tcugl cord-316244-s5ua0re3 cord-335676-7ak53hto cord-336201-fl606l3b cord-298265-elbnzgx6 cord-268527-wbfnhedy cord-310723-ogo9mvi5 cord-323730-5iawbnua cord-297469-26d8o1xk cord-313918-uv9xdp5f cord-268122-74nj66vb cord-307148-k1uo3fxm cord-032561-x3qbqy69 cord-006230-xta38e7j cord-022940-atbjwpo5 Creating transaction Updating ent table ===== Reducing parts of speech cord-001769-2sdg5ll7 cord-000799-s70onyix cord-001347-ssrs0cwf cord-004508-ok3px98z cord-005280-a23oy0sz cord-014661-mrh2pbi6 cord-102808-c7ajfvt5 cord-289034-yl3emjef cord-013415-110b95cg cord-048478-ftlb5b95 cord-012495-r6nkdeaw cord-273992-xddikzxs cord-034321-ohjik0pf cord-003841-7uaj9hmx cord-020646-s7eopu9y cord-035015-slgywe0c cord-034294-ti1cc24m cord-262759-ec2c25q3 cord-017817-ztp7w9yh cord-293319-oo0w6faj cord-278846-nqj7ctk3 cord-257514-gw9xnb4x cord-319614-4qi59pbz cord-291190-f6km3c7z cord-273093-u79r80ip cord-313825-bbjxd86y cord-291559-h6czy5bh cord-271939-m1ko4yal cord-288238-36hiiw91 cord-260348-83ftjqev cord-320591-re99v1qt cord-295459-ffi1043k cord-331673-xv1tcugl cord-316244-s5ua0re3 cord-335676-7ak53hto cord-336201-fl606l3b cord-268527-wbfnhedy cord-298265-elbnzgx6 cord-310723-ogo9mvi5 cord-323730-5iawbnua cord-297469-26d8o1xk cord-313918-uv9xdp5f cord-307148-k1uo3fxm cord-032561-x3qbqy69 cord-268122-74nj66vb cord-006230-xta38e7j cord-022940-atbjwpo5 Creating transaction Updating pos table Building ./etc/reader.txt cord-022940-atbjwpo5 cord-006230-xta38e7j cord-268122-74nj66vb cord-022940-atbjwpo5 cord-268122-74nj66vb cord-316244-s5ua0re3 number of items: 47 sum of words: 847,196 average size in words: 18,025 average readability score: 40 nouns: cells; cell; expression; protein; levels; activity; study; stress; effects; cancer; patients; role; effect; results; treatment; proteins; activation; disease; mice; dna; response; infection; production; studies; group; gene; damage; function; inflammation; system; apoptosis; virus; acid; receptor; control; analysis; pathway; tissue; lung; inhibition; genes; level; diseases; type; regulation; factor; data; model; groups; time verbs: using; induced; showed; increased; reduce; died; including; leading; compared; regulate; associated; inhibited; found; causes; activated; decreases; suggests; mediated; determined; signalling; investigated; involved; binding; indicated; based; related; demonstrate; observed; treated; plays; promotes; reveal; resulted; expressed; enhanced; containing; identified; performed; produce; affect; known; followed; preventing; provided; measured; developing; report; contribute; study; control adjectives: oxidative; human; mitochondrial; inflammatory; different; high; anti; cellular; immune; specific; dependent; important; significant; higher; viral; molecular; metabolic; several; low; chronic; non; antioxidant; reactive; many; various; therapeutic; clinical; potential; new; intracellular; acute; normal; pulmonary; present; extracellular; pro; healthy; respiratory; apoptotic; novel; functional; key; responsive; recent; major; endothelial; total; similar; diabetic; first adverbs: also; however; significantly; well; therefore; respectively; furthermore; recently; moreover; highly; directly; thereby; still; interestingly; mainly; together; previously; even; additionally; especially; widely; specifically; currently; statistically; first; often; strongly; finally; indeed; less; subsequently; now; potentially; particularly; effectively; yet; similarly; rather; far; commonly; alone; probably; mostly; consequently; possibly; hence; clearly; already; almost; rapidly pronouns: we; it; their; its; our; i; they; them; itself; us; his; themselves; one; prdx2; you; he; your; her; il-1β; she; prdx5; mtorc1; mrs; me; itsn2; il-; y€; ykl-40; trpm4; tnfsf7; pdcs; pcv2; p-450; my; mrnas; kv4.2; itselves; inhibits; imagej; ilc1s; i40a; him; euk-134; cyp2e1; caspase-1; benzo-1,2,4thiadiazine; bche; b-733d; afprbd; -alkaline proper nouns: ROS; der; NAD; von; und; C; S.; GSH; mg; COPD; T; NADPH; II; RNA; Fig; University; TNF; ATP; Turkey; SARS; werden; den; PCR; MS; mit; AE; eine; Nrf2; A; wird; IL-6; DNA; ER; sich; pH; Ca; durch; kg; α; E.; das; sind; B; C.; des; COVID-19; M.; EC; LPS; HIF-1α keywords: ros; cell; effect; dna; protein; mitochondrial; covid-19; sars; increase; atp; virus; study; rna; nadph; level; gsh; akt; activity; western; trap; tnf; tissue; table; result; pulmonary; pcr; patient; oxidative; nrf2; neutrophil; net; infection; il-6; gene; expression; copd; cancer; ace2; a549; zo-1; zinc; zellen; yun; wiseman; wirkung; wird; werden; von; viral; v79 one topic; one dimension: cells file(s): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569300/ titles(s): The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis three topics; one dimension: cells; cells; die file(s): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7164006/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504550/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7143866/ titles(s): Poster Sessions | Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment | Die Pathophysiologie der Entzündung five topics; three dimensions: cells cell expression; cells cell study; cells mitochondrial nad; responsive drug ros; die der und file(s): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7100643/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7164006/, https://doi.org/10.1038/s41392-020-00311-7, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504550/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7143866/ titles(s): Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie e.V. | Poster Sessions | NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential | Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment | Die Pathophysiologie der Entzündung Type: cord title: keyword-ros-cord date: 2021-05-25 time: 16:19 username: emorgan patron: Eric Morgan email: emorgan@nd.edu input: keywords:ros ==== make-pages.sh htm files ==== make-pages.sh complex files ==== make-pages.sh named enities ==== making bibliographics id: cord-013415-110b95cg author: Aquino-Martinez, Ruben title: Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem? date: 2020-10-09 words: 10333 sentences: 522 pages: flesch: 27 cache: ./cache/cord-013415-110b95cg.txt txt: ./txt/cord-013415-110b95cg.txt summary: Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. In contrast to transient DNA damage, persistent genomic lesions promote constitutive DNA damage signaling and cellular senescence, which is correlated with increased secretion of inflammatory signals [26, 30] In agreement with this observation, several studies have reported that premature senescence can also be induced by exposing human cells to subtoxic H 2 O 2 concentrations [31, 32] . As a consequence of chronological aging, the burden of senescent cells increases in different tissues in humans, mice, and other species, where they contribute to the development of chronic pathologies including arthritis, osteoporosis, Alzheimer''s disease, atherosclerosis, cancer, and diabetes [58, 59] Similar to other agerelated pathologies, the etiology of diabetes may be the result of the impact of different aging mechanism, including stem cell exhaustion, chronic low-grade inflammation, macromolecular damage, and cellular senescence. abstract: The recent identification of senescent cells in periodontal tissues has the potential to provide new insights into the underlying mechanisms of periodontal disease etiology. DNA damage-driven senescence is perhaps one of the most underappreciated delayed consequences of persistent Gram-negative bacterial infection and inflammation. Although the host immune response rapidly protects against bacterial invasion, oxidative stress generated during inflammation can indirectly deteriorate periodontal tissues through the damage to vital cell macromolecules, including DNA. What happens to those healthy cells that reside in this harmful environment? Emerging evidence indicates that cells that survive irreparable genomic damage undergo cellular senescence, a crucial intermediate mechanism connecting DNA damage and the immune response. In this review, we hypothesize that sustained Gram-negative bacterial challenge, chronic inflammation itself, and the constant renewal of damaged tissues create a permissive environment for the abnormal accumulation of senescent cells. Based on emerging data we propose a model in which the dysfunctional presence of senescent cells may aggravate the initial immune reaction against pathogens. Further understanding of the role of senescent cells in periodontal disease pathogenesis may have clinical implications by providing more sophisticated therapeutic strategies to combat tissue destruction. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7587987/ doi: 10.3390/ijms21207441 id: cord-004508-ok3px98z author: Armando, Federico title: Oxidative Stress in Canine Histiocytic Sarcoma Cells Induced by an Infection with Canine Distemper Virus Led to a Dysregulation of HIF-1α Downstream Pathway Resulting in a Reduced Expression of VEGF-B In Vitro date: 2020-02-11 words: 8265 sentences: 382 pages: flesch: 38 cache: ./cache/cord-004508-ok3px98z.txt txt: ./txt/cord-004508-ok3px98z.txt summary: Based on these findings, the aim of the present study was to investigate the impact of a persistent CDV-infection on oxidative stress mediated changes in the expression of hypoxia-inducible factor (HIF)-1α and its angiogenic downstream pathway in DH82 cells in vitro. In summary, these results suggest a reduced activation of the HIF-1α angiogenic downstream pathway in DH82Ond pi cells in vitro, most likely due to an excessive, unusually localized, and non-functional expression of HIF-1α triggered by a CDV-induced increased oxidative stress. In a hypothesis-driven approach, an online available microarray data set of quadruplicates of non-infected DH82 and DH82Ond pi cells (ArrayExpress; http://www.ebi.ac.uk/arrayexpress; accession number E-MTAB-3942 [11, 44] ) was investigated for differentially expressed genes related to ROS production and scavenging, ER-stress and HIF-1α pathway, with a special focus on the angiogenic downstream targets of the latter. abstract: Histiocytic sarcomas represent malignant tumors which require new treatment strategies. Canine distemper virus (CDV) is a promising candidate due to its oncolytic features reported in a canine histiocytic sarcoma cell line (DH82 cells). Interestingly, the underlying mechanism might include a dysregulation of angiogenesis. Based on these findings, the aim of the present study was to investigate the impact of a persistent CDV-infection on oxidative stress mediated changes in the expression of hypoxia-inducible factor (HIF)-1α and its angiogenic downstream pathway in DH82 cells in vitro. Microarray data analysis, immunofluorescence for 8-hydroxyguanosine, superoxide dismutase 2 and catalase, and flow cytometry for oxidative burst displayed an increased oxidative stress in persistently CDV-infected DH82 cells (DH82Ond pi) compared to controls. The HIF-1α expression in DH82Ond pi increased, as demonstrated by Western blot, and showed an unexpected, often sub-membranous distribution, as shown by immunofluorescence and immunoelectron microscopy. Furthermore, microarray data analysis and immunofluorescence confirmed a reduced expression of VEGF-B in DH82Ond pi compared to controls. In summary, these results suggest a reduced activation of the HIF-1α angiogenic downstream pathway in DH82Ond pi cells in vitro, most likely due to an excessive, unusually localized, and non-functional expression of HIF-1α triggered by a CDV-induced increased oxidative stress. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077254/ doi: 10.3390/v12020200 id: cord-310723-ogo9mvi5 author: Belinskaia, Daria A. title: The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin date: 2020-10-09 words: 13775 sentences: 724 pages: flesch: 46 cache: ./cache/cord-310723-ogo9mvi5.txt txt: ./txt/cord-310723-ogo9mvi5.txt summary: Therefore, the correct extrapolation of in vivo results obtained in rats to a human organism requires the identification of amino acids involved in protein-ligand interaction, determination of all structural and conformational features of the binding sites and comparison of the obtained characteristics in HSA vs. Therefore, the correct extrapolation of in vivo results obtained in rats to a human organism requires the identification of amino acids involved in protein-ligand interaction, determination of all structural and conformational features of the binding sites and comparison of the obtained characteristics in HSA vs. It was demonstrated by the method of electron paramagnetic resonance (EPR) that oxidation of albumin of the healthy subjects with hydrogen peroxide and tert-butyl hydroperoxide led to conformational changes in the microenvironment of the binding sites of maleimide and iodoacetamide spin labels, which interact predominantly with the thiol group of Cys34. abstract: As a carrier of many biologically active compounds, blood is exposed to oxidants to a greater extent than the intracellular environment. Serum albumin plays a key role in antioxidant defence under both normal and oxidative stress conditions. This review evaluates data published in the literature and from our own research on the mechanisms of the enzymatic and non-enzymatic activities of albumin that determine its participation in redox modulation of plasma and intercellular fluid. For the first time, the results of numerous clinical, biochemical, spectroscopic and computational experiments devoted to the study of allosteric modulation of the functional properties of the protein associated with its participation in antioxidant defence are analysed. It has been concluded that it is fundamentally possible to regulate the antioxidant properties of albumin with various ligands, and the binding and/or enzymatic features of the protein by changing its redox status. The perspectives for using the antioxidant properties of albumin in practice are discussed. url: https://doi.org/10.3390/antiox9100966 doi: 10.3390/antiox9100966 id: cord-319614-4qi59pbz author: Benej, Martin title: Quantitative Proteomics Reveal Peroxiredoxin Perturbation Upon Persistent Lymphocytic Choriomeningitis Virus Infection in Human Cells date: 2019-10-25 words: 8900 sentences: 479 pages: flesch: 45 cache: ./cache/cord-319614-4qi59pbz.txt txt: ./txt/cord-319614-4qi59pbz.txt summary: Experimental data indicate that during persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate regulatory cellular processes and alter cellular functions that are not critical for survival, but are essential for cell homeostasis. Increased levels of ROS were accompanied by changes in the pattern of telomere restriction fragments (TRFs) in infected cells and mediated activation of hypoxia-inducible transcription factor-1 (HIF-1) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways. These data suggest that LCMV maintains its replication in persistently infected cells by regulating redox signaling through modulation of local levels of H 2 O 2 and subsequent activation of cellular processes that it uses for its own benefit. Notably, the treatment with antioxidants also resulted in reduced levels of viral NP in HeLa, as well as in A549 LCMV-infected cells, suggesting a link between ROS-dependent signaling and virus replication (Figures 7B,D and Supplementary Figure S2B ). abstract: Experimental data indicate that during persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate regulatory cellular processes and alter cellular functions that are not critical for survival, but are essential for cell homeostasis. In order to shed more light on these processes, two-dimensional differential in-gel electrophoresis (2D-DIGE) and MALDI-TOF tandem mass spectrometry were used to determine the proteome response of the HeLa cell line to persistent LCMV infection. Quantitative analysis revealed 24 differentially abundant proteins. Functional analysis showed that LCMV-responsive proteins were primarily involved in metabolism, stress, and the defense response. Among identified proteins, we discovered significant changes for peroxiredoxins, a family of antioxidant enzymes. Decreased amount of these antioxidant proteins correlated with elevation of reactive oxygen species (ROS) in infected cells. Increased levels of ROS were accompanied by changes in the pattern of telomere restriction fragments (TRFs) in infected cells and mediated activation of hypoxia-inducible transcription factor-1 (HIF-1) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways. Moreover, treatment with antioxidants resulted in reduced levels of viral nucleoprotein, indicating a connection between ROS-dependent signaling and viral replication. url: https://www.ncbi.nlm.nih.gov/pubmed/31708904/ doi: 10.3389/fmicb.2019.02438 id: cord-012495-r6nkdeaw author: Bonora, Massimo title: Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology date: 2020-07-04 words: 11954 sentences: 657 pages: flesch: 34 cache: ./cache/cord-012495-r6nkdeaw.txt txt: ./txt/cord-012495-r6nkdeaw.txt summary: Mitochondrial calcium overload and ROS levels can trigger either the activation of intrinsic apoptotic pathway (left side) through the recruitment of Bcl-2 family proteins at the mitochondria, or permeability transition pore complex (PTPC) formation which could lead to mitochondrial outer membrane permeabilization (MOMP), energetic imbalance, and subsequent release of proapoptotic cofactors from the inter membrane space, such as SMAC/DIABLO, CytC, and ENDOG (right side). MPT is associated with the opening of the mitochondrial permeability transition pore complex (PTPC), a voltage-dependent, high-conductance Mitochondrial calcium overload and ROS levels can trigger either the activation of intrinsic apoptotic pathway (left side) through the recruitment of Bcl-2 family proteins at the mitochondria, or permeability transition pore complex (PTPC) formation which could lead to mitochondrial outer membrane permeabilization (MOMP), energetic imbalance, and subsequent release of proapoptotic cofactors from the inter membrane space, such as SMAC/DIABLO, CytC, and ENDOG (right side). abstract: Mitochondrial permeability transition (MPT) is the sudden loss in the permeability of the inner mitochondrial membrane (IMM) to low-molecular-weight solutes. Due to osmotic forces, MPT is paralleled by a massive influx of water into the mitochondrial matrix, eventually leading to the structural collapse of the organelle. Thus, MPT can initiate outer-mitochondrial-membrane permeabilization (MOMP), promoting the activation of the apoptotic caspase cascade and caspase-independent cell-death mechanisms. The induction of MPT is mostly dependent on mitochondrial reactive oxygen species (ROS) and Ca(2+), but is also dependent on the metabolic stage of the affected cell and signaling events. Therefore, since its discovery in the late 1970s, the role of MPT in human pathology has been heavily investigated. Here, we summarize the most significant findings corroborating a role for MPT in the etiology of a spectrum of human diseases, including diseases characterized by acute or chronic loss of adult cells and those characterized by neoplastic initiation. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408088/ doi: 10.3390/biom10070998 id: cord-307148-k1uo3fxm author: Bradshaw, Patrick C. title: COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm date: 2020-09-09 words: 20788 sentences: 1093 pages: flesch: 40 cache: ./cache/cord-307148-k1uo3fxm.txt txt: ./txt/cord-307148-k1uo3fxm.txt summary: R-BHB activates anti-inflammatory GPR109A signaling and inhibits the NLRP3 inflammasome and histone deacetylases, while a ketogenic diet has been shown to protect mice from influenza virus infection through a protective γδ T cell response and by increasing electron transport chain gene expression to restore energy metabolism. Others have also suggested that increasing systemic ketone levels may aid host defenses against respiratory viral infection, in part, by decreasing inflammation [1, 2] , including a recent comprehensive review [3] , while a clinical trial of the effects of a ketogenic diet on intubated SARS-CoV-2 patients has recently been registered (NCT04358835). Coronaviruses have been shown to increase the oxidation of phospholipids, which stimulate toll-like receptor 4 (TLR4) signaling on macrophages, leading to cytokine production and acute lung injury [163] , so HDAC inhibition with R-BHB appears to be a viable treatment to decrease cytokine levels and inflammation. abstract: Human SARS-CoV-2 infection is characterized by a high mortality rate due to some patients developing a large innate immune response associated with a cytokine storm and acute respiratory distress syndrome (ARDS). This is characterized at the molecular level by decreased energy metabolism, altered redox state, oxidative damage, and cell death. Therapies that increase levels of (R)-beta-hydroxybutyrate (R-BHB), such as the ketogenic diet or consuming exogenous ketones, should restore altered energy metabolism and redox state. R-BHB activates anti-inflammatory GPR109A signaling and inhibits the NLRP3 inflammasome and histone deacetylases, while a ketogenic diet has been shown to protect mice from influenza virus infection through a protective γδ T cell response and by increasing electron transport chain gene expression to restore energy metabolism. During a virus-induced cytokine storm, metabolic flexibility is compromised due to increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that damage, downregulate, or inactivate many enzymes of central metabolism including the pyruvate dehydrogenase complex (PDC). This leads to an energy and redox crisis that decreases B and T cell proliferation and results in increased cytokine production and cell death. It is hypothesized that a moderately high-fat diet together with exogenous ketone supplementation at the first signs of respiratory distress will increase mitochondrial metabolism by bypassing the block at PDC. R-BHB-mediated restoration of nucleotide coenzyme ratios and redox state should decrease ROS and RNS to blunt the innate immune response and the associated cytokine storm, allowing the proliferation of cells responsible for adaptive immunity. Limitations of the proposed therapy include the following: it is unknown if human immune and lung cell functions are enhanced by ketosis, the risk of ketoacidosis must be assessed prior to initiating treatment, and permissive dietary fat and carbohydrate levels for exogenous ketones to boost immune function are not yet established. The third limitation could be addressed by studies with influenza-infected mice. A clinical study is warranted where COVID-19 patients consume a permissive diet combined with ketone ester to raise blood ketone levels to 1 to 2 mM with measured outcomes of symptom severity, length of infection, and case fatality rate. url: https://www.ncbi.nlm.nih.gov/pubmed/33014275/ doi: 10.1155/2020/6401341 id: cord-297469-26d8o1xk author: Choi, Won Hyung title: The Mechanism of Action of Ursolic Acid as a Potential Anti-Toxoplasmosis Agent, and Its Immunomodulatory Effects date: 2019-05-09 words: 6997 sentences: 266 pages: flesch: 43 cache: ./cache/cord-297469-26d8o1xk.txt txt: ./txt/cord-297469-26d8o1xk.txt summary: gondii effects of ursolic acid, and analyzed the production of nitric oxide (NO), reactive oxygen species (ROS), and cytokines through co-cultured immune cells, as well as the expression of intracellular organelles of T. Furthermore, ursolic acid effectively increased the production of NO, ROS, interleukin (IL)-10, IL-12, granulocyte macrophage colony stimulating factor (GM-CSF), and interferon-β, while reducing the expression of IL-1β, IL-6, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1 (TGF-β1) in T. gondii-infected cells were treated with different concentrations (12.5-200 µg/mL) of ursolic acid (UA) and sulfadiazine (SF) at 37 • C for 24 h, respectively; their survival rates were inhibited a dose-dependent manner. We evaluated the effect of ROS and NO production induced by ursolic acid in immune cells infected with T. We evaluated the effect of ROS and NO production induced by ursolic acid in immune cells infected with T. abstract: This study was performed to investigate the mechanism of action of ursolic acid in terms of anti-Toxoplasma gondii effects, including immunomodulatory effects. We evaluated the anti-T. gondii effects of ursolic acid, and analyzed the production of nitric oxide (NO), reactive oxygen species (ROS), and cytokines through co-cultured immune cells, as well as the expression of intracellular organelles of T. gondii. The subcellular organelles and granules of T. gondii, particularly rhoptry protein 18, microneme protein 8, and inner membrane complex sub-compartment protein 3, were markedly decreased when T. gondii was treated with ursolic acid, and their expressions were effectively inhibited. Furthermore, ursolic acid effectively increased the production of NO, ROS, interleukin (IL)-10, IL-12, granulocyte macrophage colony stimulating factor (GM-CSF), and interferon-β, while reducing the expression of IL-1β, IL-6, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1 (TGF-β1) in T. gondii-infected immune cells. These results demonstrate that ursolic acid not only causes anti-T. gondii activity/action by effectively inhibiting the survival of T. gondii and the subcellular organelles of T. gondii, but also induces specific immunomodulatory effects in T. gondii-infected immune cells. Therefore, this study indicates that ursolic acid can be effectively utilized as a potential candidate agent for developing novel anti-toxoplasmosis drugs, and has immunomodulatory activity. url: https://www.ncbi.nlm.nih.gov/pubmed/31075881/ doi: 10.3390/pathogens8020061 id: cord-336201-fl606l3b author: Daryabor, Gholamreza title: The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System date: 2020-07-22 words: 13863 sentences: 715 pages: flesch: 38 cache: ./cache/cord-336201-fl606l3b.txt txt: ./txt/cord-336201-fl606l3b.txt summary: Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. T2DM, the most common form of diabetes (∼90%), is characterized by a systemic inflammatory disease accompanied by insulin resistance (IR) or decreased metabolic response to insulin in several tissues, including the adipose tissue, liver, and skeletal muscle, as well as by reduced insulin synthesis by pancreatic beta cells (4, 5) . During the progression of diabetes, hyperglycemia promotes mitochondrial dysfunction and induces the formation of reactive oxygen species (ROS) that cause oxidative stress in several tissues such as blood vessels and pancreatic beta cells (7) (8) (9) . In addition, the attachment of AGEs to their receptors [e.g., CD36, galectin-3, scavenger receptors types I (SR-A1), and II (SR-A2)] on the surfaces of immune cells in the circulation and tissues activates the expression of pro-inflammatory cytokines and increases free radical generation (18) . abstract: Metabolic abnormalities such as dyslipidemia, hyperinsulinemia, or insulin resistance and obesity play key roles in the induction and progression of type 2 diabetes mellitus (T2DM). The field of immunometabolism implies a bidirectional link between the immune system and metabolism, in which inflammation plays an essential role in the promotion of metabolic abnormalities (e.g., obesity and T2DM), and metabolic factors, in turn, regulate immune cell functions. Obesity as the main inducer of a systemic low-level inflammation is a main susceptibility factor for T2DM. Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. Hyperglycemia and the subsequent inflammation are the main causes of micro- and macroangiopathies in the circulatory system. They also promote the gut microbiota dysbiosis, increased intestinal permeability, and fatty liver disease. The impaired immune system together with metabolic imbalance also increases the susceptibility of patients to several pathogenic agents such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thus, the need for a proper immunization protocol among such patients is granted. The focus of the current review is to explore metabolic and immunological abnormalities affecting several organs of T2DM patients and explain the mechanisms, whereby diabetic patients become more susceptible to infectious diseases. url: https://www.ncbi.nlm.nih.gov/pubmed/32793223/ doi: 10.3389/fimmu.2020.01582 id: cord-003841-7uaj9hmx author: Desmonts de Lamache, D. title: Immuno-modulating properties of Tulathromycin in porcine monocyte-derived macrophages infected with porcine reproductive and respiratory syndrome virus date: 2019-08-23 words: 7978 sentences: 414 pages: flesch: 37 cache: ./cache/cord-003841-7uaj9hmx.txt txt: ./txt/cord-003841-7uaj9hmx.txt summary: The findings indicate that tulathromycin, in the absence of a direct anti-viral effect, is able to restore the phagocytic function and to attenuate the pro-inflammatory phenotype of PRRSV-infected monocyte-derived porcine macrophages. However, Immuno-modulating properties of Tulathromycin in PRRSV-infected porcine monocyte-derived macrophages PRRSV-induced IL-10 inhibition was abolished when the cells were pre-treated with tulathromycin at 2 and 12 hours post infection (Fig 6) . Another set of experiments assessed the effects of PRRSV, and of tulathromycin, on the nonopsonized and opsonized phagocytic functions of MDMs. PRRSV infection significantly Immuno-modulating properties of Tulathromycin in PRRSV-infected porcine monocyte-derived macrophages inhibited both phagocytic functions of the cells (Figs 10 and 11 ). The findings indicate that TUL inhibits PRRSV-induced inflammatory responses in porcine monocyte-derived macrophages and protects against the phagocytic impairment caused by the virus, in the absence of any direct anti-viral effects. abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) is a positive-stranded RNA virus that grows in macrophages and causes acute pneumonia in pigs. PRRSV causes devastating losses to the porcine industry. However, due to its high antigenic variability and poorly understood immunopathogenesis, there is currently no effective vaccine or treatment to control PRRSV infection. The common occurrence of PRRSV infection with bacterial infections as well as its inflammatory-driven pathobiology raises the question of the value of antibiotics with immunomodulating properties for the treatment of the disease it causes. The macrolide antibiotic Tulathromycin (TUL) has been found to exhibit potent anti-inflammatory and immunomodulating properties in cattle and pigs. The aim of this study was to characterize the anti-viral and immunomodulating properties of TUL in PRRSV-infected porcine macrophages. Our findings indicate that blood monocyte-derived macrophages are readily infected by PRRSV and can be used as an effective cellular model to study PRRSV pathogenesis. TUL did not change intracellular or extracellular viral titers, not did it alter viral receptors (CD163 and CD169) expression on porcine macrophages. In contrast, TUL exhibited potent immunomodulating properties, which therefore occurred in the absence of any direct antiviral effects against PRRSV. TUL had an additive effect with PRRSV on the induction of macrophage apoptosis, and inhibited virus-induced necrosis. TUL significantly attenuated PRRSV-induced macrophage pro-inflammatory signaling (CXCL-8 and mitochondrial ROS production) and prevented PRRSV inhibition of non-opsonized and opsonized phagocytic function. Together, these data demonstrate that TUL inhibits PRRSV-induced inflammatory responses in porcine macrophages and protects against the phagocytic impairment caused by the virus. Research in live pigs is warranted to assess the potential clinical benefits of this antibiotic in the context of virally induced inflammation and tissue injury. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707645/ doi: 10.1371/journal.pone.0221560 id: cord-014661-mrh2pbi6 author: Dumitrascu, Georgiana R. title: Critical physiological and pathological functions of Forkhead Box O tumor suppressors date: 2013-12-31 words: 9235 sentences: 419 pages: flesch: 38 cache: ./cache/cord-014661-mrh2pbi6.txt txt: ./txt/cord-014661-mrh2pbi6.txt summary: FOXO proteins are considered unique cellular targets, regulating a wide variety of critical cellular processes, such as: apoptosis, oxidative stress, DNA damage repair, cell cycle, stem cell proliferation and maintenance, metabolism, angiogenesis, vascular tone, cardiovascular development, fertility, immune response and neuronal survival 4, 20 . Hence, the FOXO transcription factors control the expression of a wide spectrum of genes that regulate essential physiological cellular processes, such as cell death/cell survival, cell cycle, cell proliferation, cell differentiation/development, angiogenesis, cell metabolism, stress response and stem cell maintenance 33,34,35,36,37,38 (Figure 2) . Moreover, the consensus FOXO recognition element (FRE) -(G/C)(T/A)AA(C/T)AA -which differs from that of other forkhead proteins, seems to have a very important role in both apoptotic pathways, since matching functional FRE sites have been identified in the promoters of FOXO target genes encoding Fas ligand (FasL), insulin like growth factorbinding protein 1 (IGFBP1), the apoptotic regulator Bcl-2 interacting mediator of cell death (Bim) and others 30 . abstract: The Forkhead box, subclass O (FOXO) proteins are critical transcription factors, ubiquitously expressed in the human body. These proteins are characterized by a remarkable functional diversity, being involved in cell cycle arrest, apoptosis, oxidative detoxification, DNA damage repair, stem cell maintenance, cell differentiation, cell metabolism, angiogenesis, cardiac development, aging and others. In addition, FOXO have critical implications in both normal and cancer stem cell biology. New strategies to modulate FOXO expression and activity may now be developed since the discovery of novel FOXO regulators and non-coding RNAs (such as microRNAs) targeting FOXO transcription factors. This review focuses on physiological and pathological functions of FOXO proteins and on their action as fine regulators of cell fate and context-dependent cell decisions. A better understanding of the structure and critical functions of FOXO transcription factors and tumor suppressors may contribute to the development of novel therapies for cancer and other diseases. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6941590/ doi: 10.15190/d.2013.5 id: cord-001769-2sdg5ll7 author: Guo, Sheng title: The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis date: 2015-09-14 words: 6529 sentences: 330 pages: flesch: 41 cache: ./cache/cord-001769-2sdg5ll7.txt txt: ./txt/cord-001769-2sdg5ll7.txt summary: We show that wild-type mice infected with murine hepatitis virus strain-3 (MHV-3), a model for viral FH, manifest with severe disease and high mortality in association with a significant elevation in IL-1β expression in the serum and liver. Further experiments show that mice deficient of p47 (phox), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit that controls acute ROS production, present with reductions in NLRP3 inflammasome activation and subsequent IL-1β secretion during viral infection, which appears to be responsible for acquiring resilience to viral FH. The hallmarks of MHV-3-induced FH in susceptible BALB/cJ and C57BL/6 mice include the appearance of liver sinusoidal thrombosis and hepatocellular necrosis, resulting from over expression of a virus-induced, monocyte/macrophage-specific procoagulant, fibrinogen-like protein-2 (FGL2). abstract: Viral fulminant hepatitis (FH) is a severe disease with high mortality resulting from excessive inflammation in the infected liver. Clinical interventions have been inefficient due to the lack of knowledge for inflammatory pathogenesis in the virus-infected liver. We show that wild-type mice infected with murine hepatitis virus strain-3 (MHV-3), a model for viral FH, manifest with severe disease and high mortality in association with a significant elevation in IL-1β expression in the serum and liver. Whereas, the viral infection in IL-1β receptor-I deficient (IL-1R1 (-/-)) or IL-1R antagonist (IL-1Ra) treated mice, show reductions in virus replication, disease progress and mortality. IL-1R1 deficiency appears to debilitate the virus-induced fibrinogen-like protein-2 (FGL2) production in macrophages and CD45(+)Gr-1(high) neutrophil infiltration in the liver. The quick release of reactive oxygen species (ROS) by the infected macrophages suggests a plausible viral initiation of NLRP3 inflammasome activation. Further experiments show that mice deficient of p47 (phox), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit that controls acute ROS production, present with reductions in NLRP3 inflammasome activation and subsequent IL-1β secretion during viral infection, which appears to be responsible for acquiring resilience to viral FH. Moreover, viral infected animals in deficiencies of NLRP3 and Caspase-1, two essential components of the inflammasome complex, also have reduced IL-1β induction along with ameliorated hepatitis. Our results demonstrate that the ROS/NLRP3/IL-1β axis institutes an essential signaling pathway, which is over activated and directly causes the severe liver disease during viral infection, which sheds light on development of efficient treatments for human viral FH and other severe inflammatory diseases. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569300/ doi: 10.1371/journal.ppat.1005155 id: cord-262759-ec2c25q3 author: Hsieh, Yi-Ting title: Glucose-6-Phosphate Dehydrogenase (G6PD)-Deficient Epithelial Cells Are Less Tolerant to Infection by Staphylococcus aureus date: 2013-11-04 words: 4838 sentences: 223 pages: flesch: 40 cache: ./cache/cord-262759-ec2c25q3.txt txt: ./txt/cord-262759-ec2c25q3.txt summary: The impairment of ROS removal is predicted to enhance apoptotic activity in G6PD-deficient cells, and this enhanced apoptosis was observed by annexin V/PI staining under a confocal fluorescence microscope and quantified by flow cytometry. We hypothesized that G6PD-deficient cells are less tolerant to oxidative stress upon bacterial infection, leading to the accumulation of more intracellular ROS when compared to the control scramble cells. To determine whether the reduced ROS accumulation and apoptotic activity, particularly in G6PD-deficient cells, was due to deceased αhemolysin expression upon VRSA infection in the presence of vancomycin, the production of intracellular ROS and cell apoptosis when the α-hemolysin inhibitor Oroxylin A was added to the media was quantified by flow cytometry. Our results presented here indicate that expression of active caspase-9, as well as the downstream caspase-3, was much higher in G6PD-deficient cells than in control scramble cells upon VRSA infection, suggesting that mitochondrial dysfunction may be the major cause of the increase in cell apoptosis (Figure 4) . abstract: Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway and provides reducing energy to all cells by maintaining redox balance. The most common clinical manifestations in patients with G6PD deficiency are neonatal jaundice and acute hemolytic anemia. The effects of microbial infection in patients with G6PD deficiency primarily relate to the hemolytic anemia caused by Plasmodium or viral infections and the subsequent medication that is required. We are interested in studying the impact of bacterial infection in G6PD-deficient cells. G6PD knock down A549 lung carcinoma cells, together with the common pathogen Staphylococcus aureus, were employed in our cell infection model. Here, we demonstrate that a lower cell viability was observed among G6PD-deficient cells when compared to scramble controls upon bacterial infection using the MTT assay. A significant increase in the intracellular ROS was detected among S. aureus-infected G6PD-deficient cells by observing dichlorofluorescein (DCF) intensity within cells under a fluorescence microscope and quantifying this signal using flow cytometry. The impairment of ROS removal is predicted to enhance apoptotic activity in G6PD-deficient cells, and this enhanced apoptosis was observed by annexin V/PI staining under a confocal fluorescence microscope and quantified by flow cytometry. A higher expression level of the intrinsic apoptotic initiator caspase-9, as well as the downstream effector caspase-3, was detected by Western blotting analysis of G6PD-deficient cells following bacterial infection. In conclusion, we propose that bacterial infection, perhaps the secreted S. aureus α-hemolysin in this case, promotes the accumulation of intracellular ROS in G6PD-deficient cells. This would trigger a stronger apoptotic activity through the intrinsic pathway thereby reducing cell viability when compared to wild type cells. url: https://www.ncbi.nlm.nih.gov/pubmed/24223971/ doi: 10.1371/journal.pone.0079566 id: cord-288238-36hiiw91 author: Keshavarz, Mohsen title: Metabolic host response and therapeutic approaches to influenza infection date: 2020-03-05 words: 8134 sentences: 425 pages: flesch: 32 cache: ./cache/cord-288238-36hiiw91.txt txt: ./txt/cord-288238-36hiiw91.txt summary: It is also reported that influenza infection significantly increases ROS production by inducing Nox4, and the proliferation of this virus in lung epithelial cells is dependent on redox-sensitive pathways activated by Nox4-derived ROS [16] . IFN can also exert its function on metabolic changes by producing several mediators including indoleamine-2,3-dioxygenase (IDO) and nitric oxide (NO), both of which appear to have either an inducible or an inhibitory role in viral replication [33] . In addition, increased temperature of cells during infection (which could be the result of virus replication and fever) causes heat stress which in turn can considerably downregulate carnitine palmitoyltransferase II (CPT II) activity and reduce the β-oxidation and ATP levels in fibroblasts of influenza-associated encephalopathy patients and healthy volunteers [110] . Through enhancing the activity of the mTORC1 complex, the influenza virus strengthens several metabolic pathways, including glycolysis, glutaminolysis, pentose phosphate, and fatty acid synthesis, to provide more ATP and structural materials for viral replication. abstract: Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid β-oxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways. url: https://www.ncbi.nlm.nih.gov/pubmed/32161622/ doi: 10.1186/s11658-020-00211-2 id: cord-295459-ffi1043k author: Khan, Naseem Ahmed title: Respiratory Syncytial Virus-Induced Oxidative Stress Leads to an Increase in Labile Zinc Pools in Lung Epithelial Cells date: 2020-05-27 words: 6785 sentences: 345 pages: flesch: 54 cache: ./cache/cord-295459-ffi1043k.txt txt: ./txt/cord-295459-ffi1043k.txt summary: Small interfering RNA (siRNA)-mediated knockdown of the ubiquitous zinc uptake transporter ZIP1 suggests that labile zinc levels are increased due to the increased uptake by RSV-infected cells as an antiviral response. Our results suggest that zinc homeostasis plays a critical role in the host response to RSV infection by regulating oxidative stress and inhibiting virus replication. As with A549 cells, we observed a time-dependent increase in labile zinc levels in SAECs infected with RSV without any effect on cell viability ( Fig. 2A and B) . To further confirm the role of oxidative stress in RSV infection, cells infected with RSV were treated with 300 M H 2 O 2 (one of the ROS) and virus titers were measured at 24 h p.i. As observed in the case of zinc chelation, addition of H 2 O 2 led to a modest but significant increase in RSV titers at 24 h p.i. abstract: Zinc supplementation in cell culture has been shown to inhibit various viruses, like herpes simplex virus, rotavirus, severe acute respiratory syndrome (SARS) coronavirus, rhinovirus, and respiratory syncytial virus (RSV). However, whether zinc plays a direct antiviral role in viral infections and whether viruses have adopted strategies to modulate zinc homeostasis have not been investigated. Results from clinical trials of zinc supplementation in infections indicate that zinc supplementation may be beneficial in a pathogen- or disease-specific manner, further underscoring the importance of understanding the interaction between zinc homeostasis and virus infections at the molecular level. We investigated the effect of RSV infection on zinc homeostasis and show that RSV infection in lung epithelial cells leads to modulation of zinc homeostasis. The intracellular labile zinc pool increases upon RSV infection in a multiplicity of infection (MOI)-dependent fashion. Small interfering RNA (siRNA)-mediated knockdown of the ubiquitous zinc uptake transporter ZIP1 suggests that labile zinc levels are increased due to the increased uptake by RSV-infected cells as an antiviral response. Adding zinc to culture medium after RSV infection led to significant inhibition of RSV titers, whereas depletion of zinc by a zinc chelator, N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN) led to an increase in RSV titers. The inhibitory effect of zinc was specific, as other divalent cations had no effect on RSV titers. Both RSV infection and zinc chelation by TPEN led to reactive oxygen species (ROS) induction, whereas addition of zinc blocked ROS induction. These results suggest a molecular link between RSV infection, zinc homeostasis, and oxidative-stress pathways and provide new insights for developing strategies to counter RSV infection. IMPORTANCE Zinc deficiency rates in developing countries range from 20 to 30%, and zinc supplementation trials have been shown to correct clinical manifestations attributed to zinc deficiency, but the outcomes in the case of respiratory infections have been inconsistent. We aimed at understanding the role of zinc homeostasis in respiratory syncytial virus (RSV) infection. Infection of lung epithelial cell lines or primary small-airway epithelial cells led to an increase in labile zinc pools, which was due to increased uptake of zinc. Zinc supplementation inhibited RSV replication, whereas zinc chelation had an opposing effect, leading to increases in RSV titers. Increases in labile zinc in RSV-infected cells coincided with induction of reactive oxygen species (ROS). Both zinc depletion and addition of exogenous ROS led to enhanced RSV infection, whereas addition of the antioxidant inhibited RSV, suggesting that zinc is part of an interplay between RSV-induced oxidative stress and the host response to maintain redox balance. url: https://doi.org/10.1128/msphere.00447-20 doi: 10.1128/msphere.00447-20 id: cord-291559-h6czy5bh author: Koirala, Prashamsa title: Recent advances in pharmacological research on Ecklonia species: a review date: 2017-08-24 words: 12240 sentences: 567 pages: flesch: 34 cache: ./cache/cord-291559-h6czy5bh.txt txt: ./txt/cord-291559-h6czy5bh.txt summary: A study investigated the protective effect of ES in alcoholic fatty liver and found that ES treatment suppressed adipogenesis and increased the expression of fatty acid oxidation-related genes, e.g., peroxisome proliferator-activated receptor (PPAR)-a and CPT-1, but decreased the expression of sterol regulatory element-binding protein (SREBP)-1, a triglyceride (TG) synthesis-related gene, suggesting that ES extract could be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver (Bang et al. Fucoidan extracted from EC exhibited prominent effects on peroxyl radical scavenging activity and 2, 2 0 -azobisdihydrochloride-induced oxidative stress in Vero cells and reduced ROS generation, lipid peroxidation, and cell death in a zebrafish model, proving its antioxidant capacities in vitro and in vivo despite being neither a polyphenol nor a flavonoid. Dieckol, isolated from the edible brown algae Ecklonia cava, induces apoptosis of ovarian cancer cells and inhibits tumor xenograft growth abstract: The genus Ecklonia (Lessoniaceae, Phaeophyceae), commonly called kelp (brown algae), is abundant on the coasts of Japan and Korea. During the past few decades, Ecklonia species have received tremendous attention for their wide range of therapeutic properties and multiple health benefits, such as great nutritional value and being rich in vitamins, minerals, dietary fiber, proteins, and polysaccharides. Several novel functional ingredients with diversified biological activities have been isolated and possess antimicrobial, antiviral, hepatoprotective, cardioprotective, anti-inflammatory, neuroprotective, anticarcinogenic, immunomodulatory, hypolipidemic, anti-diabetic, and antioxidant therapeutic properties. The present review discusses the phytochemical, pharmacological, therapeutic, nutritional, and health benefits of different species of genus Ecklonia, as well as their use in the prevention of disease and maintenance of good health. url: https://doi.org/10.1007/s12272-017-0948-4 doi: 10.1007/s12272-017-0948-4 id: cord-273093-u79r80ip author: Laforge, Mireille title: Tissue damage from neutrophil-induced oxidative stress in COVID-19 date: 2020-07-29 words: 1348 sentences: 71 pages: flesch: 35 cache: ./cache/cord-273093-u79r80ip.txt txt: ./txt/cord-273093-u79r80ip.txt summary: The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. By producing excessive ROS, deregulated neutrophils can spread a local inflammatory response so that it becomes systemic, which explains why they have been involved The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. In conclusion, the presence of oxidative stress markers (for example, lipid peroxidation, rTEM and a high neutrophil to lymphocyte ratio) in patients with COVID-19 may help to identify high-risk individuals early in the course of the disease and prevent their sudden deterioration. abstract: The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. We suggest that free radical scavengers could be beneficial for the most vulnerable patients. url: https://doi.org/10.1038/s41577-020-0407-1 doi: 10.1038/s41577-020-0407-1 id: cord-017817-ztp7w9yh author: Land, Walter Gottlieb title: Cell-Autonomous (Cell-Intrinsic) Stress Responses date: 2018-03-28 words: 17727 sentences: 855 pages: flesch: 40 cache: ./cache/cord-017817-ztp7w9yh.txt txt: ./txt/cord-017817-ztp7w9yh.txt summary: Autophagy is an evolutionarily highly conserved self-digestive process in response to environmental stress to eukaryotic cells, by which cytoplasmic components such as defective/damaged or redundant organelles or protein aggregates are delivered to the lysosome for recycling and degradation. More recent studies then revealed that these transcription factors, notably Nrf2, are activated by Keap1 as the primary negative regulator of Nrf2, that is, a molecule that simultaneously operates as a sensor protein able to perceive dyshomeostatic Subclass IIC-4 DAMPs, for example, in terms of redox changes reflecting electrophilic stress. Strikingly, a complex relationship reportedly exists between autophagy and DAMPs in cellular adaption to stress and injury and cell death characterized by a crosstalk between autophagy induction and secretion or release of DAMPs. In fact, growing evidence indicates that autophagic mechanisms are involved in regulating release and degradation of DAMPs including CALR, HMGB1, ATP, and DNA in several cell types [37, 148, 175] . abstract: In this chapter, the role of cell-intrinsic stress responses is examined which include autophagic processes, the oxidative stress response, the heat shock response, the unfolded proteins response, and the DNA damage response. Autophagy (macroautophagy, microautophagy, and chaperone-mediated autophagy) is a self-digestive process in response to environmental stress to eukaryotic cells, by which cytoplasmic components are delivered to the lysosome for recycling and degradation. The oxidative stress response is directed against any oxidative stress and is mediated by antioxidative defense systems including antioxidant enzymes such as superoxide dismutase, detoxifying enzymes such as glutathione peroxidase, and energy-dependent efflux pumps. The heat shock response is induced upon exposure of cells to any stress condition and characterized by emission of heat shock proteins which operate as DAMPs to maintain and restore homeostasis. The unfolded protein response is induced by any stress of the endoplasmic reticulum that is perceived by three sensor molecules. Under remediable endoplasmic reticulum stress conditions, the sensors trigger signalling pathways to resolve this stress. However, in severe irremediable endoplasmic reticulum stress, the unfolded protein response may lead to pro-inflammatory and pro-apoptotic responses resulting in regulated cell death. Finally, the DNA damage response is induced by any DNA damage that occurs in a variety of exogenous and endogenous conditions. When successful, this stress response leads to DNA repair and is associated with the emission of various DAMPs which contribute to restoration of homeostasis. When unsuccessful, the DNA damage response, like the unsuccessful unfolded protein response, can result in regulated cell death, either in form of apoptosis or necrosis. Together, the ultimate goal of all the stress responses is to maintain cellular homeostasis and ensure cell integrity. When they fail, the incidence of regulated cell death is frequently observed. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122488/ doi: 10.1007/978-3-319-78655-1_18 id: cord-320591-re99v1qt author: Le, Thanh Ninh title: Bioactive Compounds and Bioactivities of Brassica oleracea L. var. Italica Sprouts and Microgreens: An Updated Overview from a Nutraceutical Perspective date: 2020-07-27 words: 8182 sentences: 395 pages: flesch: 34 cache: ./cache/cord-320591-re99v1qt.txt txt: ./txt/cord-320591-re99v1qt.txt summary: Particularly, these studies mostly focused on the antioxidant and anticancer activities of broccoli sprouts and microgreens owing to the functions of glucosinolates and phenolic compounds (Tables 4 and 5 ). Particularly, these studies mostly focused on the antioxidant and anticancer activities of broccoli sprouts and microgreens owing to the functions of glucosinolates and phenolic compounds (Tables 4 and 5 ). In summary, previous studies showed that broccoli sprout extracts rich in vitamins, carotenoids, and phenolic compounds showed very high antioxidant activity in both in vitro and in vivo tests (Table 4) . Moreover, the previous studies have focused on several biological activities of broccoli seedlings, such as antioxidant, anticancer, antimicrobial, and anti-inflammatory, as well as the potentially beneficial effects for patients with cancers, diabetes, and obesity. abstract: Sprouts and microgreens, the edible seedlings of vegetables and herbs, have received increasing attention in recent years and are considered as functional foods or superfoods owing to their valuable health-promoting properties. In particular, the seedlings of broccoli (Brassica oleracea L. var. Italica) have been highly prized for their substantial amount of bioactive constituents, including glucosinolates, phenolic compounds, vitamins, and essential minerals. These secondary metabolites are positively associated with potential health benefits. Numerous in vitro and in vivo studies demonstrated that broccoli seedlings possess various biological properties, including antioxidant, anticancer, anticancer, antimicrobial, anti-inflammatory, anti-obesity and antidiabetic activities. The present review summarizes the updated knowledge about bioactive compounds and bioactivities of these broccoli products and discusses the relevant mechanisms of action. This review will serve as a potential reference for food selections of consumers and applications in functional food and nutraceutical industries. url: https://www.ncbi.nlm.nih.gov/pubmed/32727144/ doi: 10.3390/plants9080946 id: cord-032561-x3qbqy69 author: Liu, Gengqi title: Stimulus-Responsive Nanomedicines for Disease Diagnosis and Treatment date: 2020-09-02 words: 25208 sentences: 1664 pages: flesch: 46 cache: ./cache/cord-032561-x3qbqy69.txt txt: ./txt/cord-032561-x3qbqy69.txt summary: demonstrated that nanodrug carriers with diselenides could release more drugs using poly (ester carbamate) triblock copolymers (PAUR-Se-Se) with Se-Se bonds compared with poly (ester carbamate) triblock copolymers (PAUR-S-S) [54, 55] Thioether Selenium Tellurium Besides the development of drug delivery systems, pH-responsive systems can also be used for tumor detection and image-guided surgery [46] . demonstrated that nanodrug carriers with diselenides could release more drugs using poly (ester carbamate) triblock copolymers (PAUR-Se-Se) with Se-Se bonds compared with poly (ester carbamate) triblock copolymers (PAUR-S-S) [65] PBA/PBE Besides the development of drug delivery systems, pH-responsive systems can also be used for tumor detection and image-guided surgery [46] . Therefore, pH responsive system can be combined with other stimulus conditions such as light, redox, enzymes and others with the aim of improved selectivity for drug release in diseased tissues [47, 48] . In addition to photothermal therapy and PDT, light-responsive strategies have also been applied in the design of prodrug systems and drug delivery carriers. abstract: Stimulus-responsive drug delivery systems generally aim to release the active pharmaceutical ingredient (API) in response to specific conditions and have recently been explored for disease treatments. These approaches can also be extended to molecular imaging to report on disease diagnosis and management. The stimuli used for activation are based on differences between the environment of the diseased or targeted sites, and normal tissues. Endogenous stimuli include pH, redox reactions, enzymatic activity, temperature and others. Exogenous site-specific stimuli include the use of magnetic fields, light, ultrasound and others. These endogenous or exogenous stimuli lead to structural changes or cleavage of the cargo carrier, leading to release of the API. A wide variety of stimulus-responsive systems have been developed—responsive to both a single stimulus or multiple stimuli—and represent a theranostic tool for disease treatment. In this review, stimuli commonly used in the development of theranostic nanoplatforms are enumerated. An emphasis on chemical structure and property relationships is provided, aiming to focus on insights for the design of stimulus-responsive delivery systems. Several examples of theranostic applications of these stimulus-responsive nanomedicines are discussed. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504550/ doi: 10.3390/ijms21176380 id: cord-313918-uv9xdp5f author: Marí, Montserrat title: Mitochondrial Glutathione: Recent Insights and Role in Disease date: 2020-09-24 words: 10385 sentences: 524 pages: flesch: 31 cache: ./cache/cord-313918-uv9xdp5f.txt txt: ./txt/cord-313918-uv9xdp5f.txt summary: Abbreviations 2-oxoglutarate carrier (OGC; SLC25A11); adenine nucleotide translocator (ANT); alcoholic liver disease (ALD); alcoholic steatohepatitis (ASH); Alzheimer''s disease (AD); amyloid beta peptides (Aβ); amyloid precursor protein/presenilin 1 (APP/PS1); amyotrophic lateral sclerosis (ALS); Cu/Zn-superoxide dismutase (SOD1); diabetic nephropathy (DN); electron transport chain (ETC); endoplasmic reticulum (ER); free cholesterol (FC); glyoxalase II (GLO2); Glutathione (GSH); glutathione disulfide (GSSG); glutathione reductase (GR); glutathione S-transferase (GST); GSH ethyl ester (GEE); GSH peroxidases (GPx); hepatic steatosis (HS); metabolic associated fatty liver disease (MAFLD); mitochondrial dicarboxylate carrier (DIC; SLC25A10); mitochondrial glutathione (mGSH); mitochondrial NADP+-dependent isocitrate dehydrogenase (IDPm); mitochondrial permeability transition (MPT); non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); Parkinson''s disease (PD); peroxiredoxins (Prx); protein disulfide isomerase (PDI); reactive oxygen species (ROS); S-adenosyl-l-methionine (SAM); S-d-lactoylglutathione (SLG); sterol regulatory element binding protein 2 (SREBP-2); thioredoxin 2/thioredoxin reductase 2 (Trx2/TrxR2); tumor necrosis factor (TNF). abstract: Mitochondria are the main source of reactive oxygen species (ROS), most of them deriving from the mitochondrial respiratory chain. Among the numerous enzymatic and non-enzymatic antioxidant systems present in mitochondria, mitochondrial glutathione (mGSH) emerges as the main line of defense for maintaining the appropriate mitochondrial redox environment. mGSH’s ability to act directly or as a co-factor in reactions catalyzed by other mitochondrial enzymes makes its presence essential to avoid or to repair oxidative modifications that can lead to mitochondrial dysfunction and subsequently to cell death. Since mitochondrial redox disorders play a central part in many diseases, harboring optimal levels of mGSH is vitally important. In this review, we will highlight the participation of mGSH as a contributor to disease progression in pathologies as diverse as Alzheimer’s disease, alcoholic and non-alcoholic steatohepatitis, or diabetic nephropathy. Furthermore, the involvement of mitochondrial ROS in the signaling of new prescribed drugs and in other pathologies (or in other unmet medical needs, such as gender differences or coronavirus disease of 2019 (COVID-19) treatment) is still being revealed; guaranteeing that research on mGSH will be an interesting topic for years to come. url: https://www.ncbi.nlm.nih.gov/pubmed/32987701/ doi: 10.3390/antiox9100909 id: cord-335676-7ak53hto author: Meftahi, Gholam Hossein title: The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of “inflame-aging” date: 2020-06-11 words: 8208 sentences: 435 pages: flesch: 43 cache: ./cache/cord-335676-7ak53hto.txt txt: ./txt/cord-335676-7ak53hto.txt summary: It seems that "cytokine storm" phenomenon in elderly patients with severe COVID-19 infection, is associated with many age-related pathophysiologic processes, including alteration of angiotensin-converting enzyme 2 (ACE2) receptor expression [9] , excess ROS production [10] , alteration of autophagy [11] , the inflammatory phenotype of senescent cell activity, particularly adipose tissue [12] , and immune-senescence [13] , as well as lack of vitamin D content [14] . As shown in Fig. 2 , several factors, including alteration of ACE2 receptor expression, excess reactive oxygen species (ROS) production, senescent adipocytes activity, alteration of autophagy and mitophagy, immune-senescent, as well as vitamin D (VD) deficiency, may associate "inflame-aging" to cytokine storm in elderly patients of COVID-19. Furthermore, the lack of VD in aged subjects is associated with the pro-inflammatory phenotype of immune cells, leading to likely increasing the risk of elderly adults with chronic mild inflammation condition [122] . abstract: PURPOSE: Novel Coronavirus disease 2019 (COVID-19), is an acute respiratory distress syndrome (ARDS), which is emerged in Wuhan, and recently become worldwide pandemic. Strangely, ample evidences have been shown that the severity of COVID-19 infections varies widely from children (asymptomatic), adults (mild infection), as well as elderly adults (deadly critical). It has proven that COVID-19 infection in some elderly critical adults leads to a cytokine storm, which is characterized by severe systemic elevation of several pro-inflammatory cytokines. Then, a cytokine storm can induce edematous, ARDS, pneumonia, as well as multiple organ failure in aged patients. It is far from clear till now why cytokine storm induces in only COVID-19 elderly patients, and not in young patients. However, it seems that aging is associated with mild elevated levels of local and systemic pro-inflammatory cytokines, which is characterized by “inflamm-aging”. It is highly likely that “inflamm-aging” is correlated to increased risk of a cytokine storm in some critical elderly patients with COVID-19 infection. METHODS: A systematic search in the literature was performed in PubMed, Scopus, Embase, Cochrane Library, Web of Science, as well as Google Scholar pre-print database using all available MeSH terms for COVID-19, Coronavirus, SARS-CoV-2, senescent cell, cytokine storm, inflame-aging, ACE2 receptor, autophagy, and Vitamin D. Electronic database searches combined and duplicates were removed. RESULTS: The aim of the present review was to summarize experimental data and clinical observations that linked the pathophysiology mechanisms of “inflamm-aging”, mild-grade inflammation, and cytokine storm in some elderly adults with severe COVID-19 infection. url: https://doi.org/10.1007/s00011-020-01372-8 doi: 10.1007/s00011-020-01372-8 id: cord-001347-ssrs0cwf author: Michaelis, Martin title: Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A date: 2014-06-23 words: 1995 sentences: 125 pages: flesch: 43 cache: ./cache/cord-001347-ssrs0cwf.txt txt: ./txt/cord-001347-ssrs0cwf.txt summary: title: Effects of flavonoid-induced oxidative stress on anti-H5N1 influenza a virus activity exerted by baicalein and biochanin A Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Next, we investigated whether the reduction of baicalein-or biochanin A-induced enhanced ROS levels in H5N1-infected A549 cells by NAC influences the antiviral effects of these flavonoids. Notably, NAC also inhibited baicalein-and biochanin A-induced oxidative stress in H5N1-infected primary human monocytederived macrophages but did not affect H5N1 replication in this cell type (Figure 3 ). These findings emphasise that flavonoids, a class of natural compounds known to exert anti-influenza effects [16] [17] [18] [19] 28] , induce a complex range of pharmacological actions by which they modify influenza A virus replication including highly pathogenic avian H5N1 strains. Differential antiviral and anti-inflammatory mechanisms of the flavonoids biochanin A and baicalein in H5N1 influenza A virus-infected cells abstract: BACKGROUND: Different flavonoids are known to interfere with influenza A virus replication. Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Here, we investigated the effects of both compounds on H5N1-induced reactive oxygen species (ROS) formation and the role of ROS formation during H5N1 replication. FINDINGS: Baicalein and biochanin A enhanced H5N1-induced ROS formation in A549 cells and primary human monocyte-derived macrophages. Suppression of ROS formation induced by baicalein and biochanin A using the antioxidant N-acetyl-L-cysteine strongly increased the anti-H5N1 activity of both compounds in A549 cells but not in macrophages. CONCLUSIONS: These findings emphasise that flavonoids induce complex pharmacological actions some of which may interfere with H5N1 replication while others may support H5N1 replication. A more detailed understanding of these actions and the underlying structure-activity relationships is needed to design agents with optimised anti-H5N1 activity. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080993/ doi: 10.1186/1756-0500-7-384 id: cord-289034-yl3emjef author: Moro, Loredana title: Mitochondria at the Crossroads of Physiology and Pathology date: 2020-06-24 words: 3790 sentences: 197 pages: flesch: 27 cache: ./cache/cord-289034-yl3emjef.txt txt: ./txt/cord-289034-yl3emjef.txt summary: Two mitochondria quality control mechanisms are in place to meet the functional needs of any given cell under different physiological and pathological conditions: (a) mitochondrial biogenesis, fusion and fission [4] [5] [6] ; (b) mitophagy [7, 8] . The second mechanism, mitophagy, is a specific form of autophagy that removes damaged mitochondria and reduces the mitochondrial mass upon microenvironmental stresses, such as hypoxia and nutrient starvation, promoting cell survival [11] . In this context, mutations in three TCA cycle enzymes, namely succinate dehydrogenase, fumarate hydratase and isocitrate dehydrogenase, have been shown to play a causal role in carcinogenesis [54, 55] , thus providing compelling evidence for the involvement of mitochondrial metabolic alterations as cancer drivers. Mitochondrial dysfunction is implicated in several pathological conditions, ranging from neurodegenerative and cardiovascular diseases, to aging, cancer and inflammation. abstract: Mitochondria play a crucial role in cell life and death by regulating bioenergetic and biosynthetic pathways. They are able to adapt rapidly to different microenvironmental stressors by accommodating the metabolic and biosynthetic needs of the cell. Mounting evidence places mitochondrial dysfunction at the core of several diseases, notably in the context of pathologies of the cardiovascular and central nervous system. In addition, mutations in some mitochondrial proteins are bona fide cancer drivers. Better understanding of the functions of these multifaceted organelles and their components may finetune our knowledge on the molecular bases of certain diseases and suggest new therapeutic avenues. url: https://doi.org/10.3390/jcm9061971 doi: 10.3390/jcm9061971 id: cord-048478-ftlb5b95 author: Mroczek, Seweryn title: Apoptotic signals induce specific degradation of ribosomal RNA in yeast date: 2008-04-01 words: 9796 sentences: 418 pages: flesch: 45 cache: ./cache/cord-048478-ftlb5b95.txt txt: ./txt/cord-048478-ftlb5b95.txt summary: One striking characteristic, which accompanies apoptosis in both vertebrates and yeast, is a fragmentation of cellular DNA and mammalian apoptosis is often associated with degradation of different RNAs. We show that in yeast exposed to stimuli known to induce apoptosis, such as hydrogen peroxide, acetic acid, hyperosmotic stress and ageing, two large subunit ribosomal RNAs, 25S and 5.8S, became extensively degraded with accumulation of specific intermediates that differ slightly depending on cell death conditions. For example, in metazoans the programmed cell death (PCD) called apoptosis, in addition to irreversible DNA damage, which is considered an apoptotic hallmark (3) , also involves specific cleavage of several RNA species, including 28S rRNA, U1 snRNA or Ro RNP-associated Y RNAs (4) . Together, this strongly suggests that rRNA degradation observed in apoptotic and oxidative stress conditions is not simply a result of cell death but is produced in the process that requires enzymatic activity and functional cellular machinery. abstract: Organisms exposed to reactive oxygen species, generated endogenously during respiration or by environmental conditions, undergo oxidative stress. Stress response can either repair the damage or activate one of the programmed cell death (PCD) mechanisms, for example apoptosis, and finally end in cell death. One striking characteristic, which accompanies apoptosis in both vertebrates and yeast, is a fragmentation of cellular DNA and mammalian apoptosis is often associated with degradation of different RNAs. We show that in yeast exposed to stimuli known to induce apoptosis, such as hydrogen peroxide, acetic acid, hyperosmotic stress and ageing, two large subunit ribosomal RNAs, 25S and 5.8S, became extensively degraded with accumulation of specific intermediates that differ slightly depending on cell death conditions. This process is most likely endonucleolytic, is correlated with stress response, and depends on the mitochondrial respiratory status: rRNA is less susceptible to degradation in respiring cells with functional defence against oxidative stress. In addition, RNA fragmentation is independent of two yeast apoptotic factors, metacaspase Yca1 and apoptosis-inducing factor Aif1, but it relies on the apoptotic chromatin condensation induced by histone H2B modifications. These data describe a novel phenotype for certain stress- and ageing-related PCD pathways in yeast. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2396418/ doi: 10.1093/nar/gkm1100 id: cord-298265-elbnzgx6 author: Mutua, Victoria title: A Review of Neutrophil Extracellular Traps (NETs) in Disease: Potential Anti-NETs Therapeutics date: 2020-08-01 words: 10404 sentences: 565 pages: flesch: 35 cache: ./cache/cord-298265-elbnzgx6.txt txt: ./txt/cord-298265-elbnzgx6.txt summary: Studies have demonstrated that circulating neutrophils of RA patients are more easily stimulated to NETosis than those from healthy subjects [73, 74] , and as in other autoimmune conditions, NETs act as a source of extracellular autoantigens leading to excessive innate and adaptive immune responses in the joints and subsequent tissue injury [73, 75] . Inhibits ROS production, prevents thrombus formation [190] [191] [192] [193] [194] [195] Nucleases Recombinant human DNase DNA matrixes Reduces neutrophil infiltration, cleaves DNA matrixes [196] [197] [198] [199] [200] [201] [202] [203] [204] [205] [206] [207] Staphylokinase Plasminogen, alpha-defensins Converting NETs to deoxyadenosine mediating death of immune cells [208] [209] [210] [211] Notable compounds Probiotics PKC pathway run a study to evaluate the effect of inhibition of PAD4 in NETosis using an antagomiR-155, a pleiotropic microRNA important in the regulation of immune responses, demonstrating a decreased induction of PAD4 mRNA and subsequent reduced NETs in response to PMA challenge [13] . abstract: Activated neutrophils release neutrophil extracellular traps (NETs) in response to a variety of stimuli. NETosis is driven by protein-arginine deiminase type 4, with the release of intracellular granule components that function by capturing and destroying microbes, including viral, fungal, bacterial, and protozoal pathogens. The positive effects of pathogen control are countered by pro-inflammatory effects as demonstrated in a variety of diseases. Components of NETS are non-specific, and other than controlling microbes, they cause injury to surrounding tissue by themselves or by increasing the pro-inflammatory response. NETs can play a role in enhancement of the inflammation seen in autoimmune diseases including psoriasis, rheumatoid arthritis, and systemic lupus erythematosis. In addition, autoinflammatory diseases such as gout have been associated with NETosis. Inhibition of NETs may decrease the severity of many diseases improving survival. Herein, we describe NETosis in different diseases focusing on the detrimental effect of NETs and outline possible therapeutics that can be used to mitigate netosis. There is a need for more studies and clinical trials on these and other compounds that could prevent or destroy NETs, thereby decreasing damage to patients. url: https://doi.org/10.1007/s12016-020-08804-7 doi: 10.1007/s12016-020-08804-7 id: cord-291190-f6km3c7z author: Nasi, Aikaterini title: Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention date: 2020-06-18 words: 2999 sentences: 155 pages: flesch: 42 cache: ./cache/cord-291190-f6km3c7z.txt txt: ./txt/cord-291190-f6km3c7z.txt summary:  SARS-CoV has been reported to modulate PARP function and thereby NAD+ biosynthesis  Cellular homeostasis and redox imbalances by SARS-CoV2 can cause stress responses  Antioxidants such as NAC could limit ROS mediated tissue damage during COVID-19 Hereby, based on literature review from the current pandemic and previous outbreaks with corona viruses we analyze the impact of the virus infection on cell stress responses and redox balance. PLA2G2D expression was shown to be increased in the lungs of middle aged mice, resulting in decreased survival and impaired T cell responses upon infection with SARS-CoV1 [20] . Interestingly, NAC administration to aged mice, diminished PLAG2D expression in both lung cells and CD11c+ DCs. In addition, increased levels of oxidized phospholipidsare a common feature associated with acute respiratory distress syndrome (ARDS) caused by viruses including SARS and H5N1. abstract: During the current COVID-19 pandemic, a need for evaluation of already available drugs for treatment of the disease is crucial. Hereby, based on literature review from the current pandemic and previous outbreaks with corona viruses we analyze the impact of the virus infection on cell stress responses and redox balance. High levels of mortality are noticed in elderly individuals infected with SARS-CoV2 and during the previous SARS-CoV1 outbreak. Elderly individuals maintain a chronic low level of inflammation which is associated with oxidative stress and inflammatory cytokine production, a condition that increases the severity of viral infections in this population. SARS-CoV2 infection can lead to alterations of redox balance in infected cells through modulation of NAD + biosynthesis, PARP function along with altering proteasome and mitochondrial function in the cell thereby leading to enhanced cell stress responses which further exacerbate inflammation. ROS production can increase IL-6 production and lipid peroxidation resulting in cell damage. Therefore, early treatment with anti-oxidants such as NAC during COVID-19 can be a way to bypass the excessive inflammation and cell damage that lead to severe infection. url: https://www.sciencedirect.com/science/article/pii/S221475002030336X?v=s5 doi: 10.1016/j.toxrep.2020.06.003 id: cord-035015-slgywe0c author: Nunn, Alistair V. W. title: SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing date: 2020-11-09 words: 14660 sentences: 715 pages: flesch: 36 cache: ./cache/cord-035015-slgywe0c.txt txt: ./txt/cord-035015-slgywe0c.txt summary: Data is now showing that COVID-19 patients do have populations of T-cells displaying mitochondrial dysfunction, as well as altered mitochondrial markers in monocyteshinting that immune-metabolic phenotyping could be used to understand disease pathogenesis and possible treatments; this could include targeting mitochondria [32] . The underlying aetiology for "inflammaging" has long thought to be associated with mitochondrial dysfunction as suggested by Nick Lane in 2003 in his "double agent" theory [5] , and is now receiving renewed interest, for instance, in how decreasing mitochondrial function can reduce T-cell function and enhance immune senescence, as mitochondria are pivotal in metabolic reprogramming towards the Warburg effect [40] . Furthermore, as evidence indicates that many viruses, which most likely include SARs-CoV-2, modulate bioenergetics and redox in both the immune system and other cells they infect to enhance their own replication, they could potentially induce excessive stress in these systems if their mitochondria are already sub-optimally functional. abstract: Infection with SARs-COV-2 displays increasing fatality with age and underlying co-morbidity, in particular, with markers of the metabolic syndrome and diabetes, which seems to be associated with a “cytokine storm” and an altered immune response. This suggests that a key contributory factor could be immunosenescence that is both age-related and lifestyle-induced. As the immune system itself is heavily reliant on mitochondrial function, then maintaining a healthy mitochondrial system may play a key role in resisting the virus, both directly, and indirectly by ensuring a good vaccine response. Furthermore, as viruses in general, and quite possibly this new virus, have also evolved to modulate immunometabolism and thus mitochondrial function to ensure their replication, this could further stress cellular bioenergetics. Unlike most sedentary modern humans, one of the natural hosts for the virus, the bat, has to “exercise” regularly to find food, which continually provides a powerful adaptive stimulus to maintain functional muscle and mitochondria. In effect the bat is exposed to regular hormetic stimuli, which could provide clues on how to resist this virus. In this paper we review the data that might support the idea that mitochondrial health, induced by a healthy lifestyle, could be a key factor in resisting the virus, and for those people who are perhaps not in optimal health, treatments that could support mitochondrial function might be pivotal to their long-term recovery. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7649575/ doi: 10.1186/s12979-020-00204-x id: cord-278846-nqj7ctk3 author: Ogger, Patricia P. title: Macrophage metabolic reprogramming during chronic lung disease date: 2020-11-12 words: 10123 sentences: 516 pages: flesch: 31 cache: ./cache/cord-278846-nqj7ctk3.txt txt: ./txt/cord-278846-nqj7ctk3.txt summary: While these initial observations were made during steady state or using in vitro polarised macrophages, recent studies have indicated that during many chronic lung diseases (CLDs), AMs adapt their metabolic profile to fit their local niche. By generating reactive oxygen species (ROS) for pathogen defence, utilising aerobic glycolysis to rapidly generate cytokines, and employing mitochondrial respiration to fuel inflammatory responses, AMs utilise metabolic reprogramming for host defence, although these changes may also support chronic pathology. Indeed, many recent studies have indicated that in chronic lung diseases (CLDs), such as asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF), and during infection such as with Mycobacterium Tuberculosis (Mtb), there are significant alterations in AM metabolic processes and that targeting these pathways could represent an exciting therapeutic approach 6, 7 . Iron metabolism is therefore likely a key pathway in IPF-AMs and targeting it would be a viable option to decrease ROS, oxidative stress and macrophage activation. abstract: Airway macrophages (AMs) play key roles in the maintenance of lung immune tolerance. Tissue tailored, highly specialised and strategically positioned, AMs are critical sentinels of lung homoeostasis. In the last decade, there has been a revolution in our understanding of how metabolism underlies key macrophage functions. While these initial observations were made during steady state or using in vitro polarised macrophages, recent studies have indicated that during many chronic lung diseases (CLDs), AMs adapt their metabolic profile to fit their local niche. By generating reactive oxygen species (ROS) for pathogen defence, utilising aerobic glycolysis to rapidly generate cytokines, and employing mitochondrial respiration to fuel inflammatory responses, AMs utilise metabolic reprogramming for host defence, although these changes may also support chronic pathology. This review focuses on how metabolic alterations underlie AM phenotype and function during CLDs. Particular emphasis is given to how our new understanding of AM metabolic plasticity may be exploited to develop AM-focused therapies. url: https://www.ncbi.nlm.nih.gov/pubmed/33184475/ doi: 10.1038/s41385-020-00356-5 id: cord-323730-5iawbnua author: Ohl, Kim title: Oxidative stress in multiple sclerosis: Central and peripheral mode of action date: 2016-03-31 words: 9168 sentences: 438 pages: flesch: 39 cache: ./cache/cord-323730-5iawbnua.txt txt: ./txt/cord-323730-5iawbnua.txt summary: Whatever the trigger factors for lesion Experimental Neurology 277 (2016) [58] [59] [60] [61] [62] [63] [64] [65] [66] [67] Abbreviations: APCs, antigen-presenting cells; ARE, antioxidant response element; DMF, dimethyl fumarate; FAEs, fumaric acid esters; GSH, glutathione; HO, heme oxygenase; IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; Keap1, Kelch ECH associating protein 1; MDSC, myeloid-derived suppressor cells; MMF, monomethyl fumarate; NQO1, NAD(P)H: quinone oxidoreductase 1; Nrf2, nuclear factor (erythroid-derived 2)-like 2; RNS, reactive nitrogen species; ROS, reactive oxygen species; S1P, sphingosine 1-phosphate; TGF, transforming growth factor; T h , T helper cell; T reg , regulatory T cell; Trx, thioredoxin. Furthermore, redox stress is important for the functional outcome during experimentally-induced adaptive-immunity responses; e.g. in a graft-versus-host disease mouse model, free radical scavenger therapy with NecroX-7 attenuates disease severity, probably via the induction of T reg cells (Im et al., 2015) and oxidative damage regulates antigen-specific T cell responses in agerelated macular degeneration (Cruz-Guilloty et al., 2014) . abstract: Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of multiple sclerosis (MS). Reactive oxygen species (ROS), which if produced in excess lead to oxidative stress, have been implicated as mediators of demyelination and axonal damage in both MS and its animal models. One of the most studied cell populations in the context of ROS-mediated tissue damage in MS are macrophages and their CNS companion, microglia cells. However, and this aspect is less well appreciated, the extracellular and intracellular redox milieu is integral to many processes underlying T cell activation, proliferation and apoptosis. In this review article we discuss how oxidative stress affects central as well as peripheral aspects of MS and how manipulation of ROS pathways can potentially affect the course of the disease. It is our strong belief that the well-directed shaping of ROS pathways has the potential to ameliorate disease progression in MS. url: https://www.ncbi.nlm.nih.gov/pubmed/26626971/ doi: 10.1016/j.expneurol.2015.11.010 id: cord-316244-s5ua0re3 author: Park, Mi Hee title: Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases date: 2016-04-26 words: 19183 sentences: 1015 pages: flesch: 41 cache: ./cache/cord-316244-s5ua0re3.txt txt: ./txt/cord-316244-s5ua0re3.txt summary: PRDX6 is an oxidative stress inducible protein regulated by Nrf2 and activation of the gene expression was observed in mouse lungs by hyperoxia and in cultured lung epithelial cells following treatment with H 2 O 2 or paraquat . One previous study reported that hypoxia increases AR activity in prostate cancer cells, and that PRDX1, which is upregulated by hypoxia, interacts with AR to enhance the expression of androgen-regulated genes (Chhipa, Lee, Onate, Wu, & Ip, 2009; Park et al., 2006) . PRDX2 is overexpressed in colorectal carcinoma tissues compared with the matched non-cancer colorectal mucosa tissues and that expression is positively associated with tumor metastasis and the TNM stage by regulation of oxidation induced apoptosis (Lu et al., 2014a) . Other researchers also demonstrated that PRDX2 knockdown using a lentiviral vector-mediated specific shRNA inhibited cell growth, stimulated apoptosis, and augmented the production of endogenous ROS that led to an altered expression of proteins associated with the Wnt signaling pathway (Lu et al., 2014b) . abstract: Peroxiredoxins (PRDXs) are antioxidant enzymes, known to catalyze peroxide reduction to balance cellular hydrogen peroxide (H(2)O(2)) levels, which are essential for cell signaling and metabolism and act as a regulator of redox signaling. Redox signaling is a critical component of cell signaling pathways that are involved in the regulation of cell growth, metabolism, hormone signaling, immune regulation and variety of other physiological functions. Early studies demonstrated that PRDXs regulates cell growth, metabolism and immune regulation and therefore involved in the pathologic regulator or protectant of several cancers, neurodegenerative diseases and inflammatory diseases. Oxidative stress and antioxidant systems are important regulators of redox signaling regulated diseases. In addition, thiol-based redox systems through peroxiredoxins have been demonstrated to regulate several redox-dependent process related diseases. In this review article, we will discuss recent findings regarding PRDXs in the development of diseases and further discuss therapeutic approaches targeting PRDXs. Moreover, we will suggest that PRDXs could be targets of several diseases and the therapeutic agents for targeting PRDXs may have potential beneficial effects for the treatment of cancers, neurodegenerative diseases and inflammatory diseases. Future research should open new avenues for the design of novel therapeutic approaches targeting PRDXs. url: https://api.elsevier.com/content/article/pii/S0163725816300407 doi: 10.1016/j.pharmthera.2016.03.018 id: cord-331673-xv1tcugl author: Reina, Giacomo title: Hard Nanomaterials in Time of Viral Pandemics date: 2020-07-15 words: 15712 sentences: 976 pages: flesch: 44 cache: ./cache/cord-331673-xv1tcugl.txt txt: ./txt/cord-331673-xv1tcugl.txt summary: For instance, in the case of Herpesviridae and Paramyxoviridae viruses (both enveloped viruses with embedded viral-encoded glycoproteins), AgNPs can effectively reduce their infectivity, by blocking the interaction between the viral particles and the host cells with an antiviral activity strictly dependent on the size and ζ potential of the AgNPs. As a general observation, it was reported that smaller nanoparticles have better antiviral effect. cAgNPs could reduce cytopathic effects induced by RSV and showed efficient antiviral activity against infection by directly inactivating the virus prior to entry into the host cells. have reported that porous AuNPs are able to inhibit influenza A infection more efficiently than nonporous AuNPs. 39 This effect has been associated with the higher surface area of the porous material that favors their interaction with capsids and thus increases their antiviral activity ( Figure 4 ). abstract: [Image: see text] The SARS-Cov-2 pandemic has spread worldwide during 2020, setting up an uncertain start of this decade. The measures to contain infection taken by many governments have been extremely severe by imposing home lockdown and industrial production shutdown, making this the biggest crisis since the second world war. Additionally, the continuous colonization of wild natural lands may touch unknown virus reservoirs, causing the spread of epidemics. Apart from SARS-Cov-2, the recent history has seen the spread of several viral pandemics such as H2N2 and H3N3 flu, HIV, and SARS, while MERS and Ebola viruses are considered still in a prepandemic phase. Hard nanomaterials (HNMs) have been recently used as antimicrobial agents, potentially being next-generation drugs to fight viral infections. HNMs can block infection at early (disinfection, entrance inhibition) and middle (inside the host cells) stages and are also able to mitigate the immune response. This review is focused on the application of HNMs as antiviral agents. In particular, mechanisms of actions, biological outputs, and limitations for each HNM will be systematically presented and analyzed from a material chemistry point-of-view. The antiviral activity will be discussed in the context of the different pandemic viruses. We acknowledge that HNM antiviral research is still at its early stage, however, we believe that this field will rapidly blossom in the next period. url: https://doi.org/10.1021/acsnano.0c04117 doi: 10.1021/acsnano.0c04117 id: cord-271939-m1ko4yal author: Rouco, Lara title: Pursuing the Elixir of Life: In Vivo Antioxidative Effects of Manganosalen Complexes date: 2020-08-10 words: 10266 sentences: 584 pages: flesch: 37 cache: ./cache/cord-271939-m1ko4yal.txt txt: ./txt/cord-271939-m1ko4yal.txt summary: Thus, manganosalen complexes have been shown to exhibit superoxide dismutase, catalase, and glutathione peroxidase activities, and they could potentially facilitate the scavenging of excess reactive oxygen species (ROS), thereby restoring the redox balance in damaged cells and organs. Manganosalen complexes exhibit high SOD, catalase, and peroxidase activities, which has led to their development as catalytic antioxidants [6] [7] [8] [9] [10] 13, [18] [19] [20] [21] 23] , a term used for all cases in which one single molecule of catalyst induces the detoxification of numerous ROS molecules. This manganese complex and the cyclic analogue EUK-207 were used in a study with C57BL/6N Sim middle-age mice [105] , which usually exhibit a dramatic decrease in learning and memory function between 8 and 11 months of age, associated with oxidative protein damage in the brain [106] . Salen-manganese complexes for controlling ROS damage: Neuroprotective effects, antioxidant activity and kinetic studies abstract: Manganosalen complexes are coordination compounds that possess a chelating salen-type ligand, a class of bis-Schiff bases obtained by condensation of salicylaldehyde and a diamine. They may act as catalytic antioxidants mimicking both the structure and the reactivity of the native antioxidant enzymes active site. Thus, manganosalen complexes have been shown to exhibit superoxide dismutase, catalase, and glutathione peroxidase activities, and they could potentially facilitate the scavenging of excess reactive oxygen species (ROS), thereby restoring the redox balance in damaged cells and organs. Initial catalytic studies compared the potency of these compounds as antioxidants in terms of rate constants of the chemical reactivity against ROS, giving catalytic values approaching and even exceeding that of the native antioxidative enzymes. Although most of these catalytic studies lack of biological relevance, subsequent in vitro studies have confirmed the efficiency of many manganosalen complexes in oxidative stress models. These synthetic catalytic scavengers, cheaper than natural antioxidants, have accordingly attracted intensive attention for the therapy of ROS-mediated injuries. The aim of this review is to focus on in vivo studies performed on manganosalen complexes and their activity on the treatment of several pathological disorders associated with oxidative damage. These disorders, ranging from the prevention of fetal malformations to the extension of lifespan, include neurodegenerative, inflammatory, and cardiovascular diseases; tissue injury; and other damages related to the liver, kidney, or lungs. url: https://doi.org/10.3390/antiox9080727 doi: 10.3390/antiox9080727 id: cord-293319-oo0w6faj author: Seo, Youngsik title: Reactive-oxygen-species-mediated mechanism for photoinduced antibacterial and antiviral activities of Ag(3)PO(4) date: 2020-06-11 words: 2918 sentences: 148 pages: flesch: 54 cache: ./cache/cord-293319-oo0w6faj.txt txt: ./txt/cord-293319-oo0w6faj.txt summary: The antibacterial activities against Escherichia coli, Listeria innocua, and Pseudomonas syringae DC3000 in both the absence and presence of Ag(3)PO(4) under dark conditions and in the presence of Ag(3)PO(4) under red-light (625 nm) and blue-light (460 nm) irradiation were examined. The photoinduced enhancement of the Ag(3)PO(4) antibacterial activity under blue-light irradiation is explained by the formation of ROS during the antibacterial action of the Ag(3)PO(4). Moreover, the antiviral activity of Ag(3)PO(4) against amphotropic 10A1 murine leukemia virus enhanced under blue-light irradiation via ROS production. coli in the absence and presence of Ag 3 PO 4 under dark conditions and in the presence of Ag 3 PO 4 under red-light (625 nm) and blue-light (460 nm) irradiation. These data indicate that the antibacterial activity of Ag 3 PO 4 under blue-light irradiation corresponds to the amount of ROS in E. The photoinduced enhancement of the antibacterial and antiviral activities of Ag 3 PO 4 under blue-light irradiation was observed. abstract: Cubic-shaped Ag(3)PO(4) crystals with a mean size of 1 μm were synthesized by a precipitation method from a mixed solution of AgNO(3), Na(2)HPO(4), and triethanolamine. The antibacterial activities against Escherichia coli, Listeria innocua, and Pseudomonas syringae DC3000 in both the absence and presence of Ag(3)PO(4) under dark conditions and in the presence of Ag(3)PO(4) under red-light (625 nm) and blue-light (460 nm) irradiation were examined. The concentrations of reactive oxygen species (ROS) were also measured in the antibacterial action of the Ag(3)PO(4) against Escherichia coli. The photoinduced enhancement of the Ag(3)PO(4) antibacterial activity under blue-light irradiation is explained by the formation of ROS during the antibacterial action of the Ag(3)PO(4). Moreover, the antiviral activity of Ag(3)PO(4) against amphotropic 10A1 murine leukemia virus enhanced under blue-light irradiation via ROS production. These results provide an insight into extended bio-applications of Ag(3)PO(4). url: https://doi.org/10.1186/s40543-020-00220-y doi: 10.1186/s40543-020-00220-y id: cord-268527-wbfnhedy author: Smith, Sylvia B. title: Transient hyperglycosylation of rhodopsin with galactose date: 1991-10-31 words: 8560 sentences: 468 pages: flesch: 58 cache: ./cache/cord-268527-wbfnhedy.txt txt: ./txt/cord-268527-wbfnhedy.txt summary: Following subcellular fractionation of retinas, ConA purified rhodopsin from ROS was applied to one of two additional lectin columns: Ricinus communis agglutinin (RCA) or Griffonia simplicifolia I (GSA). To radiolabel existing galactose moieties on rhodopsin, bovine ROS purified by a discontinuous sucrose density gradient procedure, were subjected to enzymatic treatment with galactose oxidase followed by a reduction with tritium labeled sodium borohydride. In this method, ConA purified rhodopsin or in some cases the clarified extract of ROS from six rat retinas labeled with [35S]methionine was applied to columns of either Ricinus communis agglutinin I (RCA) or GrifSonia simplicijolia I (GSA), specific for P-linked or a-linked galactose residues, respectively. Rats injected intravitreally with [35S]methionine were maintained in darkness for 2 hr at which time 12 retinas were collected for subcellular fractionation and rhodopsin purification by ConA sepharose chromatography. abstract: Abstract Rhodopsin's oligosaccharide chains contain predominantly two types of sugar residues: mannose and N-acetylglucosamine. In the present work, bovine and rat rhodopsin were analysed biochemically for the presence of a third sugar, galactose. Treatment of bovine rod outer segments (ROS) with galactose oxidase followed by reduction with tritium-labeled sodium borohydride revealed the presence of existing molecules of galactose on rhodopsin. Rats injected intravitreally with [3H]galactose and [14C]leucine and maintained in darkness were killed 1 hr, 6 hr, 1, 3, or 5 days following the injection. Retinas were collected for subcellular fractionation and rhodopsin from each of the fractions was purified by ConA sepharose chromatography and SDS-PAGE. During the first 6 hr, galactose selectively labeled rhodopsin in the Golgi-enriched fraction resulting in increased [3H] [14C] ratios in both Golgi and ROS. The data suggested that trimming was occurring at the transition from Golgi to ROS. Furthermore, a decrease in isotope ratio in the ROS between 6 hr and 1 day suggested further trimming of rhodopsin after membrane assembly in the ROS. Additional in vivo experiments demonstrated existing molecules of galactose on rhodopsin's oligosaccharide chain using lectin affinity chromatography. Rats injected intravitreally with [35S]methionine were dark-adapted for 2 hr. Following subcellular fractionation of retinas, ConA purified rhodopsin from ROS was applied to one of two additional lectin columns: Ricinus communis agglutinin (RCA) or Griffonia simplicifolia I (GSA). Eight to nine per cent of the labeled rhodopsin was bound to and eluted from RCA, whereas none bound to GSA, indicating the presence of a β-galactoside. The RCA agarose eluted protein co-electrophoresed with a rhodopsin standard and was light sensitive. Galactose was shown to be the terminal sugar on this subset of rhodopsin and was not capped by neuraminic acid. Binding of rhodopsin's oligosaccharide to RCA was abolished by pre-treatment with β-galactosidase. Decreased binding of rhodopsin to RCA was observed following intravitreal injection of castanospermine but not swainsonine. Of those two inhibitors of glycoprotein trimming, only castanospermine would be expected to prevent the addition of galactose to the oligosaccharide. The association of galactose with rat rhodopsin appeared to be a transient one. At 2 hr, 8–9% of rhodopsin contained galactose, at 6 hr only 2·2% had galactose and by 24 hr less than 1% did. The galactose was trimmed from rhodopsin's oligosaccharide presumably after its role was complete. Separation of rhodopsin of the plasma membranes from rhodopsin of discs indicated that 75% of the galactose-containing rhodopsin was in the plasma membrane and only 25% was in the discs. These findings suggested a possible role for galactose in new disc formation with subsequent removal after the discs are sealed. url: https://www.sciencedirect.com/science/article/pii/001448359190170J doi: 10.1016/0014-4835(91)90170-j id: cord-102808-c7ajfvt5 author: Sundqvist, Martina title: Barbadin selectively modulates FPR2-mediated neutrophil functions independent of receptor endocytosis date: 2020-05-01 words: 5708 sentences: 236 pages: flesch: 34 cache: ./cache/cord-102808-c7ajfvt5.txt txt: ./txt/cord-102808-c7ajfvt5.txt summary: The formyl peptide receptor 2 (FPR2), belonging to the family of G protein-coupled receptors (GPCRs), regulates directional neutrophil migration (chemotaxis), granule secretion (degranulation), formation of F-actin filaments (through polymerization of G-actin), and activation of the reactive oxygen species (ROS) producing NADPH-oxidase [3, 5, 6] . The fact that F2Pal10 and Cmp 14 cannot induce -arrestin recruitment at these concentrations ([9-11], Fig 2A) , strongly suggests that the priming effect of Barbadin on FPR2-mediated ROS production is independent of the ability of the activating agonist to recruit -arrestin. Collectively, these results suggest that Barbadin primes neutrophils in their response to FPR2 agonists, and the increased NADPH-oxidase activation is regulated independently of FPR2 internalization and FPR2-induced -arrestin recruitment. Barbadin was added to WKYMVM-activated neutrophils at a time point when ROS production had returned to a background level; interestingly, these FPR2-desensitized cells could be resensitized to produce ROS also by Barbadin, similar to the effect of latrunculin A ( Fig 5A) . abstract: Formyl peptide receptor 2 (FPR2), a member of the family of G protein-coupled receptors (GPCRs), mediates neutrophil migration, a response that has been linked to β-arrestin recruitment. β-Arrestin regulates GPCR endocytosis and can also elicit non-canonical receptor signaling. To determine the poorly understood role of β-arrestin in FPR2 endocytosis and in NADPH-oxidase activation in neutrophils, Barbadin was used as a research tool in this study. Barbadin has been shown to bind the clathrin adaptor protein (AP2) and thereby prevent β- arrestin/AP2 interaction and β-arrestin-mediated GPCR endocytosis. In agreement with this, AP2/β-arrestin interaction induced by an FPR2-specific agonist was inhibited by Barbadin. Unexpectedly, however, Barbadin did not inhibit FPR2 endocytosis, indicating that a mechanism independent of β-arrestin/AP2 interaction may sustain FPR2 endocytosis. This was confirmed by the fact, that FPR2 also underwent agonist-promoted endocytosis in β-arrestin deficient cells, albeit at a diminished level as compared to wild type cells. Dissection of the Barbadin effects on FPR2-mediated neutrophil functions including NADPH-oxidase activation mediated release of reactive oxygen species (ROS) and chemotaxis reveled that Barbadin had no effect on chemotactic migration whereas the release of ROS was potentiated/primed. The effect of Barbadin on ROS production was reversible, independent of β-arrestin recruitment, and similar to that induced by latrunculin A. Taken together, our data demonstrate that endocytic uptake of FPR2 occurs independently of β-arrestin, while Barbadin selectively augments FPR2-mediated neutrophil ROS production independently of receptor endocytosis. Given that Barbadin binds to AP2 and prevents the AP2/β-arrestin interaction, our results indicate a role for AP2 in FPR2-mediated ROS release from human neutrophils. url: https://doi.org/10.1101/2020.04.30.070011 doi: 10.1101/2020.04.30.070011 id: cord-034321-ohjik0pf author: Vorobjeva, N. V. title: NETosis: Molecular Mechanisms, Role in Physiology and Pathology date: 2020-10-27 words: 7605 sentences: 432 pages: flesch: 43 cache: ./cache/cord-034321-ohjik0pf.txt txt: ./txt/cord-034321-ohjik0pf.txt summary: NETosis is a program for formation of neutrophil extracellular traps (NETs), which consist of modified chromatin decorated with bactericidal proteins from granules and cytoplasm. NETosis includes release of the granule components into the cytosol, modification of histones leading to chromatin decondensation, destruction of the nuclear envelope, as well as formation of pores in the plasma membrane. 1178 Abbreviations: ARDS, acute respiratory distress syndrome; CGD, chronic granulomatous disease; COPD, chronic obstructive pulmonary disease; GSDMD, gasdermin D; LPS, lipopolysaccharide of the bacterial wall; MPO, myeloper oxidase; mPTP, nonselective mitochondrial permeability tran sition pore; NE, neutrophil elastase; NETs, Neutrophil Extra cellular Traps; PCD, programmed cell death; PKC, protein kinase C; PMA, phorbol 12 myristate 13 acetate; ROS, reac tive oxygen species. At the same time, we also showed that in neutrophils isolated from the blood of patients with X linked CGD formation of NETs in response to A23187 depended on the enhanced gener ation of mtROS without participation of NADPH oxi dase [16] . abstract: NETosis is a program for formation of neutrophil extracellular traps (NETs), which consist of modified chromatin decorated with bactericidal proteins from granules and cytoplasm. Various pathogens, antibodies and immune complexes, cytokines, microcrystals, and other physiological stimuli can cause NETosis. Induction of NETosis depends on reactive oxygen species (ROS), the main source of which is NADPH oxidase. Activation of NADPH oxidase depends on increase in the concentration of Ca(2+) in the cytoplasm and in some cases on the generation of ROS in mitochondria. NETosis includes release of the granule components into the cytosol, modification of histones leading to chromatin decondensation, destruction of the nuclear envelope, as well as formation of pores in the plasma membrane. In this review, basic mechanisms of NETosis, as well as its role in the pathogenesis of some diseases including COVID-19 are discussed. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590568/ doi: 10.1134/s0006297920100065 id: cord-034294-ti1cc24m author: Wang, Cuixue title: Progress in the mechanism and targeted drug therapy for COPD date: 2020-10-27 words: 16476 sentences: 989 pages: flesch: 37 cache: ./cache/cord-034294-ti1cc24m.txt txt: ./txt/cord-034294-ti1cc24m.txt summary: Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. EPAC and PKA inhibit the human airway smooth muscle induced by a cigarette smoke extract (CSE) by blocking the activation of the NF-κB and ERK, respectively, and by releasing neutrophil chemokine IL-8, which together exert anti-inflammatory effects. 101 In COPD, increases in cAMP levels, activation of PKA and enhanced protein phosphorylation have the potential to reduce inflammation and immunomodulation, relax airway smooth muscle, inhibit chemotaxis and abnormal release of inflammatory and cytotoxic mediators, and reduce proliferation and migration of inflammatory cells. 135 The PI3K/Akt signalling pathway plays an important role in COPD by regulating inflammatory cell activation, inflammatory mediator release and airway remodelling. abstract: Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588592/ doi: 10.1038/s41392-020-00345-x id: cord-000799-s70onyix author: Wang, Ting title: Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation date: 2012-08-29 words: 5884 sentences: 363 pages: flesch: 46 cache: ./cache/cord-000799-s70onyix.txt txt: ./txt/cord-000799-s70onyix.txt summary: title: Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation OBJECTIVES: We explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction. We investigated the role of ROS and calpain in PM-induced pulmonary inflammation by examining protein leakage, white blood cell infiltration (inflammatory leukocytes), and the release of proinflammatory cytokines into BAL fluids ( Figure 5 ). These data represent the first evidence that calpain signaling, via calcium leakage from activated TRPM2 by ROS, plays a critical role in modulating endothelial cell barrier function, resulting in tight junction protein ZO-1 degradation (Additional file 1 Figure S7 ). Particulate matter induces endothelial cell intracellular oxidative stress, which leads to the activation of calpain, one of the major cytoskeletal regulators. abstract: BACKGROUND: Exposure to particulate matter (PM) is a significant risk factor for increased cardiopulmonary morbidity and mortality. The mechanism of PM-mediated pathophysiology remains unknown. However, PM is proinflammatory to the endothelium and increases vascular permeability in vitro and in vivo via ROS generation. OBJECTIVES: We explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction. METHODS: Changes in human lung EC monolayer permeability were assessed by Transendothelial Electrical Resistance (TER) in response to PM challenge (collected from Ft. McHenry Tunnel, Baltimore, MD, particle size >0.1 μm). Biochemical assessment of ROS generation and Ca(2+) mobilization were also measured. RESULTS: PM exposure induced tight junction protein Zona occludens-1 (ZO-1) relocation from the cell periphery, which was accompanied by significant reductions in ZO-1 protein levels but not in adherens junction proteins (VE-cadherin and β-catenin). N-acetyl-cysteine (NAC, 5 mM) reduced PM-induced ROS generation in ECs, which further prevented TER decreases and atteneuated ZO-1 degradation. PM also mediated intracellular calcium mobilization via the transient receptor potential cation channel M2 (TRPM2), in a ROS-dependent manner with subsequent activation of the Ca(2+)-dependent protease calpain. PM-activated calpain is responsible for ZO-1 degradation and EC barrier disruption. Overexpression of ZO-1 attenuated PM-induced endothelial barrier disruption and vascular hyperpermeability in vivo and in vitro. CONCLUSIONS: These results demonstrate that PM induces marked increases in vascular permeability via ROS-mediated calcium leakage via activated TRPM2, and via ZO-1 degradation by activated calpain. These findings support a novel mechanism for PM-induced lung damage and adverse cardiovascular outcomes. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3489700/ doi: 10.1186/1743-8977-9-35 id: cord-273992-xddikzxs author: Wiseman, A. title: Avoidance of oxidative‐stress perturbation in yeast bioprocesses by proteomic and genomic biostrategies? date: 2004-11-10 words: 2658 sentences: 122 pages: flesch: 35 cache: ./cache/cord-273992-xddikzxs.txt txt: ./txt/cord-273992-xddikzxs.txt summary: The main impact of the study is that the utilization of genetically modified (GM) yeast produced by recombinant DNA technology genomic strategies could circumvent the bioprocessing problems that otherwise result from the bioprocess perturbations: this is as a result of oxidative stress caused by ROS, which is avoidable by deployment of appropriate antioxidants such as vitamins E, C and D (and antioxidant proteins and enzymes often of microbial origin via recombinant DNA technology). Catalases ( Table 3 ) in yeasts and other micro-organisms (Antioxidants such as vitamins E and C chain terminate the formation of membrane-degrading ROS) relates to more than just structural damage that is sometimes obvious and predictable: functional damage may also follow. Avoidance biostrategies against ROS and RSS in many oxidatively stressed bioprocesses that utilise yeasts (and other micro-organisms) are essential where human therapeutic proteins are expected to be produced in high yield. abstract: Aims: Bioprocess oxidative stress caused by many reactive oxygen species (ROS) can lead to largely irreversible perturbation of yeast bioprocesses. These include the production of proteins derived from recombinant DNA yeast technology (aerobically grown Saccharomyces cerevisiae). These proteins include rennin, amyloglucosidases (glucamylases), interferons, interleukins, insulin, monoclonal antibodies, tissue plasminogen activators (t‐PA), sexually transmitted disease antigens, and measles, mumps and rubella antigens, growth hormones, somatotropin, blood clotting factors VIII and XIII. In addition, there may be a demand for severe acute respiratory syndrome–coronavirus antigens, hepatitis A, B and C viral‐selected antigens, HIV retroviral antigens, influenza antigens, trypanosomal antigens, and foot and mouth disease antigens. Prevention of oxidative stress has been achieved by application of antioxidant redox metalloenzymes such as superoxide dismutases (containing Cu/Zn cytosolic, Mn mitochondrial and Fe bacterial) glutathione peroxidases (and other Se‐containing proteins and enzymes such as the thioredoxins), catalases (Fe‐containing), cytochrome c peroxidases (Fe‐containing), ceruloplasmins (Cu‐containing), metallothionines (these cysteine thiol‐rich proteins bind ions of cadmium and mercury) and tyrosinases(Cu‐containing). Methods and Results: ROS are generated inadvertently by single metal valency couples such as FeII/FeIII and by FeIII/FeV present in 2700 (including 57 human) isoforms in cytochromes P450 mixed‐function oxidases (EC 1·14·14·1; O(2) : mono‐oxygenase NADPH/NADH requiring). In addition, mixed‐metal couples such as valency unmatched forms in CuI/FeII and FeIII/MnIV can recycle electrons. Moreover, proteins/protein chaperone couples can recycle electrons, often where futile‐recycling systems have been instigated. Furthermore, oxidized membrane phospholipids (R) can form ROOH (lipid hydroperoxides) and ROH (lipid alkoxides) that can generate ROS through Fenton chemistry (iron‐catalysed) chain reactions. Utilization of chain‐breaking antioxidants such as vitamin E (α‐tocopherol) in the lipid phase and vitamin C (ascorbate) in the aqueous phase can terminate these ROS‐producing reactions. Conclusions: The main significance of the study is that proteomic strategies of relief from bioprocess perturbation by ROS of yeast fermentations (used to manufacture proteins required in the food and therapeutic bioindustries) may become possible through addition of selected proteins (including metalloenzymes). The main impact of the study is that the utilization of genetically modified (GM) yeast produced by recombinant DNA technology genomic strategies could circumvent the bioprocessing problems that otherwise result from the bioprocess perturbations: this is as a result of oxidative stress caused by ROS, which is avoidable by deployment of appropriate antioxidants such as vitamins E, C and D (and antioxidant proteins and enzymes often of microbial origin via recombinant DNA technology). url: https://www.ncbi.nlm.nih.gov/pubmed/15613000/ doi: 10.1111/j.1472-765x.2004.01624.x id: cord-313825-bbjxd86y author: Xia, Tian title: Pulmonary diseases induced by ambient ultrafine and engineered nanoparticles in twenty-first century date: 2016-10-08 words: 8765 sentences: 389 pages: flesch: 43 cache: ./cache/cord-313825-bbjxd86y.txt txt: ./txt/cord-313825-bbjxd86y.txt summary: The lung is the first target organ for air pollution and PM exposure is associated with reduced lung function, increased lung inflammation, asthma, respiratory infections, lung cancer and exacerbation of COPD, which lead to systemic inflammation and oxidative stress affecting blood, vasculature, heart and brain, ultimately contribute to the premature mortality ( Fig. 2) [3, 8, 14, 16] . These specific features of UFPs can significantly contribute to the adverse effects through ROS over-production by the redox-active organic chemicals and metals on particle surface, resulting in cellular oxidative stress [18, 19, 21, 44, 48] . These include: (i) carbon core of PM and UFPs could induce ROS generation and oxidative stress; (ii) catalytic conversion of PAHs to quinones by cytochrome P450 in the endoplasmic reticulum; (iii) quinone redox cycling by NADPH-dependent P450 reductase in microsomes; (iv) mitochondrial perturbation leading to electron leakage in the inner membrane; and (v) NADPH oxidase activity in the macrophage surface membrane and associated phagosomes. abstract: Air pollution is a severe threat to public health globally, affecting everyone in developed and developing countries alike. Among different air pollutants, particulate matter (PM), particularly combustion-produced fine PM (PM(2.5)) has been shown to play a major role in inducing various adverse health effects. Strong associations have been demonstrated by epidemiological and toxicological studies between increases in PM(2.5) concentrations and premature mortality, cardiopulmonary diseases, asthma and allergic sensitization, and lung cancer. The mechanisms of PM-induced toxicological effects are related to their size, chemical composition, lung clearance and retention, cellular oxidative stress responses and pro-inflammatory effects locally and systemically. Particles in the ultrafine range (<100 nm), although they have the highest number counts, surface area and organic chemical content, are often overlooked due to insufficient monitoring and risk assessment. Yet, ample studies have demonstrated that ambient ultrafine particles have higher toxic potential compared with PM(2.5). In addition, the rapid development of nanotechnology, bringing ever-increasing production of nanomaterials, has raised concerns about the potential human exposure and health impacts. All these add to the complexity of PM-induced health effects that largely remains to be determined, and mechanistic understanding on the toxicological effects of ambient ultrafine particles and nanomaterials will be the focus of studies in the near future. url: https://doi.org/10.1093/nsr/nww064 doi: 10.1093/nsr/nww064 id: cord-268122-74nj66vb author: Xie, Na title: NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential date: 2020-10-07 words: 32037 sentences: 1955 pages: flesch: 39 cache: ./cache/cord-268122-74nj66vb.txt txt: ./txt/cord-268122-74nj66vb.txt summary: The NAD + decline during normal aging results in oxidative damage, metabolic disorder, circadian rhythm abnormalities, and mitochondrial dysfunction through regulating signaling pathways, such as p53, NF-κB, PGC-1α and HIF-1α, by sirtuins and PARPs. NAD + and its metabolites function as crucial regulators to maintain cellular redox homeostasis through replenishing the reducing power or modulating the activity of NAD + -consuming enzymes including sirtuins and PARPs. However, disequilibrium of NAD + metabolism could disturb physiological processes, including mitochondria function, circadian rhythm, inflammation, DNA repair and metabolism, leading to aging-associated dysfunction and cancer. c The deduced NAD + levels in kidney are attributed to the decreased expression of enzymes in NAD + de novo synthesis and increased consumption by DNA damage activated PARPs. NAD + depletion inhibits the SIRT1/PGC1α mediated mitochondrial quality control, ATP production and NAD + de novo biosynthesis. abstract: Nicotinamide adenine dinucleotide (NAD(+)) and its metabolites function as critical regulators to maintain physiologic processes, enabling the plastic cells to adapt to environmental changes including nutrient perturbation, genotoxic factors, circadian disorder, infection, inflammation and xenobiotics. These effects are mainly achieved by the driving effect of NAD(+) on metabolic pathways as enzyme cofactors transferring hydrogen in oxidation-reduction reactions. Besides, multiple NAD(+)-dependent enzymes are involved in physiology either by post-synthesis chemical modification of DNA, RNA and proteins, or releasing second messenger cyclic ADP-ribose (cADPR) and NAADP(+). Prolonged disequilibrium of NAD(+) metabolism disturbs the physiological functions, resulting in diseases including metabolic diseases, cancer, aging and neurodegeneration disorder. In this review, we summarize recent advances in our understanding of the molecular mechanisms of NAD(+)-regulated physiological responses to stresses, the contribution of NAD(+) deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention. url: https://doi.org/10.1038/s41392-020-00311-7 doi: 10.1038/s41392-020-00311-7 id: cord-260348-83ftjqev author: Xu, Yinlan title: Cepharanthine and Curcumin inhibited mitochondrial apoptosis induced by PCV2 date: 2020-09-18 words: 3752 sentences: 220 pages: flesch: 48 cache: ./cache/cord-260348-83ftjqev.txt txt: ./txt/cord-260348-83ftjqev.txt summary: The results of qPCR and Western blot showed that, compared with the PCV2 infected group, the expression of Cap in Paeonol (0.4 mg/mL and 0.2 mg/mL), Cepharanthine (0.003 mg/mL, 0.0015 mg/mL and 0.00075 mg/mL) and Curcumin (0.02 mg/mL, 0.001 mg/mL and 0.005 mg/mL) treated groups were significantly lowered in a dose-dependent manner. The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. The results showed that Compared to the PCV2-infected group, the cell apoptosis rates were significantly decreased in the group treated with Cepharanthine, Curcumin or Ribavirin, demonstrating a dose-dependent response except the group of 0.005 mg/mL Paeonol (P < 0.05) ( Fig. 3a and b). abstract: BACKGROUND: Porcine circovirus type 2 (PCV2) is an immunosuppressive pathogen with high prevalence rate in pig farms. It has caused serious economic losses to the global pig industry. Due to the rapid mutation of PCV2 strain and co-infection of different genotypes, vaccination could not eradicate the infection of PCV2. It is necessary to screen and develop effective new compounds and explore their anti-apoptotic mechanism. The 13 natural compounds were purchased, with a clear plant origin, chemical structure and content and specific biological activities. RESULTS: The maximum no-cytotoxic concentration (MNTC) and 50% cytotoxic concentration (CC(50)) of 13 tested compounds were obtained by the cytopathologic effect (CPE) assay and (3-(4,5-dimethyithiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method in PK-15 cells. The results of qPCR and Western blot showed that, compared with the PCV2 infected group, the expression of Cap in Paeonol (0.4 mg/mL and 0.2 mg/mL), Cepharanthine (0.003 mg/mL, 0.0015 mg/mL and 0.00075 mg/mL) and Curcumin (0.02 mg/mL, 0.001 mg/mL and 0.005 mg/mL) treated groups were significantly lowered in a dose-dependent manner. The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. In this study, Ribavirin was used as a positive control. CONCLUSIONS: Paeonol, Cepharanthine and Curcumin have significant antiviral effect. And the PCV2-induced Mitochondrial apoptosis was mainly remitted by Cepharanthine and Curcumin. url: https://www.ncbi.nlm.nih.gov/pubmed/32948186/ doi: 10.1186/s12917-020-02568-0 id: cord-257514-gw9xnb4x author: Yang, Mengling title: Hydrogen: A Novel Option in Human Disease Treatment date: 2020-09-05 words: 10425 sentences: 526 pages: flesch: 33 cache: ./cache/cord-257514-gw9xnb4x.txt txt: ./txt/cord-257514-gw9xnb4x.txt summary: H(2) gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. found that HW inhibited cardiomyocyte apoptosis by activating the PI3K/AKT and JAK2-STAT3 signaling pathways and can also reduce the level of oxidative stress in myocardial tissue by upregulating the expression of the nuclear erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway, which alleviated I/R injury in isolated rat hearts [39, 40, 91] . Effects of hydrogen-rich water on the PI3K/AKT signaling pathway in rats with myocardial 12 Oxidative Medicine and Cellular Longevity ischemia-reperfusion injury Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation abstract: H(2) has shown anti-inflammatory and antioxidant ability in many clinical trials, and its application is recommended in the latest Chinese novel coronavirus pneumonia (NCP) treatment guidelines. Clinical experiments have revealed the surprising finding that H(2) gas may protect the lungs and extrapulmonary organs from pathological stimuli in NCP patients. The potential mechanisms underlying the action of H(2) gas are not clear. H(2) gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. This paper reviews the basic research and the latest clinical applications of H(2) gas in multiorgan system diseases to establish strategies for the clinical treatment for various diseases. url: https://doi.org/10.1155/2020/8384742 doi: 10.1155/2020/8384742 id: cord-005280-a23oy0sz author: Yang, Shenshu title: ROS and diseases: role in metabolism and energy supply date: 2019-12-07 words: 5898 sentences: 379 pages: flesch: 38 cache: ./cache/cord-005280-a23oy0sz.txt txt: ./txt/cord-005280-a23oy0sz.txt summary: Although ROS play an important role in pathogen resistance and cellular signalling, they are also broadly recognized as harmful reactive particles to cell as they damage intracellular proteins, lipids and nucleic acids. The homeostasis of ROS plays an important role in reducing oxidative damage and fulfil energy demand. Relatively high levels of ROS may cause oxidative damage or induce apoptosis during immunological defences or pathological conditions. However, ROS themselves could activate extracellular signal-regulated kinase (ERK) by targeting proteins Gαi and Gα0 and protect cardiac cell from oxidative damage [18] . Apart from oxidative damage, ROS also serve as signalling molecules and play an important role in homeostasis, metabolism, growth and differentiation [3] . PGC-1α could protect neural cells from oxidative damage by reducing ROS level via antioxidative enzymes GPx1 and SOD2 [15] . ROS regulate vascular cell proliferation and apoptosis with their fundamental role in metabolism. abstract: Researches dedicated to reactive oxygen species (ROS) had been performed for decades, yet the outcomes remain controversial. With the relentless effort of studies, researchers have explored the role of ROS in biosystem and various diseases. ROS are beneficial for biosystem presenting as signalling molecules and enhancing immunologic defence. However, they also have harmful effects such as causing tissue and organ damages. The results are controversial in studies focusing on ROS and ROS-related diseases by regulating ROS with inhibitors or promotors. These competing results hindered the process for further investigation of the specific mechanisms lying behind. The opinions presented in this review interpret the researches of ROS from a different dimension that might explain the competing results of ROS introduced so far from a broader perspective. This review brings a different thinking to researchers, with the neglected features and potentials of ROS, to relate their works with ROS and to explore the mechanisms between their subject and ROS. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7089381/ doi: 10.1007/s11010-019-03667-9 id: cord-006230-xta38e7j author: nan title: Deutsche Gesellschaft für Experimentelle und Klinische Pharmakologie und Toxikologie e.V. date: 2012-02-22 words: 135419 sentences: 7042 pages: flesch: 43 cache: ./cache/cord-006230-xta38e7j.txt txt: ./txt/cord-006230-xta38e7j.txt summary: Here, we will present our analysis of Ca 2+ signaling following stimulation of the FcεRI receptor and application of secretagogues that are supposed to affect Ca 2+ -dependent mast cell activation such as adenosine, endothelin-1, substance P and compound 48/80 in BMMCs and PMCs derived from mouse lines with inactivation of TRPC1, TRPC3, TRPC4, TRPC5 or TRPC6 since specific antagonists are still lacking for these TRP channels. These data indicate that increased PP2A activity is associated with modified gene expression in TG hearts possibly affecting stress response and regulation of cell signalling. As demonstrated by qPCR and Western blot experiments, mesangial cells showed a marked time-and dose-dependent upregulation of CSE mRNA and protein levels after treatment with platelet-derived growth factor (PDGF-BB). The transcription factor cAMP response element (CRE)-binding protein (CREB) plays a critical role in regulating gene expression in response to activation of the cAMPdependent signaling pathway, which is implicated in the pathophysiology of heart failure. abstract: nan url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7100643/ doi: 10.1007/s00210-012-0736-0 id: cord-020646-s7eopu9y author: nan title: Die Pathophysiologie der Entzündung date: 2005 words: 30141 sentences: 4154 pages: flesch: 55 cache: ./cache/cord-020646-s7eopu9y.txt txt: ./txt/cord-020646-s7eopu9y.txt summary: Die Wirkung des Histamins auf Zielzellen erfolgt über spezifi sche Rezeptoren, von denen zwei Arten bekannt und gut studiert sind. Bei plötzlicher Aufhebung der Rezeptorblockade nach Ende einer Therapie sind die betroffenen Zellen mit einer hohen Rezeptorzahl bestückt und reagieren folglich auf Histamin verstärkt, was zum massiven Wiederauftreten der Krankheitssymptomatik führen kann (sog. Disponierte Personen, die als "Atopiker" bezeichnet werden, reagieren auf gewisse Antigene (AG) mit der Bildung spezifi scher Antikörper (AK) vom IgE-Typ. Die atopische Veranlagung ist angeboren, tritt oft familiär auf und zeigt eine Konvergenz mit gewissen MHC I Typen. Dem PAF wird heute eine wesentliche Rolle beim Pathomechanismus des Asthma bronchiale und der COPD zugeschrieben, wobei die Wirkung auch indirekt, nämlich über eine Potenzierung anderer Mediatoren wie LT, PG, Histamin zu laufen scheint. Diese Bindung ist der Mechanismus, über den die Zelle ein Partikel erkennt und von Material unterscheidet, das nicht phagozytiert werden soll, und der den Phagozytosereiz auslöst. abstract: nan url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7143866/ doi: 10.1007/3-211-29899-1_2 id: cord-022940-atbjwpo5 author: nan title: Poster Sessions date: 2016-09-07 words: 241182 sentences: 12746 pages: flesch: 47 cache: ./cache/cord-022940-atbjwpo5.txt txt: ./txt/cord-022940-atbjwpo5.txt summary: We have studied the effect of inhibition of IRE1 (inositol requiring enzyme 1), which is a central mediator of endoplasmic reticulum stress and controls cell proliferation and tumor growth, on hypoxic regulation of the expression of different proliferation related genes in U87 glioma cells. Transient inhibition of Akt and mTOR protein kinase activation in tumor cells followed by reactivation of signaling pathway did not result in a time-dependent difference on EGFR, HER2 and HER3 expression levels. In our study we aimed to determine cytotoxic effect of RES in K562 human CML cell line and to evaluate the expressions of miRNAs that are associated with genetics of leukemia after treatment with RES; to investigate target genes of miRNAs which show significant expression alterations and molecular mechanisms of RES treatment. abstract: nan url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7164006/ doi: 10.1111/febs.13808 ==== make-pages.sh questions [ERIC WAS HERE] ==== make-pages.sh search /data-disk/reader-compute/reader-cord/bin/make-pages.sh: line 77: /data-disk/reader-compute/reader-cord/tmp/search.htm: No such file or directory Traceback (most recent call last): File "/data-disk/reader-compute/reader-cord/bin/tsv2htm-search.py", line 51, in with open( TEMPLATE, 'r' ) as handle : htm = handle.read() FileNotFoundError: [Errno 2] No such file or directory: '/data-disk/reader-compute/reader-cord/tmp/search.htm' ==== make-pages.sh topic modeling corpus Zipping study carrel