# ent

id: cord-019063-mcxbl8mv
type: GGP
entity:
  specifi c antiparasitic drugs the physicians treating such diseases should be competent in tackling the specifi c issues related to lung injury and sequel that may follow such infections The lung diseases that may result from infections with


id: cord-019063-mcxbl8mv
type: TAXON
entity:
  Echinococcus multilocularis trematodes Schistosoma haematobium Schistosoma mansoni Schistosoma japonicum


id: cord-019063-mcxbl8mv
type: TAXON
entity:
  nematodes Ascaris lumbricoides Ancylostoma duodenale Necator americanus Strongyloides stercoralis Wuchereria bancrofti Brugia malayi Brugia timori


id: cord-019063-mcxbl8mv
type: DISEASE
entity:
  Ascaris lumbricoides Ancylostoma duodenale Necator americanus Strongyloides stercoralis Wuchereria bancrofti Brugia malayi Brugia timori


id: cord-018339-tyrlpl94
type: ORG
entity:
  the European Society of Blood and Marrow Transplantation the Infectious Diseases Group of the European Organization for Research and Treatment of Cancer the International Immunocompromised Host Society


id: cord-035258-nff6gfik
type: DNA
entity:
  Swan Ganz catheter Pulmonary artery pseudoaneurysm etiology presentation diagnosis and treatment Pulmonary artery


id: cord-035258-nff6gfik
type: DISEASE
entity:
  impairment of vital and functional residual capacities or other surgical factors sternotomy pleural dissection


id: cord-010078-8lkkez3n
type: WORK_OF_ART
entity:
  Clinical Guidelines for the Manual Titration of Positive Airway Pressure in Patients with Obstructive Sleep Apnea in Journal of Clinical Sleep Medicine 2008


id: cord-010078-8lkkez3n
type: DISEASE
entity:
  allergic rhinitis idiopathic pulmonary hypertension hypersensitivity pneumonitis occupational respiratory disease


id: cord-010078-8lkkez3n
type: DISEASE
entity:
  pleural and pericardial effusions pericardial thickening enlarged pulmonary artery and esophageal dilatation HRCT


id: cord-015836-ojx04jsh
type: DISEASE
entity:
  heart and lung transplantation twenty fourth offi cial adult lung and heartlung transplantation report 2007


id: cord-293613-xnos7iud
type: PROTEIN
entity:
  TGF transforming growth factor Th T helper TNF tumor necrosis factor VEGF vascular endothelial growth factor


id: cord-293613-xnos7iud
type: WORK_OF_ART
entity:
  Definition Causes Pathogenesis and Consequences of Chronic Obstructive Pulmonary Disease Exacerbations


id: cord-023311-7wqdlha4
type: CHEMICAL
entity:
  Ridl Bacopa monnieri L Pennell Ocimum gratissimum L Lawsonia inermis L Cinnamomum camphora L Sieb Aconitum napellus L Datura metel L Mimosa pudica L Achyranthes aspera L Piper betle L Randia


id: cord-023311-7wqdlha4
type: CHEMICAL
entity:
  L Agaricus albolutescens Zeller Ipomoea aquatica Forssk Stephania japonica Thunb Miers Withania somnifera L Duna Cannabis sativa L Calamus rotang L


id: cord-000268-480d3yfv
type: PROTEIN
entity:
  nTREM 1 above 2 55 MFI Sensitivity and Lung cancer 13 Staphulococcus aureus 3 Pulmonary embolism 6 Haemophilus influenzae 2 Congestive heart failure 5 Pseudomonas aeruginosa 2


id: cord-000268-480d3yfv
type: DISEASE
entity:
  noninfectious processes like peptic ulcer inflammatory bowel disease viral infections malignant pleural effusions


id: cord-006428-l9akk8i6
type: PROTEIN
entity:
  von Tuder Voelkel verwiesen 150 153 Die Lebensdauer von 51 Chrommarkierten Blutplättchen ist bei Patienten mit chronisch obstruktiven Lungenerkrankungen


id: cord-006428-l9akk8i6
type: PROTEIN
entity:
  SPH mit 2 4 d gegenüber normotensiven Patienten 3 1 d oder gesunden Probanden 3 7 d ebenso verkürzt wie bei PPH Patienten 2 3 d 141


id: cord-006428-l9akk8i6
type: CELL_TYPE
entity:
  vascular smooth muscle cell proliferation Primary pulmonary hypertension Transpulmonary angiotensin II


id: cord-006428-l9akk8i6
type: CHEMICAL
entity:
  2 4 d gegenüber normotensiven Patienten 3 1 d oder gesunden Probanden 3 7 d ebenso verkürzt wie bei PPH Patienten 2 3 d 141 Auch im Tiermodell der Monocrotalin induzierten


id: cord-290006-63sa00ju
type: PROTEIN
entity:
  CT MR DOI 10 1053 j sult 2018 12 002 sha ca234eb1ffb60b1e08f16c6ec645c9a3d188bba1 doc_id 290006 cord_uid 63sa00ju


id: cord-290006-63sa00ju
type: TAXON
entity:
  adenovirus parainfluenza respiratory syncytial virus human metapneumovirus coronavirus rhinovirus Mycoplasma pneumoniae


id: cord-290006-63sa00ju
type: ORG
entity:
  International association for the Study Of Lung Cancer American Thoracic Society European Respiratory Society


id: cord-314106-r3axl3w1
type: WORK_OF_ART
entity:
  The Acute Respiratory Distress Syndrome Mechanisms and Perspective Therapeutic Approaches Fibrinolytic


id: cord-314106-r3axl3w1
type: ORG
entity:
  INSPIRE Study Investigators International Collaboration of Aspirin Trials for Recurrent Venous Thromboembolism Aspirin


id: cord-000364-ikq38rm1
type: PROTEIN
entity:
  Puumala hantavirus nucleocapsid protein monoclonal antibody A1C5 Progen Biotechnik GmbH Heidelberg Germany For viral antigen


id: cord-323566-jck799zq
type: CELL_TYPE
entity:
  Bone B Glial nodules C Hepatoid anlage D Striated muscle E Enteric type epithelium ANSWER D 5 Congenital malformations


id: cord-323566-jck799zq
type: DISEASE
entity:
  pneumonia obliterative bronchiolitis pulmonary hemorrhage pulmonary edema pulmonary hypertension venoocclusive disease


id: cord-017016-twwa9djm
type: DISEASE
entity:
  intermittent obstruction of the precariously situated bronchi in the setting of reduced collateral ventilation of the middle lobe 208


id: cord-287544-n32iscmr
type: GGP
entity:
  Cureus DOI 10 7759 cureus 8069 sha 15e2fd4a6ed360707b770b4569f309173d267fa7 doc_id 287544 cord_uid n32iscmr Dihydropyridine calcium channel blockers CCB


id: cord-335597-anrzcsrt
type: GGP
entity:
  sargramostim GM CSF aviptadil synthetic vasoactive intestinal polypeptide DAS181 recombinant sialidase PUL042 immunostimulant TLR 2 6 9 agonist budesonide nitrogen oxide


id: cord-335597-anrzcsrt
type: CHEMICAL
entity:
  wurde eine rechtsseitige Hemikolektomie mit Anlage einer Seit zu Seit Ileotransversostomie erforderlich Nach ausgedehnter abdomineller


id: cord-335597-anrzcsrt
type: DISEASE
entity:
  cardiopulmonary comorbidities smoking history and pulmonary resting hemodynamics mPAP CO slope HR 2 84 95 CI 1 22 6 59 p 0 015 TPG CO slope HR 2 60 95 CI 1 17 5 82 p 0 020 and PAWP CO slope HR 4 92 95 CI 1 95 12 44 p 0 001


id: cord-016009-qa7bcsbu
type: CELL_LINE
entity:
  bronchus 50 Large cell undifferentiated carcinoma About 10 15 of lung cancers It can appear in any part of the lung and tends to grow and spread quickly A subtype of large cell carcinoma


id: cord-016009-qa7bcsbu
type: PROTEIN
entity:
  protein RI transforming growth factor b receptor I RII transforming growth factor b receptor II SARA Smad anchor


id: cord-016009-qa7bcsbu
type: PROTEIN
entity:
  receptor activation STAT signal transducer and activator of transcription TCF T cell factor TGF transforming growth factor


id: cord-016009-qa7bcsbu
type: GGP
entity:
  growth factor ECM extracellular matrix EGF epidermal growth factor EMT epithelial mesenchymal transition HSC hepatic stellate cell IL interleukin MMP matrix metalloproteinase TGF transforming growth factor TIMP


id: cord-016009-qa7bcsbu
type: CHEMICAL
entity:
  bananas grapes strawberries citrus fruits tomatoes nuts chocolate pineapples fish spinach fermented foods


id: cord-016009-qa7bcsbu
type: CHEMICAL
entity:
  alpha 1 antitrypsin deficiency Let s talk about Alpha 1 Antitrypsin Deficiency Alpha1 antitrypsin deficiency


id: cord-322756-ouvn71r9
type: CHEMICAL
entity:
  N 1 2 3 dioleyloxy propyl n n n trimethylammonium chloride DOTMA and 1 2 dioleoyl 3 trimethylammonium propane chloride salt


id: cord-018601-mk66097y
type: GGP
entity:
  serotonin 5 hydroxytryptamine 2B receptor in pulmonary hypertension A role for potassium channels in smooth muscle cells


id: cord-018601-mk66097y
type: DISEASE
entity:
  anomalous pulmonary venous drainage 192 Pulmonary Capillary Hemangiomatosis Pulmonary capillary hemangiomatosis


id: cord-305838-i0ck2oo0
type: ORG
entity:
  the Diagnosis Management and Prevention of Chronic Obstructive Pulmonary Disease Reevaluation of Diagnosis in Adults With


id: cord-305838-i0ck2oo0
type: ORG
entity:
  Congenital Cardiology AEPC International Society for Heart and Lung Transplantation ISHLT Cystic Fibrosis Pulmonary Guidelines Chronic Medications for Maintenance of Lung Health


id: cord-305838-i0ck2oo0
type: WORK_OF_ART
entity:
  Away From Work A New Approach for Identifying Patients with Undiagnosed Chronic Obstructive Pulmonary Disease Case


id: cord-305838-i0ck2oo0
type: ORG
entity:
  Health Towards Reliable Data Collection and Annotation to Extract Pulmonary Digital Biomarkers Using Mobile Sensors SpiroSmart


id: cord-008510-mnpu27kl
type: DISEASE
entity:
  mononuclear cell infiltration of the alveolar walls Days 4 or 5 after transplantation and 4 the destruction


id: cord-002122-s2r0en6f
type: DNA
entity:
  dog date 2016 07 07 journal Acta Vet Scand DOI 10 1186 s13028 016 0228 1 sha eb87c25391cf7493b664f98408bc230ce97198fb doc_id 2122


id: cord-002122-s2r0en6f
type: ORG
entity:
  nl 1 Department of Clinical Sciences of Companion Animals Faculty of Veterinary Medicine Utrecht University


id: cord-002122-s2r0en6f
type: ORG
entity:
  the Emergency Service of the Department of Clinical Science of Companion Animals of the Faculty of Veterinary Medicine Utrecht University


id: cord-022082-1dq623oe
type: CL
entity:
  bronchiolar and alveolar walls by collagen and hyperplastic cuboidal epithelium may line the thickened alveolar septa Air spaces


id: cord-022082-1dq623oe
type: DISEASE
entity:
  Olfactory neuroblastoma ethesioneuroblastoma olfactory neuroepithelioma olfactory neuroepithelial carcinoma


id: cord-022082-1dq623oe
type: DISEASE
entity:
  liver kidney lung and olfactory mucosa Nasal cytochrome P450 2A Identification regional localization


id: cord-022082-1dq623oe
type: DISEASE
entity:
  hypersecretion of mucus in the bronchial tree Goblet cell glycoprotein and tracheal gland hypertrophy


id: cord-331939-6okbdw7a
type: ORG
entity:
  the American College of Physicians Task Force for the Diagnosis and Management of Acute Pulmonary Embolism


id: cord-024183-1mrdjc39
type: DISEASE
entity:
  congenital neuromuscular disorders congenital myopathies congenital muscular dystrophies congenital myotonic dystrophy


id: cord-021742-sdz6d1r5
type: CELL_LINE
entity:
  Gn RH analogue Catamenial pneumothorax Catamenial pneumothorax Spontaneous pneumothorax complicating pregnancy


id: cord-005941-e4fvj54l
type: DISEASE
entity:
  impairment of the surfactant system 55 Several reports support this hypothesis In rats exposed to 0 3 ppm of ozone


id: cord-000254-bufbjdmw
type: PROTEIN
entity:
  SP C GM CSF Granulocyte macrophage colony stimulating factor Human immunodeficiency virus HP Hypersensitivity pneumonitis


id: cord-000254-bufbjdmw
type: CELL_TYPE
entity:
  paediatric pulmonary alveolar proteinosis Granulocyte macrophage colony stimulating factor autoantibodies


id: cord-000254-bufbjdmw
type: GGP
entity:
  defensins 89 90 91 92 A large number of pathological situations can impair gas exchange and contribute to progressive lung damage and ILD Consequently diagnosis approaches need to be organized by cause with a clinical evaluation requiring a careful history paying attention to exposures and systemic diseases Indeed in a number of pathological situations no final diagnosis is proposed and the conclusion reported by the physician in charge of the patient is ILD of unknown cause However information from recent studies highlights the concept that lung insults caused by substances from the environment


id: cord-000254-bufbjdmw
type: ORG
entity:
  European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias Pediatric


id: cord-000254-bufbjdmw
type: DISEASE
entity:
  respiratory manifestations lymphadenopathy skin lesions ocular and central nervous system abnormalities


id: cord-255519-tcobane8
type: ORG
entity:
  the International Diabetes Federation Task Force on Epidemiology and Prevention American Heart Association World Heart Federation International Atherosclerosis Society and International Association for the Study of Obesity American Association of Cardiovascular


id: cord-255519-tcobane8
type: ORG
entity:
  the Council on Clinical Cardiology the Councils on Cardiovascular Nursing Epidemiology and Prevention and Nutrition Physical Activity and Metabolism


id: cord-255519-tcobane8
type: ORG
entity:
  the American Heart Association Council on Clinical Cardiology Subcommittee on Exercise Cardiac Rehabilitation and Prevention Cardiac


id: cord-255519-tcobane8
type: ORG
entity:
  the National Association of Clinical Nurse Specialists the Preventive Cardiovascular Nurses Association


id: cord-255519-tcobane8
type: ORG
entity:
  the Council on Clinical Cardiology Subcommittee on Exercise Cardiac Rehabilitation and Prevention Harmonizing


id: cord-255519-tcobane8
type: WORK_OF_ART
entity:
  Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents National Heart Lung and Blood Institute


id: cord-255519-tcobane8
type: ORG
entity:
  the American Heart Association Council on Clinical Cardiology Subcommittee on Exercise Cardiac Rehabilitation and Prevention


id: cord-255519-tcobane8
type: ORG
entity:
  Rehabilitation Inter American Heart Foundation National Association of Clinical Nurse Specialists Preventive Cardiovascular Nurses Association


id: cord-255519-tcobane8
type: ORG
entity:
  the Council on Clinical Cardiology Subcommittee on Exercise Cardiac Rehabilitation and Prevention Effect


id: cord-255519-tcobane8
type: DISEASE
entity:
  orthostatic intolerance skeletal muscle changes joint contractures pulmonary atelectasis urinary stasis


id: cord-019001-ralxw4ad
type: CL
entity:
  vascular smooth muscle as a determinant of pulmonary hypertension at high altitude Endothelial and subintimal changes in rat


id: cord-335382-fk4um9nw
type: DNA
entity:
  adenosine triphosphate APT binding cassette transporter subfamily A member 3 ABCA3 chromosome 16p13 3 Defects


id: cord-335382-fk4um9nw
type: GGP
entity:
  Stage IA T1 N0 M0 Stage IB T2 N0 M0 Stage IIA T1 N1 M0 Stage IIB T2 N1 M0 T3 N0 M0 Stage IIIA T1 N2 M0 T2 N2 M0 T3 N1 M0 T3 N2 M0 Stage IIIB Any T N3 M0 T4


id: cord-335382-fk4um9nw
type: CHEMICAL
entity:
  tropomyosin TPM N terminal coiled coil domains to the ALK C terminal kinase domain producing two ALK fusion genes TPM4


id: cord-335382-fk4um9nw
type: DISEASE
entity:
  preneoplastic preinvasive bronchial epithelium reveals multiple discontinuous sites of 3p allele loss


id: cord-335382-fk4um9nw
type: DISEASE
entity:
  interstitial diseases Pulmonary fibrosis sarcoidosis histiocytosis X autoimmune pulmonary disease lymphangioleiomyomatosis Idiopathic pulmonary fibrosis


id: cord-320447-nq9f1gmu
type: FAC
entity:
  Pulmonary Vascular Remodeling in Pulmonary Hypertension Structure and Composition of Pulmonary Arteries Capillaries and Veins Interpretation


id: cord-016690-3gsq724l
type: DISEASE
entity:
  chronic obstructive pulmonary disease tuberculosis silicosis pulmonary abscess bronchiectasis cystic


id: cord-320959-sgdqhtns
type: ORG
entity:
  Wisconsin Final Report Update Interim Guidance for Health Care Providers Evaluating and Caring for Patients with Suspected


id: cord-329442-ycj6sf6z
type: PROTEIN
entity:
  Haemophilus influenzae Moraxella catarrhalis Streptocuccus pneumoniae Pseudomonas aeruginosa Staphylococcus aureus


id: cord-278846-nqj7ctk3
type: PROTEIN
entity:
  Mer tyrosine kinase MerTK sialic acid dependent adhesion molecule SiglecF hormone receptor F4 8 glycoprotein CD64


id: cord-278846-nqj7ctk3
type: GGP
entity:
  transforming growth factor beta receptor TGF βR interleukin IL 10 receptor IL 10R CD200 receptor CD200R


id: cord-278846-nqj7ctk3
type: CL
entity:
  proinflammatory host responses 2 For example severe Coronavirus disease 19 COVID 19 associated pneumonia patients may exhibit features of systemic hyper inflammation also known as macrophage activation syndrome or cytokine storm which is associated with sustained elevation of macrophage monocytederived pro inflammatory cytokines e g IL 6 IL 8 TNF α IL 1β


id: cord-278846-nqj7ctk3
type: DISEASE
entity:
  asthma chronic obstructive pulmonary disease COPD cystic fibrosis CF idiopathic pulmonary fibrosis IPF


id: cord-026005-f2khcjdy
type: CELL_TYPE
entity:
  thymus thymic branchial cysts bronchi bronchogenic cysts ectopic thyroid tissue thyroglossal duct cysts


id: cord-026005-f2khcjdy
type: CL
entity:
  Mannheimia haemolytica Pasteurella multocida parainfluenza virus 3 PI 3 adenovirus reovirus respiratory syncytial virus RSV chlamydiae


id: cord-026005-f2khcjdy
type: CL
entity:
  bronchiolar and alveolar epithelium edema and a few days later proliferation of type II pneumonocytes


id: cord-026005-f2khcjdy
type: WORK_OF_ART
entity:
  Disorders of the Conducting System Species Specific Diseases of the Nasal Cavity and Paranasal Sinuses Disorders of Dogs Mycotic Infections Neoplasms


id: cord-026005-f2khcjdy
type: DISEASE
entity:
  rhinoviruses infectious bovine rhinotracheitis bovine herpesvirus 1 feline rhinotracheitis felid herpesvirus 1 and viruses of the canine infectious respiratory disease


id: cord-026005-f2khcjdy
type: DISEASE
entity:
  infectious canine hepatitis virus reovirus type 1 canid herpesvirus 1 CaHV 1 canine respiratory coronavirus CRCoV


id: cord-026005-f2khcjdy
type: DISEASE
entity:
  respiratory syndrome virus PRRSV swine influenza virus SIV porcine circovirus 2 PCV2 porcine respiratory coronavirus PRCoV Mycoplasma hyopneumoniae


id: cord-005646-xhx9pzhj
type: DNA
entity:
  SANCH S 1L AlL GO L VARAS K FOLGADO S GARCIA E P 1 C U LA FE Valencia Spain CASE REPORT The patient was a 2 year o d gift


id: cord-005646-xhx9pzhj
type: ORG
entity:
  Mayer Sagv Division of Pediatric Critical Care Medicine Schneider Children s Hospital New Hyde Park NY


id: cord-005646-xhx9pzhj
type: DISEASE
entity:
  congenital heart disease ventricular septal defect _ other septal defects VSD atrioventricular AV canal Tetralogy of Fallot TOF


id: cord-023509-tvqpv6fp
type: PROTEIN
entity:
  tumour necrosis factor antagonists 42 43 44 48 82 83 84 85 86 87 88 89 90 The histological appearances may suggest extrinsic allergic alveolitis or sarcoidosis but the centri acinar


id: cord-023509-tvqpv6fp
type: DNA
entity:
  Sahara regions Sulla possibilita e sulla frequenza della silicosi pulmonare tra gli abitanti del deserto libico Simple siliceous pneumoconiosis


id: cord-023509-tvqpv6fp
type: ORG
entity:
  Committee of the Environmental and Occupational Health Assembly of the Committee of the Environmental and Occupational Health Assembly


id: cord-017248-a37t31u1
type: CL
entity:
  stem and spinal cord Prepare frozen sections and request Sudan stain Prepare frozen sections of one half of gland and paraffin sections of the other half Petechial hemorrhages of skin chest neck and face Wounds other traumatic lesions Bone fractures Petechiae of conjunctivas and retinas Fat may accumulate on surface ofblood


id: cord-017248-a37t31u1
type: CL
entity:
  stem encephalitis Listeria monocytogenes brain stem encephalitis viral brain stem encephalitis NOTE See also under Encephalitis limbic Brain For removal and specimen preparation see Chapter 4 Necrotizing encephalitis with or without abscess formation 1 Enterocolitis Other Types or Type Undetermined NOTE A multitude of infectious and noninfectious agents


id: cord-017248-a37t31u1
type: CL
entity:
  stem and spinal cord See also above under Skull and spine and under Possible Associated Conditions Incompetence See Insufficiency Related Terms Battered child syndrome child abuse or child neglect death NOTE Vitreous should not be aspirated until the skull has been opened and trauma ruled out because there is a risk of artifactual damage to the retina In the presence of craniocerebral trauma the pathologist can opt to examine the eyes by removal fixation and histologic study or retinal photography Follow general procedures described under Homicide and if necessary the procedures described under Rape External examination See above under Note Prepare roentgenograms of entire body See above under Note In other situations or after study of the fundus submit sample of vitreous for chemical and possible toxicologic study Umbilical cord attachment Prepare histologic sections of umbilicus and end of umbilical cord Blood Submit sample for toxicologic study Consider retaining dried blood on filter paper for possible DNA


id: cord-017248-a37t31u1
type: GGP
entity:
  Reye s syndrome differential diagnosis Prevalence and non specificity of microvesicular fatty changes


id: cord-017248-a37t31u1
type: DISEASE
entity:
  infectious angiitis necrotizing arteritis polyarteritis nodosa rheumatic arteritis rheumatoid arteritis syphilitic arteritis Takayasu s arteritis


id: cord-017248-a37t31u1
type: DISEASE
entity:
  iris cataracts retinal pigmentation Ischemic lesions Artery Patent Ductal Synonym Patent ductus arteriosus


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Atrial or ventricular septal defect coarctation ofthe aorta conotruncal anomalies necrotizing enterocolitis


id: cord-017248-a37t31u1
type: DISEASE
entity:
  ventricular and atrial walls hypoplastic left atrium mitral valve left ventricle and ascending aorta mitral atresia


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Congenital biliary atresia extrahepatic biliary atresia infantile obstructive cholangio pathy syndromic Alagille s syndrome


id: cord-017248-a37t31u1
type: DISEASE
entity:
  malrotation situs inversus preduodenal portal vein absent inferior vena cava anomalous hepatic artery


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Hemosiderosis idiopathic pulmonary Lipoproteinosis pulmonary alveolar Microlithiasis pulmonary alveolar Pneumonia lipoid


id: cord-017248-a37t31u1
type: DISEASE
entity:
  acute hypersensitivity arteritis hyperthyroidism gastrointestinal hemorrhage hypothyroidism idiopathic arterial calcification


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Dreifuss mucular dystrophy facioscapulohumeral dystrophy limb girdle dystrophy myotonic muscular dystrophy


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Barre syndrome idiopathic pulmonary fibrosis idiopathic thrombocytopenic purpura IgA deficiency lichen planus


id: cord-017248-a37t31u1
type: DISEASE
entity:
  cirrhosis biliary atresia 3 Immunodeficiency See Syndrome acquired immunodeficiency and Syndrome primary immunodeficiency Impression Basilar NOTE Basilar


id: cord-017248-a37t31u1
type: DISEASE
entity:
  acquired immunodeficiency syndrome AIDS cancer cachexia inflammatory bowel disease liver or kidney failure


id: cord-017248-a37t31u1
type: DISEASE
entity:
  reflux 3 neoplasms of lungs esophagus intestine and liver chronic liver disease inflammatory bowel disease pulmonary disease


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Pharynx and gastrointestinal tract Heart liver and kidneys Record skin changes and eye abnormalities


id: cord-017248-a37t31u1
type: DISEASE
entity:
  liver and biliary tract Pulmonary Related Terms Congenital cystic adenomatoid malformation congenital pulmonary lymphangiectasis intralobular bronchopulmonary sequestration


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Collagenous inorganic dust pneumoconiosis nodular type Silicosis Noncollagenous inorganic dust pneumoconiosis


id: cord-017248-a37t31u1
type: DISEASE
entity:
  Acute lymphocytic leukemia acute myelocytic leukemia acute megakaryocytic leukemia Cardiovascular disease


id: cord-017248-a37t31u1
type: DISEASE
entity:
  atrioventricular septal defect subpulmonary stenosis pulmonary valve atresia midline symmetric liver malrotation


id: cord-017248-a37t31u1
type: DISEASE
entity:
  cerebral arteries aortic insufficiency calcific aortic stenosis coarctation of the aorta infective endocarditis Shone s syndrome Turner s syndrome


id: cord-005814-ak5pq312
type: PROTEIN
entity:
  soluble intercellular adhesion molecule 1 sICAM 1 vascular cell adhesion molecule 1 sVCAM 1 and E selectin sELAM 1 sICAM 1 sVCAM 1 sELAM 1


id: cord-005814-ak5pq312
type: PROTEIN
entity:
  plasma soluble intercellular adhesion molecule 1 sICAM 1 vascular cell adhesion molecule 1 sVCAM 1 and E selecfin sELAM 1


id: cord-005814-ak5pq312
type: CELL_LINE
entity:
  PREHOSPITAL RESUSCITATION EFFORTS C K6ppel G Fahron H Lufft A KrUger C Th Jrk F Bertschat F Martens Dept of Nephrology add Medical Intensive Care Virchow Klinikum Humboldt Universit t D 13353 Bedin Germany Obiective The success rate of prehospital resuscitation in patients with cardiocirculatory arrest in an Emergency Medical System EMS


id: cord-005814-ak5pq312
type: CELL_LINE
entity:
  T45 T60 T65 T75 A 2 1 0 6 2 1 0 5 2 1 0 4 2 1 0 4 2 1 0 7 2 1 0 7 2 1 0 Conclusion the C slowed V L and V T


id: cord-005814-ak5pq312
type: CELL_LINE
entity:
  Swan Ganz pulmonary artery catheter Beckton Dickinson U S A Deseret 1000 Cardiac Output Computer Medical Inc U S A


id: cord-005814-ak5pq312
type: DNA
entity:
  ICU C Kotsavassiloglou D Matamis G Dadoudis J Kioumis D Riggos ICU dep G Papanicolaou Gen Hosp Exohl Thessaloniki


id: cord-005814-ak5pq312
type: PROTEIN
entity:
  pI F CACT PI7 r 0 62 CVC samples 132 88 34 22 V femoralis samples 1 28 84 29 24 p value n s n s Conclusion There is no difference in heparin


id: cord-005814-ak5pq312
type: CELL_LINE
entity:
  Swan Ganz pulmonary catheter PC requiremen t during elective cardiac surgery according to the need of sustained inotropic support after surgery Methods Three hundred patients aged from 27 to 85 89 females and 211 males were consecutively operated on for elective coronary artery bypass surgery CABG n 179 valvular replacement VR n 98 combination of both VR CABG n 15


id: cord-005814-ak5pq312
type: GGP
entity:
  LDH p 0 04 and a more marked hypoalbuminemia p O 03 Mortality was higer in Group A 52 6 than in Group B 29 6 p 0 04 Analysing the A


id: cord-005814-ak5pq312
type: GGP
entity:
  Objectives Activated endothelial cells release soluble intercellular adhesion molecule 1 sICAM 1 vascular cell adhesion molecule 1 sVCAM 1


id: cord-005814-ak5pq312
type: GGP
entity:
  fenoterol 0 2 rag For 0 5 h spirometry was repeated Results In resting pulmonary abnormalities observer in the S


id: cord-005814-ak5pq312
type: GGP
entity:
  Propanolol i v RESULTS A significant increase of the aortic diastolic pressures and a significant decrease of the left ventricle telediastolic pressures


id: cord-005814-ak5pq312
type: GGP
entity:
  FIO2 0 4 4 pH 7 45 5 heart rate 20 bm and or 6 non mental alertness and 7 other medical disorders after which adequate weaning therapy was necessary Then successful weaning after 24h was considered 1 spontaneous breathing without any forrn of mechanical assistance 2 stability in haemodynamics and 3 elimination of fever threat Results 122 pts 75 were extubated at 8h without complication 29 other pts 18 at 8h but had to be reintubated because they were hypoxic and began weaning therapy finally they were all re extubated by 48h Only 11 pts 7 proved problematic Conclusion A aesthesia wimhlw options selectkm extubation reintubation and weaning predicted quick times Propofol administration and safe rigid criteria extubation 75 8h and 18 24h exempting pts with developed post operative complications 7 extubation


id: cord-005814-ak5pq312
type: GGP
entity:
  8channel electroencephalograph 4 channel roencephalograph AD converter 16 analog inputs 12 bit resolution 60 k Hz IBM


id: cord-005814-ak5pq312
type: GGP
entity:
  MAP T0 124mmHg T8 118mmHg HR T0 177 T8 201 RAP T0 11mmHg T8 19mmHg PAP T0 26mmHg T8 31mmHg PCWP T0 14mmHg T8 15 mHg SVR T0


id: cord-005814-ak5pq312
type: WORK_OF_ART
entity:
  Laterre F Thys E Danse J P Pelgrim E Florence Z Roeseler M S R eynaert Dept of Intensive Care St Luc Univ Hospital Brussels Belgium Therapy


id: cord-005814-ak5pq312
type: WORK_OF_ART
entity:
  A Michalopoulos A Anthi K Rellos J Kriaras S Geroulanos Intensive Care Unit Onassis Cardiac Center Athens


id: cord-005814-ak5pq312
type: ORG
entity:
  Chair of Anaesthesiology Resuccitation and Medicine of Catastrophes Neurology of Ukrainian State Medical


id: cord-005814-ak5pq312
type: CHEMICAL
entity:
  CO 133_ 4 vs 144_ 8 p 0 28 and QSt AA 21 5_ 0 8 vs 22 8_ 0 9 p 0 09 The results of regional pertusion


id: cord-005814-ak5pq312
type: CHEMICAL
entity:
  xauifosted b 7 the exhaust of Lhe confulaLion nod oessel plateL heuoStasis The consuxptton of cnnpononts tbronbln


id: cord-005814-ak5pq312
type: CHEMICAL
entity:
  carbamates 5 8 imidazopyridines 5 1 cyclqpyrrol0nes 2 7 Analgesics and nonsteroidal antiinflammatories represented 6 8 of


# bib

id: cord-000254-bufbjdmw
title: Interstitial lung diseases in children
author: Clement, Annick
date: 2010-08-20
txt: ./txt/cord-000254-bufbjdmw.txt
cache: ./cache/cord-000254-bufbjdmw.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2939531/
doi: 10.1186/1750-1172-5-22
summary:
  Interstitial lung disease (ILD) in infants and children comprises a large spectrum of rare respiratory disorders that are mostly chronic and associated with high morbidity and mortality. Interstitial lung disease (ILD) in infants and children represents a heterogeneous group of respiratory disorders that are mostly chronic and associated with high morbidity and mortality (around 15%) [1, 2] . These disorders, more prevalent in young children, include diffuse developmental disorders, lung growth abnormalities, neuroendocrine cell hyperplasia and pulmonary interstitial glycogenosis, surfactant dysfunction disorders, disorders related to systemic diseases, disorders of immunocompromised host, and disorders of normal host caused by various insults such as aspiration syndrome or infections [8] . Several studies in the adult literature have reported an increased incidence of EBV and CMV infection in patients with pulmonary fibrosis, associated with virus DNA-positive lung tissue biopsies in several cases [147] .

abstract:
  Interstitial lung disease (ILD) in infants and children comprises a large spectrum of rare respiratory disorders that are mostly chronic and associated with high morbidity and mortality. These disorders are characterized by inflammatory and fibrotic changes that affect alveolar walls. Typical features of ILD include dyspnea, diffuse infiltrates on chest radiographs, and abnormal pulmonary function tests with restrictive ventilatory defect and/or impaired gas exchange. Many pathological situations can impair gas exchange and, therefore, may contribute to progressive lung damage and ILD. Consequently, diagnosis approach needs to be structured with a clinical evaluation requiring a careful history paying attention to exposures and systemic diseases. Several classifications for ILD have been proposed but none is entirely satisfactory especially in children. The present article reviews current concepts of pathophysiological mechanisms, etiology and diagnostic approaches, as well as therapeutic strategies. The following diagnostic grouping is used to discuss the various causes of pediatric ILD: 1) exposure-related ILD; 2) systemic disease-associated ILD; 3) alveolar structure disorder-associated ILD; and 4) ILD specific to infancy. Therapeutic options include mainly anti-inflammatory, immunosuppressive, and/or anti-fibrotic drugs. The outcome is highly variable with a mortality rate around 15%. An overall favorable response to corticosteroid therapy is observed in around 50% of cases, often associated with sequelae such as limited exercise tolerance or the need for long-term oxygen therapy.


id: cord-000268-480d3yfv
author: Porfyridis, Ilias
date: 2010-09-29
txt: ./txt/cord-000268-480d3yfv.txt
cache: ./cache/cord-000268-480d3yfv.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955686/
doi: 10.1186/1471-2334-10-286
summary:
  title: Diagnostic value of triggering receptor expressed on myeloid cells-1 and C-reactive protein for patients with lung infiltrates: an observational study The aim of the present study was to define whether expression of TREM-1 on cell membranes of neutrophils (nTREM-1), of monocytes (mTREM-1) and serum sTREM-1 may help in the diagnosis of acute bacterial infections for patients admitted with a new pulmonary infiltrate or pleural effusion. In conclusion, the presented results indicate that serum sTREM-1 and expression of TREM-1 on neutrophils and monocytes may serve as markers of CAP in patients with pulmonary infiltrates. Increased levels of soluble triggering receptor expressed on myeloid cells-1 in patients with acute pancreatitis Prognosis of community acquired pneumonia(CAP): value of triggering receptor expressed on myeloid cells-1 (TREM-1) and other mediators of the inflammatory response Diagnostic implications of soluble triggering receptor expressed on myeloid cells-1 in BAL fluid of patients with pulmonary infiltrates in the ICU

title:
  Diagnostic value of triggering receptor expressed on myeloid cells-1 and C-reactive protein for patients with lung infiltrates: an observational study

abstract:
  BACKGROUND: Differential diagnosis of patients with lung infiltrates remains a challenge. Triggering receptor expressed on myeloid cells (TREM)-1 is a neutrophil and monocyte receptor up-regulated during infection. The aim of this study was to evaluate the diagnostic accuracy of TREM-1 and of C-reactive protein (CRP) from patients with lung infiltrates to discern community acquired lung infections. METHODS: 68 patients admitted to a medical ward with acute respiratory illness were enrolled in the study. Neutrophil and monocyte TREM-1 expression were measured by flow cytometry, sTREM-1 by an enzyme immunoassay and C-reactive protein by nephelometry. Clinical pulmonary infection score was recorded. RESULTS: 34 patients were diagnosed with bacterial community acquired pneumonia (group A) and 34 with non-bacterial pulmonary disease (group B). Median serum TREM-1 concentration was 102.09 pg/ml in group A and lower than 15.10 pg/ml (p < 0.0001) in group B. Mean±SE neutrophil TREM-1 expression was 4.67 ± 0.53 MFI in group A and 2.64 ± 0.25 MFI (p = 0.001) in group B. Monocyte TREM-1 expression was 4.2 ± 0.42 MFI in group A and 2.64 ± 0.35 MFI (p = 0.007) in group B and mean±SE CRP was 18.03 ± 2 mg/ml in group A and 7.1 ± 1.54 mg/ml (p < 0.001) in group B. A cut-off of 19.53 pg/ml of sTREM-1 with sensitivity 82.6% and specificity 63% to discriminate between infectious and non-infectious pulmonary infiltrates was found. sTREM-1 at admission greater than 180 pg/ml was accompanied with unfavourable outcome. CONCLUSION: TREM-1 myeloid expression and sTREM-1 are reliable markers of bacterial infection among patients with pulmonary infiltrates; sTREM-1 is a predictor of final outcome.


id: cord-000364-ikq38rm1
author: Rasmuson, J.
date: 2011-01-15
txt: ./txt/cord-000364-ikq38rm1.txt
cache: ./cache/cord-000364-ikq38rm1.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075397/
doi: 10.1007/s10096-010-1141-6
summary:
  Lung computer tomography (CT) on admission revealed pronounced diffuse bilateral interstitial infiltrates with pulmonary oedema, dependant atelectasis, and moderate pleural effusions (Fig. 1 ) which were later drained (>800 ml). Hantavirus infection was verified with the detection of PUUV RNA in plasma (630,000 copies/ml) on the day of admission, while IgM and IgG were negative. Consecutive plasma samples were analysed for PUUV RNA with declining viral copy numbers until negative 16 days post onset of Fig. 1 Chest CT-scans of two European patients with hantavirus pulmonary syndrome. Concerning the cases of European hantavirus infection in our present report, there was only mild or no renal impairment at the time of admission, whereas the respiratory involvement was early and severe, consistent with acute respiratory distress syndrome (ARDS), fulfilling criteria of HPS according to CDC case definition [19] .

title:
  Time to revise the paradigm of hantavirus syndromes? Hantavirus pulmonary syndrome caused by European hantavirus

abstract:
  Hantaviruses have previously been recognised to cause two separate syndromes: hemorrhagic fever with renal syndrome in Eurasia, and hantavirus pulmonary syndrome (HPS) in the Americas. However, increasing evidence suggests that this dichotomy is no longer fruitful when recognising human hantavirus disease and understanding the pathogenesis. Herein are presented three cases of severe European Puumala hantavirus infection that meet the HPS case definition. The clinical and pathological findings were similar to those found in American hantavirus patients. Consequently, hantavirus infection should be considered as a cause of acute respiratory distress in all endemic areas worldwide.


id: cord-002122-s2r0en6f
title: Interstitial pneumonia and pulmonary hypertension associated with suspected ehrlichiosis in a dog
author: Toom, Marjolein Lisette den
date: 2016-07-07
txt: ./txt/cord-002122-s2r0en6f.txt
cache: ./cache/cord-002122-s2r0en6f.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937533/
doi: 10.1186/s13028-016-0228-1
summary:
  BACKGROUND: In dogs with canine monocytic ehrlichiosis (CME), respiratory signs are uncommon and clinical and radiographic signs of interstitial pneumonia are poorly described. Treatment with oxygen supplementation, a typed packed red blood cell transfusion and medical therapy with doxycycline, pimobendan and sildenafil was initiated and the dog improved clinically. Acta Veterinaria Scandinavica *Correspondence: M.L.denToom@uu.nl 1 Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 108, 3508 TD Utrecht, The Netherlands Full list of author information is available at the end of the article vasorum, Leishmania chagasi, Toxoplasma gondii, Pneumocystis carinii, Babesia canis, Leptospira sp., Mycoplasma sp, canine distemper virus and adenovirus [4] [5] [6] [7] [8] [9] [10] [11] [12] . This case report describes the clinical, radiographic and echocardiographic presentation of a dog with interstitial pneumonia and severe PH suspected to be associated with E.

abstract:
  BACKGROUND: In dogs with canine monocytic ehrlichiosis (CME), respiratory signs are uncommon and clinical and radiographic signs of interstitial pneumonia are poorly described. However, in human monocytic ehrlichiosis, respiratory signs are common and signs of interstitial pneumonia are well known. Pulmonary hypertension (PH) is classified based on the underlying disease and its treatment is aimed at reducing the clinical signs and, if possible, addressing the primary disease process. PH is often irreversible, but can be reversible if it is secondary to a treatable underlying etiology. CME is currently not generally recognized as one of the possible diseases leading to interstitial pneumonia and secondary PH in dogs. Only one case of PH associated with CME has been reported worldwide. CASE PRESENTATION: A seven-year-old, male intact, mixed breed dog was presented with 2 weeks history of lethargy and dyspnea. The dog previously lived in the Cape Verdean islands. Physical examination showed signs of right-sided congestive heart failure and poor peripheral perfusion. Thoracic radiography showed moderate right-sided cardiomegaly with dilation of the main pulmonary artery and a mild diffuse interstitial lung pattern with peribronchial cuffing. Echocardiography showed severe pulmonary hypertension with an estimated pressure gradient of 136 mm Hg. On arterial blood gas analysis, severe hypoxemia was found and complete blood count revealed moderate regenerative anemia and severe thrombocytopenia. A severe gamma hyperglobulinemia was also documented. Serology for Ehrlichia canis was highly positive. Treatment with oxygen supplementation, a typed packed red blood cell transfusion and medical therapy with doxycycline, pimobendan and sildenafil was initiated and the dog improved clinically. Approximately 2 weeks later, there was complete resolution of all clinical signs and marked improvement of the PH. CONCLUSION: This report illustrates that CME might be associated with significant pulmonary disease and should be considered as a possible differential diagnosis in dogs presenting with dyspnea and secondary pulmonary hypertension, especially in dogs that have been in endemic areas. This is important because CME is a treatable disease and its secondary lung and cardiac manifestations may be completely reversible.


id: cord-005646-xhx9pzhj
author: nan
date: 1996
txt: ./txt/cord-005646-xhx9pzhj.txt
cache: ./cache/cord-005646-xhx9pzhj.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095092/
doi: 10.1007/bf02316512
abstract: nan
summary:
  Aims and methods The aim of both a prospective and retrospective survey conducted in German pediatric intensive care units in 1993 was to accumulate data on the epidemiology, risk factors, natural history and treatment strategies in a large group of pediatric ARDS patients who were treated in the tt~ee year period from 1991 to 1993.All patients had acute bilateral alveolar infiltration of noncardiogenic origin and a pO2~iO2 ratio < 150mmHg. The influence of sex, underlying disease and single organ failure was analyzed using the Fischer''s exact test, the influence of additional organ failure on mortality was tested with the Cochran-Mantel-Haenszet statistics.

title:
  2nd World Congress on Pediatric Intensive Care 1996 Rotterdam, The Netherlands, 23–26 June 1996 Abstracts of Oral Presentations, Posters and Nursing Programme


id: cord-005814-ak5pq312
title: 8th European Congress of Intensive Care Medicine Athens - Greece, October 18–22, 1995 Abstracts
author: nan
date: 1995
txt: ./txt/cord-005814-ak5pq312.txt
cache: ./cache/cord-005814-ak5pq312.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095534/
doi: 10.1007/bf02426401
abstract: nan
summary:
  Results: In 5 patients with treated SS, 16 tests were performed (VL n=8; Dobu n=4; NA n=4 Method: Septic shock was defined as severe sepsis with either persistent hypotension (mean arterial pressure; MAP<70 mmHg) or the requirement for a noradrenaline (NA) infusion ~> 0.1 ~g/kg/min with a MAP _< 90mmHg. Cardiovascular support was limited to NA + dobutamine (DB), 546C88 was administered for up to 8 h at a fixed dose-rate of either i, 2.5, 5, 10 or 20 mg/kg/h iv. Methods: Fourteen cases were s~udied,their gestational age ranged from(27-32)ws.Continnous positive air way pressure was applied to six cases at Peep level from (3-6)cm H2o through nasal pronge,(group I),the other 8 cases were managed as routine,(group II).Blood gases, TcPO2,TcCo2,resp.rate,depth and pattern were monitored for assessment of tissue Oxygenation and ventilation, Results: Our rasults showed that early application of CPAP improve ventilation among (83.3%)of cases,while (16.7%)of cases need IMV.The cases of group II need IMV among (75%)of the studied cases during the second or the third day of life.


id: cord-005941-e4fvj54l
title: The surfactant system of the adult lung: physiology and clinical perspectives
author: Hamm, H.
date: 1992
txt: ./txt/cord-005941-e4fvj54l.txt
cache: ./cache/cord-005941-e4fvj54l.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095985/
doi: 10.1007/bf00180279
summary:
  Further clinical studies will be necessary to investigate the potential therapeutic benefits of surfactant substitution and the usefulness of pharmacologic manipulation of the secretory activity of alveolar type II cells in pulmonary medicine. The fate of secreted surfactant material seems to be determined by five mechanisms: -Intraalveolar catabolism -Phagocytosis and degradation by alveolar macrophages [110, 118] -Removal by the mucociliary escalator -Recycling into the alveolar type II cell -Redistribution into other surrounding tissue Clearance studies in rabbits [140] have shown that approximately 7% of radiolabeled phosphatidylcholine is removed via the upper airways in 24 h, suggesting that this pathway is only of minor importance. These studies may indicate that the acute effect of nitrogen dioxide on alveolar type II cells is enhanced surfactant lipid synthesis, while chronic low-dose exposure leads to a decrease in surfactant synthesis capacity. Effects of ozone on phospholipid synthesis by alveolar type II cells isolated from adult rat lung

abstract:
  Pulmonary surfactant is synthesized and secreted by alveolar type II cells and constitutes an important component of the alveolar lining fluid. It comprises a unique mixture of phospholipids and surfactant-specific proteins. More than 30 years after its first biochemical characterization, knowledge of the composition and functions of the surfactant complex has grown considerably. Its classically known role is to decrease surface tension in alveolar air spaces to a degree that facilitates adequate ventilation of the peripheral lung. More recently, other important surfactant functions have come into view. Probably most notable among these, surfactant has been demonstrated to enhance local pulmonary defense mechanisms and to modulate immune responses in the alveolar milieu. These findings have prompted interest in the role and the possible alterations of the surfactant system in a variety of lung diseases and in environmental impacts on the lung. However, only a limited number of studies investigating surfactant changes in human lung disease have hitherto been published. Preliminary results suggest that surfactant analyses, e.g., from bronchoalveolar lavage fluids, may reveal quantitative and qualitative abnormalities of the surfactant system in human lung disorders. It is hypothesized that in the future, surfactant studies may become one of our clinical tools to evaluate the activity and severity of peripheral lung diseases. In certain disorders they may also gain diagnostic significance. Further clinical studies will be necessary to investigate the potential therapeutic benefits of surfactant substitution and the usefulness of pharmacologic manipulation of the secretory activity of alveolar type II cells in pulmonary medicine.


id: cord-006428-l9akk8i6
title: Zelluläre Pathophysiologie der pulmonalen Hypertonie
author: Kuebler, W. M.
date: 2014-02-18
txt: ./txt/cord-006428-l9akk8i6.txt
cache: ./cache/cord-006428-l9akk8i6.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101801/
doi: 10.1007/s00398-002-0347-z
summary:
  Die endotheliale Dysfunktion bewirkt durch eine verminderte Freisetzung vasodilatierender, anti-proliferativer Mediatoren bei gleichzeitig vermehrter Produktion vasokonstriktiver, proliferativer Substanzen nicht nur eine zunehmende pulmonale Vasokonstriktion, sondern unterstützt auch die pathologischen Umbauprozesse in Gefäßintima und -media. Durch Einnahme von Appetitzüg143) kam es allerdings in den 60er, 80er und 90er Jahren des vergangenen Jahrhunderts jeweils zu einem epidemischen Auftreten der Erkrankung in Europa, in dessen Folge die Inzidenz teilweise um das 25fache anstieg (1). Mittels Oligonukleotid-Microarray-Technik wurde zudem kürzlich bei PPH-Patienten eine veränderte pulmonale Expression verschiedener Onkogene, Apoptosegene sowie von Genen diagnostiziert, die für verschiedene Angiogenese-Mediatoren, Proteine der TGF-b-Familie, Kinasen sowie spezifische Ionenkanäle kodieren (45). Auch Hypoxie, die häufig mit der PH assoziiert ist, vermindert die Aktivität spannungsabhängiger Kaliumkanäle und bedingt dadurch einen Anstieg der zytosolischen Calcium-Konzentration, dem vermutlich wesentliche Bedeutung hinsichtlich der hypoxischen pulmonalen Vasokonstriktion zukommt (123, 169) . Dysfunctional voltage-gated K + channels in pulmonary artery smooth muscle cells of patients with primary pulmonary hypertension

abstract:
  Pulmonary hypertension comprises a group of diseases with heterogeneous etiology characterized by an increase of hydrostatic pressure in the pulmonary vascular bed. While secondary pulmonary hypertension predominantly results from acute or chronic left ventricular failure, characteristic gene defects or predisposing risk factors lead to various forms of primary pulmonary hypertension. Despite its diverse pathogenesis, pulmonary hypertension exhibits a uniform cellular pathophysiology in the pulmonary microcirculation. The dysfunction of lung vascular endothelial cells, which are the front line in response to hemodynamic changes in the pulmonary circulation, is the pathophysiological driving force of pulmonary hypertension. Endothelial dysfunction is characterized by a reduced production of vasodilative, anti-proliferative mediators and an increased release of vasoconstrictive, proliferative factors. This apparent imbalance not only enhances pulmonary vasoconstriction, but supports pathologic remodeling processes in the vascular intima and media. In addition, the pulmonary endothelium recruits platelets and leukocytes, thus, contributing to further release of vasoconstrictive and proliferative mediators and characteristic thrombus formation. These endothelium-derived pathomechanisms amplify each other, further enhance pulmonary vascular resistance, and finally result in fixation of the hypertensive state. Hence, pulmonary hypertension not only describes an alteration of lung hemodynamics, but comprises a complex set of pathophysiological events in both lung parenchymal cells and circulating blood cells. For development of new therapeutical strategies, the multifactorial character of the disease should be considered.


id: cord-006586-49btg9w7
author: Golfieri, R.
date: 2000
txt: ./txt/cord-006586-49btg9w7.txt
cache: ./cache/cord-006586-49btg9w7.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102073/
doi: 10.1007/s003309900268
summary:
  The aim of this study was to evaluate the incidence, radiographic appearance, time of onset, outcome and risk factors of non-infectious and infectious pulmonary complications following liver transplantation. The aim of this study was to evaluate the incidence, radiographic appearance, time of onset, outcome and risk factors of non-infectious and infectious pulmonary complications following liver transplantation. In univariate analysis (Table 1) , a statistically significant higher risk was demonstrated in cases of AHF patients, retransplantation, immunosuppression with OKT3, prolonged stay in ICU and AMV and in protracted pulmonary oedema; instead, surgical piggyback caval anastomosis is a factor reducing hazard. The present study, performed on a wider patient population, demonstrated, in univariate analysis, a significantly increased association of pulmonary infection with the following five risk factors: caval traditional anastomosis, retransplantation, OKT3 immunosuppression, ICU stay and AMV duration, pulmonary non-inflammatory abnormalities, such as effusion and atelectasis, and oedema.

title:
  Pulmonary complications of liver transplantation: radiological appearance and statistical evaluation of risk factors in 300 cases

abstract:
  The aim of this study was to evaluate the incidence, radiographic appearance, time of onset, outcome and risk factors of non-infectious and infectious pulmonary complications following liver transplantation. Chest X-ray features of 300 consecutive patients who had undergone 333 liver transplants over an 11-year period were analysed: the type of pulmonary complication, the infecting pathogens and the mean time of their occurrence are described. The main risk factors for lung infections were quantified through univariate and multivariate statistical analysis. Non-infectious pulmonary abnormalities (atelectasis and/or pleural effusion: 86.7 %) and pulmonary oedema (44.7 %) appeared during the first postoperative week. Infectious pneumonia was observed in 13.7 %, with a mortality of 36.6 %. Bacterial and viral pneumonia made up the bulk of infections (63.4 and 29.3 %, respectively) followed by fungal infiltrates (24.4 %). A fairly good correlation between radiological chest X-ray pattern, time of onset and the cultured microorganisms has been observed in all cases. In multivariate analysis, persistent non-infectious abnormalities and pulmonary oedema were identified as the major independent predictors of posttransplant pneumonia, followed by prolonged assisted mechanical ventilation and traditional caval anastomosis. A “pneumonia-risk score” was calculated: low-risk score ( < 2.25) predicts 2.7 % of probability of the onset of infections compared with 28.7 % of high-risk ( > 3.30) population. The “pneumonia-risk score” identifies a specific group of patients in whom closer radiographic monitoring is recommended. In addition, a highly significant correlation (p < 0.001) was observed between pneumonia-risk score and the expected survival, thus confirming pulmonary infections as a major cause of death in OLT recipients.


id: cord-006608-mq4a4u40
title: Hantavirus pulmonary syndrome in the United States
author: Fabbri, Marilyn
date: 2001
txt: ./txt/cord-006608-mq4a4u40.txt
cache: ./cache/cord-006608-mq4a4u40.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102107/
doi: 10.1007/s11908-001-0028-1
summary:
  Unlike the previously characterized hantaviruses, which cause fever, hemorrhagic manifestations, and acute renal failure (hemorrhagic fever with renal syndrome), the newly named hantavirus pulmonary syndrome (HPS) presented with a brief prodromal illness followed by rapidly progressive noncardiogenic pulmonary edema [2] . In the United States, HPS is caused by at least four hantaviruses: the Sin Nombre virus (SNV, responsible for the Four Corners outbreak), the Black Creek Canal virus (isolated from the Florida cotton rat) [4] , the Bayou virus in Louisiana [5] , and the New York 1 hantavirus [6] . RNA viruses with segmented genomes, such as influenza virus, Since the first outbreak of hantavirus pulmonary syndrome (HPS) in 1993, understanding of the vast distribution and potential impact of hantaviruses has grown. A case-control study of hantavirus pulmonary syndrome during an outbreak in the southwestern United States

abstract:
  Since the first outbreak of hantavirus pulmonary syndrome (HPS) in 1993, understanding of the vast distribution and potential impact of hantaviruses has grown. At least 277 cases of HPS have been documented in the United States. The full clinical spectrum has yet to be elucidated, and one outbreak suggested the possibility of person-to-person transmission. New research has identified the β-3 integrins as cellular receptors for hantaviruses and has determined the pivotal role of the immune system in pathogenesis. Rapid diagnosis has been facilitated by a new immunoblot assay to detect Sin Nombre virus infection. Treatment remains primarily supportive; however, a placebocontrolled trial of ribavirin is ongoing. Extracorporeal membrane oxygenation may be a potential therapy in severe cases; inhaled nitric oxide needs further study. Vaccines developed against hantaviruses associated with hemorrhagic fever and renal syndrome might be effective against HPS-associated strains.


id: cord-007696-83v9yfa6
title: Pulmonary Fibrosis
author: Zisman, David A.
date: 2005
txt: ./txt/cord-007696-83v9yfa6.txt
cache: ./cache/cord-007696-83v9yfa6.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7120641/
doi: 10.1385/1-59259-940-0:003
summary:
  Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease limited to the lungs and associated with the histologic appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy. Factors that predict poor outcome include older age, male gender, severe dyspnea, history of cigarette smoking, severe loss of lung function, appearance and severity of fibrosis on radiological studies, lack of response to therapy, and prominent fibroblastic foci on histopathologic evaluation. With greater comprehension of the clinical relevance of the different histopathological subgroups that make up the idiopathic interstitial pneumonias, the term idiopathic pulmonary fibrosis (IPF) is now reserved to patients with idiopathic usual interstitial pneumonia (UIP) on surgical lung biopsy. Tang In a recent study, human T-lymphtropic virus type I (HTVL-I) positive IPF patients had more affected lung parenchyma, demonstrated traction bronchiectasis with honeycomb change, and exhibited increased levels of specific cytokines that correlated with activated T-cells in the bronchoalveolar lavage fluid (BALF).

abstract:
  Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease limited to the lungs and associated with the histologic appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy. The estimated prevalence in the United States is between 35,000 and 55,000 cases, and evidence suggests that the prevalence is increasing for IPF. Risk factors associated with pulmonary fibrosis include smoking, environmental exposures, gastroesophageal reflux disease, commonly prescribed drugs, diabetes mellitus, infectious agents, and genetic factors. The diagnosis requires a careful history and physical examination, characteristic physiological and radiological studies, and, in some cases, a surgical lung biopsy. The natural history of IPF is not known, but evidence supports the concept of a continuum of idiopathic interstitial pneumonias that may overlap in time. Most patients with IPF succumb to respiratory failure, cardiovascular disease, lung cancer, pulmonary embolism, infection, and other health problems. The median survival time for patients with IPF is less than 3 yr. Factors that predict poor outcome include older age, male gender, severe dyspnea, history of cigarette smoking, severe loss of lung function, appearance and severity of fibrosis on radiological studies, lack of response to therapy, and prominent fibroblastic foci on histopathologic evaluation. Conventional therapy (corticosteroids, azathioprine, cyclophosphamide) provides only marginal benefit. Lung transplantation should be considered for patients with IPF refractory to medical therapy. In light of the poor prognosis and lack of response to available anti-inflammatory therapy, alternative approaches to therapy are being pursued. Emerging strategies to treat patients with IPF include agents that inhibit epithelial injury or enhance repair, anticytokine approaches, agents that inhibit fibroblast proliferation or induce fibroblast apoptosis, and other novel approaches.


id: cord-007797-toam6r5y
title: Imaging of Pulmonary Infection
author: Franquet, Tomás
date: 2019-02-20
txt: ./txt/cord-007797-toam6r5y.txt
cache: ./cache/cord-007797-toam6r5y.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123565/
doi: 10.1007/978-3-030-11149-6_7
summary:
  Community acquired pneumonia refers to an acute infection of the lung in patients who did not meet any of the criteria for HCAP, presenting select clinical features (e.g., cough, fever, sputum production, and pleuritic chest pain) and accompanied by an acute infiltrate on a chest radiograph. Chest radiographs are of limited value in predicting the causative pathogen but are of good use to determine the extent of pneumonia and to detect complications (i.e., cavitation, abscess formation, pneumothorax, pleural effusion), to detect additional or alternative diagnoses, and, in some cases, to guide invasive diagnostic procedures. Risk factors for the development of staphylococcal pneumonia include underlying pulmonary disease (e.g., COPD, carcinoma), chronic illnesses (e.g., diabetes mellitus, renal failure), or viral infection. The lower lobes contrast-enhanced CT image shows a mixed opacity of consolidation (arrow) and ground-glass opacity (small arrows) consistent with lobar pneumonia tend to be affected, and the radiographic pattern is similar to that seen with S.

abstract:
  The spectrum of organisms known to cause respiratory infections is broad and constantly increasing as new pathogens are identified, and an increasing number of patients have impaired immunity due to disease or medications. The radiographic manifestations of a given organism may be variable depending on the immunologic status of the patient and the presence of pre- or coexisting lung disease. Moreover, the clinical data and radiographic findings often fail to lead to a definitive diagnosis of pneumonia because there are an extensive number of noninfectious processes associated with febrile pneumonitis. This chapter describes and illustrates the characteristic imaging manifestations of the most common community- acquired pneumonias, nosocomial pneumonias, and the various infections seen in both immunocompetent and immunocompromised patients.


id: cord-008510-mnpu27kl
title: The Regulation of Pulmonary Immunity
author: Lipscomb, Mary F.
date: 2008-04-10
txt: ./txt/cord-008510-mnpu27kl.txt
cache: ./cache/cord-008510-mnpu27kl.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7131473/
doi: 10.1016/s0065-2776(08)60634-3
summary:
  Demonstration that lung cells regulate both nonspecific inflammation and immunity through the expression of adhesion molecules and the secretion of cytokines offers hope for ways to design more effective vaccines, enhance microbial clearance in immune-suppressed hosts, and to suppress manifestations of immunologically mediated lung disease. The cells that are the major initiators and regulators of immunity in the lung include macrophages, dendritic cells (DCs), and lymphocytes, each expressing surface molecules and secretory products that depend on perturbations in the environments. The cells that are the major initiators and regulators of immunity in the lung include macrophages, dendritic cells (DCs), and lymphocytes, each expressing surface molecules and secretory products that depend on perturbations in the environments. Models to examine immune responses to various respiratory antigens were developed in many animal strains, including mice, rats, hamsters, guinea pigs, ferrets, dogs, monkeys, horses, and cattle; antigens were delivered via aerosol, intranasal, intratracheal, or intrabronchial instillation.

abstract:
  Thechapter describes the cells and structures of the lung that participate in pulmonary immunity and how the lung responds to challenges fromforeign antigens, with particular emphasis on animal models that have been developed to explore these issues. Some ligands-receptor interactions are specific while others are not, and it is the particular pattern of surface molecules and secreted factors expressed by interacting immune cells that determines the type of immune response that develops during central processing. The cells that are the major initiators and regulators of immunity in the lung include macrophages, dendritic cells (DCs), and lymphocytes, each expressing surface molecules and secretory products that depend on perturbations in the environments. Immune cells and structures of the lung and lung immunity to noninfectious particulate and soluble antigens are discussed. Several models for regulation of pulmonary immunity such as models for immunity in lung infections, models for hypersensitivity lung disease, models for lung transplantation, and graft versus host are also presented. Demonstration that lung cells regulate both nonspecific inflammation and immunity through the expression of adhesion molecules and the secretion of cytokines offers hope for ways to design more effective vaccines, enhance microbial clearance in immune-suppressed hosts, and to suppress manifestations of immunologically mediated lung disease.


id: cord-010078-8lkkez3n
title: Invited Speakers
author: nan
date: 2010-11-24
txt: ./txt/cord-010078-8lkkez3n.txt
cache: ./cache/cord-010078-8lkkez3n.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169233/
doi: 10.1111/j.1440-1843.2010.01863.x
abstract: nan
summary:
  Both modes of imaging discriminate early malignant lesions from non-specifi c infl ammation, aid in selecting appropriate sites for biopsy and better delineate tumor margins for more precise staging, but are of little value at present in clinical practice since most patients with malignant pleural effusions have extensive pleural involvement that is easy to diagnose with white light pleuroscopy For pleuroscopic guided pleural biopsies, specimens obtained with the rigid forceps are larger than those with the fl ex-rigid pleuroscope since they are limited by size of the fl exible forceps, which in turn depends on the diameter of the working channel. In the United Kingdom, a thrombosis group has been formed to promote awareness among parliamentarians about the risk and management of VTE; to increase knowledge of its causes, effects, and treatments; and to monitor the implementation of government initiatives and other researches being and this program has corrected the wrong perception that PTE is a rare disease in China Pulmonary hypertension (PH) is a common complication of chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD) or interstitial lung diseases (ILD).


id: cord-010697-0eutz8xy
author: Roumy, Aurélien
date: 2020-05-11
txt: ./txt/cord-010697-0eutz8xy.txt
cache: ./cache/cord-010697-0eutz8xy.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7216520/
doi: 10.1186/s13054-020-02937-z
summary:
  Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology that provides transient respiratory and circulatory support for patients with profound cardiogenic shock or refractory cardiac arrest. The interaction of blood components with the biomaterials of the extracorporeal membrane elicits a systemic inflammatory response which may increase pulmonary vascular permeability and promote the sequestration of polymorphonuclear neutrophils within the lung parenchyma. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology providing respiratory and circulatory support in patients with refractory cardiogenic shock or cardiac arrest [1] and which may give time to plan future therapeutic decisions such as the insertion of long-term cardiac assist devices or heart transplantation (HTX) [2] . Alveolar edema and decreased pulmonary artery perfusion lead to lung parenchymal ischemia which in turn maintains chronic inflammation and promotes neoangiogenesis and fibrosis generation and polymorphonuclear cells (PMNs), and triggers the intrinsic coagulation cascade, resulting in the rapid generation of thrombin and fibrin within the systemic circulation [13] .

title:
  Pulmonary complications associated with veno-arterial extra-corporeal membrane oxygenation: a comprehensive review

abstract:
  Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology that provides transient respiratory and circulatory support for patients with profound cardiogenic shock or refractory cardiac arrest. Among its potential complications, VA-ECMO may adversely affect lung function through various pathophysiological mechanisms. The interaction of blood components with the biomaterials of the extracorporeal membrane elicits a systemic inflammatory response which may increase pulmonary vascular permeability and promote the sequestration of polymorphonuclear neutrophils within the lung parenchyma. Also, VA-ECMO increases the afterload of the left ventricle (LV) through reverse flow within the thoracic aorta, resulting in increased LV filling pressure and pulmonary congestion. Furthermore, VA-ECMO may result in long-standing pulmonary hypoxia, due to partial shunting of the pulmonary circulation and to reduced pulsatile blood flow within the bronchial circulation. Ultimately, these different abnormalities may result in a state of persisting lung inflammation and fibrotic changes with concomitant functional impairment, which may compromise weaning from VA-ECMO and could possibly result in long-term lung dysfunction. This review presents the mechanisms of lung damage and dysfunction under VA-ECMO and discusses potential strategies to prevent and treat such alterations.


id: cord-015836-ojx04jsh
title: Idiopathic Pulmonary Fibrosis
author: Lynch, Joseph P.
date: 2011-07-12
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119915/
doi: 10.1007/978-1-4419-9771-5_10
abstract:
  Idiopathic pulmonary fibrosis (IPF) is a specific clinicopathologic ­syndrome presenting in older adults with the predominant features: dyspnea, dry cough, restrictive defect on pulmonary function tests (PFTs), hypoxemia, characteristic abnormalities on high-resolution thin section computed tomographic (HRCT) scans, usual interstitial pneumonitis (UIP) pattern on lung biopsy. Surgical lung biopsy is the gold standard of diagnosis, but the diagnosis can be established in some cases by HRCT, provided the clinical features are consistent. The cause of IPF is unknown. However, IPF is more common in adults >60 years old, smokers (current or ex), and patients with specific occupational or noxious exposures. Familial IPF, associated with several distinct genetic mutations, accounts for 1.5–3% of cases. Unfortunately, the prognosis is poor, and most patients die of respiratory failure within 3–6 years of diagnosis. However, the course is highly variable. In some patients, the disease is fulminant, progressing to lethal respiratory failure within months, whereas the course may be indolent, spanning >5 years in some patients. Therapy has not been proven to alter the course of the disease or influence mortality, but recent studies with pirfenidone and tyrosine kinase inhibitors are promising. Lung transplantation is the best therapeutic option, but is limited to selected patients with severe, life-threatening disease and no contraindications to transplant.


id: cord-016009-qa7bcsbu
title: Respiratory
author: Starkel, Julie L.
date: 2019-10-07
txt: ./txt/cord-016009-qa7bcsbu.txt
cache: ./cache/cord-016009-qa7bcsbu.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7120155/
doi: 10.1007/978-3-030-30730-1_51
summary:
  Disease that restricts airflow through either inflammation of the lining of the bronchial tubes or destruction of alveoli Increased risk of emphysema if genetic variant of alpha-1 antitrypsin deficiency and smoking or exposed to high levels of air pollution [11] Bronchiectasis A disorder of the airways that leads to airway dilation and destruction, chronic sputum production, and a tendency toward recurrent infection [39] Bronchiolitis Airway injury that can be caused by infections, irritants, toxic fumes, drug exposures, pneumonitis (typically viral), organ transplants, connective tissue disorders, vasculitis, or other insults [40] Dyspnea Shortness of breath or difficulty breathing [11] Emphysema Thinning and destruction of the alveoli, resulting in decreased oxygen transfer into the bloodstream and shortness of breath.

abstract:
  Lung disease rivals the position for the top cause of death worldwide. Causes and pathology of the myriad lung diseases are varied, yet nutrition can either affect the outcome or support treatment in the majority of cases. This chapter explores the modifiable risk factors, from lifestyle changes to dietary intake to specific nutrients, anti-nutrients, and toxins helpful for the nutritionist or dietitian working with lung disease patients. General lung health is discussed, and three major disease states are explored in detail, including alpha-1 antitrypsin deficiency, asthma, and idiopathic pulmonary fibrosis. Although all lung diseases have diverse causes, many integrative and functional medical nutrition therapies are available and are not being utilized in practice today. This chapter begins the path toward better nutrition education for the integrative and functional medicine professional.


id: cord-016690-3gsq724l
title: HIV/AIDS Related Respiratory Diseases
author: Li, Hongjun
date: 2013-09-30
txt: ./txt/cord-016690-3gsq724l.txt
cache: ./cache/cord-016690-3gsq724l.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121050/
doi: 10.1007/978-94-007-7823-8_17
summary:
  Its difference from the clinical manifestations of non-HIV infected patients is as the following: (1) More common pulmonary infi ltration with multiple involvements and rare cavities; (2) Higher incidence of dissemination (87-96 %) commonly along with blood fl ow and higher incidence of extrapulmonary tuberculosis (60-70 %); (3) More common lymph node tuberculosis, such as hilar, mediastinal and extrapleural lymphadenectasis; (4) Lower positive rate of tuberculin test (PPD); (5) More patients with no expectoration, with sputum smear for acid-fast bacilli staining is negative; (6) Higher incidence of resistant strains, high recurrence rate, and higher mortality (Table 17 .1 ). Based on the course of the disease, the diagnostic imaging demonstrations of Rhodococcus equi pulmonary infection can be divided into early stage, showing round liked fl aky blurry shadows surrounding unilateral hilum that has blurry boundary; middle stage (parenchymal change), showing central sphere liked high density shadow surrounding unilateral hilum, in parenchymal changes and with clear boundary; advanced stage (necrosis) showing secondary cavity of the pulmonary mass, possibly with hydropneumothorax and pleurisy.

abstract:
  Lungs are the most commonly involved organ by HIV/AIDS related diseases, and pulmonary infections are the main reasons for the increasing death rate from AIDS. Pathogens of HIV related pulmonary infections include parasites, fungi, mycobacteria, viruses, bacteria and toxoplasma gondii. According to international reports, pathogens have different geographical distribution, which is also closely related to the socioeconomic status of the region to produce varied AIDS related diseases spectra. For instance, in the United States, pneumocystis carnii pneumonia (PCP), tuberculosis and recurrent bacterial pneumonia (at least twice within 1 year) occur frequently in HIV infected patients. An international report published 10 years ago indicated that PCP is the most common and serious pulmonary opportunistic infections in HIV infected patients. Now its incidence has dropped with the application of antiretroviral treatment and preventive measures. PCP will continue to occur initially in patients who are aware of their HIV infection. In addition, HIV related viral and parasitic infections have been reported both domestically and internationally. In this section, the clinical manifestations and imaging findings of HIV related pulmonary infections are analyzed and discussed, which provide effective diagnosis basis, so as to reduce the incidence of HIV-related pulmonary infections.


id: cord-016973-s32jp0ej
title: Respiratory Diseases of Pregnancy
author: Menon, Nithya
date: 2016-07-21
txt: ./txt/cord-016973-s32jp0ej.txt
cache: ./cache/cord-016973-s32jp0ej.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121415/
doi: 10.1007/978-3-319-43341-7_89
summary:
  Understanding the underlying pulmonary physiologic changes that come with pregnancy as well as those conditions which are unique to the pregnant patient will help arrive at the correct diagnosis and management. Recognizing that the gravid patient has other physiologic changes that contribute to decreased respiratory reserve, increased risk of aspiration, infection, and difficult airway can help in managing these patients acutely. The most common causes of non-cardiogenic acute pulmonary edema in pregnancy are the use of tocolytic agents, fluid overload, preeclampsia, sepsis, trauma or following aspiration of gastric contents [6, 7] . A partial pressure of carbon dioxide within the normal range of 36-40 on an arterial blood gas can be a early sign of imment respiratory failure in the gravid patient. Some of the risk factors for pneumonia in pregnancy include anemia, asthma, antepartum corticosteroids given to enhance fetal lung maturity, and the use of tocolytic agents to induce labor [25] .

abstract:
  Respiratory complaints in the gravid patient are often difficult to identify as a disease state, expected physiologic changes of pregnancy or both. Understanding the underlying pulmonary physiologic changes that come with pregnancy as well as those conditions which are unique to the pregnant patient will help arrive at the correct diagnosis and management. Recognizing that the gravid patient has other physiologic changes that contribute to decreased respiratory reserve, increased risk of aspiration, infection, and difficult airway can help in managing these patients acutely.


id: cord-017016-twwa9djm
title: Aspiration, Bronchial Obstruction, Bronchiectasis, and Related Disorders
author: Tomashefski, Joseph F.
date: 2008
txt: ./txt/cord-017016-twwa9djm.txt
cache: ./cache/cord-017016-twwa9djm.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121473/
doi: 10.1007/978-0-387-68792-6_5
summary:
  These occult aspirations may lead to interstitial fibrosis, and perhaps account for the 20% to 54 % incidence of associated and unexplained pulmonary fibrosis in patients with esophageal abnormalities, most commonly hiatal hernia or simple reflux,39,40 The role of reflux in asthma, chronic bronchitis, chronic cough, recurrent pneumonia, cystic fibrosis, and sudden infant death syndrome has been reviewed by Allen et al. 130 In their reviews, Phillips and Rao l3l and Penner and colleagues130 note that similar predisposing factors as those with community-acquired pneumonia, such as aspiration and abscess formation, pertain to this entity, but the location helps distinguish it from the other typical sites of aspiration, When in the upper lobes, it appears to progress through necrotizing pneumonia with thrombosis of arteries (pulmonary and bronchial) and veins, [129] [130] [131] Although not strictly abiding by the foregoing definition (of localization in upper lobe), in one case total unilateral lung gangrene was attributed to hilar vessel involvement following treatment of a massive hilar recurrence of Hodgkin''s disease.

abstract:
  The conducting airways play a pivotal role in the spectrum of pulmonary pathology, not only as conduits for injurious agents to enter the lung, but also as an anatomic compartment that is affected by a diverse array of primary or secondary bronchocentric diseases. This chapter discusses aspiration and bronchial obstruction in detail, with emphasis on the aspiration of toxic, infective, or particulate matter. Lung abscess, a frequent complication of obstruction or aspiration, is also reviewed. Both aspiration and lung abscess are reconsidered within the context of pulmonary infectious disease mainly in Chapter 8 on bacterial infections, and to some extent in the chapters on mycobacterial (Chapter 9), fungal (Chapter 10), and parasitic diseases (Chapter 14).


id: cord-017105-mljywm9p
title: Pulmonary Complications of Obstetric and Gynecologic Conditions
author: Jain, Amisha
date: 2017-10-24
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121584/
doi: 10.1007/978-3-319-69620-1_8
abstract:
  The respiratory and the female reproductive systems are not embryologically or functionally related. However, the reproductive system can exert significant effects on the respiratory system as a result of the various hormonal changes that occur during a woman’s menstrual cycle and especially during pregnancy. In addition, there are several unique gynecologic and/or obstetric conditions that can directly affect the respiratory system. The following chapter reviews the effects of pregnancy on the respiratory system, as well as the special issues concerning the management of common respiratory conditions (e.g., pneumonia, asthma) during pregnancy. In addition it reviews several gynecologic disorders with unique pulmonary complications.


id: cord-017248-a37t31u1
title: Alphabetic Listing of Diseases and Conditions
author: nan
date: 2010-05-17
txt: ./txt/cord-017248-a37t31u1.txt
cache: ./cache/cord-017248-a37t31u1.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7121759/
doi: 10.1007/978-1-59745-127-7_17
summary:
  Possible Associated Conditions: Disseminated intravascular coagulation;* eclampsia;* glucose-6-phosphatase deficiency (G6PD); hemolytic uremic syndrome;* malignant hypertension; lymphoma* and other malignancies; paroxysmal nocturnal hemo-globinuria; sickle cell disease;*thalassemia;* thrombotic thrombocytopenic purpura.* (See also below under "NOTE.") NOTE: Hemolysis also may be caused by conditions such as poisoning with chemicals or drugs, heat injury, snake bite,* or infections or may develop as a transfusion reaction* or be secondary to adenocarcinoma, heart valve prostheses (see below), liver disease (see below), renal disease, or congenital erythropoietic porphyria. Unusual under-lying or associated conditions include chronic aortic stenosis or regurgitation; coronary artery anomalies; coronary artery dissection; coronary embolism; coronary ostial stenosis (due to calcification of aortic sinotubular junction or, rarely, to syphilitic aortitis); coronary vasculitis (for instance, in polyarteritis nodosa* or acute hypersensitivity arteritis); hyperthyroidism,* gastrointestinal hemorrhage; * hypothyroidism, * idiopathic arterial calcification of infancy; intramural coronary amyloidosis; pheochromocytoma, polycythemia vera; * pseudoxanthoma elasticum,* radiationinduced coronary stenosis; severe pulmonary hypertension (with right ventricular ischemia); sickle cell disease;* and others.

abstract:
  Part II begins with a list of special histologic stains, their for use and their corresponding references. At the end of this list is a procedure for removal of formalin precipitate from tissue sections.


id: cord-017581-6lubp7io
title: Respiratory Diseases of Pregnancy
author: Glass, Daniel M.
date: 2019-07-24
txt: ./txt/cord-017581-6lubp7io.txt
cache: ./cache/cord-017581-6lubp7io.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122174/
doi: 10.1007/978-3-030-26710-0_99
summary:
  Pregnant patients can suffer from the same respiratory diseases as the general population in addition to unique syndromes of pregnancy (such as pre-eclampsia and tocolytic induced pulmonary edema, and pregnancy induced cardiomyopathy). Low pulmonary reserves that arise from reductions in functional residual capacity (caused by the gravid uterus and changes in the chest wall morphology) [1] and increased oxygen consumption make pregnant women develop hypoxemia more rapidly during apnea [4] . The most common causes of non-cardiogenic acute pulmonary edema in pregnancy are, fluid overload, preeclampsia, tocolytic agents, sepsis, trauma or following aspiration of gastric contents [6, 7] . A partial pressure of carbon dioxide within the normal range of 36-40 on an arterial blood gas can be an early sign of imminent respiratory failure in the gravid patient. Some of the risk factors for pneumonia in pregnancy include anemia, asthma, antepartum corticosteroids given to enhance fetal lung maturity, and the use of tocolytic agents to induce labor [27] .

abstract:
  Pregnant patients can suffer from the same respiratory diseases as the general population in addition to unique syndromes of pregnancy (such as pre-eclampsia and tocolytic induced pulmonary edema, and pregnancy induced cardiomyopathy). Pregnancy by itself may add certain challenges such as difficult intubation. The critically ill pregnant patient requires a multidisciplinary approach and early inclusion of obstetrical expertise is paramount in managing these patients especially in the third trimester.


id: cord-017771-g72qaoub
title: Imaging of ICU Patients
author: Lohan, Rahul
date: 2019-01-15
txt: ./txt/cord-017771-g72qaoub.txt
cache: ./cache/cord-017771-g72qaoub.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122429/
doi: 10.1007/978-981-13-2544-1_7
summary:
  Besides the evaluation of these conditions, imaging is routinely used for the assessment of various catheters and tubes commonly used in ICUs. The common pulmonary parenchymal disease processes in ICU patients include hydrostatic pulmonary edema, acute respiratory distress syndrome (ARDS), atelectasis, pneumonia, aspiration, and pulmonary hemorrhage. Indistinctness of pulmonary vasculature is subtle but often the most useful radiographic sign of early interstitial edema in ICU patients. The CT findings of hydrostatic pulmonary edema include smooth interlobular septal thickening, ground-glass opacities, consolidation, and pleural effusions ( Fig. 7.4) . The diagnosis of pneumonia in ICU patients is often challenging as the airspace opacities seen on chest radiographs in these patients can be caused by atelectasis, aspiration, pulmonary hemorrhage, noninfectious lung inflammation (e.g., drug reaction), pulmonary edema, or ARDS [12] . The radiographic abnormalities commonly seen with aspiration are patchy ill-defined ground-glass opacities, nodular opacities, or consolidation in the dependent regions of the lungs (Fig. 7.10 ).

abstract:
  Imaging in intensive care unit (ICU) is integral to patient management. The portable chest radiograph is the most commonly requested imaging examination in ICU, and, despite its limitations, it significantly contributes to the decision-making process. Multidetector CT (MDCT) is reserved for relatively complex and challenging clinical scenarios. Bedside ultrasound is emerging as a promising imaging modality as it does not subject the patients to risks and resources involved in the transportation of these patients to the CT facility. Ultrasound is an effective modality to triage patients and is being increasingly incorporated into the emergency and intensive care management algorithms.


id: cord-017983-ehxpdavo
title: Acute Exacerbation of Idiopathic Pulmonary Fibrosis
author: Lee, Joyce S.
date: 2013-09-13
txt: ./txt/cord-017983-ehxpdavo.txt
cache: ./cache/cord-017983-ehxpdavo.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122696/
doi: 10.1007/978-1-62703-682-5_17
summary:
  Often, patients are found to have impaired gas exchange with a decrease in SP-D Marker of alveolar type II cell injury and/or proliferation Plasma levels higher in AEx compared to stable [ 42 ] Thrombomodulin Membrane protein expressed on the surface of endothelial cells which serves as a receptor for thrombin Plasma levels higher in AEx compared to stable and log change in thrombomodulin was predictive of survival [ 42 ] von Willebrand factor Marker of endothelial cell injury and is involved in hemostasis Higher plasma % in AEx compared to stable [ 42 ] AEx acute exacerbation, IPF idiopathic pulmonary fi brosis, KL-6 Previous or concurrent diagnosis of idiopathic pulmonary fi brosis Unexplained development or worsening of dyspnea within 30 days High-resolution computed tomography with new bilateral ground-glass abnormality and/or consolidation superimposed on a background reticular or honeycomb pattern consistent with usual interstitial pneumonia No evidence of pulmonary infection by endotracheal aspirate or bronchoalveolar lavage Exclusion of alternative causes, including left heart failure, pulmonary embolism, and other identifi able causes of acute lung injury a Patients who do not meet all fi ve criteria should be termed "suspected acute exacerbation"

abstract:
  Acute exacerbation of idiopathic pulmonary fibrosis (IPF) is a clinically important complication of IPF that carries a high morbidity and mortality. In the last decade, we have learned much about this event, but there are many remaining questions: What is it? Why does it happen? How can we prevent it? How can we treat it? This chapter attempts to summarize our current understanding of the epidemiology, etiology, and management of acute exacerbation of IPF and point out areas where additional data are sorely needed.


id: cord-017998-tcf2mr1h
title: Acute and Chronic Right Ventricular Failure
author: Sayer, Gabriel
date: 2017-02-22
txt: ./txt/cord-017998-tcf2mr1h.txt
cache: ./cache/cord-017998-tcf2mr1h.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122716/
doi: 10.1007/978-1-4471-4219-5_4
summary:
  While both echocardiography and CMRI can provide some assessment of RV hemodynamics, invasive measurement of intracardiac pressures by right heart catheterization is often required to diagnose the etiology of RV failure and determine the appropriate therapeutic approach. Severe RV dilation predictor of death, VT, advanced NYHA class CMRI cardiac magnetic resonance imaging, HF heart failure, LV left ventricle, LVEF left ventricular ejection fraction, LVESV left ventricular end systolic volume, MI myocardial infarction, NYHA New York Heart Association, OHT orthotopic heart transplantation, PAH pulmonary arterial hypertension, PAP pulmonary artery pressure, PVR pulmonary vascular resistance, RIMP right ventricular index of myocardial performance, RV right ventricle, RVEF right ventricular ejection fraction, RVESV right ventricular end systolic volume, TAPSE tricuspid annular plane systolic excursion, TOF tetralogy of Fallot, V E /V CO2 ratio of minute ventilation to production of carbon dioxide, VT ventricular tachycardia of RV dysfunction are addressed. Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure

abstract:
  Right ventricular failure is the subject of renewed attention as the importance of RV function in a variety of disease states has been recognized. The RV is highly compliant, and is able to accommodate a wide range of preload conditions. Yet, it is afterload-sensitive, and normal physiology is dependent on its association with the low resistance of the pulmonary vasculature. Changes in the pulmonary vascular resistance, either acutely or over time, provoke a series of adaptations that are designed to maintain a normal cardiac output, but ultimately lead to decompensation and RV failure. Through ventricular interdependence, RV failure may impair left ventricular diastolic and systolic function, further reducing cardiac performance. Both echocardiography and magnetic resonance imaging can provide detailed information about RV structure, with MRI providing better assessment of ventricular volumes and RV function. Right heart catheterization is often necessary for definitive diagnosis of the etiology of RV failure and for determining the best therapeutic options. The treatment of RV failure is highly dependent on the underlying etiology, which should be corrected if possible. Targeted medical therapy is particularly useful in cases of pulmonary arterial hypertension, and is under investigation for broader use in other causes of pulmonary hypertension.


id: cord-018168-j85m7wno
title: MMPs, inflammation and pulmonary arterial hypertension
author: d’Ortho, Marie-Pia
date: 2008
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122977/
doi: 10.1007/978-3-7643-8585-9_6
abstract:
  Pulmonary arterial hypertension (PAH) is characterised by remodelling of small pulmonary arteries leading to a progressive increase in pulmonary vascular resistance and right ventricular failure [1]. PAH can be idiopathic, familial, or associated with a number of conditions or diseases, such as connective tissue disease. Its prognosis is poor, less than 3 yr from diagnosis. The aetiology of severe unexplained pulmonary hypertension remained largely unknown until a few years ago. The gene underlying familial PAH was identified in 2000, the BMPR-2 gene. However its mutations are not always present, and it probably does not explained the full scope of the disease. PAH is associated with structural alterations in pulmonary arteries including intimal fibrosis, medial hypertrophy and adventitial changes, pointing towards extracellular matrix remodelling which have raised the question of involvement of the matrix degrading enzymes. Among them, serine proteases, such as plasmina and endogenous vascular elastase (EVE), and matrix metalloproteases have been studied. In experimental models, the three of them are increased. Accordingly, their inhibition has preventing and in some cases therapeutic effects. However it should be stressed that opposite consequence of protease inhibition on PAH can be observed depending on the experimental model, either chronic hypoxia-induced PAH (deleterious) or toxic moncrotalin-induced PAH (positive). In humans, only sparse reports exist, that found increase in the MMP inhibitor, TIMP-1, and MMP-2 expression and decreased collagenase (MMP-1). Inflammation is part of the PAH, and accordingly, protease production is a well known part of the inflammatory response. Answering the question whether protease inhibition might represent a therapeutic option in human PAH is however certainly too early.


id: cord-018209-v2crgj5w
title: What Has Been Learned from Postmortem Studies?
author: Pastores, Stephen M.
date: 2010-08-19
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123032/
doi: 10.1007/978-3-642-15742-4_20
abstract:
  Infectious and noninfectious pulmonary diseases are commonly found on postmortem autopsy studies in patients with hematological malignancy. Despite the technological advances in diagnostic testing and imaging modalities, obtaining an accurate clinical diagnosis remains difficult and often not possible until autopsy. Major diagnostic discrepancies between clinical premortem diagnoses and postmortem autopsy findings have been reported in these patients. The most common missed diagnoses are due to opportunistic infections and cardiopulmonary complications. These findings underscore the importance of enhanced surveillance, monitoring and treatment of infections and cardiopulmonary disorders in these patients. Autopsies remain important in determining an accurate cause of death and for improved understanding of diagnostic deficiencies, as well as for medical education and quality assurance.


id: cord-018243-hyvu9nuq
author: Salman, Huda
date: 2010-08-19
txt: ./txt/cord-018243-hyvu9nuq.txt
cache: ./cache/cord-018243-hyvu9nuq.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123073/
doi: 10.1007/978-3-642-15742-4_42
summary:
  This chapter will address the chronic lung complications that lead to pulmonary fibrosis and persistent organ dysfunction in each context with specific focus on hematologic malignancy patients treated using HSCT. Hematologic malignancy patients treated with chemotherapy or chest wall radiation therapy, or those who proceed to receive a HSCT may develop a wide variety inflammatory noninfectious lung disorders that ultimately may lead to pulmonary fibrosis. The diagnosis of drug-induced respiratory disease often is complex because: (1)1 patients may be exposed to several pneumo-toxic drugs concurrently or in sequence due to earlier treatment failure; (2)2 time to onset of pulmonary toxicity may be delayed, making it difficult to ascertain which agent is responsible for the pulmonary reaction; (3)3 the combination of drugs to treat malignant hematologic conditions may lead to unexpected drug interactions, producing enhanced toxicity compared with the toxicity of each agent considered separately; and (4)4 radiation therapy to the chest or TBI.

title:
  Fibrosing Alveolitis in Hematologic Malignancy Patients Undergoing Hematopoietic Cell Transplantation

abstract:
  Although advances in antineoplastic therapy have considerably improved the survival of patients with hematological malignancies, current treatment modalities increase the risk of late complications. Several forms of chronic pulmonary dysfunction due to infectious or noninfectious causes commonly occur in the months to years after chemo-radiotherapy and can be fatal or result in long-term morbidity. The judicious use of prophylactic antimicrobial agents has tipped the balance toward noninfectious etiologies. Hence, while opportunistic infections still contribute to chronic lung disease, late sequelae resulting from antineoplastic therapy have been identified and reported. Patients who proceed to receive hematopoietic cell transplantation (HSCT) are particularly prone to developing lung complications. Pulmonary dysfunction occurring after HSCT may manifest with obstructive or restrictive pulmonary mechanics and may range in severity from subtle, subclinical functional changes to frank respiratory failure. Insights generated using animal models suggest that the immunologic mechanisms contributing to lung inflammation after HSCT may be similar to those responsible for graft-versus host disease. In sum, chronic fibrotic pulmonary dysfunction is a frequent and significant complication facing survivors of hematologic malignancies and their practitioners. The high incidence and suboptimal response to current support care and immunosuppressive therapy underscore the need for heightened awareness and continued research in this area.


id: cord-018339-tyrlpl94
title: Late Noninfectious Pulmonary Complications in Hematopoietic Stem Cell Transplantation
author: Dsouza, Kevin
date: 2019-07-09
txt: ./txt/cord-018339-tyrlpl94.txt
cache: ./cache/cord-018339-tyrlpl94.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123191/
doi: 10.1007/978-3-319-74588-6_51
summary:
  A recent prospective study to evaluate the epidemiology of late non onset noninfectious complications after allogenic stem cell transplant reported a cumulative incidence of BOS 36 months posttransplant at 10.7% [9] . In a study of 9550 patients of post-allogenic HCST recipients, HLA disparity, female-to-male HSCT, and peripheral blood stem cell transplant (PBSCT) were associated with an increased risk of developing OP. Association between acute and chronic graft-versus-host disease and bronchiolitis obliterans organizing pneumonia in recipients of hematopoietic stem cell transplants Concurrent treatment with a tumor necrosis factor-alpha inhibitor and veno-venous extracorporeal membrane oxygenation in a post-hematopoietic stem cell transplant patient with idiopathic pneumonia syndrome: a case report Incidence, clinical features, and risk factors of idiopathic pneumonia syndrome following hematopoietic stem cell transplantation in children Bronchiolitis obliterans syndrome (BOS), bronchiolitis obliterans organizing pneumonia (BOOP), and other late-onset noninfectious pulmonary complications following allogeneic hematopoietic stem cell transplantation

abstract:
  Hematopoietic stem cell transplantation (HSCT) is an established therapeutic modality for a number of malignant and nonmalignant conditions. Pulmonary complications following HSCT are associated with increased mortality and morbidity. These complications may be classified into infectious versus noninfectious, and early versus late based on the time of occurrence post-transplant. Thus, exclusion of infectious etiologies is the first step in the diagnoses of pulmonary complications. Late onset noninfectious pulmonary complications typically occur 3 months post-transplant. Bronchiolitis obliterans is the major contributor to late-onset pulmonary complications, and its clinical presentation, pathogenesis, and current therapeutic approaches are discussed. Idiopathic pneumonia syndrome is another important complication which usually occurs early, although its onset may be delayed. Organizing pneumonia is important to recognize due to its responsiveness to corticosteroids. Other late onset noninfectious pulmonary complications discussed here include pulmonary venoocclusive disease, pulmonary cytolytic thrombi, pleuroparenchymal fibroelastosis, thoracic air leak syndrome, and posttransplant lymphoproliferative disorders.


id: cord-018414-6ffhm895
title: Anesthesia Management of Liver Transplantation
author: Kang, Yoogoo
date: 2016-07-22
txt: ./txt/cord-018414-6ffhm895.txt
cache: ./cache/cord-018414-6ffhm895.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123279/
doi: 10.1007/978-3-319-07209-8_9
summary:
  Specifically, patients with fulminant hepatic failure develop significant changes in cerebral function, and cerebral perfusion is maintained by monitoring cerebral blood flow and cerebral metabolic rate of oxygen, and intracranial pressure. Small-for-size syndrome develops in a patient who received a donor graft that was less than 1 % of the recipient''s body weight and is caused by decreased hepatic arterial flow in response to increased portal venous flow and pressure. The major criteria for the diagnosis of the hepatorenal syndrome are as follows: (1) advanced hepatic disease and portal hypertension; (2) low glomerular filtration rate (serum creatinine >1.5 mg/dL or creatinine clearance <40 mL/ min); (3) absence of nephrotoxic drug use, shock, systemic infection, or recent fluid losses; (4) lack of sustained improvement after diuretic withdrawal and volume resuscitation with 1.5 L of normal saline; (5) proteinuria (<500 mg/dL); and (6) no ultrasound evidence of urinary obstruction or parenchymal disease.

abstract:
  Anesthesia for liver transplantation pertains to a continuum of critical care of patients with end-stage liver disease. Hence, anesthesiologists, armed with a comprehensive understanding of pathophysiology and physiologic effects of liver transplantation on recipients, are expected to maintain homeostasis of all organ function. Specifically, patients with fulminant hepatic failure develop significant changes in cerebral function, and cerebral perfusion is maintained by monitoring cerebral blood flow and cerebral metabolic rate of oxygen, and intracranial pressure. Hyperdynamic circulation is challenged by the postreperfusion syndrome, which may lead to cardiovascular collapse. The goal of circulatory support is to maintain tissue perfusion via optimal preload, contractility, and heart rate using the guidance of right-heart catheterization and transesophageal echocardiography. Portopulmonary hypertension and hepatopulmonary syndrome have high morbidity and mortality, and they should be properly evaluated preoperatively. Major bleeding is a common occurrence, and euvolemia is maintained using a rapid infusion device. Pre-existing coagulopathy is compounded by dilution, fibrinolysis, heparin effect, and excessive activation. It is treated using selective component or pharmacologic therapy based on the viscoelastic properties of whole blood. Hypocalcemia and hyperkalemia from massive transfusion, lack of hepatic function, and the postreperfusion syndrome should be aggressively treated. Close communication between all parties involved in liver transplantation is also equally valuable in achieving a successful outcome.


id: cord-018601-mk66097y
title: Pulmonary Arterial Hypertension
author: Michelakis, Evangelos D.
date: 2007
txt: ./txt/cord-018601-mk66097y.txt
cache: ./cache/cord-018601-mk66097y.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7123519/
doi: 10.1007/978-1-84628-715-2_108
summary:
  18 Primary PHT was defined as mean pulmonary artery (PA) pressure >25 mm Hg at rest (or >30 mm Hg with exercise) in the absence of secondary causes for PHT, a definition different from the current definition of PAH, which includes PHT due to more common diseases like collagen vascular disease, HIV infection, portal hypertension, congenital heart disease as PAH (Table 105 .2). The following tests should be obtained in all patients in whom the cause of PHT is not evident: electrocardiogram (ECG), chest radiograph, arterial blood gases, complete blood count, electrolytes and liver function tests, pulmonary function tests (PFTs), ventilation/ perfusion lung scan, serology for rheumatic diseases (e.g., fluorescent antinuclear antibody, FANA), serology for HIV, ventilation perfusion (V/Q) scan, and an echocardiogram with Doppler assessment of PA acceleration time and tricuspid regurgitation velocity as well as an echo-contrast study, to exclude shunting.

abstract:
  The first description of the circulation of blood through the lungs has been attributed to Ibn Nafis (1210–1288).1 The concept was rediscovered by Michael Servetus, a Spanish physician during the Renaissance (1511–1553) and recorded, oddly enough, in two pages of his religious treatise, Christianismi Restitutio (1553).2 The definitive exposition of the pulmonary circulation was made by William Harvey in DeMotu Cordis (1628).3 The first observation of the pulmonary capillaries was first reported by Marcellus Malpighi (1661).4 Heart catheterization in humans, driven by a desire to obtain the perfect mixed venous specimen and measure cardiac output, was first performed in 1929 by the German urologist Forssmann,5 using a ureteral catheter to access his own right atrium. Over a decade later, Cournand and Richards at Columbia University in New York subsequently used right heart catheterization to record pulmonary artery pressure (PAP) in patients with shock and secondary forms of pulmonary hypertension (PHT). For these accomplishments, which were inspired by an interest in the pulmonary circulation and PHT related to mitral stenosis, Forssmann, Cournand, and Richards received the Nobel Prize in 1956.


id: cord-019001-ralxw4ad
title: Diseases of the Pulmonary Vascular System
author: Oishi, Peter
date: 2008-11-15
txt: ./txt/cord-019001-ralxw4ad.txt
cache: ./cache/cord-019001-ralxw4ad.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7124039/
doi: 10.1007/978-1-84800-925-7_20
abstract: nan
summary:
  In addition, physical expansion of the lung results in the release of vasoactive substances, such as PGI 2 , which increases pulmonary blood fl ow and decreases pulmonary vascular resistance in the fetal goat and lamb independent of the changes in oxygen tension [35] [36] [37] [38] [39] [40] . In humans, endothelial dysfunction, including histologic abnormalities of the endothelium, impairment of endothelium-dependent pulmonary vasodilation, and increased plasma ET-1 concentrations have been described in children with congenital heart defects and pulmonary hypertension before the development of signifi cant vascular remodeling [22, 98, 101] . In addition, neonates with PPHN and adults with advanced pulmonary vascular disease have evidence of endothelial dysfunction, impairment of endothelium-dependent pulmonary vasodilation, increased plasma ET-1 concentrations, and decreased prostacyclin production [23, 24, 62, 99] . The oral formulation is currently being investigated for chronic pulmonary hypertensive therapy, and recent short-term studies demonstrate benefi cial effects in children with advanced pulmonary vascular disease [164] .


id: cord-019063-mcxbl8mv
title: Diagnosis of Pulmonary Parasitic Diseases
author: Vijayan, Vannan K.
date: 2013-06-05
txt: ./txt/cord-019063-mcxbl8mv.txt
cache: ./cache/cord-019063-mcxbl8mv.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7124114/
doi: 10.1007/978-3-642-37609-2_1
summary:
  The lung diseases that may result from these infections range from asymptomatic phase to life-threatening acute respiratory distress syndrome. The diagnosis of leishmaniasis is based on the microscopical demonstration of Leishmania amastigotes in the relevant tissue aspirates or biopsies such as bone marrow, spleen, lymph nodes, or liver, skin slit smears, or in the peripheral blood buffy coat [ 19 ] . The important helminthic parasites that cause lung diseases include cestodes ( Echinococcus granulosus and Echinococcus multilocularis ), trematodes ( Schistosoma haematobium , Schistosoma mansoni , Schistosoma japonicum , and Paragonimus westermani ), and nematodes ( Ascaris lumbricoides , Ancylostoma duodenale , Necator americanus , Strongyloides stercoralis , Wuchereria bancrofti , Brugia malayi , Brugia timori , Dirofi laria immitis , Dirofi laria repens , Toxocara canis or cati , and Trichinella spiralis ). A diagnosis of pulmonary disease due to ascariasis can be made in an endemic region in a patient who presents with dyspnea, dry cough, fever, and eosinophilia.

abstract:
  The protozoal and helminthic parasites that traverse the respiratory tract during their life cycles can cause lung diseases, though the most common habitats of these parasites are the gastrointestinal tract and the blood or lymphatic circulations. These diseases are commonly encountered in the tropical regions of the world. However, parasitic lung diseases are increasingly being reported from other parts of the world due to an increase in the occurrence of immunosuppression (acquired immunodeficiency syndrome, organ transplantations, the use of immunosuppressive drugs) and transcontinental travel. The lung diseases that may result from these infections range from asymptomatic phase to life-threatening acute respiratory distress syndrome. These diseases can also mimic common respiratory diseases such as bacterial pneumonias, pulmonary tuberculosis, lung cancer, bronchial asthma, interstitial lung disease, and pulmonary hypertension. The diagnosis of parasitic lung diseases is a challenge to physicians, if they are not aware of the entity or these diseases are not investigated properly. The diagnosis of these diseases is based on the identification of the causative organism in the stool, sputum, other body fluids, or tissue specimens. Radiological imaging studies of the thorax including chest radiographs, high-resolution computerized tomograms, and ultrasonograms may aid in the diagnosis. In certain situations, invasive investigations such as fiberoptic bronchoscopic evaluation (transbronchial lung biopsies and bronchoalveolar lavage studies) and thoracic surgical procedures (thoracoscopy and open lung biopsy) may be required for a diagnosis and also to exclude other lung diseases. Serologic and molecular diagnostic methods are being developed for accurate diagnosis of the parasitic diseases.


id: cord-021742-sdz6d1r5
title: Pneumothorax and Barotrauma
author: Karnik, Ankur A.
date: 2009-05-15
txt: ./txt/cord-021742-sdz6d1r5.txt
cache: ./cache/cord-021742-sdz6d1r5.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151955/
doi: 10.1016/b978-032304841-5.50050-9
abstract: nan
summary:
  Pneumothorax Secondary to Underlying Lung Disease In adults, SP has been reported to occur as a result of a large variety of diseases including asthma, staphylococcal septicemia, pulmonary infarction, sarcoidosis, idiopathic pulmonary hemorrhage, pulmonary alveolar proteinosis, familial fi brocystic pulmonary dysplasia, tuberous sclerosis, cryptogenic fi brosing alveolitis, eosinophilic granuloma, coccidioidomycosis, echinococcal disease, chronic obstructive pulmonary disease (COPD), Shaver''s disease (bauxite pneumoconiosis), lymphangioleiomyomatosis, von Recklinghausen''s disease, gastropleural and colopleural fi stulas through the diaphragm into the left pleural cavity, radiation therapy to the thorax, Wegener''s granulomatosis, cystic fi brosis, acute bacterial pneumonia, and as a complication of the chemotherapy used in the treatment of malignancy and pulmonary metastases from a variety of malignancies. In those patients whose pneumothorax is large (more than 20% to 25%), progressive, or tension type; who are symptomatic; have an underlying chronic lung disease; are on a ventilator; or who have a recurrent pneumothorax, the pleural space air needs to be removed by various therapeutic means rather than be allowed to be absorbed spontaneously.


id: cord-022082-1dq623oe
title: Respiratory Tract
author: Greaves, Peter
date: 2007-09-28
txt: ./txt/cord-022082-1dq623oe.txt
cache: ./cache/cord-022082-1dq623oe.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152448/
doi: 10.1016/b978-044452771-4/50007-9
summary:
  In the case of tulobuterol, a 32-adrenergic receptor agonist, it was argued that the nasal inflammation induced in rats in a one month inhalation toxicity study was the result of a particularly high exposure of the nasal epithelium to drug, not representative of the likely human exposure to tulobuterol by inhalation, where little or no nasal exposure would occur.^^ RP73401 [3cyclopentyloxy)-Ar-(3,5-dichloro-4-pyridy)-4-methoxybenzamide], a novel type IV phosphodiesterase inhibitor which was being developed for the treatment of asthma and rheumatoid arthritis, was also reported to produce degeneration of the olfactory epithelium in rats but neither dogs nor mice after single and repeated oral doses and by inhalation.^^ Histologically, the olfactory epithelium showed necrosis of the superflcial epithelial layers including the sustentacular and sensory cells, with sparing of the basal cell layer.

abstract:
  The chapter describes different aspects of the respiratory tract. In preclinical safety studies, pathologies of the respiratory system can be a result of an intercurrent disease or can be induced by systemically administered drugs. Intranasal or inhalation modes of therapy pose particular challenges in terms of the formulations and technologies required to administer a drug. A complex technology is developed to support the assessment of adverse effects of inhaled substances in rodent and nonrodent species, and the extrapolation of experimental findings to humans. The nasal chambers are the structures that are first to be subjected to the effects of inhaled substances, whether microorganisms or chemical substances. In rodents, the relatively small size of the nose and nasal sinuses facilitates a histological examination. Findings show that infectious agents cause inflammation in the nose and nasal sinuses, and this may be associated with inflammation in the conjunctiva, the middle ear, and the oral cavity. It has been observed that a particular response of the rodent nasal mucosa to some irritant substances, including pharmaceutical agents, is the formation of rounded eosinophilic inclusions in the cytoplasm of sustentacular cells of the olfactory epithelium, and to a lesser extent in respiratory and glandular epithelial cells.


id: cord-022173-kb6mez61
title: Hematologic neoplasms: Interpreting lung findings in chest computed tomography()
author: Calvillo Batllés, P.
date: 2015-11-06
txt: ./txt/cord-022173-kb6mez61.txt
cache: ./cache/cord-022173-kb6mez61.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153726/
doi: 10.1016/j.rxeng.2015.09.001
summary:
  Chest HRCT plays a fundamental role---urgent when there are clinical signs of severity and early (<24 h) in the absence of a response to antibiotics therapy in 72---96 h because treatment of a possible invasive fungal infection (IFI) requires an early administration, a determinant factor for prognosis. 20, 40 Noninfectious complications secondary to treatment In the 6 h following the transfusion of blood products, the sudden appearance of consolidations simulating an edema and accompanying a respiratory failure usually reflect acute pulmonary damage (APD) called TRALI (transfusion-related alveolar lung injury) which associates high mortality rates. In patients with HP the thoracic HRCT helps us come close to the differential diagnosis of infectious and non-infectious pulmonary complications by integrating image findings and clinical data.

abstract:
  Lung disease is very common in patients with hematologic neoplasms and varies in function of the underlying disease and its treatment. Lung involvement is associated with high morbidity and mortality, so it requires early appropriate treatment. Chest computed tomography (CT) and the analysis of biologic specimens are the first line diagnostic tools in these patients, and sometimes invasive methods are necessary. Interpreting the images requires an analysis of the clinical context, which is often complex. Starting from the knowledge about the differential diagnosis of lung findings that radiologists acquire during training, this article aims to explain the key clinical and radiological aspects that make it possible to orient the diagnosis correctly and to understand the current role of CT in the treatment strategy for this group of patients.


id: cord-023311-7wqdlha4
title: Oral Session
author: nan
date: 2010-11-24
txt: ./txt/cord-023311-7wqdlha4.txt
cache: ./cache/cord-023311-7wqdlha4.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169143/
doi: 10.1111/j.1440-1843.2010.01864.x
abstract: nan
summary:
  Methods We determined the usefulness of preoperative lung function by spirometry in predicting regression of pulmonary hypertension after surgical correction of mitral stenosis among 20 patients who underwent mitral valve surgery at Philippine Heart Center from July to December 2009. Elderly patients exhibited a signifi cantly higher mortality rate that was independently associated with the following: age; residence status; confusion, urea, respiratory frequency and blood pressure (CURB) score; comorbid conditions; and failure of initial therapy. Methods A total of 40 patients (Male: 50%; Female: 50%) admitted and diagnosed with HAP at our Center were followed up to investigate the rate of adherence of physicians on the diagnosis and treatment of HAP based on Level I and II ATS/IDSA 2008 recommendations and to determine its association with outcome (mortality, mechanical ventilation, ICU stay, hospital stay).


id: cord-023509-tvqpv6fp
title: Occupational, environmental and iatrogenic lung disease
author: Corrin, Bryan
date: 2011-03-02
txt: ./txt/cord-023509-tvqpv6fp.txt
cache: ./cache/cord-023509-tvqpv6fp.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170212/
doi: 10.1016/b978-0-7020-3369-8.00007-0
abstract: nan
summary:
  As a general rule, exposure to silica dust extends over many years, often 20 or more, before the symptoms of silicosis first appear: by the time the disease becomes overt clinically, much irreparable damage has been inflicted on the lungs. Confusingly, the term ''acute silicosis'' has since been applied to a further effect of heavy dust exposure in tunnellers, sand blasters and silica flour workers, namely pulmonary alveolar lipoproteinosis (see below), 71, 72 whilst the terms ''accelerated silicosis'' or ''cellular phase silicosis'' have been substituted for ''acute silicosis'' in referring to the rapid development of early cellular lesions. Asbestosis is defined as diffuse interstitial fibrosis of the lung caused by exposure to asbestos dust. The finely divided fume of several metals is highly toxic to the lungs and capable of producing severe acute and chronic damage to both the conductive airways and the alveoli, resulting in acute tracheobronchitis and bronchiolitis, diffuse alveolar damage, obliterative bronchiolitis and pulmonary fibrosis.


id: cord-024183-1mrdjc39
title: The Respiratory System
author: Hutchison, Alastair A.
date: 2013-10-08
txt: ./txt/cord-024183-1mrdjc39.txt
cache: ./cache/cord-024183-1mrdjc39.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7193717/
doi: 10.1007/978-3-642-01219-8_4
summary:
  After airway occlusion at mid-expiration, there is a biphasic change in P ao : the immediate rapid rise in P ao represents the resistive pressure drop across the conducting airways and is followed by a secondary slower increase in P ao (often referred to as P dif ) generally attributed to stress recovery in the respiratory tissues (lung and chest wall) and gas redistribution associated with ventilation inhomogeneity (Bates et al. To describe flow (F), lung volumes (V), and respiratory pressure (P) measurements together with resistance (R) and compliance (C) measurements in restrictive lung diseases, obstructive lung diseases, and neuromuscular disorders (NMD) decrease in TLC, in general, is relatively less than that of VC because of normal chest wall recoil and inspiratory muscle function in most patients (Martinez and Flaherty 2006) .

abstract:
  This chapter addresses upper airway physiology for the pediatric intensivist, focusing on functions that affect ventilation, with an emphasis on laryngeal physiology and control in breathing. Effective control of breathing ensures that the airway is protected, maintains volume homeostasis, and provides ventilation. Upper airway structures are effectors for all of these functions that affect the entire airway. Nasal functions include air conditioning and protective reflexes that can be exaggerated and involve circulatory changes. Oral cavity and pharyngeal patency enable airflow and feeding, but during sleep pharyngeal closure can result in apnea. Coordination of breathing with sucking and nutritive swallowing alters during development, while nonnutritive swallowing at all ages limits aspiration. Laryngeal functions in breathing include protection of the subglottic airway, active maintenance of its absolute volume, and control of tidal flow patterns. These are vital functions for normal lung growth in fetal life and during rapid adaptations to breathing challenges from birth through adulthood. Active central control of breathing focuses on the coordination of laryngeal and diaphragmatic activities, which adapts according to the integration of central and peripheral inputs. For the intensivist, knowledge of upper airway physiology can be applied to improve respiratory support. In a second part the mechanical properties of the respiratory system as a critical component of the chain of events that result in translation of the output of the respiratory rhythm generator to ventilation are described. A comprehensive understanding of respiratory mechanics is essential to the delivery of optimized and individualized mechanical ventilation. The basic elements of respiratory mechanics will be described and developmental changes in the airways, lungs, and chest wall that impact on measurement of respiratory mechanics with advancing postnatal age are reviewed. This will be follwowed by two sections, the first on respiratory mechanics in various neonatal pathologies and the second in pediatric pathologies. The latter can be classified in three categories. First, restrictive diseases may be of pulmonary origin, such as chronic interstitial lung diseases or acute lung injury/acute respiratory distress syndrome, which are usually associated with reduced lung compliance. Restrictive diseases may also be due to chest wall abnormalities such as obesity or scoliosis (idiopathic or secondary to neuromuscular diseases), which are associated with a reduction in chest wall compliance. Second, obstructive diseases are represented by asthma and wheezing disorders, cystic fibrosis, long term sequelae of neonatal lung disease and bronchiolitis obliterans following hematopoietic stem cell transplantation. Obstructive diseases are defined by a reduced FEV1/VC ratio. Third, neuromuscular diseases, mainly represented by DMD and SMA, are associated with a decrease in vital capacity linked to respiratory muscle weakness that is better detected by PImax, PEmax and SNIP measurements.


id: cord-026005-f2khcjdy
title: Respiratory System, Mediastinum, and Pleurae
author: López, Alfonso
date: 2017-02-17
txt: ./txt/cord-026005-f2khcjdy.txt
cache: ./cache/cord-026005-f2khcjdy.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7271179/
doi: 10.1016/b978-0-323-35775-3.00009-6
abstract: nan
summary:
  Microscopic examination of properly collected, stored, and processed samples may reveal many erythrocytes and siderophages in pulmonary hemorrhage or left-sided heart failure; inclusion bodies or syncytial cells in viral pneumonias; increased number of leukocytes in pulmonary inflammation; abundant mucus in asthma or equine recurrent airway obstruction (RAO); the presence of pulmonary pathogens, such as parasites, fungi, and bacteria; or tumor cells in cases of pulmonary neoplasia. The portal of entry for the respiratory form is typically aerogenous, and the disease is generally transient; thus the primary viral-induced lesions in the nasal mucosa and lungs are rarely seen at necropsy unless complicated by secondary bacterial rhinitis, pharyngitis, or bronchopneumonia. Laryngeal edema occurs in pigs with edema disease; in horses with purpura hemorrhagica; in cattle with acute interstitial pneumonia; in cats with systemic anaphylaxis; and in all species as a result of trauma, improper endotracheal tubing, inhalation of irritant gases (e.g., smoke), local inflammation, and animal species is classified as fibrinous, catarrhal, purulent, or granulomatous (Figs.


id: cord-034294-ti1cc24m
title: Progress in the mechanism and targeted drug therapy for COPD
author: Wang, Cuixue
date: 2020-10-27
txt: ./txt/cord-034294-ti1cc24m.txt
cache: ./cache/cord-034294-ti1cc24m.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588592/
doi: 10.1038/s41392-020-00345-x
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.


id: cord-034406-i1hbx3pz
title: Developing inhaled protein therapeutics for lung diseases
author: Matthews, Abigail A.
date: 2020-10-30
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7595758/
doi: 10.1186/s43556-020-00014-z
abstract:
  Biologic therapeutics such as protein/polypeptide drugs are conventionally administered systemically via intravenous injection for the treatment of diseases including lung diseases, although this approach leads to low target site accumulation and the potential risk for systemic side effects. In comparison, topical delivery of protein drugs to the lung via inhalation is deemed to be a more effective approach for lung diseases, as proteins would directly reach the target in the lung while exhibiting poor diffusion into the systemic circulation, leading to higher lung drug retention and efficacy while minimising toxicity to other organs. This review examines the important considerations and challenges in designing an inhaled protein therapeutics for local lung delivery: the choice of inhalation device, structural changes affecting drug deposition in diseased lungs, clearance mechanisms affecting an inhaled protein drug’s lung accumulation, protein stability, and immunogenicity. Possible approaches to overcoming these issues will also be discussed.


id: cord-035258-nff6gfik
title: Pulmonary Complications of Cardiac Surgery
author: Tanner, Tristan George
date: 2020-11-11
txt: ./txt/cord-035258-nff6gfik.txt
cache: ./cache/cord-035258-nff6gfik.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655908/
doi: 10.1007/s00408-020-00405-7
summary:
  Pulmonary complications are common in patients who undergo cardiac surgery with outcomes such as pneumonia, pulmonary embolism, ventilation longer than 24 h, and pleural effusions necessitating drainage being reportable to the Society of Thoracic Surgeons [1] . Risk factors for postoperative bleeding in cardiac surgery patients include advanced age, low body weight, nonelective surgery, CPB time over 150 min, high complexity of procedure, perioperative use of antiplatelet agents, and use of over 5 bypass grafts [58] . Operative risk factors include low cardiac output syndrome, more than 3 U of packed RBCs (or massive transfusion), isolated valve surgery, and development of postoperative pneumonia [68, 69] . While routine use of the pulmonary artery catheter became less prevalent over the previous decades, it still holds a central role in the postoperative care of cardiac surgery patients. The incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of cardiac surgery patients: a prospective nested casecontrol study

abstract:
  Cardiothoracic surgery posits an arrangement of large, significant hemodynamic, and physiologic alterations upon the human body, which predisposes a patient to develop pathology. The care of these patients in the postoperative realm requires an astute physician with deep understanding of the cardiopulmonary system, who is able to address subtle developing problems promptly, before the patient suffers further sequelae. In this review, we describe the presentation and management of an assortment of important complications which occur in the pulmonary system. In addition, we aim to shed better light upon how the physiology of a patient responds to the condition of cardiothoracic surgery.


id: cord-253722-6jsaxirt
author: Lan, Yanqiu
date: 2020-09-11
txt: ./txt/cord-253722-6jsaxirt.txt
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extension: .txt
mime: text/plain
url: https://doi.org/10.1097/md.0000000000022016
doi: 10.1097/md.0000000000022016
summary:
  title: Danhong injection in the treatment of idiopathic pulmonary fibrosis: A protocol for systematic review and meta-analysis RESULTS: This study will provide high-quality comprehensive evidence for the effectiveness and safety of danhong injection in the treatment of idiopathic pulmonary fibrosis. CONCLUSIONS: The results obtained from this study will define the basis for the effectiveness and safety of danhong injection in the treatment of idiopathic pulmonary fibrosis. [13] To further evaluate the efficacy and safety of danhong injection in the management of patients with Idiopathic pulmonary fibrosis, a meta-analysis of related randomized controlled trials (RCTs) was conducted. A comprehensive search of electronic databases such as PubMed, MEDLINE, EMbase, Web of Science, Cochrane Library, China National Knowledge Infrastructure, WanFang, the Chongqing VIP Chinese Science and Technology Periodical Database, and China biomedical literature database was effected to collect RCTs on the integration of danhong injection in the treatment of idiopathic pulmonary fibrosis. Effectiveness and safety of Chinese medicine for idiopathic pulmonary fibrosis: a systematic review and meta-analysis

title:
  Danhong injection in the treatment of idiopathic pulmonary fibrosis: A protocol for systematic review and meta-analysis

abstract:
  BACKGROUND: Many studies have reported that the effects of danhong injection on idiopathic pulmonary fibrosis. However, its effects are still not well understood. The aim of this study is to assess the effects of danhong injection in the management of idiopathic pulmonary fibrosis. METHODS: Electronic databases such as PubMed, MEDLINE, EMbase, Web of Science, Cochrane Library, China National Knowledge Infrastructure, WanFang, the Chongqing VIP Chinese Science and Technology Periodical Database, and China biomedical literature database will be searched without limitations of language and geographical location. Two researchers will independently conduct research selection, data extraction, and research quality assessment. The RevMan 5.3 software and Stata 14.0 software are used for statistical analysis. RESULTS: This study will provide high-quality comprehensive evidence for the effectiveness and safety of danhong injection in the treatment of idiopathic pulmonary fibrosis. CONCLUSIONS: The results obtained from this study will define the basis for the effectiveness and safety of danhong injection in the treatment of idiopathic pulmonary fibrosis.


id: cord-255519-tcobane8
title: Acute Medical Conditions: Cardiopulmonary Disease, Medical Frailty, and Renal Failure
author: Bartels, Matthew N.
date: 2020-10-02
txt: ./txt/cord-255519-tcobane8.txt
cache: ./cache/cord-255519-tcobane8.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/B9780323625395000278
doi: 10.1016/b978-0-323-62539-5.00027-8
summary:
  The population of patients who benefit from both cardiac and pulmonary rehabilitation is increasing as the population ages and heart disease remains a leading cause of global morbidity and mortality. Many patients with stroke, vascular disease, or other conditions can be included in active cardiac and pulmonary rehabilitation programs or benefit from the application of cardiopulmonary rehabilitation principles to their rehabilitation. For secondary prevention in patients with known cardiopulmonary disease, exercise should be at a safe level at 60% or more of the maximum heart rate to achieve a training effect. 82 Rehabilitation is focused on a program that resembles exercise for patients with heart failure, with the addition of close monitoring of oxygen saturation and the use of appropriate levels of supplemental oxygen to prevent hypoxemia. Individuals who are disabled tend to have lower activity levels, which puts them at increased risk of cardiac and pulmonary disease and may present obstacles for a standard rehabilitation program for a person who is newly disabled and who has preexisting cardiopulmonary limitations.

abstract:
  Cardiopulmonary rehabilitation includes essential interventions that help patients maximize functional potential due to progressive deconditioning or acute decompensation following an acute medical event. The population of patients who benefit from both cardiac and pulmonary rehabilitation is increasing as the population ages and heart disease remains a leading cause of global morbidity and mortality. The principles of exercise physiology when applied to this population can reverse deconditioning, build cardiopulmonary reserve, and ultimately reduce morbidity and mortality in these populations. The physically disabled also benefit from exercise conditioning. The model of cardiac rehabilitation can also be applied to improve functional status of stroke patients, and this is an emerging area of interest supported by the shared pathophysiology and risk factors of cardiovascular conditions. The benefits of supervised exercise can also be extended to patients with clinically recognized frailty and post-transplant decline in function. Frailty is a complex diagnosis with multiple tools and approaches used to describe this syndrome.


id: cord-272034-fvii5nsv
author: McNaughton, Amanda
date: 2020-09-11
txt: ./txt/cord-272034-fvii5nsv.txt
cache: ./cache/cord-272034-fvii5nsv.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32982205/
doi: 10.2147/copd.s267268
summary:
  title: Taking Charge: A Proposed Psychological Intervention to Improve Pulmonary Rehabilitation Outcomes for People with COPD We offer a different perspective drawn from clinical experience of PR, quantitative and qualitative studies of singing groups for people with COPD, and stroke rehabilitation research that gives psychological factors a more central role in determining outcomes after PR. [38] [39] [40] [41] [42] [43] [44] [45] Two randomized controlled trials of singing group interventions in COPD report improvements in quality of life and reduction in anxiety, although not in lung function. 49 Arnold and colleagues showed that improvements in quality of life scores after PR were associated with increases in measures of self-efficacy and suggested that "focussing more explicitly on the enhancement of perceptions of personal control in COPD patients may be an important aim of pulmonary rehabilitation". Taking Charge after stroke: promoting self-directed rehabilitation to improve quality of life -a randomized controlled trial

title:
  Taking Charge: A Proposed Psychological Intervention to Improve Pulmonary Rehabilitation Outcomes for People with COPD

abstract:
  Pulmonary rehabilitation (PR) is an important, evidence-based treatment that improves outcomes for people with COPD. Individualized exercise programmes aim to improve exercise capacity; self-management education and psychological support are also provided. Translating increased exercise capacity into sustained behavioural change of increased physical activity is difficult. Other unresolved problems with PR programmes include improving uptake, completion, response and sustaining long-term benefit. We offer a different perspective drawn from clinical experience of PR, quantitative and qualitative studies of singing groups for people with COPD, and stroke rehabilitation research that gives psychological factors a more central role in determining outcomes after PR. We discuss Take Charge; a simple but effective psychological intervention promoting self-management––that could be used as part of a PR programme or in situations where PR was declined or unavailable. This may be particularly relevant now when traditional face-to-face group programmes have been disrupted by COVID-19 precautions.


id: cord-273149-b1qsnxr1
title: ERS International Congress, Madrid, 2019: highlights from the Pulmonary Vascular Diseases Assembly
author: Ramjug, Sheila
date: 2020-10-13
txt: ./txt/cord-273149-b1qsnxr1.txt
cache: ./cache/cord-273149-b1qsnxr1.txt
extension: .txt
mime: text/plain
url: https://doi.org/10.1183/23120541.00304-2020
doi: 10.1183/23120541.00304-2020
summary:
  The use of risk stratification in relation to pulmonary arterial hypertension (PAH) was heavily featured and the scientific sessions informing the respiratory community of potential biomarkers and targets for future therapies were thought-provoking. It is also important to consider risk factors for possible chronic thromboembolic pulmonary hypertension (CTEPH) or chronic thromboembolic disease in both the symptomatic and asymptomatic patient, which are helpfully listed in the new guidance [17] [18] [19] . [24] also demonstrated that ILD-related PH patients, at right heart catheterisation, had lower mPAP and PVR when compared to their idiopathic pulmonary arterial hypertension (PAH) cohort; despite these findings, mortality was high in both groups. Prognostic value of right ventricular dysfunction or elevated cardiac biomarkers in patients with low-risk pulmonary embolism: a systematic review and meta-analysis A dynamic prognostic model to predict survival and determine treatment goals in pulmonary arterial hypertension (PAH): the EFORT study Risk stratification of pulmonary arterial hypertension (PAH) associated with adult congenital heart disease (ACHD)

abstract:
  The 2019 European Respiratory Society (ERS) International Congress, held in Madrid, Spain, had exciting sessions regarding the field of pulmonary vascular disease. The symposia related to the new ERS/European Society of Cardiology (ESC) Guidelines for the diagnosis and management of acute pulmonary embolism were well received, as were sessions on pulmonary hypertension related to lung disease, demonstrating the concept of pulmonary hypertension not being the rarity that it was previously thought to be. The use of risk stratification in relation to pulmonary arterial hypertension (PAH) was heavily featured and the scientific sessions informing the respiratory community of potential biomarkers and targets for future therapies were thought-provoking. This article discusses highlights of the 2019 pulmonary vascular disease sessions as a summary of current knowledge and practice. We have summarised the key points from the sessions pertaining to the new ERS/ESC Guidelines for the management of acute pulmonary embolism. We have also focused on prognostic factors and potential therapies in pulmonary hypertension related to interstitial lung disease. Relating to PAH, we have reviewed the symposia on risk stratification, along with the use of noninvasive measures and the sessions relating to biomarkers in PAH.


id: cord-278846-nqj7ctk3
title: Macrophage metabolic reprogramming during chronic lung disease
author: Ogger, Patricia P.
date: 2020-11-12
url: https://www.ncbi.nlm.nih.gov/pubmed/33184475/
doi: 10.1038/s41385-020-00356-5
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.


id: cord-287544-n32iscmr
author: Solaimanzadeh, Isaac
date: 2020-05-12
txt: ./txt/cord-287544-n32iscmr.txt
cache: ./cache/cord-287544-n32iscmr.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32411566/
doi: 10.7759/cureus.8069
summary:
  title: Nifedipine and Amlodipine Are Associated With Improved Mortality and Decreased Risk for Intubation and Mechanical Ventilation in Elderly Patients Hospitalized for COVID-19 A retrospective review was conducted on CCB use in hospitalized patients in search of any difference in outcomes related to specific endpoints: survival to discharge and progression of disease leading to intubation and mechanical ventilation. Nifedipine and amlodipine were found to be associated with significantly improved mortality and a decreased risk for intubation and mechanical ventilation in elderly patients hospitalized with COVID-19. Nifedipine and amlodipine were found to be associated with significantly improved mortality and a decreased risk for intubation and mechanical ventilation in elderly patients hospitalized with COVID-19. A retrospective review of patients on either nifedipine or amlodipine was conducted in search of any difference in outcomes, including survival to discharge and progression of disease leading to intubation and mechanical ventilation.

title:
  Nifedipine and Amlodipine Are Associated With Improved Mortality and Decreased Risk for Intubation and Mechanical Ventilation in Elderly Patients Hospitalized for COVID-19

abstract:
  Dihydropyridine calcium channel blockers (CCB) are typically used agents in the clinical management of hypertension. Yet, they have also been utilized in the treatment of various pulmonary disorders with vasoconstriction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been implicated in the development of vasoconstrictive, proinflammatory, and pro-oxidative effects. A retrospective review was conducted on CCB use in hospitalized patients in search of any difference in outcomes related to specific endpoints: survival to discharge and progression of disease leading to intubation and mechanical ventilation. The electronic medical records for all patients that tested positive for SARS-CoV-2 that were at or above the age of 65 and that expired or survived to discharge from a community hospital in Brooklyn, NY, between the start of the public health crisis due to the viral disease up until April 13, 2020, were included. Of the 77 patients that were identified, 18 survived until discharge and 59 expired. Seven patients from the expired group were excluded since they died within one day of presentation to the hospital. Five patients were excluded from the expired group since their age was above that of the eldest patient in the survival group (89 years old). With 65 patients left, 24 were found to have been administered either amlodipine or nifedipine (CCB group) and 41 were not (No-CCB group). Patients treated with a CCB were significantly more likely to survive than those not treated with a CCB: 12 (50%) survived and 12 expired in the CCB group vs. six (14.6%) that survived and 35 (85.4%) that expired in the No-CCB treatment group (P<.01; p=0.0036). CCB patients were also significantly less likely to undergo intubation and mechanical ventilation. Only one patient (4.2%) was intubated in the CCB group whereas 16 (39.0%) were intubated in the No-CCB treatment group (P<.01; p=0.0026). Nifedipine and amlodipine were found to be associated with significantly improved mortality and a decreased risk for intubation and mechanical ventilation in elderly patients hospitalized with COVID-19. Further clinical studies are warranted. Including either nifedipine or amlodipine in medication regimens for elderly patients with hypertension hospitalized for COVID-19 may be considered.


id: cord-290006-63sa00ju
title: Approach to Peribronchovascular Disease on CT
author: Ko, Jane P.
date: 2018-12-20
url: https://api.elsevier.com/content/article/pii/S0887217118301306
doi: 10.1053/j.sult.2018.12.002
abstract:
  Diseases that are predominantly peribronchovascular in distribution on computed tomography by definition involve the bronchi, adjacent vasculature, and associated lymphatics involving the central or axial lung interstitium. An understanding of diseases that can present with focal peribronchovascular findings is useful for establishing diagnoses and guiding patient management. This review will cover clinical and imaging features that may assist in differentiating amongst the various causes of primarily peribronchovascular disease.


id: cord-293613-xnos7iud
author: Ritchie, Andrew I.
date: 2020-08-12
txt: ./txt/cord-293613-xnos7iud.txt
cache: ./cache/cord-293613-xnos7iud.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32800196/
doi: 10.1016/j.ccm.2020.06.007
summary:
  The 2017 Global Initiative for Chronic Obstructive Lung Disease (GOLD) document AECOPD definition slightly differs from this as "an acute worsening of respiratory symptoms that results in additional therapy." This definition requires the patient to seek or use treatment and is an example of a health care use (HCU) exacerbation in which the patient or clinician decides whether treatment is warranted. This approach has been widely accepted in research, using several validated patient-reported outcome (PRO) tools such as symptom/treatment diary cards and questionnaire tools such as the EXACT (Exacerbations of Chronic Obstructive Pulmonary Disease Tool) and CAT (The COPD Assessment Test). Analysis of viral infection and biomarkers in patients with acute exacerbation of chronic obstructive pulmonary disease

title:
  Definition, Causes, Pathogenesis, and Consequences of Chronic Obstructive Pulmonary Disease Exacerbations

abstract:
  Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are episodes of symptom worsening which have significant adverse consequences for patients. Exacerbations are highly heterogeneous events associated with increased airway and systemic inflammation and physiological changes. The frequency of exacerbations is associated with accelerated lung function decline, quality of life impairment and increased mortality. They are triggered predominantly by respiratory viruses and bacteria, which infect the lower airway and increase airway inflammation. A proportion of patients appear to be more susceptible to exacerbations, with poorer quality of life and more aggressive disease progression than those who have infrequent exacerbations. Exacerbations also contribute significantly to healthcare expenditure. Prevention and mitigation of exacerbations are therefore key goals of COPD management.


id: cord-305838-i0ck2oo0
title: CHEST Reviews: Addressing reduced laboratory-based pulmonary function testing during a pandemic
author: Kouri, Andrew
date: 2020-07-08
txt: ./txt/cord-305838-i0ck2oo0.txt
cache: ./cache/cord-305838-i0ck2oo0.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S0012369220318675
doi: 10.1016/j.chest.2020.06.065
summary:
  Home measurement of peak expiratory flow (PEF) using an inexpensive portable handheld device is already a guideline-recommended option to facilitate patient self-management in asthma and in the diagnosis of occupational asthma, but its role is less well defined in COPD. 37 Electronic portable spirometers have been studied and found to be comparable to conventional laboratory spirometry in several chronic respiratory conditions, such as asthma and COPD, cystic fibrosis, idiopathic pulmonary fibrosis, and post-lung and hematopoietic stem cell transplant monitoring. Oscillometry is emerging as an alternative form of pulmonary function testing that offers some advantages over conventional PFTs. 54 It has been shown to be more sensitive than spirometry in early diagnosis of COPD, 55, 56 to correlate better with respiratory symptoms and asthma control 57,58 as well as in identifying spirometrically silent episodes of biopsy-proven acute graft rejection following lung transplant.

abstract:
  Abstract To reduce the spread of SARS-CoV-2, many pulmonary function testing (PFT) laboratories have been closed or have significantly reduced their testing capacity. As these mitigation strategies may be necessary for the next 6-18 months to prevent recurrent peaks in disease prevalence, fewer objective measurements of lung function will alter the diagnosis and care of patients with chronic respiratory diseases. PFTs, which include spirometry, lung volumes, and diffusion capacity measurement, are essential to the diagnosis and management of patients with asthma, COPD, and other chronic lung conditions. Both traditional and innovative alternatives to conventional testing must now be explored. These may include peak expiratory flow devices, electronic portable spirometers, portable exhaled nitric oxide measurement, airwave oscillometry devices, as well as novel digital health tools such as smartphone microphone spirometers, and mobile health technologies along integration of machine learning approaches. The adoption of some novel approaches may not merely replace but could improve existing management strategies and alter common diagnostic paradigms. With these options come important technical, privacy, ethical, financial, and medicolegal barriers that must be addressed. However, the COVID-19 pandemic also presents a unique opportunity to augment conventional testing by including innovative and emerging approaches to measuring lung function remotely in patients with respiratory disease. The benefits of such an approach have the potential to enhance respiratory care and empower patient self-management well beyond the current global pandemic.


id: cord-312978-i41l4mtx
title: Hydropneumothorax Revealing a Pneumoblastoma in Children
author: El Fakiri, Karima
date: 2020-09-09
txt: ./txt/cord-312978-i41l4mtx.txt
cache: ./cache/cord-312978-i41l4mtx.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/32963869/
doi: 10.1155/2020/8879661
summary:
  A thoracic CT scan searching an underlying pathology revealed overdistension of the right hemithorax with parenchymal air cystic lesions involving the external segment of the middle lobe conducting to a malformation cystic adenomatoid, a fairly abundant right hydropneumothorax responsible for a compressive effect on the adjacent pulmonary parenchyma, and inflammation of the pleura ( Figure 2 ). Regarding the localization, the right lung is more frequently affected by pulmonary blastoma than the left, which is consistent with a previous study involving adult patients [6] . When performing a lobectomy for type II or III PPB, involved pleural surfaces should be resected with the primary tumor and involved pulmonary lobe. Pneumoblastoma in children is a rare, aggressive tumor that shows up with nonspecific clinical and radiological signs which may often delay diagnosis, so the prognosis may be so bad. Pulmonary blastoma in children: report of a rare case and review of the literature

abstract:
  Pneumoblastoma is a rare primary childhood tumor. We report the observation of an infant aged 2 years and 8 months who presented with dry cough and dyspnea. The physical examination found mixed pleural effusion syndrome on the right. The chest X-ray revealed a right pneumothorax. Biology has shown leukocytosis at 16,000/mm(3). The CT scan revealed parenchymal air cystic lesions affecting the outer segment of the middle lobe mimicking a pulmonary malformation. Thoracic drainage brought back 100 ml of the fluid. Two months later, when a pyopneumothorax appeared, a medium lobectomy was performed. Pathological study specimen showed a high-grade type II pneumoblastoma The extension assessment identified a secondary hepatic location. Chemotherapy has been indicated. This observation illustrates the diagnosis challenge of pneumoblastoma in children.


id: cord-314106-r3axl3w1
title: Pulmonary Artery Thrombosis: A Diagnosis That Strives for Its Independence
author: Porembskaya, Olga
date: 2020-07-18
url: https://doi.org/10.3390/ijms21145086
doi: 10.3390/ijms21145086
abstract:
  According to a widespread theory, thrombotic masses are not formed in the pulmonary artery (PA) but result from migration of blood clots from the venous system. This concept has prevailed in clinical practice for more than a century. However, a new technologic era has brought forth more diagnostic possibilities, and it has been shown that thrombotic masses in the PA could, in many cases, be found without any obvious source of emboli. Chronic obstructive pulmonary disease, asthma, sickle cell anemia, emergency and elective surgery, viral pneumonia, and other conditions could be complicated by PA thrombosis development without concomitant deep vein thrombosis (DVT). Different pathologies have different causes for local PA thrombotic process. As evidenced by experimental results and clinical observations, endothelial and platelet activation are the crucial mechanisms of this process. Endothelial dysfunction can impair antithrombotic function of the arterial wall through downregulation of endothelial nitric oxide synthase (eNOS) or via stimulation of adhesion receptor expression. Hypoxia, proinflammatory cytokines, or genetic mutations may underlie the procoagulant phenotype of the PA endothelium. Both endotheliocytes and platelets could be activated by protease mediated receptor (PAR)- and receptors for advanced glycation end (RAGE)-dependent mechanisms. Hypoxia, in particular induced by high altitudes, could play a role in thrombotic complications as a trigger of platelet activity. In this review, we discuss potential mechanisms of PA thrombosis in situ.


id: cord-320447-nq9f1gmu
title: Assessment of small pulmonary blood vessels in COVID-19 patients using HRCT
author: Lins, Muriel
date: 2020-07-25
txt: ./txt/cord-320447-nq9f1gmu.txt
cache: ./cache/cord-320447-nq9f1gmu.txt
extension: .txt
mime: text/plain
url: https://www.sciencedirect.com/science/article/pii/S1076633220304426?v=s5
doi: 10.1016/j.acra.2020.07.019
summary:
  Results: Compared to healthy volunteers, COVID-19 patients showed significant reduction in BV5 (pulmonary blood volume contained in blood vessels of <5 mm(2)) expressed as BV5/(Total pulmonary blood volume) (p<0.0001), and significant increases in BV5-10 and BV 10 (pulmonary blood volumes contained in vessels between 5 and 10 mm(2) and above 10 mm(2), respectively) (p<0.0001). Conclusions: COVID-19 patients display striking anomalies in the distribution of blood volume within the pulmonary vascular tree, consistent with increased pulmonary vasculature resistance in the pulmonary vessels below the resolution of CT. These results suggest that while the pathological changes to the pulmonary vasculature implicated in pulmonary vascular disease (PVD), collectively termed "pulmonary vascular remodeling", occur primarily below the resolution of CT scans, those processes do have a measurable effect on larger, more proximal vessels. In this study we assessed the use of novel CT-derived measures of pulmonary blood volume and pulmonary vascular density in patients with COVID-19.

abstract:
  Background: Mounting evidence supports the role of pulmonary hemodynamic alternations in the pathogenesis of COVID-19. Previous studies have demonstrated that changes in pulmonary blood volumes measured on CT are associated with histopathological markers of pulmonary vascular pruning, suggesting that quantitative CT analysis may eventually be useful in the assessment pulmonary vascular dysfunction more broadly. Methods: Building upon previous work, automated quantitative CT measures of small blood vessel volume and pulmonary vascular density were developed. Scans from 103 COVID-19 patients and 107 healthy volunteers were analyzed and their results compared, with comparisons made both on lobar and global levels. Results: Compared to healthy volunteers, COVID-19 patients showed significant reduction in BV5 (pulmonary blood volume contained in blood vessels of <5 mm(2)) expressed as BV5/(Total pulmonary blood volume) (p<0.0001), and significant increases in BV5-10 and BV 10 (pulmonary blood volumes contained in vessels between 5 and 10 mm(2) and above 10 mm(2), respectively) (p<0.0001). These changes were consistent across lobes. Conclusions: COVID-19 patients display striking anomalies in the distribution of blood volume within the pulmonary vascular tree, consistent with increased pulmonary vasculature resistance in the pulmonary vessels below the resolution of CT.


id: cord-320959-sgdqhtns
title: Vitamin E Acetate as Linactant in the Pathophysiology of EVALI
author: Lee, Hanjun
date: 2020-08-12
txt: ./txt/cord-320959-sgdqhtns.txt
cache: ./cache/cord-320959-sgdqhtns.txt
extension: .txt
mime: text/plain
url: https://api.elsevier.com/content/article/pii/S0306987720315188
doi: 10.1016/j.mehy.2020.110182
summary:
  In membrane biophysics, Vitamin E is a linactant and a potent modulator of lateral phase separation that effectively reduces the line tension at the two-dimensional phase boundaries and thereby exponentially increases the surface viscosity of the pulmonary surfactant. Supplementation of pulmonary surfactants which retain moderate level of cholesterol and 10 controlled hypothermia for patients are recommended when the hypothesis that the line-active property of the vitamin derivative drives the pathogenesis of EVALI holds. Currently, there are 5 five established non-antioxidative properties of Vitamin E in the biological system: i) its ability to induce gel-liquid crystalline phase transition, ii) its active deposition in the lipid droplet of macrophages, iii) its modulation of the antidiabetic cascade involving diacylglycerol kinase (DGK) and protein kinase C (PKC), iv) its activation of the xenobiotic-sensing pregnane X receptor (PXR) signaling, and v) its ability to modulate lateral phase separation.

abstract:
  The recent identification of Vitamin E acetate as one of the causal agents for the e-cigarette, or vaping, product use associated lung injury (EVALI) is a major milestone. In membrane biophysics, Vitamin E is a linactant and a potent modulator of lateral phase separation that effectively reduces the line tension at the two-dimensional phase boundaries and thereby exponentially increases the surface viscosity of the pulmonary surfactant. Disrupted dynamics of respiratory compression-expansion cycling may result in an extensive hypoxemia, leading to an acute respiratory distress entailing the formation of intraalveolar lipid-laden macrophages. Supplementation of pulmonary surfactants which retain moderate level of cholesterol and controlled hypothermia for patients are recommended when the hypothesis that the line-active property of the vitamin derivative drives the pathogenesis of EVALI holds.


id: cord-322756-ouvn71r9
title: Inhaled RNA Therapy: From Promise to Reality
author: Chow, Michael Y.T.
date: 2020-09-04
url: https://www.sciencedirect.com/science/article/pii/S0165614720301802
doi: 10.1016/j.tips.2020.08.002
abstract:
  RNA-based medicine is receiving growing attention for its diverse roles and potential therapeutic capacity. The largest obstacle in its clinical translation remains identifying a safe and effective delivery system. Studies investigating RNA therapeutics in pulmonary diseases have rapidly expanded and drug administration by inhalation allows the direct delivery of RNA therapeutics to the target site of action while minimizing systemic exposure. In this review, we highlight recent developments in pulmonary RNA delivery systems with the use of nonviral vectors. We also discuss the major knowledge gaps that require thorough investigation and provide insights that will help advance this exciting field towards the bedside.


id: cord-322919-5ty35rsy
title: Non‐invasive hemodynamic profile of early COVID‐19 infection
author: Busana, Mattia
date: 2020-10-28
txt: ./txt/cord-322919-5ty35rsy.txt
cache: ./cache/cord-322919-5ty35rsy.txt
extension: .txt
mime: text/plain
url: https://www.ncbi.nlm.nih.gov/pubmed/33113285/
doi: 10.14814/phy2.14628
summary:
  When stratifying for SVRI, patients with an SVRI value below the cohort median had also more severe oxygenation impairment and lower TPR, despite a similar degree of CXR infiltrates. CONCLUSIONS: In the early stages of COVID‐19 infection the hemodynamic profile is characterized by a hyperdynamic circulatory state with high CI and low SVRI, while the right heart is functionally unaffected. In this study, we found that in the early stages of the disease, COVID-19 infection leads to a hyperdynamic circulatory state characterized by an elevated CI and low SVRI. The right heart function was unaffected, and pulmonary pressures were normal, despite the high CI, particularly in the low SVRI range. Lung recruitability in COVID-19 is moderately low (Pan et al., 2020) and blood diversion with cardiac output reduction may justify the reported oxygenation improvement at high Positive End Expiratory Pressure (PEEP).

abstract:
  INTRODUCTION: Little is known about the systemic and pulmonary macrohemodynamics in early COVID‐19 infection. Echocardiography may provide useful insights into COVID‐19 physiopathology. METHODS: Twenty‐three COVID‐19 patients were enrolled in a medical ward. Gas exchange, transthoracic echocardiographic, and hemodynamic variables were collected. RESULTS: Mean age was 57 ± 17 years. The patients were hypoxemic (PaO(2)/FiO(2) = 273.0 ± 102.6 mmHg) and mildly hypocapnic (PaCO(2) = 36.2 ± 6.3 mmHg, pH = 7.45 ± 0.03). Mean arterial pressure was decreased (86.7 [80.0–88.3] mmHg). Cardiac index was elevated (4.32 ± 0.90 L∙min(‐1)∙m(‐2)) and the resulting systemic vascular resistance index low (1,458 [1358–1664] dyn∙s∙cm(‐5)∙m(‐2)). The right heart was morphologically and functionally normal, with pulmonary artery pressure (PAPm, 18.0 ± 2.9 mmHg) and Total Pulmonary Resistances (TPR, 2.3 [2.1–2.7] mmHg∙l(‐1)∙min(‐1)) within normal limits. When stratifying for SVRI, patients with an SVRI value below the cohort median had also more severe oxygenation impairment and lower TPR, despite a similar degree of CXR infiltrates. Oxygen delivery index in this group resulted supranormal. CONCLUSIONS: In the early stages of COVID‐19 infection the hemodynamic profile is characterized by a hyperdynamic circulatory state with high CI and low SVRI, while the right heart is functionally unaffected. Our findings suggest that hypoxemia, viral sepsis or peripheral shunting are possible mechanisms for the vasodilation that dominates at this stage of the disease and may itself worsen the gas exchange.


id: cord-323566-jck799zq
title: Acute Lung Injury
author: Cheung, Oi-Yee
date: 2017-11-05
url: https://api.elsevier.com/content/article/pii/B9780323442848000065
doi: 10.1016/b978-0-323-44284-8.00006-5
abstract:
  A wide variety of insults can produce acute lung damage, inclusive of those that injure the lungs directly. The clinical syndrome of acute onset respiratory distress, dyspnea, and bilateral infiltrates is referred to as acute respiratory distress syndrome. The histologic counterpart of acute respiratory distress syndrome is diffuse alveolar damage, classically characterized by hyaline membranes. Other histologic features of acute lung injury include intraalveolar fibrin, organization, interstitial edema, and reactive pneumocytes. Diffuse alveolar damage and other histologic features of acute lung injury are nonspecific as to etiology, and once identified require the pathologist to search the biopsy for further features that may help identify a specific etiology. This chapter reviews the temporal sequence of acute lung injury and explores the large variety of specific etiologic causes with emphasis on helpful histologic features to identify.


id: cord-325461-q8igdvq4
title: Pulmonary vascular dysfunction in ARDS
author: Ryan, Donal
date: 2014-08-22
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url: https://doi.org/10.1186/s13613-014-0028-6
doi: 10.1186/s13613-014-0028-6
summary:
  We consider the factors that influence pulmonary arterial pressure, both in normal lungs and in the presence of ARDS, including the important effects of mechanical ventilation. (Am J Respir Crit Care Med 182:1123–1128, 2010) have recently reported that elevated pulmonary vascular resistance (PVR) and TPG were independently associated with increased mortality in ARDS, in a large trial with protocol-defined management strategies and using lung-protective ventilation. Studies were identified after a literature search using key terms (ARDS or acute respiratory distress or ALI or acute lung injury) together with any of the following: pulmonary haemodynamics, pulmonary artery pressure, pulmonary vascular resistance, pulmonary vascular dysfunction, right ventricle, right ventricular failure, acute cor pulmonale, or pulmonary artery catheter. There are very few studies which have measured pulmonary vascular resistance in ARDS patients ventilated with lower tidal volumes, perhaps due to the reduction in the use of the pulmonary artery catheter just as lung-protective ventilation was gaining widespread acceptance [60] .

abstract:
  Acute respiratory distress syndrome (ARDS) is characterised by diffuse alveolar damage and is frequently complicated by pulmonary hypertension (PH). Multiple factors may contribute to the development of PH in this setting. In this review, we report the results of a systematic search of the available peer-reviewed literature for papers that measured indices of pulmonary haemodynamics in patients with ARDS and reported on mortality in the period 1977 to 2010. There were marked differences between studies, with some reporting strong associations between elevated pulmonary arterial pressure or elevated pulmonary vascular resistance and mortality, whereas others found no such association. In order to discuss the potential reasons for these discrepancies, we review the physiological concepts underlying the measurement of pulmonary haemodynamics and highlight key differences between the concepts of resistance in the pulmonary and systemic circulations. We consider the factors that influence pulmonary arterial pressure, both in normal lungs and in the presence of ARDS, including the important effects of mechanical ventilation. Pulmonary arterial pressure, pulmonary vascular resistance and transpulmonary gradient (TPG) depend not alone on the intrinsic properties of the pulmonary vascular bed but are also strongly influenced by cardiac output, airway pressures and lung volumes. The great variability in management strategies within and between studies means that no unified analysis of these papers was possible. Uniquely, Bull et al. (Am J Respir Crit Care Med 182:1123–1128, 2010) have recently reported that elevated pulmonary vascular resistance (PVR) and TPG were independently associated with increased mortality in ARDS, in a large trial with protocol-defined management strategies and using lung-protective ventilation. We then considered the existing literature to determine whether the relationship between PVR/TPG and outcome might be causal. Although we could identify potential mechanisms for such a link, the existing evidence does not allow firm conclusions to be drawn. Nonetheless, abnormally elevated PVR/TPG may provide a useful index of disease severity and progression. Further studies are required to understand the role and importance of pulmonary vascular dysfunction in ARDS in the era of lung-protective ventilation.


id: cord-329442-ycj6sf6z
author: Perotin, Jeanne‐Marie
date: 2013-02-27
url: https://www.ncbi.nlm.nih.gov/pubmed/23447038/
doi: 10.1002/jmv.23495
title:
  Detection of multiple viral and bacterial infections in acute exacerbation of chronic obstructive pulmonary disease: A pilot prospective study

abstract:
  Few studies have evaluated the contribution of multiple virus and bacterial infections in acute exacerbation of chronic obstructive pulmonary disease. This study estimated the burden of multiple viral and bacterial respiratory infections in moderate to very severe chronic obstructive pulmonary disease patients that were prospectively followed‐up during a 12‐month pilot study. Clinical data were collected monthly and sputum was collected at the time of each acute exacerbation event. Classical culture techniques for bacteria and multiplex polymerase chain reaction (PCR) and microarray detection assays were performed to identify viral and atypical bacterial pathogens in the sputum. Overall, 51 patients were included and 45 acute exacerbation events were investigated clinically and microbiologically. Among the 45 acute exacerbation events, 44% had evidence of viral infection involving human rhinovirus (HRV) and metapneumovirus (hMPV) in 20% and 18%, respectively. Intracellular bacteria were not found in sputum by PCR. Common bacterial pathogens were identified in 42% of acute exacerbation patients, most frequently Branhamella catarrhalis, Streptococcus pneumoniae and Haemophilus influenzae. Viral or virus and bacteria co‐infections were detected in 27% of acute exacerbation events (n = 12) with HRV and hMPV involved in 92% of cases. Patients with co‐infections did not present greater clinical severity scores at exacerbation and more recurrence of acute exacerbation events at 3 and 6 months than those with single infections (P > 0.4). These results suggest that HRV and hMPV may be contributors or cofactors of AECOPD. These findings indicate that viral or virus and bacterial co‐infections do not impact significantly on the clinical severity of acute exacerbation of chronic obstructive pulmonary disease and recurrence at 3 and 6 months. J. Med. Virol. 85:866–873, 2013. © 2013 Wiley Periodicals, Inc.


id: cord-331910-s474ecvk
author: Thota, Sai Manohar
date: 2020-08-17
url: https://doi.org/10.1002/ptr.6794
doi: 10.1002/ptr.6794
title:
  Natural products as home‐based prophylactic and symptom management agents in the setting of COVID‐19

abstract:
  Coronavirus disease (COVID‐19) caused by the novel coronavirus (SARS‐CoV‐2) has rapidly spread across the globe affecting 213 countries or territories with greater than six million confirmed cases and about 0.37 million deaths, with World Health Organization categorizing it as a pandemic. Infected patients present with fever, cough, shortness of breath, and critical cases show acute respiratory infection and multiple organ failure. Likelihood of these severe indications is further enhanced by age as well as underlying comorbidities such as diabetes, cardiovascular, or thoracic problems, as well as due to an immunocompromised state. Currently, curative drugs or vaccines are lacking, and the standard of care is limited to symptom management. Natural products like ginger, turmeric, garlic, onion, cinnamon, lemon, neem, basil, and black pepper have been scientifically proven to have therapeutic benefits against acute respiratory tract infections including pulmonary fibrosis, diffuse alveolar damage, pneumonia, and acute respiratory distress syndrome, as well as associated septic shock, lung and kidney injury, all of which are symptoms associated with COVID‐19 infection. This review highlights the potential of these natural products to serve as home‐based, inexpensive, easily accessible, prophylactic agents against COVID‐19.


id: cord-331939-6okbdw7a
title: Acute pulmonary embolism multimodality imaging prior to endovascular therapy
author: Sin, David
date: 2020-08-30
url: https://doi.org/10.1007/s10554-020-01980-9
doi: 10.1007/s10554-020-01980-9
abstract:
  The manuscript discusses the application of CT pulmonary angiography, ventilation–perfusion scan, and magnetic resonance angiography to detect acute pulmonary embolism and to plan endovascular therapy. CT pulmonary angiography offers high accuracy, speed of acquisition, and widespread availability when applied to acute pulmonary embolism detection. This imaging modality also aids the planning of endovascular therapy by visualizing the number and distribution of emboli, determining ideal intra-procedural catheter position for treatment, and signs of right heart strain. Ventilation–perfusion scan and magnetic resonance angiography with and without contrast enhancement can also aid in the detection and pre-procedural planning of endovascular therapy in patients who are not candidates for CT pulmonary angiography.


id: cord-334528-xenq90xj
title: Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations
author: Chen, Hsing I
date: 2011-03-17
txt: ./txt/cord-334528-xenq90xj.txt
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url: https://www.ncbi.nlm.nih.gov/pubmed/22783284/
doi: 10.3724/sp.j.1263.2011.00044
summary:
  This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS. [33, 34] In addition to the aforementioned animal experimentations and clinical observations that NO production through the iNOS may be involved in the lung injury due to various causes, our research team demonstrated that endotoxemia produced in anesthetized rats by intravenous administration of lipopolysaccharide (LPS, endotoxin) provoked systemic hypotension, endothelial damage and ALI accompanied by increased plasma nitrate/nitrite and expression of iNOS mRNA, TNF α and IL-1 β . The detrimental role of inducible nitric oxide synthase in the pulmonary edema caused by hypercalcemia in conscious rats and isolated lungs

abstract:
  Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALI or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS.


id: cord-335382-fk4um9nw
title: Molecular Basis of Pulmonary Disease
author: Farver, Carol F.
date: 2012-08-10
txt: ./txt/cord-335382-fk4um9nw.txt
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url: https://api.elsevier.com/content/article/pii/B9780123744197000184
doi: 10.1016/b978-0-12-374419-7.00018-4
summary:
  When lung cancer is suspected, evaluation of the patient includes a thorough clinical, radiologic, and laboratory assessment, with collection of tissue or cytology samples to establish a pathologic diagnosis of malignancy and to classify the tumor type. Development of lung cancer occurs with multiple, complex, stepwise genetic and epigenetic changes involving allelic losses, chromosomal instability and imbalance, mutations in tumor suppressor genes (TSGs) and dominant oncogenes, epigenetic gene silencing through promoter hypermethylation, and aberrant expression of genes participating in control of cell proliferation and apoptosis [7] . In recent years, atypical adenomatous hyperplasia (AAH) has been recognized as a precursor lesion for peripheral pulmonary ACs. This lesion is defined as "a localized proliferation of mild to moderately atypical cells lining involved alveoli and, sometimes, respiratory bronchioles, resulting in focal lesions in peripheral Part IV Molecular Pathology of Human Disease alveolated lung, usually less than 5 mm in diameter and generally in the absence of underlying interstitial inflammation and fibrosis" (Figure 18 .8) [36] .

abstract:
  Pulmonary pathology includes a large spectrum of both neoplastic and non-neoplastic diseases that affect the lung. Many of these are a result of the unusual relationship of the lung with the outside world. Every breath that a human takes brings the outside world into the body in the form of infectious agents, organic and inorganic particles, and noxious agents of all types. Although the lung has many defense mechanisms to protect itself from these insults, these are not infallible; therefore, lung pathology arises. Damage to the lung is particularly important given the role of the lung in the survival of the organism. Any impairment of lung function has widespread effects throughout the body, since all organs depend on the lungs for the oxygen they need. Pulmonary pathology catalogs the changes in the lung tissues and the mechanisms through which these occur. This chapter presents a review of lung pathology and the current state of knowledge about the pathogenesis of each disease. It suggests that a clear understanding of both morphology and mechanism is required for the development of new therapies and preventive measures.


id: cord-352532-xqphom6x
title: 1 Tropical Lung Diseases
author: Papanikolaou, Ilias C
date: 2013-12-31
txt: ./txt/cord-352532-xqphom6x.txt
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url: https://api.elsevier.com/content/article/pii/B9781416043904000011
doi: 10.1016/b978-1-4160-4390-4.00001-1
abstract: nan
summary:
  The following are the common tropical pulmonary conditions: l pneumonia: typical and atypical l eosinophilic pneumonias and tropical pulmonary eosinophilia l bronchiectasis, asthma and chronic obstructive pulmonary disease (COPD) l pleural effusion l nontuberculous granulomatous lung disease l occupational lung diseases. A reasonable approach to the patient with lung disease in the tropic starts with age, occupational exposure, physical examination, HIV status, chest x-ray and blood tests. • If wheezing (even if it disappeared after rapidly acting bronchodilator) give an inhaled bronchodilator for 5 days* • Soothe the throat and relieve the cough with a safe remedy • If coughing for more than 3 weeks or if having recurrent wheezing, refer for assessment for TB or asthma • Advise the mother when to return immediately • Follow-up in 5 days if not improving A blood count usually reveals leukocytosis in bacterial pneumonia, leukopenia in viral infection, and eosinophilia in parasitic infestation.


