Orthotopic Implantation with Immature Mouse Fetal Lung Did Not Self-Organize Airways Structures, but Improved Prognosis of Mice with Paraquat-Induced Severe Lung Injury

2019 ◽  
Vol 38 (4) ◽  
pp. S257
Author(s):  
R. Okabe ◽  
T. Chen-Yoshikawa ◽  
A. Yoshizawa ◽  
T. Hirashima ◽  
F. Gochi ◽  
...  
Keyword(s):  
Lung Injury ◽  
Fetal Lung ◽  
Orthotopic Implantation ◽  
Immature Mouse ◽  
Severe Lung

Severe Lung Injury after Exposure to Chloramine Gas from Household Cleaners

1999 ◽  
Vol 341 (11) ◽  
pp. 848-849 ◽  
Author(s):  
David A. Tanen ◽  
Kimberlie A. Graeme ◽  
Robert Raschke
Keyword(s):  
Lung Injury ◽  
Severe Lung

scholarly journals Do sex-specific immunobiological factors and differences in angiotensin converting enzyme 2 (ACE2) expression explain increased severity and mortality of COVID-19 in males?

Diagnosis ◽  
2020 ◽  
Vol 7 (4) ◽  
pp. 385-386 ◽  
Author(s):  
Jens Vikse ◽  
Giuseppe Lippi ◽  
Brandon Michael Henry
Keyword(s):  
Mortality Rate ◽  
Severe Acute Respiratory Syndrome ◽  
Lung Injury ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Sars Coronavirus ◽  
Immunomodulatory Treatment ◽  
Angiotensin Converting Enzyme 2 ◽  
Cytopathic Effects ◽  
Severe Lung

AbstractCoronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2), shares similarities with the former SARS outbreak, which was caused by SARS-CoV-1. SARS was characterized by severe lung injury due to virus-induced cytopathic effects and dysregulated hyperinflammatory state. COVID-19 has a higher mortality rate in men both inside and outside China. In this opinion paper, we describe how sex-specific immunobiological factors and differences in angiotensin converting enzyme 2 (ACE2) expression may explain the increased severity and mortality of COVID-19 in males. We highlight that immunomodulatory treatment must be tailored to the underlying immunobiology at different stages of disease. Moreover, by investigating sex-based immunobiological differences, we may enhance our understanding of COVID-19 pathophysiology and facilitate improved immunomodulatory strategies.

“BOWEL GANGRENE-AN UNUSUAL PRESENTATION OF COVID 19”

2021 ◽  
pp. 1-2
Author(s):  
Irfan Rasool Bhat ◽  
Manish Gupta ◽  
Komal Goel
Keyword(s):  
Case Report ◽  
Tract Infection ◽  
Lung Injury ◽  
Respiratory Tract ◽  
Venous Thrombosis ◽  
Lower Respiratory Tract ◽  
Emergency Laparotomy ◽  
Present Case Report ◽  
Bowel Gangrene ◽  
Severe Lung

The Covid 19 disease caused by novel corona virus was rst reported in Wuhan, China in December 2019 with 5% patients having severe lung injury. Though this disease primilary presents as the lower respiratory tract infection, multiple digestive manifestation have been reported which are often overlooked. The present case report describes the unusual progression of the Covid 19 disease from pneumonia to a procoagulant state leading to abdominal venous thrombosis and subsequent gut ischemia necessitating emergency laparotomy.

scholarly journals Lung and gut microbiota are altered by hyperoxia and contribute to oxygen-induced lung injury in mice

2020 ◽  
Vol 12 (556) ◽  
pp. eaau9959 ◽  
Author(s):  
Shanna L. Ashley ◽  
Michael W. Sjoding ◽  
Antonia P. Popova ◽  
Tracy X. Cui ◽  
Matthew J. Hoostal ◽  
...  
Keyword(s):  
Lung Injury ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Bacterial Communities ◽  
Adult Mouse ◽  
Relative Growth ◽  
Germ Free ◽  
The Relationship ◽  
Systemic Antibiotic Treatment ◽  
Severe Lung

Inhaled oxygen, although commonly administered to patients with respiratory disease, causes severe lung injury in animals and is associated with poor clinical outcomes in humans. The relationship between hyperoxia, lung and gut microbiota, and lung injury is unknown. Here, we show that hyperoxia conferred a selective relative growth advantage on oxygen-tolerant respiratory microbial species (e.g., Staphylococcus aureus) as demonstrated by an observational study of critically ill patients receiving mechanical ventilation and experiments using neonatal and adult mouse models. During exposure of mice to hyperoxia, both lung and gut bacterial communities were altered, and these communities contributed to oxygen-induced lung injury. Disruption of lung and gut microbiota preceded lung injury, and variation in microbial communities correlated with variation in lung inflammation. Germ-free mice were protected from oxygen-induced lung injury, and systemic antibiotic treatment selectively modulated the severity of oxygen-induced lung injury in conventionally housed animals. These results suggest that inhaled oxygen may alter lung and gut microbial communities and that these communities could contribute to lung injury.

Rat Model to Investigate the Treatment of Acute Nitrogen Dioxide Intoxication

1992 ◽  
Vol 11 (3) ◽  
pp. 179-187 ◽  
Author(s):  
J. Meulenbelt ◽  
J.A.M.A. Dormans ◽  
M. Marra ◽  
P.J.A. Rombout ◽  
B. Sangster
Keyword(s):  
Lung Injury ◽  
Nitrogen Dioxide ◽  
Lung Tissue ◽  
Rat Model ◽  
Therapeutic Interventions ◽  
Nitrite Concentration ◽  
Therapeutic Measures ◽  
Severe Lung

1 The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2 A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO 2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2=1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3 An adequate NO 2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4 Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5 The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6 Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.

A preliminary study on fetal lung injury in a rat model of acute pancreatitis in pregnancy

2017 ◽  
Vol 213 (11) ◽  
pp. 1370-1377 ◽  
Author(s):  
Liang Zhao ◽  
Teng Zuo ◽  
Qiao Shi ◽  
Fang-chao Mei ◽  
Yu-pu Hong ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Lung Injury ◽  
Rat Model ◽  
Fetal Lung ◽  
Preliminary Study ◽  
In Pregnancy

The influence of genetic variation in surfactant protein B on severe lung injury in African American children*

2011 ◽  
Vol 39 (5) ◽  
pp. 1138-1144 ◽  
Author(s):  
Mary K. Dahmer ◽  
Peggy OʼCain ◽  
Pallavi P. Patwari ◽  
Pippa Simpson ◽  
Shun-Hwa Li ◽  
...  
Keyword(s):  
Genetic Variation ◽  
African American ◽  
Lung Injury ◽  
Surfactant Protein ◽  
African American Children ◽  
Surfactant Protein B ◽  
American Children ◽  
Severe Lung ◽  
Protein B

Strategies for ventilation in acute, severe lung injury after combat trauma

2013 ◽  
Vol 161 (1) ◽  
pp. 14-21
Author(s):  
Thomas G Brogden ◽  
J Bunin ◽  
H Kwon ◽  
J Lundy ◽  
A McD Johnston ◽  
...  
Keyword(s):  
Lung Injury ◽  
Combat Trauma ◽  
Severe Lung

TNF-α causes reversible in vivo systemic vascular barrier dysfunction via NO-dependent and -independent mechanisms

1997 ◽  
Vol 273 (6) ◽  
pp. H2565-H2574 ◽  
Author(s):  
Neil K. Worrall ◽  
Kathy Chang ◽  
Wanda S. Lejeune ◽  
Thomas P. Misko ◽  
Patrick M. Sullivan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Water Content ◽  
Selective Inhibition ◽  
No Production ◽  
Barrier Dysfunction ◽  
Barrier Integrity ◽  
Tnf Α ◽  
Severe Lung

Tumor necrosis factor (TNF-α) and nitric oxide (NO) are important vasoactive mediators of septic shock. This study used a well-characterized quantitative permeation method to examine the effect of TNF-α and NO on systemic vascular barrier function in vivo, without confounding endotoxemia, hypotension, or organ damage. Our results showed 1) TNF-α reversibly increased albumin permeation in the systemic vasculature (e.g., lung, liver, brain, etc.); 2) TNF-α did not affect hemodynamics or blood flow or cause significant tissue injury; 3) pulmonary vascular barrier dysfunction was associated with increased lung water content and impaired oxygenation; 4) TNF-α caused inducible nitric oxide synthase (iNOS) mRNA expression in the lung and increased in vivo NO production; 5) selective inhibition of iNOS with aminoguanidine prevented TNF-α-induced lung and liver vascular barrier dysfunction; 6) aminoguanidine prevented increased tissue water content in TNF-α-treated lungs and improved oxygenation; and 7) nonselective inhibition of NOS with N G-monomethly-l-arginine increased vascular permeation in control lungs and caused severe lung injury in TNF-α-treated animals. We conclude that 1) TNF-α reversibly impairs vascular barrier integrity through NO-dependent and -independent mechanisms; 2) nonselective NOS inhibition increased vascular barrier dysfunction and caused severe lung injury, whereas selective inhibition of iNOS prevented impaired endothelial barrier integrity and pulmonary dysfunction; and 3) selective inhibition of iNOS may be beneficial in treating increased vascular permeability that complicates endotoxemia and cytokine immunotherapy.

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