scholarly journals Gender-specific associations between polymorphisms in the Toll-like receptor (TLR) genes and lung function among workers in swine operations

2018 ◽  
Vol 81 (22) ◽  
pp. 1186-1198 ◽  
Author(s):  
Zhiwei Gao ◽  
James A. Dosman ◽  
Donna C. Rennie ◽  
David A. Schwartz ◽  
Ivana V. Yang ◽  
...  
2013 ◽  
Vol 110 (1) ◽  
pp. 44-50.e1 ◽  
Author(s):  
Zhiwei Gao ◽  
James A. Dosman ◽  
Donna C. Rennie ◽  
David A. Schwartz ◽  
Ivana V. Yang ◽  
...  

2014 ◽  
Vol 134 (2) ◽  
pp. 485-488.e5 ◽  
Author(s):  
Zhiwei Gao ◽  
James A. Dosman ◽  
Donna C. Rennie ◽  
David A. Schwartz ◽  
Ivana V. Yang ◽  
...  

2013 ◽  
Vol 74 (12) ◽  
pp. 1649-1655 ◽  
Author(s):  
F. Haerynck ◽  
J.M. Mahachie John ◽  
K. Van Steen ◽  
P. Schelstraete ◽  
S. Van daele ◽  
...  

2007 ◽  
Vol 42 (7) ◽  
pp. 631-639 ◽  
Author(s):  
Yunxian Yu ◽  
Rajesh Kumar ◽  
Scott Venners ◽  
Jacqueline Pongracic ◽  
Binyan Wang ◽  
...  

Author(s):  
Siavash Bolourani ◽  
Max Brenner ◽  
Ping Wang

AbstractPulmonary fibrosis is a chronic debilitating condition characterized by progressive deposition of connective tissue, leading to a steady restriction of lung elasticity, a decline in lung function, and a median survival of 4.5 years. The leading causes of pulmonary fibrosis are inhalation of foreign particles (such as silicosis and pneumoconiosis), infections (such as post COVID-19), autoimmune diseases (such as systemic autoimmune diseases of the connective tissue), and idiopathic pulmonary fibrosis. The therapeutics currently available for pulmonary fibrosis only modestly slow the progression of the disease. This review is centered on the interplay of damage-associated molecular pattern (DAMP) molecules, Toll-like receptor 4 (TLR4), and inflammatory cytokines (such as TNF-α, IL-1β, and IL-17) as they contribute to the pathogenesis of pulmonary fibrosis, and the possible avenues to develop effective therapeutics that disrupt this interplay.


2020 ◽  
Author(s):  
Mélany Pierard ◽  
Alexandra Tassin ◽  
Antoine Legrand ◽  
Alexandre Legrand

Abstract Background: Disease progression in COPD patient is associated to lung function decline, leading to a higher risk of hypoxaemia and associated comorbidities, notably cardiovascular diseases (CV). Gender is also known to influence CV risk. Adiponectin (Ad), a cardio-protective hormone, was suggested as a biomarker for COPD risk management. However, determinants and consequences of Ad pathway modulation in COPD are unknown and gender specificities are poorly understood. We postulated that hypoxaemia and gender could influence Ad pathway and contribute to the appearance of a distinct endotype associated to an altered CV risk.Methods: The Ad plasmatic (Adpl) level and proportion of its different forms were evaluated in hypoxemic and non-hypoxemic COPD men or women. The relationship between these measures and BMI, blood gas analysis (PaO2, PaCO2), or lung function (FEV1, FEV1/FVC, TLCO, TLC, RV) were tested.Results: Despite similar age, BMI and obstruction severity, women had a higher TLC and RV than men. Adpl level was higher in women and negatively associated with hyperinflation and hypercapnia. The proportion of the most active forms of Ad (HMW) is increased in hypoxemic women but not in men. A positive correlation between TLCO and HMW form proportion was observed in hypoxemic men, whereas a negative correlation was detected in non-hypoxemic men.Conclusion: Physiopathology of COPD seems to be gender specific. Hypoxaemia, hypercapnia and hyperinflation are associated to gender-specific Ad pathway alterations. Given CV properties of Ad, the impact of such modulation on co-morbidities development have to be considered in future studies.


2020 ◽  
Vol 19 (4) ◽  
pp. 608-613 ◽  
Author(s):  
Susanna Kosamo ◽  
Katherine B. Hisert ◽  
Victoria Dmyterko ◽  
Catherine Nguyen ◽  
R. Anthony Black ◽  
...  

2020 ◽  
Vol 109 (8) ◽  
pp. 1634-1641
Author(s):  
Riikka Riikonen ◽  
Matti Korppi ◽  
Sari Törmänen ◽  
Kirsi Nuolivirta ◽  
Merja Helminen ◽  
...  

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