Important predictors for the development of and mortality in ARDS were identified. Packed red blood cell transfusion was associated with an increased development of and increased mortality in ARDS.

Aims: To investigate the acute systemic inflammatory response to welding fume exposure. Methods: Twenty four welders (42% smokers) and 13 non-exposed controls (23% smokers) were monitored at a welding school. Exposure to fine particulate matter (PM 2.5 ) was assessed using cyclone samplers. Markers of systemic inflammation, including C-reactive protein (CRP), fibrinogen, and white blood cell (WBC) levels, were determined in peripheral blood samples collected at baseline and after 5.3 (SD 1.0) hours of exposure. Results: The median PM 2.5 concentration for welders was 1.66 mg/m 3 , which was significantly greater than that for controls (0.04 mg/m 3 ). Compared to non-smokers, smokers had a significantly higher baseline WBC count, but comparable levels of CRP and fibrinogen. In non-smokers, welding fume exposure was associated with a significant increase in WBC and neutrophil counts immediately following exposure (+0.8610 3 /ml, 95% CI 0.1 to 1.6, and +1.0610 3 /ml, 95% CI 0.4 to 1.7, respectively). A significant decrease in fibrinogen levels was observed in non-smokers (232 mg/dl, 95% CI 263 to 21). No significant changes in WBC, neutrophil, and fibrinogen levels were found in smokers. Sixteen hours after welding exposure, CRP levels were found to be significantly increased in both non-smokers and smokers (0.90 mg/l, 95% CI 0.17 to 1.64). PM 2.5 concentrations were found to be significantly associated with absolute neutrophil counts in non-smokers, and CRP levels in both non-smokers and smokers. Conclusions: High levels of welding fume exposure induce acute systemic inflammation in a relatively young, healthy working population. These results also suggest that smoking may modify the effect of welding fume exposure on specific inflammatory markers.

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HIV prevention with men who have sex with men in India has, in large part, been premised on the reification of "cultural categories"--kothi being among the most popularized terms in this context, broadly designating men who have a feminine sense of self and who enact "passive" sexual roles. Countering prevailing research trends, this article explores ways in which local, national, and global processes inform contemporary kothi sexual subjectivities--disrupting simplistic perspectives on the cultural coherence of the category. Derivative uses of anthropological knowledge in public health and activist milieux are seen to have propounded limited representations of men who have sex with men in India. Drawing on ethnographic research in Calcutta, conceptualization of time in ethnography is examined and a critique of positivist epistemologies is put forward as a basis for advancing more conceptually cogent and effective HIV prevention research and programming strategies, especially those that aim to address sexuality between men.

COVID-19 has caused unprecedented health, economic and societal impacts across the world, including many low- and middle-income countries (LMICs). The pandemic and its fallout have laid bare deep-seated social and economic inequalities with marginalised groups being at greater risk of infection and being disproportionately affected by containment measures and their socioeconomic consequences. Stigma is a central element to such inequalities but remains largely overlooked in the debate on the response to COVID-19, including in LMICs. Yet we know from experiences with other infectious diseases such as HIV/AIDS and Ebola that disease-related stigma is detrimental to halting and controlling pandemics and achieving equitable development. Emerging evidence suggests that stigma associated with COVID-19 is already taking hold. This paper assesses potential driving factors of COVID-19-related stigma, and how this intersects with existing stigma fault lines and explores mechanisms through which COVID-19-related stigma may be counteracted, with a focus on LMICs.

The -308GA and TNFB1/2 polymorphisms of the tumour necrosis factor genes have been associated with increased susceptibility to, and mortality in sepsis, although, prior studies are not consistent. Their role in acute respiratory distress syndrome (ARDS) has not been evaluated. The current authors hypothesised that the -308A allele and TNFB22 genotype would be associated with increased susceptibility to, and mortality in ARDS.The above hypothesis was investigated in a nested case-control study of 441 Caucasian controls and 212 cases admitted to an intensive care unit with sepsis, trauma, aspiration or hypertransfusions.The -308A and TNFB1 alleles were in linkage disequilibrium. These polymorphisms were not associated with ARDS susceptibility on crude analysis. On subgroup analyses, they were associated with either increased or decreased odds of developing ARDS depending on whether the clinical risk for ARDS results in direct or indirect pulmonary injury. The -308A allele was associated with increased 60-day mortality in ARDS, with the strongest association found among younger patients. There was no association between the TNFB polymorphism and ARDS mortality.The -308GA, but not the TNFB12, polymorphism was associated with increased mortality in acute respiratory distress syndrome, but their association with acute respiratory distress syndrome susceptibility depended on the site of injury predisposing to acute respiratory distress syndrome.

Patients with acute respiratory distress syndrome have a high prevalence of elevated cardiac markers. The presence of elevated cardiac markers is independently associated with increased 60-day mortality and increased organ failure. This association is most pronounced among patients with lower severity of illness. These results indicate that occult myocardial injury may be an important factor in acute respiratory distress syndrome morbidity and mortality. Further study of the relevant causal relationships and mechanisms is warranted.

Previous work has shown that impaired exercise tolerance in children with cystic fibrosis (C.F.) is related to the severity of airway obstruction without elucidating the possible roles of hypoxia or malnutrition. It has been suggested that poor nutrition leads to abnormalities in serum fatty acids composition, which may lead to tissue hypoxia. We investigated the roles of hypoxia, pulmonary mechanics, nutritional status, and serum fatty acid composition in limiting exercise tolerance in C.F. In 20 children with C.F., exercise tolerance, while breathing air and while breathing oxygen, was evaluated on a cycle ergometer and compared to pulmonary function tests, anthropometric data, serum lipid compostition, and clinical condition. The mean percent work expected from height (Wmax) was 75, and was unchanged by O2. Wmax correlated significantly with the degree of respiratory impairement, the discrepancy between height and weight, and the clinical score but not serum fatty acid composition. Where measured, no child at any time had an elevated end tidal CO2(PetCO2). We conclude that nutritional status and airway obstruction are closely correlated with exercise tolerance in C.F. and that, unlike the case in adults with chronic obstructive pulmonary disease, exercise-limiting dyspnea occurs in the presence of a normal PetCO2.