In China, air pollution has become a significant environmental threat to human health in recent years. Airborne bacteria are critical constituents of microbial aerosols, which contain numerous pathogens. However, the effects of seasonal variations, environmental factors such as air pollution, and meteorological factors on microbial diversity are poorly understood. In this study, fine particulate matter (PM 2.5 ) samples (n = 12) were collected using a high-volume air sampler over 24-hour periods during all four seasons from April 2017 to January 2018. Concurrently, the average daily concentrations of various air pollutants and the meteorological conditions were monitored. High-throughput sequencing of 16s rRNA was then employed to profile PM 2.5 bacterial communities. The results showed that the bacterial communities varied significantly by season. Proteobacteria (35.5%), Firmicutes (23.0%), and Actinobacteria (16.2%) were the most abundant bacterial phyla in the PM 2.5 samples. At the genus level, the diversity of the bacterial communities was significantly correlated with the ozone (O 3 ) concentration (r = 0.920, p = 0.001) and air temperature (T) (r = 0.534, p = 0.023). The results of this study can be used as a reference by other bioaerosol research that focuses on the health effects of atmospheric particulate matter.

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IntroductionDiabetic nephropathy (DN) develops in about 40% of patients with type 2 diabetes and remains the leading cause of end-stage renal disease. The mechanisms of DN remain to be elucidated. Oxidative stress is thought to be involved in the development of DN but antioxidant therapy has produced conflicting results. Therefore, we sought to define the role of antioxidant in retarding the development of DN in this study.Research design and methodsWe generated a new antioxidant/diabetes mouse model, LiasH/HLeprdb/db mice, by crossing db/db mice with LiasH/H mice, which have overexpressed Lias gene (~160%) compared with wild type, and also correspondingly increased endogenous antioxidant capacity. The new model was used to investigate whether predisposed increased endogenous antioxidant capacity was able to retard the development of DN. We systemically and dynamically examined main pathological alterations of DN and antioxidant biomarkers in blood and kidney mitochondria.ResultsLiasH/HLeprdb/db mice alleviated major pathological alterations in the early stage of DN, accompanied with significantly enhanced antioxidant defense. The model targets the main pathogenic factors by exerting multiple effects such as hypoglycemic, anti-inflammation, and antioxidant, especially protection of mitochondria.ConclusionThe antioxidant animal model is not only very useful for elucidating the underlying mechanisms of DN but also brings insight into a new therapeutic strategy for clinical applications.

Oxidative stress is proposed to be involved in non-alcoholic fatty liver disease (NAFLD). However, antioxidant therapy results in controversial outcomes. Therefore, we generated a new antioxidant/NAFLD mouse model, LiasHigh/HighLeprdb/db mice, by crossbreeding Leprdb/dbmice, an obesity mouse model, with LiasHigh/High mice, generated by overexpression of lipoic acid synthase gene (Lias) and having increased endogenous antioxidant capacity, to investigate whether the new model could block the development of NAFLD. We have systemically characterized the novel model based on the main features of human NAFLD, determined the impact of enhanced endogenous antioxidant capacity on the retardation of NAFLD and elucidated the underlying mechanisms using various biological and pathological methods. We found that LiasHigh/HighLeprdb/db mice ameliorated many pathological changes of NAFLD compared with the control. In particular, LiasHigh/HighLeprdb/db mice displayed the improved liver mitochondrial function, reflecting the decline of mitochondrial microvesicular steatosis, and reduced oxidative stress, which mainly contribute to alleviation of pathologic alterations of the NAFLD progression. Our new model shows that mitochondrial dysfunction is a major pathogenesis for liver steatosis. Overexpression of Lias gene effectively reduces oxidative stress and protects mitochondria, and consequently attenuates NAFLD/NASH.