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Träfflista för sökning "WFRF:(Tong Wen) "

Sökning: WFRF:(Tong Wen)

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  • 2019
  • Tidskriftsartikel (refereegranskat)
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  • Yu, Haiyang, et al. (författare)
  • Association between Parkinson’s Disease and Diabetes Mellitus : From Epidemiology, Pathophysiology and Prevention to Treatment
  • 2022
  • Ingår i: Aging and Disease. - 2152-5250. ; 13:6, s. 1591-1605
  • Tidskriftsartikel (refereegranskat)abstract
    • Diabetes mellitus (DM) and Parkinson’s disease (PD) are both age-related diseases of global concern being among the most common chronic metabolic and neurodegenerative diseases, respectively. While both diseases can be genetically inherited, environmental factors play a vital role in their pathogenesis. Moreover, DM and PD have common underlying molecular mechanisms, such as misfolded protein aggregation, mitochondrial dysfunction, oxidative stress, chronic inflammation, and microbial dysbiosis. Recently, epidemiological and experimental studies have reported that DM affects the incidence and progression of PD. Moreover, certain antidiabetic drugs have been proven to decrease the risk of PD and delay its progression. In this review, we elucidate the epidemiological and pathophysiological association between DM and PD and summarize the antidiabetic drugs used in animal models and clinical trials of PD, which may provide reference for the clinical translation of antidiabetic drugs in PD treatment.
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  • Chang, Li, et al. (författare)
  • Recent progress in research on PM2.5 in subways.
  • 2021
  • Ingår i: Environmental Science. - : Royal Society of Chemistry (RSC). - 2050-7887 .- 2050-7895. ; 23:5, s. 642-663
  • Tidskriftsartikel (refereegranskat)abstract
    • Nowadays, PM2.5 concentrations greatly influence indoor air quality in subways and threaten passenger and staff health because PM2.5 not only contains heavy metal elements, but can also carry toxic and harmful substances due to its small size and large specific surface area. Exploring the physicochemical and distribution characteristics of PM2.5 in subways is necessary to limit its concentration and remove it. At present, there are numerous studies on PM2.5 in subways around the world, yet, there is no comprehensive and well-organized review available on this topic. This paper reviews the nearly twenty years of research and over 130 published studies on PM2.5 in subway stations, including aspects such as concentration levels and their influencing factors, physicochemical properties, sources, impacts on health, and mitigation measures. Although many determinants of station PM2.5 concentration have been reported in current studies, e.g., the season, outdoor environment, and station depth, their relative influence is uncertain. The sources of subway PM2.5 include those from the exterior (e.g., road traffic and fuel oil) and the interior (e.g., steel wheels and rails and metallic brake pads), but the proportion of these sources is also unknown. Control strategies of PM mainly include adequate ventilation and filtration, but these measures are often inefficient in removing PM2.5. The impacts of PM2.5 from subways on human health are still poorly understood. Further research should focus on long-term data collection, influencing factors, the mechanism of health impacts, and PM2.5 standards or regulations.
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  • Fu, Jianxin, et al. (författare)
  • Loss of intestinal core 1-derived O-glycans causes spontaneous colitis in mice.
  • 2011
  • Ingår i: The Journal of clinical investigation. - 1558-8238. ; 121:4, s. 1657-66
  • Tidskriftsartikel (refereegranskat)abstract
    • Mucin-type O-linked oligosaccharides (O-glycans) are primary components of the intestinal mucins that form the mucus gel layer overlying the gut epithelium. Impaired expression of intestinal O-glycans has been observed in patients with ulcerative colitis (UC), but its role in the etiology of this disease is unknown. Here, we report that mice with intestinal epithelial cell-specific deficiency of core 1-derived O-glycans, the predominant form of O-glycans, developed spontaneous colitis that resembled human UC, including massive myeloid infiltrates and crypt abscesses. The colitis manifested in these mice was also characterized by TNF-producing myeloid infiltrates in colon mucosa in the absence of lymphocytes, supporting an essential role for myeloid cells in colitis initiation. Furthermore, induced deletion of intestinal core 1-derived O-glycans caused spontaneous colitis in adult mice. These data indicate a causal role for the loss of core 1-derived O-glycans in colitis. Finally, we detected a biosynthetic intermediate typically exposed in the absence of core 1 O-glycan, Tn antigen, in the colon epithelium of a subset of UC patients. Somatic mutations in the X-linked gene that encodes core 1 β1,3-galactosyltransferase-specific chaperone 1 (C1GALT1C1, also known as Cosmc), which is essential for core 1 O-glycosylation, were found in Tn-positive epithelia. These data suggest what we believe to be a new molecular mechanism for the pathogenesis of UC.
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