著者

Weidong Liu Wei Yu De Xie Qiang Wang Hairong Zhao Jiaming Lv Furong He Chenxi Xu Binyang Chen Tetsuya Yamamoto Hidenori Koyama Jidong Cheng

出版者

Japan Atherosclerosis Society

雑誌

Journal of Atherosclerosis and Thrombosis (ISSN:13403478)

巻号頁・発行日

pp.63645, (Released:2022-11-26)

参考文献数

32

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Aims: Acute rupture or erosion of unstable atherosclerotic plaques is a major cause of adverse consequences of atherosclerotic cardiovascular disease, often leading to myocardial infarction or stroke. High uric acid (HUA) is associated with the increasing risk of cardiovascular events and death. However, the mechanism by which HUA promotes atherosclerosis and whether HUA affects plaque stability are still unclear. Methods: We constructed an atherosclerotic Apoe−/− mouse model with HUA. The progression of atherosclerosis and plaques was determined by Oil Red O staining, hematoxylin and eosin (H&E) staining, and Masson staining. TdT-mediated dUTP nick-end labeling assay and immunohistochemistry were used to observe the changes of apoptosis and autophagy in plaques, respectively. Then, we validated the in vivo results with RAW 264.7 cell line. Results: HUA promoted atherosclerosis and exacerbated plaque vulnerability, including significantly increased macrophage infiltration, lipid accumulation, enlarged necrotic cores, and decreased collagen fibers. HUA increased cell apoptosis and inhibited autophagy in plaques. In vitro results showed that HUA decreased cell viability and increased cell apoptosis in foam cells macrophages treated with oxidized low-density lipoprotein. An activator of autophagy, rapamycin, can partially reverse the increasing apoptosis. Conclusion: HUA promoted atherosclerosis and exacerbated plaque vulnerability, and HUA facilitates foam cell apoptosis by inhibiting autophagy.

著者

Bin Wang Wei Li Qiang Wang Wei Zhang

出版者

International Research and Cooperation Association for Bio & Socio-Sciences Advancement

雑誌

BioScience Trends (ISSN:18817815)

巻号頁・発行日

pp.2022.01320, (Released:2022-11-19)

参考文献数

52

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Kidney transplantation remains the best treatment for patients with end-stage kidney disease, and it could partially mitigate systemic disorders of mineral and bone metabolism caused by secondary hyperparathyroidism. However, persistent hyperparathyroidism is still observed in 30-60% of patients 1 year after kidney transplantation, leading to impairment of allograft function and a disturbance of mineral metabolism. The timing of parathyroidectomy varies among transplant centers because the possible negative effects of parathyroidectomy on allograft outcomes are still unclear. This review provides a comprehensive and detailed overview of the natural course of hyperparathyroidism following kidney transplantation and the effects of the timing and extent of parathyroidectomy on allograft function. It aims to provide useful information for surgeons to propose an appropriate intervention strategy to break the vicious cycle of post-kidney transplantation hyperparathyroidism and deterioration of allograft function.

著者

Hui Zhu Dong Zeng Qiang Wang Ning Wang Bo Zeng Lili Niu Xueqin Ni

出版者

Japanese Society of Microbial Ecology · The Japanese Society of Soil Microbiology

雑誌

Microbes and Environments (ISSN:13426311)

巻号頁・発行日

pp.ME17163, (Released:2018-07-25)

被引用文献数

14

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Diarrhea is often associated with marked alterations in the intestinal microbiota, termed dysbiosis; however, limited information is currently available on the intestinal microbiota in captive golden snub-nosed monkeys (Rhinopithecus roxellana) with diarrhea. We herein characterized the fecal microbiota in diarrhea and healthy monkeys using the Illumina MiSeq platform. The concentrations of fecal short-chain fatty acids (SCFAs) and copy numbers of virulence factor genes were also assessed using gas chromatography and quantitative PCR (qPCR), respectively. The results obtained showed that diarrhea monkeys harbored a distinctive microbiota from that of healthy monkeys and had 45% fewer Bacteroidetes. Among healthy subjects, old monkeys had the lowest relative abundance of Bacteroidetes. Linear discriminant analysis coupled with the effect size (LEfSe) and canonical correlation analysis (CCA) identified significant differences in microbial taxa between diarrhea and healthy monkeys. A PICRUSt analysis revealed that several pathogenic genes were enriched in diarrhea monkeys, while glycan metabolism genes were overrepresented in healthy monkeys. A positive correlation was observed between the abundance of nutrition metabolism-related genes and the individual digestive capacities of healthy monkeys. Consequently, the abundance of genes encoding heat stable enterotoxin was significantly higher in diarrhea monkeys than in healthy monkeys (P<0.05). In healthy subjects, adult monkeys had significant higher concentrations of butyrate and total SCFAs than old monkeys (P<0.05). In conclusion, the present study demonstrated that diarrhea had a microbial component and changes in the microbial structure were accompanied by altered systemic metabolic states. These results suggest that pathogens and malabsorption are the two main causes of diarrhea, which are closely related to the microbial structure and functions.