Characteristics of Gut Microbial Profiles of Offshore Workers and Its Associations With Diet.

The composition of gut microbiota is not a static state in humans but fluctuates in response to changes in environments, diet, and lifestyle factors. Here, we explored differences in gut microbiota between populations worked offshore and onshore and further studied microbiota-associated variables in offshore workers (OFWs). We investigated the gut microbiota of 168 healthy subjects (offshore: 145 and onshore: 23) using 16S rRNA sequencing. Our results indicated that the marine environment caused significant changes in intestinal microbial structure, which was mainly reflected in the increase in bacterial diversity, changes in composition, and the emergence of more specific bacteria in OFWs. In addition, characteristics of gut microbiota in OFWs were further explored, and the genus Holdemanella was considered a potential contributor to the stable state of health. Besides, some dietary factors, namely, duck, mutton, dairy products, and algae vegetables were identified as the gut microbial covariates in the OFWs cohort and were positively correlated with the genus Holdemanella. This suggests the positive intervention of diet on Holdemanella. Our data highlight, for the first time to our knowledge, that the marine geographical environment plays an important role in shaping the gut mycobiome composition. And diet could be considered as the targeted intervention that alters the composition of the microbiome to improve host health.

Soluble Flt-1 in AMI Patients Serum Inhibits Angiogenesis of Endothelial Progenitor Cells by Suppressing Akt and Erk's Activity.

In acute myocardial infarction (AMI), endothelial progenitor cells (EPCs) are essential for the recovery of collateral circulation via angiogenesis. Clinical research has shown that the poor prognosis of the patients with AMI is closely associated with the cell quantity and function of EPCs. Whether there are differences in the biological features of EPCs from AMI patients and healthy subjects is worth exploring. In this study, EPCs were isolated from human peripheral blood and identified as late-stage EPCs by flow cytometry, immunofluorescence, and blood vessel formation assay. Compared to healthy subjects, AMI patients had more EPCs in the peripheral blood compared to healthy subjects. In addition, EPCs from AMI patients exhibited higher migration ability in the transwell assay compared to EPCs from healthy subjects. However, no difference in the angiogenesis of EPCs was observed between AMI patients and healthy subjects. Further studies revealed that soluble vascular endothelial growth factor receptor 1 (sFlt-1) in the serum of AMI patients was involved in the inhibition of EPCs angiogenesis by suppressing the Akt and Erk pathways. In conclusion, this study demonstrated that elevated serum sFlt-1 inhibits angiogenesis of EPC in AMI patients. Our findings uncover a pathogenic role of sFlt-1 in AMI.

Transition of Hypertriglyceridemic-Waist Phenotypes and the Risk of Type 2 Diabetes Mellitus among Middle-Aged and Older Chinese: A National Cohort Study.

The rapid economic growth and nutritional changes in China have brought an increased burden of type 2 diabetes mellitus (T2DM). This study aimed to assess the effects of hypertriglyceridemic-waist (HTW) and its dynamic transitions on incident T2DM among middle-aged and older Chinese. Data were extracted from the China Health and Retirement Longitudinal Study (CHARLS). Participants were classified into three HTW phenotypes, namely NTNW (normal triglyceride (TG) and waist circumference (WC)), NTEW/ETNW (normal TG and enlarged WC, or elevated TG and normal WC) and ETEW (elevated TG and enlarged WC). Multivariable Cox frailty models were used to assess the associations of HTW phenotypes and their transitions over time with the risk of T2DM. A total of 7397 subjects without T2DM were included, of which 849 developed T2DM during 2011-2018. Compared with individuals with NTNW, people in the NTEW/ETNW group and ETEW group were at a significantly higher risk of T2DM (HRNTEW/ETNW = 1.28, 95% CI: 1.06-1.54 and HRETEW = 1.61, 95% CI: 1.26-2.06). For subjects with NTNW at baseline, the risk of developing T2DM increased by 38% and 83% if their metabolic status changed to NTEW/ETNW and ETEW, respectively. For subjects with NTEW/ETNW, the risk of T2DM decreased by 33% when their metabolic status changed to normal (NTNW); but the risk increased by 49% if the status became more serious (ETEW). NTEW/ETNW, ETEW and their transitions to adverse states were risk factors for T2DM.

TRAIL facilitates cytokine expression and macrophage migration during hypoxia/reoxygenation via ER stress-dependent NF-κB pathway.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is known as a key molecule to induce cancer cell apoptosis, has also been found to participate in the process of ischemia/reperfusion (I/R) injury. Infiltrated macrophages play dual roles in inflammatory injury and healing following I/R. Whether TRAIL has any effect on macrophages during this process remains elusive. Here we showed that I/R triggered the expressions of TRAIL, DR5 and cytokines (IL-1ß, TNFα, CCL-2 and ICAM-1), in addition to macrophage infiltration, which could be abolished by TRAIL neutralizing antibody. In vitro, TRAIL enhanced DR5 expression and facilitated the macrophages migration following hypoxia/reoxygenation (H/R) treatment in a dose-dependent manner via ER stress and NF-κB signaling pathways, which is accompanied by inflammatory factors expression. The increased cytokines production (such as TNFα and IL-1ß) stimulated by TRAIL can be blocked by the NF-κB and ER stress inhibitor. The results also suggested that NF-κB activation of macrophages during H/R was regulated by ER stress. Thus, our research present that TRAIL affects functional activities of macrophages during I/R injury, which may be a potential therapeutic target for ischemic heart disease.