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Background Recently, it has been found that the gut microbiota may affect the development of lung cancer through the “gut‐lung axis.” To investigate this relationship, we performed this study to determine whether the gut microbiota in non‐small‐cell lung cancer (NSCLC) patients is different from that in healthy adults. Methods Quantitative PCR (qPCR) was used to detect the expression levels of eight gut butyrate‐producing bacteria in healthy adults and NSCLC patients. We enrolled 30 patients with NSCLC and 30 subjects from 100 healthy adults after matching for age and sex. Results Compared to healthy adults, most of the gut butyrate‐producing bacteria in NSCLC patients were significantly decreased; these included Faecalibacterium prausnitzii, Clostridium leptum, Clostridial cluster I, Ruminococcus spp., Clostridial Cluster XIVa, and Roseburia spp. Among the gut butyrate‐producing bacteria, we analyzed Clostridial cluster IV and Eubacterium rectale were not decreased in NSCLC patients. Conclusions We conclude that NSCLC patients had gut butyrate‐producing bacteria dysbiosis. Further studies should be performed to investigate the underlying mechanisms of how these specific bacteria affect lung cancer progression and prognosis.

Objective FK866 is an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which exhibits neuroprotective effects in ischemic brain injury. However, in traumatic brain injury (TBI), the role and mechanism of FK866 remain unclear. The present research was aimed to investigate whether FK866 could attenuate TBI and clarified the underlying mechanisms. Methods A controlled cortical impact model was established, and FK866 at a dose of 5 mg/kg was administered intraperitoneally at 1 h and 6 h, then twice per day post‐TBI until sacrifice. Brain water content, Evans blue dye extravasation, modified neurological severity scores (mNSS), Morris water maze test, enzyme‐linked immunosorbent assay (ELISA), immunofluorescence staining, and western blot were performed. Results The results demonstrated that FK866 significantly mitigated the brain edema, blood–brain barrier (BBB) disruption, and ameliorated the neurological function post‐TBI. Moreover, FK866 decreased the number of Iba‐1‐positive cells, GFAP‐positive astrocytes, and AQP4‐positive cells. FK866 reduced the protein levels of proinflammatory cytokines and inhibited NF‐κB from translocation to the nucleus. FK866 upregulated the expression of Bcl‐2, diminished the expression of Bax and caspase 3, and the number of apoptotic cells. Moreover, p38 MAPK and ERK activation were significantly inhibited by FK866. Interpretation FK866 attenuated TBI‐induced neuroinflammation and apoptosis, at least in part, through p38/ERK MAPKs signaling pathway.

BACKGROUND: Current management of patients with atrial fibrillation (AF) is limited by low detection of AF, nonadherence to guidelines and lack of consideration of patient's preferences, thus highlighting the need for a holistic and integrated approach to AF management. The present study aims to determine whether a mHealth technology-supported AF integrated management strategy will reduce AF-related adverse events.METHODS/DESIGN: The mAFA II trial is a prospective, cluster randomized controlled trial. The 40 sites will be randomized to mAFA-integrated care intervention or usual care arms. Prior to randomization, study sites will be paired to be matched in size and the proportion of study eligible patients. All AF patients aged over 18 years old with CHA2 DS2 -VASc score ≥2 will be enrolled. Assuming a composite adverse event rate of 10% pre-intervention, reduced to 5% after intervention, we aim to recruit 3660 patients assuming a 10% loss to follow-up. The primary study endpoint is a composite of stroke/thromboembolism, all-cause death, and rehospitalization. Ancillary analyses would determine patient-related outcome measures, health economics and cost effectiveness, as well as an embedded qualitative study.DISCUSSION: The mAFA II trial will provide evidence for an integrated care approach to holistic AF care, supported by mobile health technology to improve screening, patient involvement and optimization of management. This article is protected by copyright. All rights reserved.

Diabetic cardiovascular complication is a major cause of mortality in type 2 diabetic patients. Hyperglycemia markedly increases the risk of cardiovascular disease. Endothelial dysfunction is common in type 2 diabetes mellitus (DM) and is an early indicator of diabetic vascular disease. Therefore, it is necessary to identify the effect of different hypoglycemic agents on vascular endothelium. The aim of the study was to examine and compare the effects of metformin and gliquidone on atherosclerotic lesions in streptozotocin-induced diabetic rats.Forty male Sprague-Dawley rats (age, 8 weeks; weight, 180-200 g) were included in this study and fed with a normal chow diet for 1 week. Rats (n = 10) served as the normal control group (NC group) were fed with a normal chow for another 2 weeks and received an injection of saline. The rest 30 rats fed with a high-fat diet for 2 weeks and injected streptozotocin were randomly assigned to three groups (n = 10 rats per group) as follow: type 2 DM group (DM group), DM + gliquidone group (GLI group) and DM + metformin group (MET group). Five weeks later, all rats were fasted overnight and taken tail blood samples for biochemical determinations. Then rats in the NC and DM groups were administrated with normal saline, while rats in the MET and GLI groups were administrated with metformin (100 mg/kg) or gliquidone (10 mg/kg), respectively. All medicines were given via intragastric administration for 8 weeks. After 16 weeks, plasma triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) were measured. The aortic arch was isolated from diabetic rats and was assessed by pathological sectioning using HE staining.Metformin treatment prevented weight gain ((315.80 ± 52.16) g vs. (318.70 ± 68.48) g, P = 0.773), improved plasma TG, HDL-C and LDL-C levels (P = 0.006, 0.003, 0.001, respectively, all P0.05). However, gliquidone showed no significant effects on plasma TG and TC levels (P = 0.819, 0.053, respectively). LDL-C and HDL-C in the GLI group changed ((0.46 ± 0.10) mmol/L vs. (0.36 ± 0.14) mmol/L, P = 0.007; (0.99 ± 0.27) mmol/L vs. (1.11 ± 0.18) mmol/L, P = 0.049). Both metformin and gliquidone treatment lowered blood glucose levels (P = 0.001, 0.004, respectively, P0.05). Under light microscopy, no changes were observed in the aortic wall structure of each layer; the intima was smooth and the membrane elastic fibers were normal in the NC group. In the DM group, the aortic wall structure was unclear, the intima was thickened with irregular intima, and membrane elastic fibers collapsed. The aortic intima in the MET and GLI groups was smoother compared with the DM group, but the endothelial structure of the MET group was closer to that of the NC group.Both metformin and gliquidone have anti-atherosclerotic effects. But the endothelial structure of the MET group was closer to that of the NC group. Metformin and gliquidone therapy can reduce serum level of LDL-C and increase level of HDL-C, whereas gliquidone therapy did not lose weight and decrease serum level of TG. These data may have important implications for the treatment of patients with type 2 DM.