Gut microbiome profile of Chinese hypertension patients with and without type 2 diabetes mellitus.

BACKGROUND: The coexistence of hypertension and type 2 diabetes mellitus (T2DM) may largely increase the risk for cardiovascular disease. However, there is no clear consensus on the association between hypertension and the risk of diabetes. Gut microbiota plays important roles in the development of hypertension and T2DM, but whether there is difference between hypertension patients with or without T2DM has not been explored yet. METHODS: We recruited 101 hypertension patients in this study (72 patients without T2DM named HT group and 29 patients with T2DM named HT-T2DM group). Their blood samples were collected for testing clinical characteristics and fecal samples were tested for bacterial DNA using 16 S ribosomal RNA gene sequencing targeting the V3 and V4 region. The data of 40 samples were downloaded from project PRJNA815750 as health control (HC group) in this study. The community composition and structure of the microbiome, taxonomic difference, co-occurrence network and functional enrichment were analyzed by alpha/beta diversity, LEfSe, Fruchterman Reingold's algorithm and PICRUSt2 functional analysis, respectively. RESULTS: Alpha and beta diversity analysis showed significant differences in microbial community richness and composition among the three groups. The HC group had a significantly higher Simpson index and a distinct microbiota community compared to the HT and HT-T2DM groups, as demonstrated by significant differences in unweighted and weighted UniFrac distances. The LEfSe analysis identified specific taxa that had significantly different abundance among the groups, such as Bacteroides uniformis, Blautia wexlerae, Alistipes putredinis, and Prevotella stercorea in the HC group, Prevotella copri and Phascolarctobacterium faecium in the HT group, and Klebsiella pneumoniae in the HT-T2DM group. Co-occurrence network analysis indicates that Prevotella copri, Mediterraneibacter gnavus, Alistipes onderdonkii and some unidentified species act as key nodes in the network. Differentially functional pathway identified by PICRUSt2 were concentrated in nutrition and energy metabolism, as well as the biosynthesis of other secondary metabolites. CONCLUSIONS: Our study found significant differences in microbial community richness, composition, and function among the healthy controls, hypertension patients with and without T2DM. Some specific taxa may explain this difference and serve as potential therapeutic targets for hypertension, T2DM, and their coexistence.

Dual-ATME: Dual-Branch Attention Network for Micro-Expression Recognition.

Micro-expression recognition (MER) is challenging due to the difficulty of capturing the instantaneous and subtle motion changes of micro-expressions (MEs). Early works based on hand-crafted features extracted from prior knowledge showed some promising results, but have recently been replaced by deep learning methods based on the attention mechanism. However, with limited ME sample sizes, features extracted by these methods lack discriminative ME representations, in yet-to-be improved MER performance. This paper proposes the Dual-branch Attention Network (Dual-ATME) for MER to address the problem of ineffective single-scale features representing MEs. Specifically, Dual-ATME consists of two components: Hand-crafted Attention Region Selection (HARS) and Automated Attention Region Selection (AARS). HARS uses prior knowledge to manually extract features from regions of interest (ROIs). Meanwhile, AARS is based on attention mechanisms and extracts hidden information from data automatically. Finally, through similarity comparison and feature fusion, the dual-scale features could be used to learn ME representations effectively. Experiments on spontaneous ME datasets (including CASME II, SAMM, SMIC) and their composite dataset, MEGC2019-CD, showed that Dual-ATME achieves better, or more competitive, performance than the state-of-the-art MER methods.

A case report of successful atrioventricular junction pacing in Ebstein's anomaly.

We report a case of atrioventricular junction (AVJ) pacing in a patient with Ebstein's anomaly (EA). The patient was a 68-year-old man who suffered from pacemaker syndrome and complained of heart failure symptoms. He was initially diagnosed with EA in his thirties and received right ventricular (RV) apex pacing for safe during a surgery because of low heart rate atrial fibrillation (AF) 9 years ago. However, since the patient felt discomfort, the pacing rate was then programed down to 45-55 per/min. During recent years, he was often admitted for dyspnea, dizziness, or edema and was advised to undergo intracardiac repair, but he rejected this due to the high risk of the surgery. We believed that the patient's low heart rate and ventricular pacing burden (47.8%) might be important causes of the symptoms. Therefore, we suggested that the patient undergo an upgrade of the pacing mode. In consideration of possible abnormal cardiac coronary veins, we tried His bundle pacing (HBP) to upgrade pacing. However, the SelectSecure 3830 lead was fixed at the AVJ region and obtained steady pacing parameters. After the upgrading of the AVJ pacing mode. The patient's symptoms, exercise capacity and quality of life were all improved at the 2-year follow-up. Thus, we presented the first case of AVJ pacing in a patient with EA.

Effect of implantation site of the His bundle pacing leads on pacing parameters: a single-center experience.

BACKGROUND: HB pacing is a promising approach to achieve physiological pacing, but its efficacy and long-term effects require further validation. In current study, we deemed to investigate the effect of the His bundle pacing (HBP) lead location on pacing parameters. METHODS: 2D echocardiography imaging was performed after successful implantation, according to which the patients were divided into groups A (whose His lead tips were at the atrial side) and B (whose His lead tips were at the ventricular side). The capture thresholds, sensing values, and H-V intervals between the two groups were compared. RESULTS: Thirteen patients were in group A and 16 patients were in group B. The average capture thresholds during, 1 month, and 1 year after operation were 1.20 ± 0.34, 0.69 ± 0.29, and 0.92 ± 0.80 V/0.5 ms for group A and 1.14 ± 0.43, 0.81 ± 0.39, and 0.98 ± 0.59 V/0.5 ms for group B, respectively. The difference between the two groups was not significant. The threshold values in both groups decreased significantly in 1 month and slightly increased in 1 year. The sensing values of group A were 1.87 ± 0.82, 1.95 ± 0.76, and 1.88 ± 0.75 mV, while those of group B were 4.53 ± 1.37, 4.69 ± 1.38, and 4.59 ± 1.42 mV. The difference among the three time points was not significant. However, the sensing values in group A were consistently significantly lower than those in group B. The HV interval in group A was significantly longer than that in group B. CONCLUSIONS: The implantation site of HBP leads has a significant effect on sensing values for that His leads crossing the tricuspid annulus toward the ventricle are associated with higher sensing values, compared to a more proximal location. Meanwhile, lead location has no evident effect on capture thresholds that is improved significantly shortly after operation.

Ginseng polysaccharide inhibits MDA-MB-231 cell proliferation by activating the inflammatory response.

Ginseng polysaccharide (GPS) is known for its efficacy in cancer therapy; however, its regulatory mechanism in breast cancer (BC) remains unclear. To analyze the effect of GPS on BC cell proliferation, cell proliferation rate calculations, western blotting, plasmid transfections, electrophoretic mobility shift assays and chromatin immunoprecipitation assays were performed. GPS treatment in the culture cell medium inhibited cell proliferation in the BC cell line MDA-MB-231. In addition, the E-cadherin level was enhanced while the vimentin level was suppressed following GPS treatment (both P<0.05). Furthermore, the levels of apoptotic markers, including cleaved-Caspase-3 and p53, and inflammatory response markers, including plasminogen activator inhibitor and TNF-α, were induced by GPS treatment in MDA-MB-231 cells (all P<0.05). These results indicated that GPS supplementation activated the inflammatory response and apoptosis in BC cells. GPS treatment activated the phosphorylation levels of c-Jun N-terminal kinase, Akt and NF-κB. In MDA-MB-231 cells, GPS resulted in the accumulation of the NF-κB components p65, p50 and Ikaros family zing finger protein 1 (IKZF1; all, P<0.05). Chromatin immunoprecipitation and electrophoretic mobility shift assays indicated that p65 bound to the IKZF1 promoter. The overexpression of IKZF1 or p65 inhibited MDA-MB-231 cell proliferation (P<0.05), indicating that GPS treatment may inhibit BC cell proliferation by the activation of IKZF1. Taken together, these results suggested that GPS significantly inhibited BC cell proliferation via the control of the biological processes, including the activation of p65-IKZF1 signaling and apoptosis. The data indicated a novel mechanism for further understanding of cancer cell proliferation.

Monocytic cell junction proteins serve important roles in atherosclerosis via the endoglin pathway.

The formation of atherosclerosis is recognized to be caused by multiple factors including pathogenesis in monocytes during inflammation. The current study provided evidence that monocytic junctions were significantly altered in patients with atherosclerosis, which suggested an association between cell junctions and atherosclerosis. Claudin­1, occludin­1 and ZO­1 were significantly enhanced in atherosclerosis, indicating that the tight junction pathway was activated during the pathogenesis of atherosclerosis. In addition, the gene expression of 5 connexin members involved in the gap junction pathway were quantified, indicating that connexin 43 and 46 were significantly up­regulated in atherosclerosis. Furthermore, inflammatory factors including endoglin and SMAD were observed, suggesting that immune regulative factors were down­regulated in this pathway. Silicon­based analysis additionally identified that connexins and tight junctions were altered in association with monocytic inflammation regulations, endoglin pathway. The results imply that reduced expression of the immune regulation pathway in monocytes is correlated with the generation of gap junctions and tight junctions which serve important roles in atherosclerosis.