HRV changes before and after radiofrequency ablation in patients with different origin of right ventricular outflow tract ventricular premature contraction

Objective:To observe the HRV changes before and after the radiofrequency current catheter ablationventricular premature beats originated from different site of right ventricular outflow tract.Methods:A total of 102 patients with frequent RVOT-VPC admitted to our hospital were accepted radiofrequency current catheter ablation (RF). According to the origin of RVOT-VPC, it was divided into 2 groups, one is from ventricular septum, and the other one is from free wall, and in each group, male and female are observed separately.Results:(1) HRV before RF ablation: 1) rMSSD in the female patients with RVOT-VPC from free wall was significantly lower than those from septum;2) frequency domain index (W, LF) were higher than normal range, and in male patients, LF/HF<1 were found, but in female patients, LF/HF>1. (2) HRV after RF ablation: 1) Significant changes were found in female patients with RVOT-VPC from septum, rMSSD, PNN50, HF and LF decreased;2) In female patients with RVOT-VPC from free wall, rMSSD decreased;3) In male patients, there were no significant HRV changes found before and after RF ablation. (3) Heart rate changes: 1) In female patients with RVOT-VPC from septum, heart rate decreased significantly ((76.47±9.47) bpm vs (69.29±14.59) bpm)2) No significant changes were found in male patients.Conclusion:In patients with RVOT-PVC sympathetic and vagus excitability increased, and after catheter ablation, in female patients with RVOT-PVC originated from septum, the HRV index relating to sympathetic and vagus excitability significantly decreased.

VSL#3 can prevent ulcerative colitis-associated carcinogenesis in mice

AIM To investigate the effects of VSL#3 on tumor formation, and fecal and intestinal mucosal microbiota in azoxymethane/dextran sulfate sodium(AOM/DSS) induced mice model. METHODS C57 BL/6 mice were administered AOM/DSS to develop the ulcerative colitis(UC) carcinogenesis model. Mice were treated with 5-ASA(75 mg/kg/d), VSL#3(1.5 × 109 CFU/d), or 5-ASA combined with VSL#3 by gavage from the day of AOM injection for three months(five days/week). The tumor load was compared in each group, and tumor necrosis factor(TNF-α) and interleukin(IL)-6 levels were evaluated in colon tissue. The stool and intestinal mucosa samples were collected to analyze the differences in the intestinal microbiota by 16 s rDNA sequencing method.RESULTS VSL#3 significantly reduced the tumor load in AOM/DSS-induced mice model and decreased the level of TNF-α and IL-6 in colon tissue. The model group had a lower level of Lactobacillus and higher level of Oscillibacter and Lachnoclostridium in fecal microbiota than the control group. After the intervention with 5-ASA and VSL#3, Bacillus and Lactococcus were increased, while Lachnoclostridium and Oscillibacter were reduced. 5-ASA combined with VSL#3 increased the Lactobacillus and decreased the Oscillibacter. The intestinal mucosal microbiota analysis showed a lower level of Bifidobacterium and Ruminococcaceae_UCG-014 and higher level of Al oprevotel a in the model group as compared to the control group. After supplementation with VSL#3, Bifidobacterium was increased. 5-ASA combined with VSL#3 increased the level of both Lachnoclostridium and Bifidobacterium. CONCLUSION VSL#3 can prevent UC-associated carcinogenesis in mice, reduce the colonic mucosal inflammation levels, and rebalance the fecal and mucosal intestinal microbiota.

Upregulated insulin receptor tyrosine kinase substrate promotes the proliferation of colorectal cancer cells via the bFGF/AKT signaling pathway

Background:Some recent studies on insulin receptor tyrosine kinase substrate(IRTKS)have focused more on its functions in diseases.However,there is a lack of research on the role of IRTKS in carcinomas and its mechanism remains ambiguous.In this study,we aimed to clarify the role and mechanism of IRTKS in the carcinogenesis of colorectal cancer(CRC).Methods:We analysed the expression of IRTKS in CRC tissues and normal tissues by researching public databases.Cancer tissues and adjacent tissues of 67 CRC patients who had undergone radical resection were collected from our center.Quantitative real-time polymerase chain reaction and immunohistochemistry were performed in 52 and 15 pairs of samples,respectively.In vitro and in vivo experiments were conducted to observe the effect of IRTKS on CRC cells.Gene Set Enrichment Analysis and Metascape platforms were used for functional annotation and enrichment analysis.We detected the protein kinase B(AKT)phosphorylation and cell viability of SW480 transfected with small interfering RNAs(siRNAs)with or without basic fibroblast growth factor(bFGF)through immunoblotting and proliferation assays.Results:The expression of IRTKS in CRC tissues was higher than that in adjacent tissues and normal tissues(all P<0.05).Disease-free survival of patients with high expression was shorter.Overexpression of IRTKS significantly increased the proliferation rate of CRC cells in vitro and the number of tumor xenografts in vivo.The phosphorylation level of AKT in CRC cells transfected with pLVX-IRTKS was higher than that in the control group.Furthermore,siRNA-IRTKS significantly decreased the proliferation rate of tumor cells and the phosphorylation level of AKT induced by bFGF.Conclusion:IRTKS mediated the bFGF-induced cell proliferation through the phosphorylation of AKT in CRC cells,which may contribute to tumorigenicity in vivo.