Effects of vasoactive drugs on hepatic and intestinal circulation and intestinal barrier in patients with septic shock.

In this study, 60 patients with septic shock were selected over the course of 1 year, and the effects of dopamine and norepinephrine combined with dobutamine on hepatic and intestinal circulation and intestinal barrier in patients with septic shock were studied by comparison between the control group and the experimental group. All patients received mechanical ventilation to maintain breathing at 14 to 20 times/min. The experimental group was treated with vascular active drugs after adequate rehydration, and the control group only received adequate rehydration. There were extremely significant differences (p<0.01) in the total effective rate of each group. There were significant differences in the hemodynamic indexes in each group (p<0.05). There was a significant difference in total 24-hour bile output (p<0.01). There were significant differences in liver function and blood lipid values in patients (p<0.01). There were significant differences in the repair of epithelial injury at 0 hour, 48 hours and 96 hours (p<0.01). There were significant differences in the transmembrane resistance of monolayer cells (p<0.01). The expression differences of three proteins ZO-1, occludin and ß-actin were also significant, among which the three proteins in the control group were weak, while those in groups A and B were strong. The expression of tight junction protein in monolayer cells was weakly positive in expression and strong in other proteins. In conclusion, vasoactive drugs had significant effects on hepatic and intestinal circulation and intestinal barrier in patients with septic shock.

HIF-1α rs11549465 C>T polymorphism contributes to increased cancer susceptibility: Evidence from 49 studies.

HIF-1α (hypoxia-inducible factor-1α) is a transcriptional factor that participates in the regulation of oxygen homeostasis. Despites numbers of case-control studies working on this area, the actual relationship of HIF-1α gene generic variant rs11549465 C>T imposing on cancer susceptibility remains unveiled. To get a better understanding of such relationship, this meta-analysis was carried out by incorporating all eligible case-control studies. Qualified articles were acquired from PubMed, CNKI, EMBASE, PMC, and Wanfang database update to April 2019. Odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were employed to estimate the relationship of interest. Heterogeneity tests, sensitivity analyses and publication bias assessments were also carried out to ensure the strength of our conclusion. A total of 46 articles with 49 studies including 12920 cases and 13363 controls were included. The results indicated that HIF-1α rs11549465 C>T was significantly related to the increased risk of overall cancer under four genetic models (TT vs. CC: OR=2.06, 95% CI=1.34-3.16; TT vs. CC/CT: OR=2.42, 95% CI=1.60-3.65; CT/TT vs. CC: OR=1.21, 95% CI=1.04-1.40; T vs. C: OR=1.29, 95% CI=1.12-1.48). Furthermore, enhanced cancer risk was detected after stratification by cancer type, ethnicity, the source of controls and HWE. These results suggest that HIF-1α rs11549465 C>T polymorphism may predispose to cancer susceptibility.

miR­146a­5p suppresses ATP­binding cassette subfamily G member 1 dysregulation in patients with refractory Mycoplasma pneumoniae via interleukin 1 receptor­associated kinase 1 downregulation.

In the present study, we examined the function of microRNA (miR)­146a­5p in patients with refractory Mycoplasma pneumoniae pneumonia. In brief, the expression of miR­146a­5p was reduced in patients with refractory Mycoplasma pneumoniae pneumonia. Downregulation of miR­146a­5p reduced inflammation in an in vitro model of refractory Mycoplasma pneumoniae pneumonia, whilst overexpression of miR­146a­5p promoted inflammation. Downregulation of miR­146a­5p induced the protein expression of ATP­binding cassette subfamily G member 1 (ABCG1) and interleukin 1 receptor­associated kinase 1 (IRAK­1), while suppressed expression was observed of the aforementioned proteins following overexpression of miR­146a­5p in an in vitro model of refractory Mycoplasma pneumoniae pneumonia. The administration of small interfering RNA against RXR or IRAK­1 attenuated the effects of miR­146a­5p on inflammation in an in vitro model of refractory Mycoplasma pneumoniae pneumonia. Collectively, these results suggested that miR­146a­5p reduced ABCG1 expression in refractory Mycoplasma pneumoniae pneumonia via downregulation of IRAK­1.