A meta-analysis of randomized controlled trials: efficiency and safety of ondansetron in preventing post-anesthesia shivering during cesarean section.

OBJECTIVE: Although ondansetron was considered to prevent post-anesthesia shivering during cesarean section, its efficiency remained controversial. Our review was conducted to estimate the efficiency and safety of ondansetron in preventing post-anesthesia shivering during cesarean section. METHODS: The literature were searched from their inception to October 2020 without restriction of language. All randomized controlled trials investigating the efficacy of ondansetron versus placebo in preventing shivering during cesarean section under neuraxial anesthesia were included. The meta-analysis was conducted using Stata software. RESULTS: Eleven randomized controlled studies with a total of 748 individuals were finally included in our meta-analysis. Our results manifested that intravenous ondansetron compared with intravenous placebo significantly reduced the incidence of post-anesthesia shivering (PAS) (RR 0.53, 95% CI 0.14-0.68). Subgroup analysis according to doses of ondansetron indicated that the efficacy of 4 mg doses of ondansetron (RR 0.37, 95% CI 0.21-0.64) is equivalent to that of 8 mg doses of ondansetron (RR 0.61, 95% CI 0.47-0.81) in preventing PAS. In addition, the intravenous ondansetron led to a lower incidence of hypotension than intravenous placebo (OR 0.47, 95% CI 0.32-0.70). We could not demonstrate differences in the incidence of bradycardia between intravenous ondansetron and intravenous placebo. CONCLUSION: Our results found that intravenous ondansetron was effective in preventing shivering during cesarean section under neuraxial anesthesia, and had an advantage in reducing the incidence of hypotension compared with intravenous placebo.

Targeting Tristetraprolin Expression or Functional Activity Regulates Inflammatory Response Induced by MSU Crystals.

The RNA-binding protein tristetraprolin (TTP) is an anti-inflammatory factor that prompts the mRNA decay of target mRNAs and is involved in inflammatory diseases such as rheumatoid arthritis (RA). TTP is regulated by phosphorylation, and protein phosphatase 2A (PP2A) can dephosphorylate TTP to activate its mRNA-degrading function. Some small molecules can enhance PP2A activation. Short interfering RNA (siRNA) targeting TTP expression or PP2A agonist (Arctigenin) was administered to monosodium urate (MSU) crystal-induced J774A.1 cells, and the expression of inflammatory related genes was detected by RT-PCR and Western blot assays. The effects of Arctigenin in mouse models of acute inflammation induced by MSU crystals, including peritonitis and arthritis, were evaluated. The data indicated that TTP expression levels and endogenous PP2A activity were increased in MSU-crystal treated J774A.1 cells. TTP knockdown exacerbated inflammation-related genes expression and NLRP3 inflammasome activation. However, PP2A agonist treatment (Arctigenin) suppressed MSU crystal-induced inflammation in J774A.1 cells. Arctigenin also relieved mitochondrial reactive oxygen species (mtROS) production and improved lysosomal membrane permeability in MSU crystal-treated J774A.1 cells. Moreover, TTP knockdown reversed the anti-inflammatory and antioxidant effects of Arctigenin. Oral administration of Arctigenin significantly alleviated foot pad swelling, the number of inflammatory cells in peritoneal lavage fluids and the production of IL-1ß in the mouse model of inflammation induced by MSU crystals. Collectively, these data imply that targeting TTP expression or functional activity may provide a potential therapeutic strategy for inflammation caused by MSU crystals.

Research Progress on Epigenetics of Diabetic Cardiomyopathy in Type 2 Diabetes.

Diabetic cardiomyopathy (DCM) is characterized by diastolic relaxation abnormalities in its initial stages and by clinical heart failure (HF) without dyslipidemia, hypertension, and coronary artery disease in its last stages. DCM contributes to the high mortality and morbidity rates observed in diabetic populations. Diabetes is a polygenic, heritable, and complex condition that is exacerbated by environmental factors. Recent studies have demonstrated that epigenetics directly or indirectly contribute to pathogenesis. While epigenetic mechanisms such as DNA methylation, histone modifications, and non-coding RNAs, have been recognized as key players in the pathogenesis of DCM, some of their impacts remain not well understood. Furthering our understanding of the roles played by epigenetics in DCM will provide novel avenues for DCM therapeutics and prevention strategies.

MiR-34b-3 and miR-449a inhibit malignant progression of nasopharyngeal carcinoma by targeting lactate dehydrogenase A.

MicroRNA expression profiling assays have shown that miR-34b/c and miR-449a are down-regulated in nasopharyngeal carcinoma (NPC); however, the targets and functions of miR-34b/c and miR-449a in the pathologenesis of NPC remain elusive. In this study, we verified miR-34b/c and miR-449a were significantly reduced with the advance of NPC. Overexpression of miR-34b-3 and miR-449a suppressed the growth of NPC cells in culture and mouse tumor xenografts. Using tandem mass tags for quantitative labeling and LC-MS/MS analysis to investigate protein changes after restoring expression of miR-34b-3, 251 proteins were found to be down-regulated after miR-34b-3 transfection. Through 3 replicate experiments, we found that miR-34b-3 regulated the expression of 15 potential targeted genes mainly clustered in the key enzymes of glycolysis metabolism, including lactate dehydrogenase A (LDHA). Further investigation revealed that miR-34b-3 and miR-449a negatively regulated LDHA by binding to the 3' untranslated regions of LDHA. Furthermore, LDHA overexpression rescued the miR-34b-3 and miR-449a induced tumor inhibition effect in CNE2 cells. In addition, miR-34b-3 and miR-449a suppressed LDH activity and reduced LD content, which were directly induced by downregulation of the LDHA. Our findings suggest that miR-34b-3 and miR-449a suppress the development of NPC through regulation of glycolysis via targeting LDHA and may be potential therapeutic targets for the treatment of NPC.

Electroencephalogram and electrocardiograph assessment of mental fatigue in a driving simulator.

Mental fatigue is a contributing factor to some serious transportation crashes. In this study, we measured mental fatigue in drivers using electroencephalogram (EEG) and electrocardiograph (ECG). Together, thirteen healthy subjects performed a continuous simulated driving task for 90 min with simultaneous ECG and multi-channel EEG recording of each subject. Several important physiological parameters were investigated using preprocessed ECG and EEG signals. The results show that the EEG alpha and beta, the relative power, the amplitude of P300 wave of event-related potential (ERP), the approximated entropy of the ECG, and the lower and upper bands of power of heart rate variability (HRV) are significantly different before and after finishing the driving task (p<0.05). These metrics are possible indices for measuring simulated driving mental fatigue.

Clinical efficiency and safety analysis of transcatheter interventional therapy for compound congenital cardiovascular abnormalities.

OBJECTIVE: To investigate the efficiency and safety of transcatheter interventional therapy for compound congenital cardiovascular abnormalities. METHODS: From Nov 2001 to Jun 2006, a total of 36 patients (17 male, 19 female), aged 17.20 +/- 10.52, with compound congenital cardiovascular abnormalities underwent transcatheter interventional procedure. These patients included 11 with perimembranous ventricular septal defect (PVSD) and patent ductus arteriosus (PDA), 8 patients with PVSD and atrial septal defect (ASD), 8 patients with ASD and PDA, 7 patients with ASD and pulmonary stenosis (PS), 1 patient with ASD and mitral stenosis(MS), 1 patient with coarctation of aorta (COA) and PDA. According to the principle of "easy first, hard second," balloon valvuloplasties of PS or MS were performed before the closure of PVSD, and of PDA and ASD. Electrocardiogram and transthoracic echocardiogram were examined at 4 days, 1, 2, 6 and 12 months, respectively, after each procedure. RESULTS: Transcatheter interventional therapy for compound congenital cardiovascular abnormalities was successful in all patients. Among these, 2 occluders were planted in each of 27 patients, 7 patients with ASD combined with PS and 1 patient with ASD combined with MS underwent successfully performed balloon valvuloplasty and ASD closure, 1 patient with COA combined with PDA underwent successfully performed balloon valvuloplasty and subsequent covered stent implantation. No patient encountered serious adverse events during the (30.5 +/- 14.6) months of follow-up. CONCLUSIONS: Transcatheter interventional therapy for compound congenital cardiovascular abnormalities could obtain satisfactory results with technical feasibility.