BackgroundAlthough a few studies have been reported on predictive factors of postoperative diabetes remission, the conclusions remain inconsistent. This meta-analysis aimed to assess the preoperative clinical factors for type 2 diabetes mellitus (T2DM) remission after bariatric surgery.MethodsThe Cochrane Library, PubMed, MEDLINE, Embase, and CINAHL databases were searched. All human studies published in English between 1 January 1992 and 1 September 2013 reporting on the parameters of interest were included.ResultsIn total, 15 studies involving 1,753 bariatric surgery patients were selected. Analyses were performed separately for the parameters of interest. T2DM remission was observed to be negatively correlated with age, diabetes duration, insulin use, and HbA1c levels. Baseline body mass index (BMI) and C-peptide levels were positively associated with the remission rate in Asian patients. However, there was no significant association between gender and remission rate.ConclusionsPatients with younger age, short diabetes duration, better glucose control, and better β cell function were more likely to achieve T2DM remission after bariatric surgery. However, further randomized controlled trials with uniform remission criteria should be conducted to provide more reliable evidence.
Premature ovarian failure (POF) contributes to amenorrhoea, infertility, early onset of menostasia and osteoporosis. This study profiled differentially expressed miRNAs for association with POF development. Ovarian tissue samples from 4-vinylcyclohexene diepoxide (VCD)-induced rat POF and normal rats were profiled for differentially expressed miRNAs using miRNA microarrays. A total of 63 miRNAs were up-regulated and 20 miRNAs were down-regulated in rat POF tissues versus the control tissues. qRT-PCR verified some of these altered miRNAs, i.e. miR-29a and miR-144 were down-regulated in POF tissues, which may target expression of PLA2G4A that is involved in prostaglandin biosynthesis, whereas miR-27b and miR-190 were up-regulated in POF tissues by negative control of PAPPA and CCL2 expression, respectively, both of which have been shown to relate to response to hormone stimulus. Moreover, the up-regulated miR-151 and miR-672 can also target expression of TNFSF10 and FNDC1, which have been shown to positively regulate cell apoptosis. Profiling of differentially expressed miRNAs in POF provided a novel insight into the molecular events involving the role of miRNAs in POF development with specific emphasis upon miR-27b, miR-190, miR-151, miR-672, miR-29a and miR-144.
We aimed to explore whether maternal chronic hepatitis B virus (HBV) infection certainly affects preterm labor (birth) in pregnant women. Four databases were systematically searched up to May 31, 2017, without language restriction. Any study was included if it clearly defined exposure to chronic HBV infection, reported risk of preterm labor or birth in pregnant women, and reported relative risks (RRs) or odds ratios (ORs) or provided data for estimation. RRs (or ORs) with 95% confidence intervals were pooled using random-effects models. Statistical heterogeneity was assessed with Cochran's Q statistic and I 2 statistic. Twenty-two observational studies involving 6 141 146 pregnant women (three prospective cohort studies, n = 1 116 799;15 retrospective cohort studies, n = 5 022 513 and four case-control studies, n = 1834)were included. The risk of preterm labor was significantly intensified with chronic HBV infection compared with uninfected women, with substantial heterogeneity. Chronic HBV infection was also significantly associated with a 16% increase in the risk of preterm birth, with substantial heterogeneity. The risk of preterm birth significantly increased by 21% in HBsAg+/HBeAg+ pregnant women compared with uninfected pregnant women. Chronic HBV infection intensifies the risk of preterm labor and birth in pregnant women, but this conclusion should be interpreted with caution given the possibility of residual confounding and be confirmed by well-designed studies in the future.
K E Y W O R D Shepatitis B virus infection, preterm birth, preterm labor, pregnancy outcome
Objectives:The primary objective of this study was to investigate whether dexmedetomidine could potentiate the analgesic efficacy of ropivacaine, when added to ropivacaine for wound infiltration in patients undergoing open gastrectomy.Methods:Fifty patients scheduled for open gastrectomy were divided into 2 equal groups that were received wound infiltration using 20 mL 0.3% ropivacaine plus 2 mL normal saline (group R) or 20 mL 0.3% ropivacaine plus 2 mL 1.0 μg/kg dexmedetomidine (group DR). Visual analogue scale (VAS) pain score, patient-controlled analgesia (PCA) pump press number, sufentanil consumption, postoperative nausea and vomiting (PONV), and wound healing score were recorded.Results:The VAS pain score were comparable between the 2 groups at the observation time points (P > .05), PCA pump press number and sufentanil consumption were higher in group R than that in group DR at 0 to 2, 2 to 4, 4 to 6 time intervals (P < .05) except for 6 to 8, 8 to 10, 10 to 12 time intervals (P > .05), meanwhile, the 24 hours total sufentanil consumption was also higher in group R than that in group DR (90.4 ± 20.5 vs 79.2 ± 9.4) (P < .05), there were no significant differences in PONV and wound healing score between the 2 groups (P > .05).Conclusions:Dexmedetomidine as an adjuvant to ropivacaine for wound infiltration promoted the analgesic efficacy of ropivacaine, reduced sufentanil consumption, and had no effect on wound healing; it could be as an ideal adjuvant which could potentiate the analgesic efficacy of local anesthetics.
Objective
To investigate the role of miR‐424 in diabetic nephropathy (DN) and its relationship with Rictor in mammalian target of rapamycin (mTOR) C2/Akt signaling.
Methods
The western blot analysis and real‐time polymerase chain reaction were used to determine the differential expression of Rictor, mTOR, and miR‐424 in DN rats. The upregulation of miR‐424 was achieved by caudal vein injection of miR‐424 mimics. The renal lesion was evaluated by hematoxylin‐eosin staining (H&E) and periodic acid schiff staining. The dual‐luciferase reporter assay was conducted to determine the binding target of miR‐424. The effect of miR‐424 upregulation on apoptosis was detected by the terminal deoxynucleotidyl transferase‐mediated 2‐Deoxyuridine‐5‐Triphosphate (dUTP) nick‐end labeling assay and western blot analysis.
Results
A significantly lower expression of miR‐424 and a significantly higher expression of Rictor and mTOR were found in renal tissues of DN rats. The upregulation of miR‐424 improved renal lesion and DN symptoms of blood glucose level, urine protein level, body weight, creatinine level, blood urea nitrogen, and KW/BW ratio. The upregulation of miR‐424 could significantly reduce apoptosis rates of tissue cells by decreasing the expression levels of caspase‐3 and Bax as well as increasing the level of Bcl‐2. Furthermore, Rictor was the direct target for miR‐424, and upregulation of miR‐424 inhibited Rictor through Akt signaling in renal tissue of DN rats and high‐glucose‐treated human glomerular mesangial cells.
Conclusion
miR‐424 contributes to alleviating the symptoms in DN rat models by targeting Rictor through mTORC2/Akt signaling.
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