Background:Osteoporotic vertebral compression fractures (OVCFs) commonly afflicts most aged people resulting back pain, substantial vertebral deformity, functional disability, decreased quality of life, and increased adjacent spinal fractures and mortality. Percutaneous vertebral augmentation (PVA) included percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP), nerve block (NB), and conservative treatment (CT) are used for the nonsurgery treatment strategy of OVCFs, however, current evaluation of their efficacy remains controversial.Methods and analysis:A systematic literature search was carried out in PubMed, EMBASE, Web of Knowledge, and the Cochrane Central Register of Controlled Trials up to October 31, 2017. Randomized controlled trials (RCTs) were compared PVP, PKP, NB, or CT for treating OVCFs. The risk of bias for each trial was rated according to the Cochrane Handbook. Mean differences (MDs) with 95% confidence intervals (CIs) were utilized to express VAS (visual analog scale) outcomes. The network meta-analysis (NMA) of the comparative efficacy measured by change of VAS on acute/subacute and chronic OVCFs was conducted for a short-term (<4 weeks) and long-term (≥6–12months) follow-up with the ADDIS software.Results:A total of 18 trials among 1994 patients were included in the NMA. The PVA (PVP and PKP) had better efficacy than CT. PKP was first option in alleviating pain in the case of the acute/subacute OVCFs for long term, and chronic OVCFs for short term and long term, while PVP had the most superiority in the case of the acute/subacute OVCFs for short term. NB ranks higher probability than PKP and PVP on acute/subacute OVCFs in short and long-term, respectively.Conclusions:The present results suggest that PVA (PVP/PKP) had better performance than CT in alleviating acute/subacute and chronic OVCFs pain for short and long-term. NB may be used as an alternative or before PVA, as far as pain relief is concerned. Various nonsurgery treatments including CT, PVA (PVP/PKP), NB, or a combination of these treatments are performed with the goal of reducing pain, stabilizing the vertebrae, and restoring mobility.

Background Although recent studies have shown that botulinum toxin‐A (BTX‐A) has a good analgesic effect on trigeminal neuralgia (TN) and peripheral neuropathic pain (PNP), the quality of evidence is low due to limited data. This meta‐analysis is used to synthesize existing evidence for the treatment of these conditions with BTX‐A. Methods Relevant trials were accessed by using an electronic search in databases (Web of Science, PubMed, EMBASE, Cochrane Library, and http://ClinicalTrials.gov). Data from included randomized controlled trials (RCTs) on the efficacy and safety of BTX‐A in treating TN and PNP were extracted for meta‐analysis. Results Finally, 10 RCTs (n = 391) were included in this meta‐analysis. The pooled effect of BTX‐A was superior to placebo based on pain intensity (SMD = −0.48, 95% CI [−0.74, 0.23] at 1 month, SMD = −0.58, 95% CI [−0.91, −0.24] at 2 months, and SMD = −0.55, 95% CI [−0.87, −0.22] at 3 months). Number needed to treat (NNT) for 50% pain intensity reduction showed better effect of BTX‐A on TN and postherpetic neuralgia (PN). Adverse events associated with BTX‐A were similar to placebo (OR = 1.58, 95% CI [0.51, 4.87], p = .424). Conclusion Pooled data from our meta‐analysis suggest that BTX‐A is efficacious and safe in treating TN and PNP. However, due to the limited sample size and heterogeneity, further larger and well‐designed RCTs are imperative to validate these findings.

Objectives:Alzheimer’s Disease (AD), characterized by deficits in memory and cognition and by behavioral impairment, is a progressive neurodegenerative disorder that influences more than 47 million people worldwide. Currently, no available drug is able to stop AD progression. Therefore, novel therapeutic strategies need to be investigated.Measurements:We analyzed the RNA sequencing data (RNA-seq) derived from the Gene Expression Omnibus (GEO) database to identify the differentially expressed mRNAs in AD. The AD mouse model Tg2576 was used to verify the effects of IGF-2. The Morris Water Maze was administered to test the role of IGF-2 in memory consolidation. In addition, we quantified cell apoptosis by the TUNEL assay. The levels of amyloid plaques and the levels of Aβ40 and Aβ42 in the hippocampus were also determined by immunohistochemistry and ELISA, respectively.Results:RNA-seq analysis revealed that IGF-2 was remarkably reduced in AD. The expression of the upstream genes PI3K and AKT and the downstream gene CREB in the PI3K signaling pathway was significantly increased in the hippocampus of Tg2576 mice cells treated with IGF-2. The Morris water maze test showed that IGF-2 improved memory consolidation in Tg2576 mice. The activity of caspase-3 was decreased in Tg2576 mice treated with IGF-2. Amyloid plaques in the hippocampus were reduced, and the levels of Aβ40 and Aβ42 were decreased. The above effects of IGF-2 on AD were blocked when the PI3K signaling pathway inhibitor wortmannin was added.Conclusions:IGF-2 attenuates memory decline, oxidative stress, cell apoptosis and amyloid plaques in the AD mouse model Tg2576 by activating the PI3K/AKT/CREB signaling pathway.

Recent study has reported that microRNA‐628‐5p (miR‐628‐5p) is involved in the development of epithelial ovarian cancer; however, the mechanisms of miR‐628‐5p in glioma remain unclear. In this study, we explored the potential biological roles of miR‐628‐5p in glioma. First, we found that miR‐628‐5p was decreased in the tissues and cells (U87 and T98) of glioma. Second, overexpressing miR‐628‐5p reduced the ability of glioma cells' proliferation and induced glioma cells' cycle arrest in G1. Then, we found that miR‐628‐5p directly bound to the 3′‐untranslated region of DDX59 and decreased the protein level of DDX59. The decrease of DDX59 was found to lead to the decrease of p‐AKT. Mechanistic studies revealed that restoring the expression of DDX59 alleviated miR‐628‐5p‐induced inhibition of proliferation of glioma. These findings suggest that the miR‐628‐5p/DDX59 axis has a key role in the development of glioma, and miR‐628‐5p might be a new therapeutic target against glioma.