Background:Hyperglycemia is associated with dismal outcomes in patients with traumatic brain injury (TBI), which is frequently treated with insulin therapy. In this study, a systematic review and meta-analysis of the published randomized controlled trials (RCTs) was performed to assess the safety and efficacy of intensive glycemic control (IGC) versus conventional glycemic control (CGC) for patients following TBI.Methods:Databases, including PubMed, Embase, and the Cochran database, were retrieved up to January 2018. The outcomes evaluated in this study included mortality, neurological outcome, infection rate, hypoglycemia episode, and length of stay (LOS) in intensive care unit (ICU). The enrolled trials were analyzed using the Review Manager 5.3 software.Results:A total of 7 randomized controlled trials (RCTs) involving 1013 cases were enrolled in this study, and the results indicated no significant difference in 6-month mortality (risk ratio [RR], 0.92; 95% confidence interval [CI] 0.76–1.10; P = .34). Subsequently, IGC was associated with a better neurological outcome (RR, 1.22; 95% CI 1.05–1.43; P = .01), lower infection rate (RR, 0.65; 95% CI 0.51–0.82; P = .0003) and shorter LOS in ICU (mean difference [MD] = –1.37; 95%CI = –2.11, –0.63; P = .0003). In addition, IGC would also increase the risk of hypoglycemia episode (RR, 4.53; 95% CI 2.18–9.42; P < .001).Conclusions:IGC plays a protective role in improving neurological outcome, decreasing infection rate and reducing the LOS in ICU. However, IGC therapy can also remarkably increase the risk of hypoglycemia, but it will not affect the mortality in TBI patients.

Cerebral ischemia–reperfusion (I/R) injury is a terrible disease which results in the dysfunction and structural damage of brain tissues. Growing evidence implies that miR-455-5p is implicated in the regulation of pathogenesis of several diseases. The aim of this study is to reveal the role of miR-455-5p in cerebral I/R injury and the regulatory mechanism. We established a vitro model by inducing SH-SY5Y and PC-12 cells with oxygen-glucose deprivation and reoxygenation. The experimental cerebral I/R rat model was established by middle cerebral artery occlusion operation. The findings indicated that miR-455-5p expression was downregulated in oxygen-glucose deprivation and reoxygenation induced cells and I/R rat model. In addition, miR-455-5p upregulation inhibited SH-SY5Y cell apoptosis and cerebral damage, whereas miR-455-5p silencing promoted SH-SY5Y cell apoptosis and cerebral damage. Mechanistically, luciferase reporter assay corroborated that miR-455-5p could bind with feline mcDonough sarcoma-like tyrosine kinase 3 (FLT3) mRNA. However, the role of FLT3 in cerebral I/R injury was rarely investigated. Real-time polymerase chain reaction revealed that FTL3 expression was negatively regulated by miR-455-5p. FTL3 upregulation reversed the inhibitory effects of miR-455-5p upregulation on PC-12 and SH-SY5Y cell apoptosis. Therefore, our study verified that miR-455-5p improved cerebral I/R injury by targeting FLT3, which suggests a potential new target for the prevention of cerebral I/R injury.

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Microvascular decompression (MVD) is a widely adopted neurosurgery in treating cranial nerve diseases providing long-term pain relief. Improving surgical techniques has been a focus of recent studies. Venous structures such as the sigmoid sinus are essential to protect, and whose risk of destruction during surgery increases with size. The medical records of patients who went through MRI ahead of MVD surgery between Dec 2020 and Dec 2021 were reviewed. Section area of sigmoid sinus calculated from the MRI plane of auditory nerve showed a right dominance of the sinus. The improved method concerning the relationship between affected side and the dominant sigmoid sinus offered a better bone window and surgical field by planning the operation incision in advance. Intraoperative adjustment of the bone flap was avoided, and the risk of destructing the sigmoid sinus was reduced.

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