Lumbar puncture as possible cause of sudden paradoxical herniation in patient with previous decompressive craniectomy: report of two cases.

BACKGROUND: Lumbar puncture is often used for the diagnosis and treatment of subarchnoid hemorrhage, infection of Cerebro-spinal Fluid (CSF), hydrocephalus in neurosurgery department patients. It is general that paradoxical herniation followed by lumbar puncture is quite rare in decompressive craniectomy cases; the related reports are very few. Moreover, most of the paradoxical herniation cases are chronic, which often occur weeks or even months after the lumbar puncture, to date, barely no reports on the acute onset paradoxical herniation have been found. CASE PRESENTATION: Two traumatic brain injury patients with decompressive craniectomy (DC) and hydrocephalus suffered from a sudden paradoxical herniation after lumbar puncture. The symptoms of herniation were improved by treated with Trendelenburg position and rapid intravenous infusion. CONCLUSIONS: Lumbar puncture may have a potential risk of inducing sudden paradoxical herniation in patients with DC. CSF drainage during lumbar puncture should be in small volume for patients with DC. Once a paradoxical herniation occurs after lumbar puncture, an immediate Trendelenburg position and rapid intravenous infusion treatment may be effective.

Effects of reminiscence therapy on psychological outcome among older adults without obvious cognitive impairment: A systematic review and meta-analysis.

Introduction: Reminiscence therapy has been a high-benefit and low-cost measure of psychosocial intervention for older adults in recent years. It has attracted much attention in the intervention study of older adults without obvious cognitive impairment. This study aimed to evaluate the effects of reminiscence therapy on psychosocial outcomes among older adults without obvious cognitive impairment and analyze the divergences of different intervention programs (form, duration, and setting) on outcomes. Methods: We searched the commonly used databases and used RevMan 5.4 in the meta-analysis (PROSPERO-ID: CRD42022315237). All eligible trials used the Cochrane Risk of Bias Tool and the Effective Public Health Practice Project quality assessment tool to identify the quality and determine the bias risk grade. Results: Twenty-seven studies were included, involving 1,755 older adults. Meta-analysis showed that reminiscence therapy has a significant effect on both depression and life satisfaction. Group reminiscence played a significant role in improving life satisfaction. Depression symptoms were not affected by the intervention duration (P = 0.06), while life satisfaction was significantly improved after more than 8 weeks of intervention (P < 0.00001). Intervention settings drove differences in depressive symptoms (P = 0.02), and the effect size of the community was larger. Conclusion: Reminiscence therapy can significantly reduce depressive symptoms and improve life satisfaction. There are different effects of reminiscence therapy in different intervention schemes on psychological outcomes among older adults. More well-designed trials with large sample sizes and long-term follow-ups are necessary to confirm and expand the present results. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=315237, identifier: CRD42022315237.

MicroRNA-562 negatively regulated c-MET/AKT pathway in the growth of glioblastoma cells.

BACKGROUND: MicroRNA-562 (miR-562) has been found to possess anti-cancer function in certain tumors. However, the function of miR-562 in glioblastoma (GBM) is still not fully understood. PURPOSE: The aim at present study is to analyze the function of miR-562 and its possible target in GBM cells. PATIENTS AND METHODS: In the present study, a total of 80 GBM samples and 16 adjacent noncancerous tissues were used to examine the expression of miR-562 and c-MET. In order to gain a deep insight into the molecular network of miR-562 and c-MET in GBM, the miR-562 mimic and inhibitor were transfected into two GBM cell lines (U251 and U87), respectively. Meanwhile, lentiviral vector was used to mediate overexpression of c-MET. Cell proliferation was examined via Cell Counting Kit-8 (CCK-8) assays. Meanwhile, cell apoptosis was analyzed by Annexin V-FTTC/PI staining assay. RESULTS: Our results indicated that the level of miR-562 was downregulated in GBM tissues and the expression of c-MET was upregulated in tumors. Cell proliferation analysis indicated that miR-562 was an anti-proliferation effector in GBM cells. Moreover, cell apoptosis analysis suggested the pro-apoptosis function of miR-562 in GBM cells. CONCLUSION: Our results demonstrated that miR-562 negatively regulated the c-MET/AKT signal pathway. In addition, caspase-3 might also serve as another target for miR-562 in GBM cells. This research not only obtained a deep understanding of miR-562 but also provided evidence in terms of developing new prognostic biomarker for GBM.

Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma Cells via Suppression of Wnt/ß-Catenin Pathway.

Human glioblastoma multiforme (GBM) accounts for the majority of human brain gliomas. Several TMEM proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However, the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of TMEM168 were overexpressed in GBM patients (n = 85) when compared with healthy people (n = 10), which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan-Meier analysis of Gene Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with shorter survival time. To investigate whether and how TMEM168 functioned in the tumorigenesis of human GBM cells, two human GBM cell lines (U87 and U373) were used for study. Lithium chloride (LiCl), an activator for Wnt/ß-catenin pathway, was used for the treatment. Our data suggested that siRNA-TMEM168 (siTMEM168) prevented viability of U87 and U373 cells, induced cell cycle arrest (G0/G1 phase) and promoted apoptosis, and the mechanisms involved in blocking Wnt/ß-catenin pathway, as evidenced by reducing expression of ß-catenin, C-myc, cyclin D1, and survivin. Furthermore, the inhibited effect of siTMEM168 on human GBM cell growth was significantly alleviated with additional LiCl treatment, substantiating the involvement of the Wnt/ß-catenin pathway in this process. In summary, our data demonstrated that TMEM168 may represent a therapeutic target for the treatment of human GBM.

MiR-223-3p overexpression inhibits cell proliferation and migration by regulating inflammation-associated cytokines in glioblastomas.

Glioblastoma(GBM) is most common brain tumor in adults. Currently standard treatments have limited effect to increase the survival, because there are still largely unclear mechanisms in glioblastoma development. miR-223 was involved in various types of cancer, however, the function of miR-223-3p in GBM was still unclear. In our study, real-time PCR was performed to exam the expression level of miR-223-3p and NLRP3 (Nucleotide-binding oligomerization domain(NOD)-like receptor family PYRIN domain containing-3) in GBM tissues. Following that, mimic or inhibitor of miR-223-3p were used to modulate miR-223-3p expression in GBM cell lines respectively. Then, we analyzed cell proliferation and migration by cell counting kit and transwell assay. Further, western blot was performed to detect several inflammation-associated cytokines level in GBM cell lines. We found that miR-223-3p was decreased but NLRP3 was increased in GBM tissues. Treatment with miR-223-3p mimic inhibits cell proliferation and migration via decreasing several inflammation-associated cytokines, including interleukin-1ß (IL-1ß), monocyte chemoattractant protein-1 (MCP-1), IL-8 and IL-18. Importantly, these effects induced by miR-223-3p could be attenuated by NLRP3 overexpression, which was considered as one of target genes of miR-223-3p. In conclusion, these results indicated that miR-223-3p might act as a suppressor and a potential therapy target of GBM.

Effects of Intracranial Pressure Monitoring on Mortality in Patients with Severe Traumatic Brain Injury: A Meta-Analysis.

BACKGROUND: The Brain Trauma Foundation (BTF) guidelines published in 2007 suggest some indications for intracranial pressure (ICP) monitoring in severe traumatic brain injury (TBI). However, some studies had not shown clinical benefit in patients with severe TBI; several studies had even reported that ICP monitoring was associated with an increased mortality rate. The effect of ICP monitoring has remained controversial, regardless of the ICP monitoring guidelines. Here we performed a meta-analysis of published studies to assess the effects of ICP monitoring in patients with severe TBI. METHODS: We searched three comprehensive databases, the Cochrane Library, PUBMED, and EMBASE, for studies without limitations published up to September 2015. Mortality, ICU LOS, and hospital LOS were analyzed with Review Manager software according to data from the included studies. RESULTS: Eighteen eligible studies involving 25229 patients with severe TBI were included in our meta-analysis. The results indicated no significant reduction in the ICP monitored group in mortality (hospitalized before 2007), hospital mortality (hospitalized before 2007), mortality in randomized controlled trials. However, overall mortality, mortality (hospitalized after 2007), hospital mortality (hospitalized after 2007), mortality in observational studies (hospitalized after 2007), 2-week mortality, 6-month mortality, were reduced in ICP monitored group. Patients with an increased ICP were more likely to require ICP monitoring. CONCLUSION: Superior survival was observed in severe TBI patients with ICP monitoring since the third edition of "Guidelines for the Management of Severe Traumatic Brain Injury," which included "Indications for intracranial pressure monitoring," was published in 2007.