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Background: There is a mutual hemodynamic and pathophysiological basis between the heart and brain. Glutamate (GLU) signaling plays an important role in the process of myocardial ischemia (MI) and ischemic stroke (IS). To further explore the common protective mechanism after cardiac and cerebral ischemic injuries, the relationship between GLU receptor-related genes and MI and IS were analyzed. Results: A total of 25 crosstalk genes were identified, which were mainly enriched in the Toll-like receptor signaling pathway, Th17 cell differentiation, and other signaling pathways. Protein-protein interaction analysis suggested that the top six genes with the most interactions with shared genes were IL6, TLR4, IL1B, SRC, TLR2, and CCL2. Immune infiltration analysis suggested that immune cells such as myeloid-derived suppressor cells and monocytes were highly expressed in the MI and IS data. Memory B cells and Th17 cells were expressed at low levels in the MI and IS data; molecular interaction network construction suggested that genes such as JUN, FOS, and PPARA were shared genes and transcription factors; FCGR2A was a shared gene of MI and IS as well as an immune gene. Least absolute shrinkage and selection operator logistic regression analysis identified nine hub genes: IL1B, FOS, JUN, FCGR2A, IL6, AKT1, DRD4, GLUD2, and SRC. Receiver operating characteristic analysis revealed that the area under the curve of these hub genes was > 65% in MI and IS for all seven genes except IL6 and DRD4. Furthermore, clinical blood samples and cellular models showed that the expression of relevant hub genes was consistent with the bioinformatics analysis. Conclusions: In this study, we found that the GLU receptor-related genes IL1B, FOS, JUN, FCGR2A, and SRC were expressed in MI and IS with the same trend, which can be used to predict the occurrence of cardiac and cerebral ischemic diseases and provide reliable biomarkers to further explore the co-protective mechanism after cardiac and cerebral ischemic injury. [ABSTRACT FROM AUTHOR]

Background: Aneurysmal subarachnoid hemorrhage is a relatively rare cause of stroke, carrying a bad prognosis of mortality and disability. The current standard procedure, neurosurgical clipping, has failed to achieve satisfactory outcomes. Therefore, endovascular detachable coils have been tested as an alternative. This meta-analysis was aimed to compare the outcomes of surgical clipping and endovascular coiling in aneurysmal subarachnoid hemorrhage. Materials and Methods: Relevant randomized trials up to June 2018 were identified from Medline, Central, and Web of Science. Data for poor outcomes (Modified Rankin Scale [mRS] scores 3 to 6) at 2–3 months, 1 year, and 3–5 years were extracted and analyzed as odds ratios (ORs) with 95% confidence intervals (CIs), using RevMan software. Results: Five studies (2780: 1393 and 1387 patients in the coiling and clipping arms, respectively) were included in the current analysis. The overall effect estimate favored endovascular coiling over surgical clipping in terms of reducing poor outcomes (death or dependency, mRS > 2) at 1 year (OR = 0.67, 95% CI: 0.57–0.79) and 3–5 years (OR = 0.8, 95% CI: 0.67–0.96). Moreover, coiling was associated with a significantly lower rate of cerebral ischemia (OR = 0.37, 95% CI: 0.16–0.86). Postprocedural mortality (OR = 0.79, 95% CI: 0.6–1.05) and rebleeding (OR = 1.15, 95% CI: 0.75–1.78) rates were comparable between the two groups. However, technical failure was significantly more common with coiling interventions than with clipping surgeries (OR = 2.84, 95% CI: 1.86–4.34). Conclusion: Our analysis suggests that coiling can be a better alternative to clipping in terms of surgical outcomes. Further improvements in the coiling technique and training may improve the outcomes of this procedure. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to investigate the nuclear expression status of cyclin dependent kinase like 2 (CDKL2) in glioma and its correlation with the characteristics of clinical pathology, including patient survival., Methods and Results: In the present study, the expression of CDKL2 mRNA was detected by real-time QPCR in freshly collected glioma and para-carcinoma tissues. Moreover, immunohistochemistry was used to identified nuclear expression of CDKL2, and the characteristics of clinical pathology from glioma cases (n = 144) and non-cancerous brain tissues (n = 32) were counted. Low mRNA and nuclear protein expression of CDKL2 was observed in glioma tissues compared to non-cancerous tissues. Glioma patients with negative nuclear expression of CDKL2 were correlated with histologic type, clinical World Health Organization (WHO) grade, tumor location, and KI-67 expression status. Negative nuclear expression of CDKL2 in glioma patients predicted an observably shorter overall survival time than did positive expression. However, as demonstrated by multivariate analysis, nuclear expression of CDKL2 was not an independent prognostic biomarker for the survival of patients with glioma., Conclusions: Our study indicated that negative nuclear expression of CDKL2 may represent a potential unfavorable marker for progression and poor prognostic in glioma., Competing Interests: None., (IJCEP Copyright © 2018.)