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Abstract Whether restarting anticoagulation (RA) treatment after intracranial hemorrhage (ICH) is still controversial. We performed a systematic review and meta‐analysis to summarize the relationship between anticoagulation after ICH with the recurrence of hemorrhagic events, ischemic events, and long‐term mortality. Medline, Embase, and the Cochrane Central Register of Controlled Trials, from inception to November 2020. We searched the published medical literature to ensure cohort studies involving ICH associated with anticoagulation in adults. Primary outcomes were long‐term mortality, hemorrhagic events, and ischemic events (myocardial infarction, pulmonary embolism, ischemic stroke, or systemic embolization). We concluded seven retrospective cohorts, including 1876 intracranial hemorrhage patients with indications of anticoagulation. The ratio of the anticoagulant restart was 35.3% (664n). RA was associated with a significantly lower incidence of recurrent ischemic events (pooled odds ratio [OR] 0.29, 95% confidence interval [CI] 0.19% to 0.45%, p = 0.97) and death events (pooled OR 0.56, 95% CI 0.40%–0.79%, p = 0.27). There is no evidence that early recovery of anticoagulation (within 2 weeks or 1 month) is associated with the occurrence of hemorrhagic events (within 2 weeks: pooled OR 0.80, 95% CI 0.3–2.12, p = 0.52 vs. within 1 month: pooled OR 1.14, 95% CI 0.77–1.68, p = 0.82). Based on these, recovery of anticoagulation after ICH is beneficial for long‐term mortality and recurrence of ischemic events. The meta‐analysis showed a resumption of oral anticoagulation within 2 weeks or 1 month in patients who had a cerebral hemorrhage was beneficial and did not increase the risk of hemorrhagic events and reduced the occurrence of ischemic and fatal endpoint events.

Abstract To screen out the prospective biomarkers of viral encephalitis (VE), analyze the biological process and signaling pathways involved by differentially expressed proteins (DEPs). A total of 11 cerebrospinal fluid (CSF) samples with VE and 5 with non‐nervous system infection were used to perform label‐free proteomic techniques. Then, the bioinformatic analysis of DEPs was applied by Interproscan software. Moreover, 73 CSF samples in the VE group and 53 in the control group were used to verify the changes of some DEPs by enzyme‐linked immunosorbent assay (ELISA). Thirty‐nine DEPs were identified, including 18 upregulated DEPs and 21 downregulated DEPs. DEPs were mainly enriched in cell adhesion molecules by Kyoto Encyclopedia of Genes and Genomes analysis pathway analysis. The DEPs related to axon tissue were obviously downregulated and the most significant downregulated proteins were neurexin 3, neurofascin, and neuroligin 2 (NLGN2). Moreover, the protein expression of NLGN2 in the VE group was significantly higher than that in the control group by ELISA. The correlation analysis of NLGN2 in the VE group revealed that there was a weak positive correlation with CSF protein and a weak negative correlation with CSF chloride. The clinical VE may be closely related to NLGN2 and the cell adhesion molecule pathway.

Objective Study the principle and possible mechanism of Ginkgo biloba in the treatment of Alzheimer's disease (AD) which is based on network pharmacology. Methods The potential targets of active ingredients of Ginkgo biloba were collected by Traditional Chinese Medicine Integrated Database platform (TCMSP). TCMSP is a pharmacological system for drug discovery from Chinese herbal medicine. The disease targets of AD were searched and collected by the database of gene‐disease associations (DisGeNET) and literature. The obtained targets were standardized by the UniProt database. STING network platform and Cytoscape were used to construct protein‐protein interaction network (PPI) of the key targets. According to Materscape, we clarify the possible mechanism of action including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) enrichment analysis. Results The compound‐target network contains 27 active ingredients, 191 related targets, 18 key targets, including PLAU, HMOX1, TNF, INSR, MPO, MAOB, IGF2, IL1B, ESR1, BCL2, ACHE, BAX, GSK3B, PPARG, SLC2A4, NOS3, CASP3, VEGFA. GO enrichment analysis has got a total of 640 GO items, including 609 biological process (BP) items (95.1%), 16 molecular function (MF) items (2.5%) and 15 cellular component (CC) items (2.4%). After KEGG enrichment, 44 pathways were obtained. Conclusion Through the construction of “component‐target‐pathway”, GO biological function and KEGG pathway enrichment analysis were performed on core targets, and the possibility of Ginkgo biloba for the treatment of AD was explored from multiple targets and pathways, which provided a new approach for multi‐target treatment.

Background Cerebral stroke is the second leading cause of death with high mortality and morbidity worldwide, currently it lacks effective therapies to improve the prognosis. This study was aimed to explore the role of bone marrow mesenchymal stem cells (BMSCs) transplantation in the recovery of brain structure and function after ischemic cerebral infarction by magnetic resonance imaging (MRI). Methods By applying internal carotid artery embolization, the ischemic cerebral infarction model in rats was established. MRI was performed to detect the imaging changes in the brain tissue after modeling, and the successful modeling was evidenced by the presence of obvious high‐signal infarct areas in the brain. BMSCs were then injected into the lateral ventricles of rats, and the recovery of brain tissue and function were quantitatively evaluated by T2‐weighted image (T2WI) and voxel‐based morphology (VBM) after 28 days. Results The results showed that BMSCs were cell subsets with multiple differentiation potentials. Deficits caused by Ischemic cerebral infarction were relieved by BMSCs transplantation, including increase in damaged cerebral tissue and recovery of cerebral function. In addition, the combined imaging technology of VBM and T2WI quantitatively revealed the effectiveness of BMSCs in repairing damaged brain tissue structure and function. Conclusion Taken together, the results revealed that the transplantation of BMSCs into the lateral ventricle was beneficial to repair the structure and function of the damaged brain tissue after ischemic cerebral infarction. Moreover, the combination of VBM and T2WI technology can detect the level of brain injury in ischemic cerebral infarction dynamically and noninvasively, and evaluate the recovery of structure and function of damaged brain tissue.