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Stroke imposes a substantial burden worldwide. With the rapid economic and lifestyle transition in China, trends of the prevalence of stroke across different geographic regions in China remain largely unknown. Capitalizing on the data in the National Health Services Surveys (NHSS), we assessed the prevalence and risk factors of stroke in China from 2003 to 2018. In this study, data from 2003, 2008, 2013, and 2018 NHSS were collected. Stroke cases were based on participants’ self-report of a previous diagnosis by clinicians. We estimated the trends of stroke prevalence for the overall population and subgroups by age, sex, and socioeconomic factors, then compared across different geographic regions. We applied multivariable logistic regression to assess associations between stroke and risk factors. The number of participants aged 15 years or older were 154,077, 146,231, 230,067, and 212,318 in 2003, 2008, 2013, and 2018, respectively, among whom, 1435, 1996, 3781, and 6069 were stroke patients. The age and sex standardized prevalence per 100,000 individuals was 879 in 2003, 1100 in 2008, 1098 in 2013, and 1613 in 2018. Prevalence per 100,000 individuals in rural areas increased from 669 in 2003 to 1898 in 2018, while urban areas had a stable trend from 1261 in 2003 to 1365 in 2018. Across geographic regions, the central region consistently had the highest prevalence, but the western region has an alarmingly increasing trend from 623/100,000 in 2003 to 1898/100,000 in 2018 (Ptrend

Introduction. Rising studies indicate that the apolipoprotein E (APOE) gene is related to the susceptibility of ischemic stroke (IS). However, certain consensus is limited by the lack of a large sample size of researches. This meta-analysis was performed to explore the potential association between the APOE gene and IS. Methods. To identify relevant case control studies in English publications by October 2020, we searched PubMed, Embase, Web of Science, and the Cochrane Library. Pooled odds ratios (ORs) with fixed- or random-effect models and corresponding 95% confidence intervals (CIs) were calculated to analyze potential associations. Results. A total of 55 researches from 32 countries containing 12207 IS cases and 27742 controls were included. The association between APOE gene ε4 mutation and IS was confirmed (ε4 vs. ε3 allele: pooled OR = 1.374 , 95% CI, 1.214-1.556; ε2/ε4 vs. ε3/ε3: pooled OR = 1.233 , 95% CI, 1.056-1.440; ε3/ε4 vs. ε3/ε3: pooled OR = 1.340 , 95% CI, 1.165-1.542; ε4/ε4 vs. ε3/ε3: pooled OR = 1.833 , 95% CI, 1.542-2.179; and APOE ε4 carriers vs. non-ε4 carriers: pooled OR = 1.377 ; 95% CI, 1.203-1.576). Interestingly, APOE ε4 mutation showed a dose-response correlation with IS risk (ε4/ε4 vs. ε2/ε4: pooled OR = 1.625 ; 95% CI, 1.281-2.060; ε4/ε4 vs. ε3/ε4: pooled OR = 1.301 ; 95% CI, 1.077-1.571). Similar conclusions were drawn in the small artery disease (SAD) subtype, but not in large artery atherosclerosis (LAA) or in cardioaortic embolism (CE), by subgroup analysis. Conclusions. These observations reveal that specific APOE ε4 mutation was significantly associated with the risk of IS in a dose-dependent manner, while APOE ε4 mutation was related to SAD subtype onset without a cumulative effect.

Rising studies indicate that the apolipoprotein E (APOE) gene is related to the susceptibility of ischemic stroke (IS). However, certain consensus is limited by the lack of a large sample size of researches. This meta-analysis was performed to explore the potential association between the APOE gene and IS.To identify relevant case control studies in English publications by October 2020, we searched PubMed, Embase, Web of Science, and the Cochrane Library. Pooled odds ratios (ORs) with fixed- or random-effect models and corresponding 95% confidence intervals (CIs) were calculated to analyze potential associations.A total of 55 researches from 32 countries containing 12207 IS cases and 27742 controls were included. The association between APOE geneThese observations reveal that specific APOE

Objective To explore dynamic changes of peripheral blood lymphocyte subsets in patients with acute ischemic stroke (AIS) and the relationship with stroke severity and long‐term outcomes. Methods A total of 96 consecutive patients with AIS and 28 age‐ and gender‐matched healthy controls were recruited. Peripheral blood samples were collected, and the percentages of lymphocyte subsets were analyzed by flow cytometry. The dynamic changes in lymphocyte subsets and their correlation with clinical parameters, such as National Institutes of Health Stroke Scale (NIHSS) scores at onset and modified Rankin scale (mRS) scores 3 months later, were evaluated. Results In our study, we observed a decrease in the percentages of T‐lymphocytes (T cells), helper/inducible T‐lymphocytes (Th cells) and suppressor/cytotoxic T‐lymphocytes (Ts cells) in AIS patients as compared to controls. The frequencies of T cells and Ts cells on day 8–14 after stroke in NIHSS ≤4 group were significantly higher than those in NIHSS >4 group. The percentages of T cells and Th cells on day 1–3 after stroke in the mRS ≤2 group were higher than those in the mRS >2 group. Conclusion The frequencies of T cells, Th cells, and Ts cells in AIS are declined dramatically at least 14 days after stroke. Lower frequencies of T cells and Ts cells on day 8–14 after stroke represent more severe disease conditions, and the percentages of T cells and Th cells within 72 hr after stroke are negatively correlated with 3‐month outcomes, which might have a potential for predicting long‐term prognosis of stroke., In this work, we prospectively enrolled patients admitted within 14 days of ischemic stroke onset and investigated the temporal dynamic changes of peripheral blood lymphocyte subsets over different infarction time in relation to clinical severity and prognosis of stroke, aiming to identify the potential prognostic value in patients with AIS.

Proteasome inhibition has been observed in many neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Here, the effect of proteasome inhibition on the morphology of cultured rat cortical astrocytes was investigated. Increasing evidence suggests that the function of astrocytes is related closely to its morphology. Lactacystin, a specific inhibitor of the 20S proteasome, can induce astrocytes stellation in a dose dependent manner and reorganize the cytoskeleton of astrocytes. Furthermore, decreased levels of expression of Rho A, total Akt, and Phospho-Akt were found in the process of astrocytes stellation and lysophosphatidic acid, an activator of Rho A, can largely reverse the astrocytes stellation caused by lactacystin. This suggests that proteasome inhibition in astrocytes could stabilize signals of morphological changes that might be processed through Rho and Akt signaling cascade. Our results suggest that proteasome inhibition might function as a factor regulating astrocytes morphology in some pathophysiological conditions.

Rationale:Multiple cerebral gliomas (MCGs), usually classified into multifocal and multicentric subtypes, represent major diagnostic challenges as their clinical, radiologic, and pathohistological features are not uniform, often mimicking brain metastatic tumors or central nervous system inf

Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regulated in activated astrocytes around ischemic infarct. Furthermore, under ischemic conditions either in vitro or in vivo, Gal-1 was found to inhibit the proliferation of astrocytes in a dose-dependent manner, attenuate astrogliosis and down-regulate the astrogliosis associated expression of nitric oxide synthase and interleukin-1β after the ischemia. All these changes were blocked by lactose, suggesting a lectin dependent manner of Gal-1's function. Moreover, 7-day Gal-1 treatment reduced apoptosis of neurons, decreased brain infarction volume and improved neurological function induced by the ischemia. Together, these findings indicate that through reducing astrogliosis related damages, Gal-1 is a potential therapeutical target for attenuating neuronal damage and promoting recovery of brain ischemia.

Stroke and traumatic injury to the nerve system may trigger axonal destruction and the formation of scar tissue, cystic cavitations and physical gaps. Olfactory ensheathing cells (OECs) can secrete neurotrophic factors to promote neurite growth and thus act as a prime candidate for autologous transplantation. Biological scaffolds can provide a robust delivery vehicle to injured nerve tissue for neural cell transplantation strategies, owing to the porous three-dimensional structures (3D). So transplantation of the purposeful cells seeded scaffolds may be a promising method for nerve tissue repair. This study aimed to evaluate the compatibility of a novel collagen-heparan sulfate biological scaffold with olfactory ensheathing cells in vitro.Collagen-heparan sulfate (CHS) biological scaffolds were made, and then the scaffolds and OECs were co-cultured in vitro. The viability of OECs was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay at days 1, 3, 5 and 7. Statistical analysis was evaluated by student's t test. Significance was accepted at P0.05. OECs were labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE), and the CFSE-labeled OECs were seeded into CHS scaffolds. The attachment and growth of OECs in CHS scaffolds were observed and traced directly by fluorescent microscopy and environmental scanning electron microscope (ESEM).CHS biological scaffolds had steady porous 3D structures and no cytotoxicity to OECs (F = 0.14, P = 0.9330). CHS biological scaffolds were good bridging materials for OECs attachment and proliferation, and they promoted the axonal growth.The compatibility of CHS biological scaffolds with OECs is pretty good and CHS biological scaffold is a promising cell carrier for the implantation of OECs in nerve tissue bioengineering.

Increasing evidence indicates that proteasome inhibition occurs in multiple central nervous system (CNS) disorders, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Compared with the extensive studies on neurons, little attention is paid on the proteasome inhibition in astrocytes. Here, we demonstrated that lactacystin inhibited proteasome dose-dependently in cultured astrocytes. Simultaneously, lactacystin suppressed the expression of cell cycle proteins in astrocytes and caused the proliferating astrocytes arrested at G1/S checkpoint. Western blots showed that proteasome inhibition led to a decrease in cdk-2, cdk-4, cyclin D1 expression accompanied with an increase in p21waf1/cip1 expression. The effect of chronic low-level proteasome inhibition on astrocytes was consistent with that in acute proteasome inhibition. Furthermore, increased levels of interleukin-6 (IL-6) secretion, STAT-3 and phospho-STAT-3 expression were found, suggesting that proteasome inhibition in astrocytes could stabilize signals of grow arrest through the JAK/STAT signaling cascade.