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Objective:To investigate the relationship between cerebrovascular variation and the occurrence and recurrence of cerebral infarction, and provide a theoretical basis for the precise prevention and treatment of cerebral infarction.Methods:Totally 13 939 patients who underwent magnetic resonance imaging(MRI) and magnetic resonance angiography(MRA) examination at the Second Affiliated Hospital of Shandong First Medical University from January 2020 to December 2021 were grouped according to clinical symptoms combined with the imaging report, including 4 412 cases in the cerebral infarction group and 9 527 cases in the control group.2 048 patients in the cerebral infarction group were eventually enrolled in the study according to the inclusion and exclusion criteria, including 1 479 cases of initial cerebral infarction and 569 cases of recurrent cerebral infarction.SPSS 25.0 statistical software was used for data analysis.The χ2 test was used to compare the incidence of cerebral infarction with different cerebrovascular variations.Univariate analysis of suspected risk factors for recurrent cerebral infarction was performed with χ2 test, nonparametric test and t test.The binary logistic regression was used to analyze independent risk factors of recurrent cerebral infarction. Results:The incidence of cerebral infarction in the dual-system cerebrovascular variant patients, the single-system cerebrovascular variant patients, and the non-cerebrovascular variant patients were 40.9%, 30.7% and 31.8% respectively.The incidence of cerebral infarction in the dual-system cerebrovascular variant patients was the highest compared with those in the single-system cerebrovascular variant patients and the non-cerebrovascular variant patients (both P<0.05). The incidence rates of embryonic posterior cerebral artery, vertebral artery dominance, and bilateral common origin anterior cerebral arteries were 14.09%, 10.76% and 5.32%, respectively.The incidence of bilateral common origin anterior cerebral arteries in the cerebral infarction group was significantly higher than that in the control group and the difference was statistically significant.Patients with cerebral infarction who were familial aggregation ( OR=2.207, 95% CI=1.591-3.062), hyperhomocysteinemia ( OR=1.262, 95% CI=1.014-1.570), hypertension ( OR=1.461, 95% CI=1.114-1.918), diabetes mellitus ( OR=1.348, 95% CI=1.072-1.694), coronary heart disease ( OR=1.491, 95% CI=1.196-1.858) were more likely to recurrent cerebral infarction ( P<0.05), and patients with cerebral infarction had a significantly increased risk of recurrent cerebral infarction with age ( OR=1.031, 95% CI=1.020-1.042, P<0.05). Conclusion:Dual-system cerebrovascular variation and bilateral common origin anterior cerebral arteries are risk factors for cerebral infarction.
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Objective:To investigate the differential expression of cyclooxygenase (COX) gene between familial aggregated atherosclerotic large-artery atherosclerosis(LAA) cerebral infarction patients and sporadic LAA cerebral infarction patients.Methods:Twenty-five patients with familial aggregation LAA cerebral infarction (familial aggregation LAA group) and 25 sporadic LAA cerebral infarction patients (sporadic LAA group) were collected.Another 25 patients with non-cardiovascular and cerebrovascular diseases were selected as control group.Real-time quantitative PCR and ELISA were used to detect COX-1 and COX-2 protein in the supernatant of samples.Results:The expression level of COX-1 gene was 0.5436±0.2737, 0.2400±0.1656 and 0.8340±0.3799 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with control group, COX-1 gene expression in sporadic LAA cerebral infarction group and familial aggregation LAA cerebral infarction group was significantly down-regulated, the differences were significant( P<0.05). The expression level of COX-2 gene was 1.3672±0.8249, 1.3932±0.7158 and 0.7212±0.9623 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with the normal control group, the expression of COX-2 gene in familial aggregation LAA cerebral infarction group and sporadic LAA cerebral infarction group increased significantly( P<0.05). The expression of COX-1 protein was 2.9956±0.5672, 2.5572±1.0289 and 2.6721±0.7944 in the familial aggregation, sporadic cerebral infarction and control groups.The expression of COX-2 protein was 16.63±4.06, 16.86±7.93 and 15.94±5.94 in the familial aggregation, sporadic cerebral infarction and control groups.There was no significant difference in the relative expression of COX-1 and COX-2 proteins among familial aggregation LAA cerebral infarction group, sporadic LAA cerebral infarction group and control group(all P>0.05). Conclusion:There is significant difference in COX-1 gene expression between patients with familial LAA and sporadic LAA cerebral infarction.
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Objective To investigate the effect of miR-141 up-regulation through miR-141 mimic transfection on proliferation,apoptosis and cell cycle of hepatocellular carcinoma (HCC) cells.Methods Real-time polymerase chain reaction (qPCR) was employed to detect differential expression of miR-141 in normal hepatic epithelial cells (L02) and hepatocellular carcinoma cells (HepG2).Furthermore,miR-141 mimics were used to transfect into HepG2 to up-regulate the expression of niR-141 (experimental group).Blank group (CON) and negative control group (miR-NC) were used as control group.qPCR was used to detect expression of miR-141.CCK8 assay was used to detect the proliferation of HepG2 cells.Flow cytometry was used to detect the apoptosis and cell cycle of HepG2 cells.Results The results of qPCR showed that miR-141 was significantly down-regulated in HepG2 cells (0.64 ± 0.13) compared to L02 cells (1.00 ± 0.18),and the difference was significant (P ＜ 0.05).Relative expression of miR-141 was significantly increased after transfection (3.33 ± 0.66),compared to CON group (1.00 ± 0.17,P ＜ 0.05) and miR-NC group (1.08 ±0.14,P ＜0.05).CCK8 assay showed that the absorbance values of HepG2 of miR141 group at 48,72,96 h (0.67 ± 0.07,1.17 ± 0.05,1.36 ± 0.03) were all decreased significantly compared with those in CON group (0.81 ±0.02;1.42±0.03;1.73 ±0.05,all P＜0.05) and miR-NC group (0.78 ±0.01;1.38 ±0.02;1.69 ±0.01,all P ＜0.05).The results showed that miR-141 group [(11.81 ± 0.23)％] had significantly increased apoptosis rate compared to CON group [(4.18 ± 0.18) ％] and miR-NC group [(4.04 ± 0.08) ％],and the difference was statistically significant (P ＜ 0.05).miR-141 group had decreased percentage of S phase cells [(19.89 ± 2.78) ％] compared to CON group [(31.87 ± 1.00) ％,P ＜ 0.05] and miR-NC group [(30.49 ± 1.73) ％,P ＜ 0.05],while miR-141 group had significantly increased percentage of G1 phase cells [(74.74 ±2.03)％] compared to CON group (60.85 ± 1.69) ％ and miR-NC group (60.93 ± 1.95) ％,and the differences were all statistically significant (all P ＜ 0.05).Conclusions miR-141 was in low expression in HepG2 cells.Upregulation of miR-141 could specifically inhibit proliferation and promote apoptosis of HepG2 and change the distribution of cell cycle.
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Objective To evaluate the role of adiponectin (ADP) and adiponectin receptor-1(ADPR1) in limb ischemic precondi-tioning(LIPC) against apoptosis after myocardial ischemia-reperfusion injury(MIRI) .Methods SD rats were divided into 3 groups (n=10 ,4 rats of every group were prepared for detecting apoptosis ) .Group sham (group in sham operated) were processed identi-cally except the left coronary artery was not be ligated ;group MIRI (group in ischemia reperfusion) were subjected to occlusion of the left coronary artery anterior descending (LAD) followed by reperfusion ,occlusion for 30 min and reperfusion for 120 min;group LIPC (group in limb ischemic preconditioning) were subjected to ischemia and reperfusion on the left hind limb for 5 min in turn for 3 d .LAD were performed ischemia for 30 min and reperfusion for 120 min at the 4th day .The expression of the level of myocardial ADP and ADPR1 mRNA of group sham ,group MIRI and group LIPC were determined by reverse transcriptase polymerase chain reaction(RT-PCR) .The apoptosis index of every group were determined by mothod of terminal-deoxynucleoitidyl transferase medi-ated nick end labeling(TUNEL)respectively .Results Compared with group sham ,the expression of ADP and ADPR1 mRNA in group MIRI lessened apparently (P<0 .05);compared with group MIRI ,the expression of ADP and ADPR1 mRNA in group LIPC increased statistically significant(P<0 .05);compared with group sham ,the apoptosis index(AI) of myocardial cells in group MIRI increased apparently(P<0 .05);compared with group MIRI ,the AI of myocardial cells in group LIPC decreased significantly (P<0 .05) .Conclusion Limb ischemic preconditioning ;decreased apoptosis after myocardial ischemia-reperfusion injury via activating ADP signaling pathways ,which played a protective role in myocardial tissue .
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Glioma is the most frequent type of intracranial tumors,which is always associated with epilepsy.The type,location and pathological grade of glioma is closely related to incidence and efficacy of epilepsy.Recent re search shows that glioma and the factors around it may effect on the balance between excitation and inhibition system of brain.The detailed pathogenesis of epilepsy remains to be studied.
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The research and application of astrocytes have developed into a frontier of neuroscience in recent years.This review describes the shapes,regulation mechanism and function of astrocytes,and their relation to neurological diseases.Astrocytes play an important role in growth and reparation of the nervous system.
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Aim To observe the effect of sodium nitrop russide (SNP)on glial fibrillary acidic protein(GFAP) synthesis in the gerbil hippocampus. Method lmmunofluorescent histochemical staining method was used. Result SNP increased GFAP synthesis in rediatum layer,molecular layer and dentate gyrus.There were not GFAP positive cells in rediatum layer and mol ecular layer.Number of GFAP positive cells related to dose of SNP.Conclu sion SNP increased GFAP synthesis.
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The impairment of learning and memory function in the central nervous system(CNS)is one of the main features of aging and Alzheimer's disease(AD).Many experimental results have showed that long- term memory( LTM) is related to long- term potentiation( LTP) and long- term depression(LTD).They influence each other.The relationship between LTP and LTD is complex.Therefore,it is important to study the learning and memory mechanism from LTP、LTD and gene expression in the CNS.
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The purpose of the present work is to observe cGMP positive cells after cerebral ischemia-reperfusion in the gerbil hip-pocampus. Immunofluorescent methods were used in gerbil hippocampal tissue slices. The results showed that after cerebral is-chemia cGMP synthesis in the CAi-a subfields was increased, cGMP positive cells were distributed mainly in CA1 subfield. Mostof cGMP positive cells were astrocytes. The number of small round cGMP positive cells were increased after recirculation follow-ing ischemia in the dentate gyrus. These results indicate that after cerebral ischemia cGMP synthesis was increased in the CA1-asubfield, It is possible that astrocytes play an important role in the regulation of metabolism in the early stage after ischemia-reperfusion.
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The impairment of learning and memory function in the central nervous system(CNS)is one of the main features of aging and Alzheimer' s disease (AD). Many experimental results have showed that long- term memory(LTM) is related to long- term potentiation(LTP) and long- term depression (LTD). They intluenee each other. The relationship between LTP and LTD is complex. Therefore, it is important to study the learning and memory mechanism from LTP、LTD and gene expression in the CNS.
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This review describes the application of stem cells.Stem cells have proliferating and (multipotential) differentiation properties.Stem cells play an important role in the repair tissue and organs.
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AIM: To observe the effects of IBMX on cGMP production in gerbil hippocampus after recirculation following ischemia. METHODS: Bilateral occlusion of common carotid arteries and immunofluorescent staining methods in gerbil hippocampal tissue slice were used. RESULTS: Recirculation following ischemia caused a rise in hippocampus cGMP concentration. IBMX increased cGMP production. cGMP positive cells mainly distributed in rediatum layer and molecular layer in the CA_1 subfield. CONCLUSION: IBMX increased cGMP production in gerbil hippocampus after recirculation following ischemia.
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OBJECTIVE：To observe effect of L-NAME on apoptosis in the gerbil hippocampus after recirculation following ischemia.METHOD：Bilateral occlusion of common carotid arteries and TUNEL stain methods in gerbitil hippocampal tissue slice were used.RESULTS：L-NAME inhibited apoptosis in the CA1 subfield.CONCLUSION:Endogenous NO mediated apoptosis is inhibited by the L-NAME.
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AIM To observe the effects of L NNA on glial fibrillary acidic protein (GFAP) production in the gerbil hippocampus after recirculation following ischemia. METHODS Both vessels occlusion and immunofluorescent methods in gerbil hippocampal tissue slices incubated in vitro were used. RESULTS Recirculation following ischemia led to a rise on GFAP concentration in the hippocampus. GFAP positive cells mainly distributed in rediatum layer and molecullar layer in the hippocampus, L NNA decreased GFAP synthesis. CONCLUSION L NNA is a strong inhibitor of nitric oxide synthase(NOS). It is possible that the role of endogenous NO mediated GFAP synthesis is inhibited by L NNA.
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AIM To observe effects of IBMX on cGMP and GFAP production in gerbil hippocampus after recirculation following ischemia. METHODS Bilateral occlusion of common carotid arteries and immunofluorescent stain methods in gerbil hippocampal tissue slice were used. RESULTS Recirculation following ischemia leads to a rise in hippocampus cGMP and GFAP concentration. cGMP and GFAP positive cells mainly distributed in rediatum layer and molecular layer in the CA 1 subfield, Most of cGMP positive cells are astrocytes under double immunofluorescent stain. Most of cGMP strong positive cells are also those of GFAP strong positive cells. IBMX increased cGMP and GFAP production. CONCLUSION cGMP is possible to play an important role in the activation or regulation of GFAP in the hippocampus.
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AIM:To observe the relation between astroglial activation state and ischemic tolerance in the gerbil hippocampus. METHOD: Bilateral occlusion of common carotid arteries and immunofluorescent methods in the gerbil hippocampal tissue. Slices were used. The morphological changes of the neurons were observed by light microscopy.RESULTS:Pretreatment with 2 minute bilateral carotid artery occlusion produced protective effects of CA 1 neurons. Glial fibrillary acidic protein (GFAP) staining showed weak positive cells in control group. Most of GFAP positive cells showed weak and middle positive cells after recirculation 1d and 2d following ischemic 3.5 min and preconditioning of the brain with sublethal ischemia respectively.CONCLUSION:Astroglial played an important role in cerebral ischemia. It is possible that state of astroglial activation related to neuronal survival in ischemic tolerance.
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Neuralstemcells (NSCs)maintainthepotentialofproliferationanddifferentiationin nervesystem .TheresearchandapplicationofNSCshavedevelopedintoafrontierofneuroscienceinrecent years .Thisreviewdescribesthespecificity ,contribution ,regulationmechanismandapplicationofNSCs . Neuralstemcellsplayanimportantroleinthenervoussystemofgrowthandreparation . [