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Objective To investigate the relationship between maximum blood pressure and the prognosis after discharged from the hospital,among patients with ischemic stroke.Methods A cohort study was conducted which including 471 cases of ischemic stroke patients that were collected from February 2014 to December 2014 at the Second Affiliated Hospital of Harbin Medical University.Values of everyday blood pressure were measured on each patient at the first six days after admitted to the hospital.Maximum blood pressure value of the 6 days was taken as an indicator of the blood pressure levels.The ability on daily living was measured by the modified Rankin score (mRs).Data were analyzed by Chi-square test,t test and multivariate logistic regression analysis.Results Confounding factors would include age,gender,culture,physical activity,income,smoking,alcohol,hypertension,diabetes,coronary heart disease,stroke history,hospitalization mrs,lipid parameters,homocysteine and blood sugar and were adjusted.Results from multivariate logistic regression analysis showed that the maximum SBP was associated with adverse outcomes.Compared with 140-159 mmHg for SBP,OR(95％CI) was 2.51 (1.30-4.85) for 160-179 mmHg,OR (95％ CI) was 2.68 (1.27-5.65) for those pressure levels higher than 180 mmHg,after multiple factors were adjusted.Compared with 90-99 mmHg for DBP,OR(95％CI) was 1.92 (1.00-3.67) for 100-109 mmHg,OR (95％ CI) was 2.78 (1.35-5.69) for the ones higher than 110 mmHg.Conclusion Maximum blood pressure during hospitalization might be associated with adverse outcome of ischemic stroke patients.
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Objective To investigate the therapeutic potential of brain-derived neurotrophic factor (BDNF) and Schwann cells(SCs) in experimental autoimmune neuritis (EAN) and assess the effect and mechanism.Methods EAN model was established by immunization of Lewis rats with 400 μg of specific peptide P2(57-81)and complete Freund adjuvant.In the therapy group,the SCs (n =28) and the combination of BDNF administration and SCs (n =48) were labeled by the nuclear fluorescent dye injected into the intracerebroventricularly in 14 d after immunization.Transplanted cell migration tracking respectively were at 25,35 and 45 days after immunization.The rats were observed for signs of disease daily and subjected to clinical score,of which the sciatic nerves were subjected to histopathological examination (hematoxylin eosinstaining,luxol-fast-green and immunohistochemical staining).The inflammatory cell infiltration and demyelination were assessed,and the CD4,CD8,CD68,S-100 and nerve growth factor (NGF) positive cells numbers were compared among the 3 different groups.Results AIl the rats had the neurological deficits.Compared with control group,there were no significant differences in SCs therapy group.In SCs + BDNF therapy group,the recovery of paralytic symptom was faster and the score was lower after immunization 45 d.After immunization 25 and 35 days,both the inflammatory cells infiltration (EAN model group:325.8 ±10.8,221.4 ± 35.2;SCs + BDNF transplantation group:307.3 ±4.6,197.2 ± 16.8; t =2.172,P =0.031 ;t=3.756,P=0.000) and the expression of CD4+,CD8+ T cells and CD68+ macrophages were reduced.After immunization 35,45 days,the demyelination degree (EAN model group:3.4 ± 0.5,2.9 ± 0.8 ; SCs +BDNF transplantation group:2.9 ±0.8,2.3 ±0.5) was reduced (t =-7.408,P =0.000;t =-6.092,P =0.000),the expression of S-100 is higher,and NGF was lower than the control group in each time point after immunization.Conclusions SCs transplanted into the cerebellar ventricle of animals can migrate into the sciatic nerve.The combination of BDNF administration and SCs transplantation may represent an effective strategy by reducing inflammation reaction,improving the expression of S-100 in the donor cell,and reducing NGF irritability heighten in sciatic nerve.However,delivery of SCs alone is inefficiency to the treatment of EAN.
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We changed the form of literature reading from simple reading and translation to comprehensive lecture,analysis,discussion and exchange under the guidance of teachers in order to promote postgraduates' capability of learning professional English and to enhance their overall quality.The new form not only improves students' English proficiency but also enhances their overall quality,such as literature quality,teaching ability,competitive consciousness,psychological quality,etc.At the same time,it is also beneficial for teachers.
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Objective To investigate the correlation between neuronal injury and the expression of caspase-3 and caspase-activated deoxyribonuclease (CAD) after focal cerebral ischemia-reperfusion in rats, also to study the effect of caspase-3 particular inhibitor. Methods The focal cerebral ischemia model (occluding middle cerebral artery of the rats) was made by using modified inserting thread method and reperfusion after embolizing for one hour. Using HE staining, TUNEL staining and microscopy to observe the morphological changes of ischemic neurons at six different time points including 6,12,24,48 and 72 h, using immunohistochemistry to observe the changes of caspase-3 and CAD protein in two groups (model group and interfere group). Results There was no significant difference between the two groups using HE staining and microscopy. While there was difference of TUNEL staining positive cells in all time points, except 6 h time point; Both the two groups reached the expression peak of caspase-3 in 24 h, and the number was 2. 360± 0. 318 and 0. 804 ± 0. 206 respectively(t' = 10. 039, P < 0. 01), there was statistical significance from 12 h to 48 h between the two groups ; The expression peak time of CAD protein in two groups was 48 h, and the number was 3.061 ± 0. 567 and 0. 812 ± 0. 240 respectively (t' = 8. 960, P < 0. 01), there was statistical significance from 12 to 72 h between two groups. Conclusions Caspase-3-CAD-DNA degradation is one important way of neuronal injury in cerebral ischemia-reperfusion of rats, caspase-3 inhibitor can protect neuron in a certain degree.
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Bone marrow mesenchymal stem cells have received great attention in the studies of therapeutic methods of cerebral ischemia in recent years. This article reviews its research Status Quo and some unsolved problems.
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5-lipoxygenase-activating protein Gene (ALOX5AP) on chromosome 13q12-13 encodes 5-lipoxygenase-activating protein (FLAP). The latter plays a key role in regulating the synthesis of leukotriene. Studies have suggested that the subjects who carry this gene may increase stroke risk by two times. Therefore, ALOX5AP plays an important role in the pathogenesis of stroke.
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Interleukin-17 (IL-17) is a newly discovered proinflammatory cytokine in recent years. It has wide biological activities; therefore it may be one of the important factors in the occurrence and development of certain diseases. The article mainly reviews the current situation of the study on the related roles of IL-17 in nervous system diseases.
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BACKGROUND: Nuclear factor-kappa B (NF-κB) is an important transcription factor, which can promote the transcription of many target genes after activated.OBJECTIVE: To investigate the expressions of NF-κB in local cerebral ischemia-reperfusion and the influence of the pretreatment of the N-acetylcysteine.DESIGN: Randomized grouping experiment with animals as subjects.SETTING: Department of Neurology, the Second Clinical Medical College, Harbin Medical University.MATERIALS: The experiment was finished in the Animal Experimental Center and Laboratory of Pathology of Harbin Medical University. Ninetynine male healthy Wister rats were randomly divided into 3 groups: Sham-operated group(n=l 1), saline control group(n=44), N-acetylcysteine group(n=44).METHODS: Rat models of cerebral ischemia were made with the method of thread blocking improved by Longa et al in rats of the three groups. A nylon line with a smooth spherical captular end of 0.26 mm in diameter made by heating was inserted through the cut of crotch of the common carotid artery. The prepared line for common carotid artery was tied tightly and the arteriole clamp of internal carotid artery was unclamped. The nylon line entered the common carotid artery and the inserted length of the saline control group and the N-acetylcysteine group from the crotch of the internal and external carotid artery was calculated about (18.5±0.5)mm in order to obstruct the blood supply of the middle cerebral artery. The inserted depth in sham-operated group was less than 15 mm and the blood supply of the middle cerebral artery was kept normal. Intraperitoneal injection of N-acetylcysteine was given with 150 mg/kg at 30 minutes before ischemia in N-acetylcysteine group and injection of normal saline was given with equal volume at 30 minutes before ischemia in saline control group.Eleven rats each time in saline control group and N-acetylcysteine group were killed by cutting off heads at the time points of ischemia 6, 24 hours,and reperfusion 1 hour after ischemia 6, 24 hours. The express of NF-κB of brain tissue was observed with immunchistochemical method. Percentage of cerebral infarction of rats in each group was determined by dyeing of tetrachloro red tetrazoline. Apoptosis of brain tissue cells was detected with terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL).MAIN OUTCOME MESURES: Percentage of cerebral infart volume of rats in each group, the activity of combination of the NF-κB and apoptosis of cells.RESULTS: Ninety-nine animals attended the experiment, all of them entered the final analysis. ① Percentages of infarct volume at 1 hour of ischemia and 6, 24 hours of reperfusion in N-acetylcysteine group were (8.39±2.54)%, (24.54±6.02)% respectively, and that of corresponding saline control group were (15.50±4.18)%,(32.22±3.99)%. The focus of infartion with ischemia for 24 hours in each group was increased as compared with that for 6 hours and the infarct volume in group with N-acetylcysteine was obviously decreased as compared with that in saline control group (P ＜ 0.01). ② NF-κB p56 transfered from the kytoplasm to the nucelus after the ischemia and reperfusion. The rates of p56 masculine cells in N-acetylcysteine group of ischemia for 6 and 24 hours were (0.462±0.022)%, (0.452±0.015)% respectively, the express of which was decreased as compared with that in saline control group [(0.563±0.028 )%,(0.554±0.013)%] (P ＜ 0.01 ). ③ Cells of apoptosis pretreated with N-acetylcysteine were obviously decreased as compared with that pretreated with normal saline.CONCLUSION: Focal cerebral ischemia and reperfusion can activate NF-κB p65, which participate in the damage of cerebral ischemia and reperfusion. NF-κB can inhibit the express of p65, and relieve the nerve injury and so have the effct of protection for brain.
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BACKGROUND: Some studies suggest that pre-injection of tumor necrosis factor-α (TNF-α)can protect focal cerebral ischemia in mice. Cerebral ischemia tolerance is related to the increase of TNF-α level; on the other hand, TNF-α is an injurious cytokine associated with stroke. Circulating antibody against anti-TNF-α can protect reperfused injury.OBJECTIVE: To study the effects of TNF-α pretreatment and post-treatment on cerebral ischemia-reperfusion injury and explore possible mechanism.DESIGN: Randomized controlled study.SETTING: Neurological Department, the Second Hospital Affiliated to Harbin Medical University.MATERIALS: The experiment was conducted at the Animal Experiment Center of Harbin Medical University from January to April 2002. Totally 120 healthy adult male Wistar rats were randomly divided into the following 8 groups: TNF-α 0.05 μg, 0.5 μg and 1.0 μg pretreatment groups and PBS group, TNF-α 0.05 μg, 0.5 μg and 1.0 μg post-treatment groups and PBS group with 15 in each group.METHODS: The focal brain ischemia model of middle cerebral artery occlusion (MCAO) was made using inserting thread method. TNF-α of different doses (0.05 μg, 0.5 μg or 1.0 μg) or PBS was injected intracisternally and 22-hour reperfusion, 8 rats from each group were killed. Then the perhour reperfusion, 7 rats from each group were killed. Then pathological changes were observed, glial fibrillary acidic protein (GFAP) and intercellular adhesion molecule-1 (ICAM-1) expression were inspected by immunohistochemical method. Histopathological and immunohistochemical evaluation was made with the computer-assisted image analyzing system,and the number of GFAP positive cells and ICAM-1 positive vessels in each hemisphere was counted.riliary acidic protein and ICAM-1.infarct volume: TNF-α 0.5 μg and TNF-α 1.0 μg pretreatment groups showed reduced volume of lesion; infarct volume reduced by 70.9% in TNF-α 0.5 μg pretreatment rats and 66.5% in TNF-α 1.0 μg pretreatment rats. TNF-α 0.5 μg and TNF-α 1.0 μg post-treatment groups showed increased volume of lesion; infarct volume increased by 22.3% in TNF-α 0.5 μg post-treatment rats and 46.7% in TNF-α 1.0 μg post-treatment rats.TNF-α 0.05 μg and 1.0 μg pretreatment groups did not differ significantly (P ＞ 0.05), but there was an obvious difference between TNF-α 0.5 μg and pared with PBS pretreatment group, TNF-α 0.5 μg and 1.0 μg pretreatment groups showed lessened tissue damage and edema. Compared with PBS post-treatment group, TNF-α 0.5 μg and TNF-α 1.0 μg post-treatment fibriliary acidic protein and ICAM-1: TNF-α 0.5 μg and TNF-α 1.0 μg pretreatment groups showed reduced volume of glial fibriliary acidic protein and ICAM-1 (P ＜ 0.05); but TNF-α 0.5 μg and TNF-α 1.0 μg posttreatment groups showed increased volume of glial fibriliary acidic protein and ICAM-1 (P ＜ 0.05). TNF-α 0.05 μg and 1.0 μg pretreatment groups did not differ significantly (P ＞ 0.05); but there was an obvious difference between TNF-α 0.5 μg and 1.0 μg post-treatment groups (P ＜ 0.05).cerebral ischemia reperfusion injury. This effect is not related to the repair given after cerebral ischemia reperfusion, ischemia exacerbates, which is α are determined by whether TNF-αis given before or after cerebral ischemia in a dose-dependent manner.
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Objective To investigate the expression of nuclear factor kappa B (NF-?B ) in focal cerebral ischemia and reperfusion and effects of N-acetylcysteine (NAC) pretreatment.Methods The focal cerebral ischemia and reperfusion model was made by suture occlusion of right middle cerebral artery. The rats were randomly assigned to nine groups: sham operated group, 6 hours and 24 hours ischemia groups, 6 hours and 24 hours reperfusion groups, corresponding NAC treatment groups. NAC groups’ rats were treated with NAC (150 mg/kg) prior to occlusion. NF-?B p65 were detected by immunohistochemistry. Brain was stained with 1% triphenyltetrazolium chloride for assessment of the volume of infarction. Apoptosis was detected by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL).Results The translocation of NF-?B from cytoplasm to nucleus increased significantly after ischemia and reperfusion. The expression of NF-?B p65 decreased in NAC pretreatment groups, which were respectively (0.462% ? 0.022%) in 6 hours ischemia-reperfusion groups, (0.452% ? 0.015%) in 24 hours ischemia-reperfusion groups, as compared with saline control groups which were (0.563% ? 0.028%) and (0.554% ? 0.013%) (P
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0.05) ;TNF-? 0.5 ?g and TNF-? 1.0 ?g pretreatment groups showed reduced volume of lesion(all P
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AIM: To study the effect of nasal mucosal tolerance to E-selectin on cerebral ischemia-reperfusion injury.METHODS: Two different doses(single and booster) of E-selectin or PBS were dropped into membrana mucosa nasi of rats.The middle cerebral artery occlusion(MCAO) model referring to Zea Longa method with modifications was performed 48 h after the last dose of E-selectin or PBS.After 2 h ischemia and 22 h reperfusion,the numbers of CD3+CD4+T-lymphocyte and CD3+CD8+T lymphocyte subgroup in the blood were examined with flow cytometry.Rats were killed,then part of the animals was used to measure the cerebral infarction volume by TTC staining.mRNA expressions of E-selectin,ICAM-1 and lymphocyte function-associated antigen-1(LFA-1) were determined by RT-PCR and activity of SOD was determined by xanthinoxidanse method in ischemic cortex of the other part of animals.RESULTS: The ratio of the numbers of CD3+CD4+T-lymphocytes and CD3+CD8+T-lymphocytes increased in E-selectin single pretreatment group(P