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Objective To investigate the association of lipid accumulation product (LAP) and visceral fat index (VAI) with nonalcoholic fatty liver disease (NAFLD) and the value of LAP and VAI in predicting the risk of NAFLD. Methods A total of 708 subjects who underwent physical examination in China-Japan Friendship Hospital from September 2018 to May 2019 were enrolled and divided into NAFLD group ( n =426) and non-NAFLD group ( n =282), and the two groups were compared in terms of LAP, VAI, and related biochemical parameters. The independent samples t -test was used for comparison of normally distributed continuous data between groups, and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between groups.The chi-square test was used for comparison of categorical data between groups. The Spearman test was used for correlation analysis. The subjects were divided into L1-L4 groups based on LAP and V1-V4 groups based on VAI, and the distribution of NAFLD was compared between groups; a logistic regression analysis was used to calculate the risk of NAFLD at different levels of LAP and VAI, and the receiver operating characteristic (ROC) curves were plotted for LAP, VAI, waist circumference (WC), and body mass index (BMI) in predicting NAFLD in different sex and body weight subgroups, so as to evaluate the value of each index in the prediction and diagnosis of NAFLD. Results Compared with the non-NAFLD group, the NAFLD group had significantly higher age, proportion of male subjects, proportion of subjects with a smoking history, and levels of LAP, VAI, WC, BMI, systolic blood pressure, diastolic blood pressure, alanine aminotransferase, aspartate aminotransferase, total cholesterol, triglyceride, low-density lipoprotein cholesterol, fasting blood glucose, and serum uric acid, as well as a significantly lower level of high-density lipoprotein cholesterol (all P 0.7 in predicting the onset of NAFLD in different sex and body weight subgroups; the AUCs of LAP and VAI in the female subgroup were significantly higher than those in the male subgroup (LAP: 0.886 vs 0.785, P < 0.05; VAI: 0.824 vs 0.748, P < 0.05), and the corresponding sensitivities and specificities of LAP and VAI in the female subgroup were also higher than those in the male subgroup (sensitivity: LAP: 79.8% vs 63.7%; VAI: 77.9% vs 77.0%; specificity: LAP: 85.0% vs 81.1%; VAI: 77.6% vs 62.3%). Conclusion The risk of NAFLD increases with the increase in the levels of LAP and VAI. Both LAP and VAI have a good value in predicting NAFLD in different sex and body weight subgroups, especially in predicting NAFLD in the female population.
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Objective:To investigate the clinical, neuropsychological and regional cerebral blood flow (rCBF) characteristics in patients with psychiatric symptoms caused by nitrous oxide abuse.Methods:Twelve patients with psychiatric symptoms caused by nitrous oxide abuse were enrolled from February 2018 to February 2020 in the Department of Neurology, China-Japan Friendship Hospital and the First Hospital of Tsinghua University.All patients were scored with the brief psychiatric rating scale (BPRS), Hamilton depression scale (HAMD), Hamilton anxiety scale (HAMA), mini-mental state examination (MMSE) and Montreal cognitive assessment (MoCA). The SPECT/CT images were collected with low-energy and high-resolution collimator.After the pictures were reconstructed, 18 brain regions were automatically sketched and calculated by Database Comparison software.The statistical value of the difference between the general mean value of each brain region and that of the corresponding region of interest in the same age group was estimated.Results:(1)The clinical manifestations of 12 patients were anxiety, depression, hallucination, delusion, and 7 patients were accompanied by cognitive decline.(2)Neuropsychological examination: BPRS score was 57.83±11.15 (anxiety depression factor was 3.94±0.47; lacking active factor was 3.25±0.85; thinking disturbance factor was 3.21±1.27; activity factor was 2.28±0.56; hostility factor was 3.14±1.24). The score of self-knowledge impairment was 2.92±1.08, the score of inability to work was 4.50±1.17, the score of HAMD was 32.75±10.13, the score of HAMA was 18.67±5.80, the score of MMSE was 27.67±2.50, and the score of MoCA was 24.58±3.78.(3)SPECT showed that compared with the general mean value of the corresponding regions of interest of normal people, the patients showed hypoperfusion in the frontal lobe (7 patients, 58.30%) and the temporal lobe (8 patients, 66.70%).Conclusion:Nitrous oxide abuse has an obvious effect on rCBF.The psychiatric symptoms include anxiety, depression, hallucination, delusion and so on, which affect the ability to work and learn.SPECT has important value in the diagnosis of nitrous oxide abuse, and indicates changes in local brain functional activity.
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Objective To analyze the clinical manifestation,imaging data and genetics mutation variants of late onset familial Alzheimer's disease concomitant with a novel mutation of presenilin 1.Methods The clinical manifestations and auxiliary examination recordings of the pedigree were analyzed.DNA was extracted from peripheral blood samples of the proband and her sons.Mutational analysis was performed by the next-generation sequencing technology and the mutation event was confirmed by Sanger sequencing technology.Results Two patients of the family presenting as Alzheimer's dementia were late onset.MRI of the proband showed extensive cerebral microbleeds.The gene detection showed p.S289P mutation in the exon 8 of presenilin 1 of the proband.Conclusion Mutation of p.S289P in the presenilin 1 gene may contribute to late onset Alzheimer's disease accompanied by amyloid angiopathy.
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Objective To investigate the protective effects of isopimaric acid ( ISO), the BKCa channel activator, on cognitive function and synaptic plasticity in APP/PS1 mice. Methods Alzet osmotic pump was loaded with ISO or DMSO only and assembled with ALZET Brain Infusion Kit III. The cannula was implanted into the lateral ventricle of 4-month-old male APP/PS1 mice or matched wild type ( WT) mice. Two weeks later, open field test and Morris water maze were conducted. Paired-pulse facilitation ( PPF) and TBS-induced long-term potentiation ( LTP ) were recorded in CA1 region of hippocampus. Results The open field test showed that there was no significant difference among the four groups in spontaneous activities and vertical plane movement distance within 30 minutes. Floor plane movement distance was significantly greater in APP/PS1+DMSO group than that in WT+DMSO group(P<0.05) . Compared with the WT+DMSO group, APP/PS1+DMSO group had significantly longer escape latency from the third to fifth day and lower percentage of time spent in the target quadrant ((43.27±3.24)% vs (34.19±2.56)%) and the number of crossing through the platform ((4.25±0.66)times vs (1.93±0.33)times)(P<0.05). Compared with the APP/PS1+DMSO group, the APP/PS1+ISO group had significantly shorter escape latency from the fourth to fifth day and higher percentage of time spent in the target quadrant ((46.16±3.51)%) and the number of crossing through the platform ((3.41±0.34) times) (P<0.05). PPF in APP/PS1+DMSO group significantly reduced compared with that in WT+DMSO group at 30-50ms interstimulus interval(P<0.05). PPF in APP/PS1+ISO group((224.50±13.79)%) was significantly augment compared with APP/PS1+DMSO ((174.99 ±6.68)%) group at 40 ms interstimulus interval (P<0.05). The LTP at 60 min post-TBS was significantly smaller in the APP/PS1+DMSO group ((135.19±1.32)%) than that in the WT+DMSO group ((172.17± 4.15)%)(P<0.001). The LTP of the APP/PS1+ISO group((160.48±1.19)%) became significantly in-creased compared with that in the APP/PS1+DMSO group(P<0.001).Conclusion BKCa channel activator ISO improve the learning and memory function of APP/PS1 mice by promoting PPF and increasing LTP to recover synaptic plasticity in the hippocampus.
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Objective To investigate the early onset of learning and memory function of 4-month-old APP/PS1/Tau Alzheimer' s disease (3×Tg-AD) model mice and explore the pathogenesis of AD in early stage through evaluating neuron excitability and BKCa channel activity in cingulate cortex pyramidal cells.Methods Ten 4-month-old male 3×Tg-AD mice and matched ten wild type (WT) mice.Behavior was tested with the novel object recognition task to observe the ability of learning and memory.Whole-cell patch-clamp recordings were performed to assess the excitability of cingulate cortex pyramidal cells in terms of resting membrane potential and frequencies of spikes evoked by current injection.A train of five pulses of depolarizing currents were injected at 100 Hz to assess the spike width,which was used as an index for BKCa channel activity.Results Compared with the WT group (0.72±0.03),the novel object recognition index significantly decreased in 3 × Tg-AD group (0.55 ± 0.04) (P =0.004).Compared to the WT group((-66.03±0.43) mV),the resting membrane potential in cingulate cortex neurons of 3×Tg-AD group((-62.31±0.54)mV) was significantly depolarized(P=0.000).In contrast to WT group,the action potential firing frequencies evoked by depolarizing current injections were higher in neurons from 3×Tg-AD group(P=0.000),demonstrating that excitability of cingulate cortex neurons was elevated by intracellular Aβ.Spikes were broader in the 3×Tg-AD group than those in the WT group(P＜0.01).Suppression of BKCa channels in cingulate cortex neurons from the 3×Tg-AD group was confirmed on the basis of the spike half-width,since BKCa channels affect the descending phase of spikes.Conclusion Compared to WT mice,4-month-old 3×Tg-AD mice are impaired in learning and memory.The suppression of BKCa channels by intracellular Aβ leads to increase of excitability in cingulate cortex pyramidal cells.
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Objective To investigate the effect of curcumin on the expression of heat shock protein 70 (HSP70) in the hippocampus and spatial learning ability in APPswe/PS1△9 transgenic mice,and provide a new theoretical basis for the treatment of Alzheimer' s disease (AD).Methods Mice were divided into wild-type (WT) group,APP/PS1 transgenic group,curcumin-treated group,quercetin combined with curcumin-treated group.The 5-month-old mice in curcumin-treated group received 150 mg · kg-1 · d-1 curcumin by intraperitoneal injection for four consecutive weeks.In addition to curcumin,the mice in quercetin combined with curcumin-treated group also received quercetin 50 mg· kg-1 · d-1 intraperitoneally for four consecutive weeks.The expression of HSP70 in the hippocampus of APP/PS1 mice was detected by Western blot.Learning and memory ability of APP/ PS1 mice were measured by Morris water maze test.The latency of finding the platforms and the number of crossing the platforms were observed.Results The results of Western blot analyses showed that the expression of HSP70 in the hippocampus of APP/PS1 transgenic mice decreased significantly compared with that of WT mice (OD:APPswe/PS1△9:0.31±0.14;WT:1.14±0.51;P＜0.01).The expression of HSP70 in curcumin-treated group significantly increased compared with that of APP/PS1 transgenic group (OD:0.91±0.20 in curcumin-treated group;P＜0.05).The results of water maze test showed that compared with WT group,in APP/PS1 group,the latency of finding the platforms was significantly longer (APPswe/PS 1 △9:(82.3 ± 6.8) s;WT:(19.5±4.4) s),and the number of crossing tbe platforms were significantly decreased (APPswe/PS1 △9:(2.7± 1.1);WT:(5.2± 2.1)).In curcumin-treated group,the latency of finding the platform ((47.7±7.6) s) was significantly shorter and the number of crossing platform ((4.5±1.9) s) was more than those in APP/ PS1 group.However,in quercetin combined with curcumin-treated group,the latency of finding the platform was significantly longer ((69.7±9.1) s) and the number of crossing platform (3.2±1.6) was decreased compared with those in curcumin-treated group.Conclusion Curcumin can promote the expression of HSP70 in the hippocampus of APP/PS1 transgenic mice,thus improve spatial learning ability of APP/PS1 transgenic mice.These results provide evidences that curcumin may have potential therapeutic value for the treatment of AD.
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Objective Toinvestigatetheoperativeeffectandsafetyofendovascularstentingfor thetreatmentofsymptomaticvertebralarteryostialstenosis.Methods Fortypatientswithsymptomatic vertebral artery ostial stenosis and stenosis rate ≥70% were admitted to the Department of Neurology, China-Japan Friendship Hospital from November 2010 to January 2013 were enrolled retrospectively. All patients received endovascular stenting therapy,15 of them were implanted bare metal stents,and 25 were implanted drug eluting stents. The technical successful rate of operation,perioperation complications,and symptom remission rate of the patients were analyzed. At the same time,stroke and death incident as well as the related ischemic symptoms of the stent vascular feeding area in the follow-up period (13 to 36 months)wereobservedandtherestenosisratewasdocumented.Results Atotalof42stentswereimplanted in 40 patients,and the technical success rate was 100. 0%. The preoperative stenosis rate of vertebral artery ostial stenosis was 75% to 99%(mean 85 ± 7%);the postoperative stenosis rate was 0% to 20%(mean 6 ± 4%). There was no perioperative complication. The clinical symptoms of 19 patients disappeared completely,16 were improved significantly within the follow-up period,and the symptom remission rate was 87. 5%. No stent vascular feeding area related stroke and death occurred. Four patients had transient ischemic attack in posterior circulation,13 had restenosis after procedure (10 of them with bare mental stents and 3 with drug eluting stents). There was significant difference in restenosis rate between the bare mental stents andthedrugelutingstents(10/15vs3/25,P=0.001).Conclusion Endovascularstentingforthe treatment of the severe symptomatic vertebral artery ostial stenosis is a safe and efficient method. Although its restenosis rate is high,but it can improve the symptom of posterior circulation ischemia effectively.
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Objective To explore effects of atorvastatin on the expressions of cyclooxygenase-2(COX-2) and membrane-associated prostaglandin E2 synthase-1 (mPGES-1) in the carotid atherosclerotic plaques of rabbits.Methods Totally 33 male New Zealand white rabbits(≥ 36months of age ) were assigned into normal control group (n=8) and animal model group with carotid atherosclerotic stenosis (n =25).The rabbit models were randomly divided into non-intervention group,celecoxib treatment group (15 mg · kg-1 · d-1,twice daily) and atorvastatin treatment group (5 mg · kg-1 · d-1,once daily) (n=8 each).Four weeks after treatment,the mRNA and protein expressions of COX-2 and mPGES-1 in carotid plaques were determined by RT-PCR and Western blot,respectively.Results The mRNA expressions of COX-2 (0.97±0.09,0.44±0.05,0.60±0.04vs.0.23±0.04,F=66.77,P＜0.01) and mPGES-1 (0.92±0.07,0.41±0.04,0.61±0.03 vs.0.17±0.03,F=54.87,P＜0.01)in carotid atherosclerotic plaques were significantly higher in non intervention group,celecoxib treatment group and atorvastatin treatment group than in normal control group.The mRNA expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group ( both P ＜ 0.01 ).The protein expressions of COX-2 (0.89±0.06,0.42±0.07,0.62±0.04 vs.0.18±0.05,F=61.75,P ＜0.01) and mPGES-1(0.91±0.05,0.44±0.05,0.63±0.05 vs.0.21±0.04,F=86.44,P＜0.01)in carotid atherosclerotic plaques in non-intervention group,celecoxib treatment group and atorvastatin treatment group were increased as compared with those in normal control group.The mRNA and protein expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group(all P＜0.01 ).The expressions of COX-2 and mPGES-1 in carotid atherosclerotic plaques were reduced in celecoxib treatment group as compared with atorvastatin treatment group (P ＜ 0.01).Conclusions As COX-2 inhibitor celecoxib,atorvastatin may inhibit the expressions of COX-2 and mPGES-1,and interfere with the inflammatory response which plays key role in the pathological progress of carotid atherosclerotic plaques,and thus slow the progress of carotid atherosclerosis.
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ObjectiveTo investigate the mechanisms and the effects of magnesium Valproate on the expressions of the kinin B1 and B2 receptors in the hippocampus of the juvenile rats submitted to pilocarpine model of epilepsy.Methods 35 healthy Wistar juvenile rats were randomly divided into six groups,that is the model groups:Ⅰ group,Ⅱ group,Ⅲ group,and intraperitoneal injection of saline water control groups:Ⅰ a group,Ⅱ a group,Ⅲ a group,after succession of 15 rats to kindle to establish the model of epilepsy by pilocarpine.To collect hippocampus tissue after the rats were to put to death,and to compared the expression levels of kinin B1 and B2 receptor mRNA by RT-PCR and western blot in the hippocampus of rats.ResultsBy treated with magnesium valproate,kinin B1 receptor mRNA (0.38 ± 0.051 ) and protein expressions(0.58 ± 0.057 ) decreased and kinin B2 receptor mRNA (0.48 ±0.056 ) and protein expressions(0.48 ± 0.044 ) increased in Ⅰ group,compared with that (0.76 ±0.068,0.89 ± 0.034;0.28 ± 0.034,0.32 ± 0.039 ) of Ⅰ a group(P ＜ 0.05 ).Compared with control group,there were more significant upregulation of kinin B1 receptor mRNA and protein expressions (P＜0.05) in the Ⅰ and the Ⅱ groups and there were no alteration in Ⅲ group.The expressional levels of B2 receptor mRNA and protein were upregulated in the Ⅰ,Ⅱ and Ⅲ groups.ConclusionThe kinin B1 and B2 receptor may play a role in the onset and maintenance of epilepsy.The magnesium valproate increased the expressional levels of kinin B2 receptor,and decreased the expressional levels of kinin B1 receptor.
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Objective To study the effects of peroxisome prolifterator-activated receptor gamma (PPARγ) agonist on the expression of ICAM-1 mRNA in the ischemia-reperfusion brain tissues. Methods Adult male SD rats were randomly divided into: sham-operation + normal saline group (NS,n = 6 ), ischemia-reperfusion tion. The expression of ICAM-1mRNA was measured by RT-PCR at 24 h after ischemia. Results The expression of ICAM-1 mRNA of the low-dose PGZ group (0.571±0.032) and the high-dose PGZ group (0. 396±0.024)were significantly reduced compared with that of the I/R + NS group (0.847±0. 028 ) (P<0.05).Conclusion PPARγ agonists can downregulate the the expression of ICAM-1mRNA in the ischemia brain tissue.
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Intravenous thrombolysis is the only treatment that has the evidence of evidence-based medicine in acute ischemic stroke. However, the narrow time window has limited the treatment opportunities of many patients. Transcranial ultrasound thrombolysis is a very promising thrombolysis-assisted method, and transcranial ultrasound plus microbubble-assisted thrombolysis is the research hotspot in recent years. At present, more suitable ultrasonic instruments for thrombolysis and a number of ways of ultrasound-assisted thrombolysis are being developed.
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BACKGROUND: Alginic sodium diester (ASD) possesses neuroprotective function because of its selective calcium antagonist effects.OBJECTIVE: To compare the influences of ASD on intraneuronal Ca2+content and nerve cell apoptosis before and after reperfusion in focal cerebral ischemic rats.DESIGN: Randomized controlled observation.SETTING: Neurological Department of Xiangya Hospital Affiliated to South China University; Laser Orthopedic Surgery of the First Hospital Affiliated to Southern China University.MATERIALS: This experiment was carried out between November 2003and April 2004 at the Neurological Department of Xiangya Hospital Affiliated to South China University. A total of 65 male SD rats were recruited and randomized into 6 groups; 17 got lost during the experiment, and the other 48 rats completed the experiment with 8 rats in each group.METHODS: In sham operation group, an incision was made on rats' cervical skin and sutured. Right cerebral middle artery was occluded in rats of ischemic group, ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group, and ASD 10 mg/kg postischemic group. After that, rats in all but ischemic group were subjected to intraperitoneal injection of various dosage of ASD or excipient 30minutes before reperfusion and 5 hours after reperfusion. FCM was used to determine intraneuronal Ca2+ content and rate of nerve cell apoptosis;meanwhile, neurological dysfunction was scored.MAIN OUTCOME MEASURES: [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia. [2]Correlation of behavioral obstacle score with intraneuronal Ca2+ fluorescence intensity and neuronal apoptosis in rats with right cerebral middle artery ischemia.RESULTS: Totally 65 rats were enrolled in this study, 17 of which got lost and the other 48 rats entered the result analysis. [1] Influence of ASD on the score for neurological dysfunction, intraneuronal Ca2+ fluorescence intensity, and neuronal apoptosis in rats with right cerebral middle artery ischemia: The score was obviously reduced in ASD 5 mg/kg preischemic group, ASD 5 mg/kg postischemic group, ASD 10 mg/kg preischemic group and ASD 10 mg/kg postischemic group as compared with ischemic group (1.80±0.21, 2.20±0.23, 1.20±0.11, 2.00±0.22, 3.40±0.65); moreover,functional improvement was more obvious due to pre-reperfusional administration than post-reperfusional administration. Intraneuronal Ca2+ concentration was reduced after ASD administration at different degrees and lower than that of ischemic group. Decrement of intraneuronal Ca2+ concentration was found most obvious due to 10 mg/kg ASD administration 30 minutes before reperfusion, approximately reduced by 70%; moreover, neuronal apoptosis rate on the ischemic side was obviously suppressed by ASD administration, displaying time-dependent manner, with apoptotic suppression effect more obvious in pre-reperfusional group than in post-reperfusional group (5.68%, 10.03%; 4.00%, 9.91%). [2] Correlation of behavioral obstacle score of right cerebral middle artery ischemic rats with intraneuronal Ca2+ fluorescence intensity and membrane associated protein/propidium iodide apoptosis: Obvious positive correlation was found between behavioral obstacle score and intraneuronal Ca2+ fluorescence intensity and detection rate of membrane associated protein/propidium iodide apoptosis (r=0.51,0.62, P ＜ 0.05); intraneuronal Ca2+ fluorescence intensity was also positively correlated with the detection rate of membrane associated protein/propidium iodide apoptosis (r=0.84, P ＜ 0.05).CONCLUSION: [1] ASD can exert anti-apoptosis effect by suppressing the increment of intraneuronal Ca2+ concentration, thus having neuroprotective function and ultimately improving neurological dysfunction. [2] Its effect displays time-dependent manner, and neurological functional improvement is more obvious by pre-reperfusional administration than by post-operational administration.
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BACKGROUND: It is manifested in epidemiology and clinical observation that lipoprotein (a) is a new risk factor of cerebrovascular disease and is closely related to cerebral ischemic stroke.OBJECTIVE: To discuss the relationship between levels of high serum lipoprotein (a) and stroke.DESIGN: Case controlled analysis.SETTING: Neurological Institute of Xiangya Hospital of Central South University.METHODS: Totally 294 patients with stroke were selected from Neurological Department of Xiangya Hospital of Central So, uth University between September 1999 and March 2002. Of them, 159 cases were regarded as cerebral infarction group and other 135 cases as acute hypertensive cerebral hemorrhage group. In cerebral infarction group, 109 patients had atherosclerotic cerebral infarction and 50 patients had lacunar cerebral infarction, and 94patients with contimuous health examination were regarded as health examination group. Serum lipoprotein (a) in each group was assayed with "sandwich enzyme-linked immuno-sorbent assay". According to whether the value of lipid was normal or not, patients with atherosclerotic cerebral infarction and acute hypertensive cerebral hemorrhage were divided into two groups. Comparisons between the two groups were assayed with single sample t test, and multiple liner regression was used to assay whether sex, hypertension and value of lipid were related to the level of serum lipoprotein (a).MAIN OUTCOME MEASURES: ① Comparisons of serum lipoprotein (a)among atherosclerotic cerebral infarction group, lacunar cerebral infarction group, acute hypertensive cerebral hemorrhage group and health examination group. ② Correlated analysis between serum lipoprotein (a) and lipid.RESULTS: Among 294 patients, 94 cases in control group entered the final analysis. ① Comparisons of serum lipoprotein (a) among atherosclerotic cerebral infarction group, lacunar cerebral infarction group, acute hypertensive cerebral hemorrhage group and health examination group: Levels of serum lipoprotein (a) in atherosclerotic cerebral infarction group and cerebral hemorrhage group were higher than those in health control group (P ＜ 0.05), and concentration of lipoprotein (a) in atheroosclerotic cerebral infarction group was increased as compared with that in acute hypertensive cerebral hemorrhage group (P ＜ 0.05). Also, level of lipoprotein (a) in lacunar cerebral infarction group was a little higher than that in control group,but the difference was not significant (P ＞ 0.05). ② Correlated analysis between serum lipoprotein (a) and lipid: Levels of lipoprotein (a) in both normal lipid group and abnormal lipid group were assayed with single sample t test, and the results showed that levels in the two groups were similar (P ＞ 0.05). Multiple liner regression was used to assay whether sex,hypertension and value of lipid were related to level of serum lipoprotein (a).CONCLUSION: Levels of lipoprotein (a) may be an independent risk factor for cerebral hemorrhage and atherosclerotic cerebral infarction.
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Objective To study the effect of intervention on blood pressure and incidence of cerebrovascular diseases. Methods In 1987, two cohorts population were selected in urban areas of Changsha . One was intervention group , another was control group. Baseline blood pressure levels were investigated and the events of stroke were collected. Results After 14 years, the cumulative stroke events were 89 in the intervention group and 128 in the control group; the mean blood pressure increased with statistical significance in each group except diastolic pressure in intervention group, but the control group increased more significantly; the analysis of Kaplan-Meier displayed that the rate of non-stroke events were higher in intervention group than that in control group and the analysis of COX regression indicated that the risk for stroke-events were 1.4 times higher in control group. Conclusions The intervention of risk factors can delay the increase of blood pressure by aging and reduce the risk of stroke-events.