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.

Objective To study the level of CD4+ CD25+ Foxp3+ regulatory T cells in peripheral blood of non-small-cell lung cancer patients.Methods The ratio of CD4+ CD25+ Foxp3+ T cells inperipheral blood of lung cancer group and control group were determined by flow cytometry.Its clinic significance was analyzed,Results The ratio of CD4+ CD25+ Foxp3+ Treg cells [the ratio of CD4+ CD25+ T and CD4+ CD25+ Foxp3+ T cells were (14.42 ± 1.22) ％ and (5.34 ± 0.45) ％] inperipheral blood was higher in the non-small-cell lung cancer group than in control group [the ratio of CD4+ CD25+T and CD4+ CD25+Foxp3+ T cells were (10.67 ±0.98)％ and (3.98 ±0.68)％] (t =2.431,2.273,all P ＜ 0.05).It was also higher in adenocarcinoma [CD4+ CD25+ T/CD4+ T to (15.05 ± 0.92) ％,CD4+ CD25+ Foxp3+ T/CD4+ T to (5.99 ± 0.38) ％] than squamous carcinoma [CD4+ CD25+ T/CD4+ T to (13.03 ± 1.64) ％,CD4+ CD25+ Foxp3+ T/CD4+ T to (3.91 ± 0.62) ％] (t =2.264,2.109,all P ＜ 0.05),and stage IV higher than stage m (t =2.165,2.058,all P ＜ 0.05).Conclusion The level of CD4+ CD25+ Foxp3+ Treg cells in peripheral blood of non-small cell lung cancer was significantly higher than that of healthy subjects,related with the pathological type and clinical stage.The CD4+ CD25+ Foxp3+ Treg cells may participate in the occurrence and development of non-small cell lung cancer.

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.

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.

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.

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.

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.

Objective To observe the effect of WeChat -based health education on young patients with initial treatment of pulmonary tuberculosis(TB).Methods A total of 180 TB patients were randomly divided into control group and observation group,90 cases in each group.All patients received health education for six months under the guidance of specialist nurses and physicians,but WeChat-based health education for the observation group and telephone health education for control group.Patients of the two groups were evaluated with TB cognitive level and compliance at 6 months after discharge.Results The pulmonary tuberculosis knowledge level of the observer group was significantly higher than that of the control group (89.8%vs 73.3%),the difference was statistically significant (χ2 =11.07,P<0.01);And after 6 months of follow-up,in the observation group,the compliances of patients taking medicine on time(97.8%vs 80.0%,χ2 =15.59,P<0.01),reasonable diet(95.5%vs 81.1%,χ2 =23.24, P<0.01),moderate exercise(97.8%vs 83.4%,χ2 =36.51,P<0.01) and timely referral(96.7% vs 82.2%,χ2 =20.63,P<0.01) were higher than those in the control group,the differences were statistically significant (all P<0.01).Conclusion WeChat -based health education is effective for improving TB cognitive level and the compliance of the patients.Since WeChat has been widely used,WeChat-based health education can be promoted.

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.

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.