Objective To study the neuroprotective effects of adeno viral mediated glial cell line derived neurotrophic factor(GDNF) gene transfer in the treatment of Parkinson's disease. Methods Thirty five SD rats were divided into 3 groups which received perinigral injections of recombinant adenovirus encoding GDNF (Ad GDNF)/ LacZ(Ad LacZ) and PBS, respectively. One week later, intrastriatal injection of 6 hydroxydopamine (6 OHDA) was made to induce progressive degeneration of dopaminergic neurons. The neuroprotective effects of Ad GDNF were evaluated by apomorphine induced rotational behavior, immunohistochemical assay of the tyrosine hydroxylase(TH) positive neurons in the midbrain and measurement of monoamine level in the striatum. RT PCR and ELISA were performed to check the expression of the exogenous GDNF gene in the brain. Results Ad GDNF treated rats showed improved motor functions, better survival of TH positive cells in the lesioned substantia nigra (70% vs 30%) and higher DA levels in the lesioned striatum. The exogenous GDNF gene was efficiently expressed in the midbrain. GDNF protein level in the injection site reached 1 ng/10 mg wet tissue 5 weeks after the adenoviral vector delivery, being 16 20 times of that of the Ad LacZ delivery or PBS treated groups. Conclusions Adeno viral mediated GDNF gene intracerebral transfer significantly protected the dopaminergic neurons of nigrostriatal system from 6 OHDA induced injury and is valuable in the treatment of Parkinson's disease.

Prophylactic effect of magnesium sulfate on reperfusion-airhythmias was studied using a left anterior descending coronary artery occlusion followed by reperfusion in the isolated rat hearts. In the first part of the present work, we observed a bell-shaped relationship between the incidence of reperfusion-induced ventricular fibrillation (VF) and the duration of preceding ischemia. In the second part, the concentration of magnesium sulfate in perfusate was increased to 3.6, 4.8 and 6.0mmol/L, respectively, 1 min before coronary ligation, VF fell in a dose-dependent manner from its control total incidence of 100% to 82%, 73% and 18% (P

AIM: To investigate the role of proliferation and apoptosis in hypertensive left ventricular hypertrophy (LVH) and the effect of AT 1 blockade with losartan. METHODS: Left ventricles (LV) from 12, 24-week-old SHR (SHR 12 , SHR 24 ), 24-week-old SHR treated with losartan (15 mg?kg -1 ?d -1 , SHR-L 24 ) during 12 weeks, and age-matched WKY rats (WKY 12 , WKY 24 ) were studied. Expression of PCNA was examined by immunohistochemistry. Apoptotic cells in LV sections were assessed by TUNEL method. Levels of fas mRNA were quantitated by RT-PCR. RESULTS: Compared with age-matched WKY, SHR 12 and SHR 24 showed increased LV hypertrophied index (HI), increased apoptotic index (AI) of myocytes ( P

Objective To explore the role of long-term enriched environment in promoting the recovery of motor and social function in mice after ischemic brain injury. Methods Sixteen adult male ICR mice underwent permanent middle cerebral artery occlusion (MCAO). The first day after operation, they were divided into enriched environment group (n=8) and standard condition group (n=8). The mice were tested with modified Neurological Severity Score (mNSS), rotarod test and smart cage 7, 14, 21, 28 days after modeling. Results The score of mNSS and the result of rotarod test improved more in the enriched environment group than in the standard condition group 28 days after MCAO (t>2.927, P<0.05). The occupancy time in the middle of smart cage was longer in the enriched environment group than in the stan-dard condition group 7 to 28 days after MCAO (t>2.480, P<0.05) in the general move test. There was a trend of being more interested in strange mice in the enriched environment group than in the standard condition group, but the difference was not statistically significant (P>0.05) in the social behavior test; however, the occupancy time in the middle of smart cage was longer in the enriched environment group than in the standard condition group 14 to 28 days after MCAO (t>3.472, P<0.01), and the velocity of moving was higher 14 days after MCAO (P<0.05). Conclusion Enriched environment could promote the recovery of motor function, somehow of social function, in mice af-ter ischemic brain injury.

Aim To evaluate neuroprotective effects of stearic acid on primarily cultured hippocampal neurons and to study the mechanism of neuroprotection afforded by stearic acid.Methods Primarily cultured hippocampal neurons were insulted by OGD(oxygen-glucose deprivation),H_2O_2,glutamate and NaN_3;MTT assay was utilized to evaluate cell viability;Inhibitors of PPAR?and PI-3K signal pathway were used to study mechanisms of neuroprotection of stearic acid.Results Compared with control neurons,A_(570) in MTT assay were increased significantly by stearic acid in hippocampal neurons insulted by OGD(oxygen-glucose deprivation),H_2O_2 and glutamate(P

Objective To investigate the effects of the free radical scavenger,edaravone,on patients undergoing cardiac valve replacement under cardiopulmonary bypass (CPB). Methods Thirty patients,including 7 males and 23 females,at a mean age of 41.4?10.4 (23 to 63),undergoing mitral or/and aortic valve replacement (MVR or AVR) under CPB from March to December 2009 in our hospital were subjected,and then divided into 2 matched groups by means of random number table,study group (n=14) and control group (n=16).Inclusion criteria: patients received valve replacement surgery under CPB; aging from 20 to 65; heart function: class Ⅰto Ⅲ; liver,kidney and lung function properly; blood gas and electrolyte properly. Exclude criteria: preoperatively used scavenger and the like; there was a history of cerebrovascular or neuropsychiatric symptoms; had a history of myocardial infarction or other coronary artery disease. In the intervention group,0.5 mg/kg of edaravone was diluted to 20 ml and introduced into CPB unit at the beginning,while the same dose of saline water was given in control group in the same way. Blood samples were collected from radial artery at following 5 time points,the beginning of CPB (T0),the end of CPB (T1),30 min (T2),6 h (T3),and 24 h (T4) after CPB. After the blood samples of all cases were collected,the serum level of hematocrit (HCT),malondialdehyde (MDA),inducible nitric oxide synthase (iNOS),cardiac troponin I (cTnI),creatine kinase-MB (CK-MB),myoglobin (Myo),S100 protein and neuron-specific enolase (NSE) was detected. Cardiac resuscitation and critically postoperative complications were observed. Results The level of HCT at T1-T3,cTnI at T4 was lower in study group than that in control (P

Objective To evaluate the therapeutic effect of small bone flap craniotomy decompression of posterior cranial fossa and duraplasty in the treatment of Chiari malformation type Ⅰ.Methods The clinical data of 45 Chiari malformation type Ⅰ patients who were treated with small bone flap craniotomy decompression of posterior cranial fossa and duraplasty were retrospectively analyzed,31 cases among them with syringomyelia.Results According to Tator etc.standard,1 month after surgery,the excellent in 30 cases,good in 15 cases.Follow up from 6 months to 6 years,the excellent in 37 cases,good in 8 cases.Among 31 patients with syringomyelia,26 cases were syringomyelia subsided,5 cases were not obvious change.Conclusion The small bone flap craniotomy decompression of posterior cranial fossa and duraplasty can make the craniocervical decompression,and has obvious effect of treating syringomyelia,is safe and effective in treatment of Chiari malformation type Ⅰ.

Objective: To investigate the effect of human vascular endothelial growth factor on restenosis after angioplasty. Methods: A rabbit model of injured carotid artery was established using percutaneous transluminal angioplasty. The pcDNA3/hVEGF165（500 μg,n=12） and pcDNA3 （500 μg,n=12） were separately transfected into injured arterial wall with 30 min incubation. The carotid artery was imaged by arotic angiography at the end of week 2 and week 4. Pathology analysis and Northern blot analysis were performed for harvested injured artery segment. Results: Arotic angiography showed carotid artery diameter narrowness were obviously lessened at week 2 and week 4 in experimental group than that in control group; H-E stains showed lumina narrow ratio were obviously reduced at week 2 and week 4 in experimental group than that in control group［（9.58±1.35）% vs (31.72±1.72)%；(18.09±2.93)% vs (44.05±3.28)%， P<0.01 ］; By Northern blot analysis, the expression of hVEGF165mRNA in experimental group were upregulated than in contol group. Conclusion: pcDNA3/hVEGF165 can be transfected into smooth muscle cell and continue to secret bioactivity protein at least for 4 weeks; it can accelerate reendothelialization and prevent restenosis.

Objective: To observe the effects of angina pector is on severe ventricular arrhythmia and QTd in patients with first acute myocard ial infarction(AMI). Methods: One hundred and eight-four cases of first AMI were divided into 2 groups: PA group, angina pectoris occurred with in 24 h before AMI onset (n=58), NPA group, no preceeding angina pectori s occurred (n=126). Occurrence of complications and QTd were investigated du ring hospitalization. Results: The basic clinical characteristic s, coronary risk factors, medication before infarction, treatments after admissi on with antiarrhythmic agents, site of infarction, successful rate of thrombolys is and peak CK, CK-MB were not statistically different. Early QTd in PA group and NPA group were (56.22±18.40) ms vs (84.45±21.90) ms, respectively, P <0.05, late QTd in PA group and NPA group were (50.67± 16.34) ms vs (64.1 8(16.41) ms, respectively, P<0.05. Comparison with NPA group, incidence of severe ventricular arrhythmia, heart failure, cardiogenic shock and rate of car diac mortality in-hospital was lower in PA group. Conclusion: P reinfarction angina pectoris can significantly reduce the incidence of severe ve ntricular arrhythmia and QTd in the patients with first AMI, sugges ting that these favorable effects might be associated with protective effects of ischemic preconditioning on myocardium and ventricular pump function and improv ement of repolarizative asynchronism in ventricular myocardium.