The purpose of this research work is to find out the longitudinal distribution of the preganglionic neurons which project to the superior cervical sympathetic ganglion (SCSG). Experiments were performed on 12 adult rabbits and a monkey. Under sodium pentobarbital anesthesia, 20 microliters of 10% HRP were injected slowly into the rabbit's SCSG. In the monkey, 20 microliters of 15% HRP was injected.After a postoperative survival time of 3～6 days, the animals were perfused through,the ascending aorta with a cold fixative mixture composed of 2% paraformaldehyde and 1.25% glutaraldyhyde in 0.1mol phosphatebuffer at pH 7.4. The spinal cord segments C_1～L_3 were cut serially in transverse plane on a cryostat at 48 micra.The HRP reaction product was demonstrated according to Mesulam's (1976) benzidine blue reaction method, and counterstained with neutral red.HRP labeled neurons in the spinal cord were located exclusively on the side ipsilateral to the injected SCSG. The total number of labeled cells were 7908 in 12 rabbits, but the number of labeled cells varied from animal to animal. The highest amount was 1690 (423~#) and the lowest amount was 71 (425~#). The longitudinal distribution of the labeled cells in 12 rabbits was 12 segaments of the spinal cord (C_6～T_9), but the largest proportion (86.18%) of them was concentrated from T_1 to T_4, especially at the level of T_2 and T_3 (56.22%), and with a peak at T_2 (29.10%).In cross section of the spinal cord. HRP-labeled cells were concentrated in four cell groups, they are: nucleus intermediolateralis pars principalis (ILp), nucleus intermediolateralis pars funicularis (ILf), nucleus intercalatus (IC) and nucleus intercalatus pars paraependymalis (ICpe). The latter is subdivided into dorsal portion and ventral portion. HRP positive cells were mainly located in the ILp, In 12 rabbits about 92.99% cells were located in it. A small portion of labeled cells(6.25%) were seen in the ILf. A few labeled neurons could be detected within,the IC (0.68%) and ICpe (0.08%). Furthermore, occasionally, very few labeled cells were found at the dorsol portion of the anterior horn.In the monkey, generally speaking, the pattern of the distribution of labeled cells was the same as the rabbit.

AIM: To investigate the platelet aggregations in patients with coronary heart disease(CHD) and the effect of ticlopidine treatment. METHODS: Platelet aggregations induced by adenosine diphosphate(ADP), epinephrine(EPI), collagen(Coll), arachidonic acid(ACA) in CHD group before and after ticlopidine treatment were measured by turbidity assay. RESULTS: Maximum ratios of platelet aggregations (max%) induced by ADP,EPI in CHD group (0.78?0.23,0.86?0.25) were significantly higher than that of control group (0.65?0.19,0.73?0.21, P

Objective To explore the inheritance characteristics of SCN1A gene in familial severe myoclome epilepsy in infancy.Methods The clinical information and blood of the patients and their relatives who had febrile seizure(FS)or epilepsy history were collected.Blood genome DNA were extracted.All exons of SeN1A gene were PCR amplified and screened with denaturing high Performance liquid chromatography(DHPLC)technology,and sequence analysis was performed.Results Fourteen SME patients had FS or epilepsy family history.Five were found positive history in first class relatives and 2 of them had inherited mutations of SCN1A(C.4284+2T>C and e.1216G>T):Other9 were found positive history in second class relatives and 2 of them had de novo mutations of SCN1A.Condusions SCN1A is the pathogenic gene for SME.The same muatation of SCN1A gene can be related to different clinical phenotypes.SME patients whose first class relatives with FS or epilepsy history should be taken as the focus of SCN1A inherited mutation screening.

Objective To stuay the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1,and the expression of CD40L of the CD4+T cells in patients withacute coronary syndrome(ACS),and to explore the relationship between CD40L and inflammatory factors and the effects of CD40/CD40L on ACS.Method Thirty-two coronary heart disease patients without history of other discernible systemic disease and medicine of steroids or immunosuppressants taken were divided into acute myocardial infarction group(AMI,n=11),unstable angina pectoris group(USP,n=14)and stable angina pectoris group(SAP,n=7).The control group was composed of eight healthy volunteers(CON group).Theexpression of CD40L Was determined by flow cytometry(FCM).Serum sCD40L.ICAM-1 and VCAM-1 were determined by using ELISA.The serum hsCRP was assayed by using immunoturbidimetry.Data were analyzed with SPSS 11.0 software for windows.Results The expression percentage(%)of CD40L of the CD4+T cells,and the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1were sifnificantly higher in patients of AMI group than those in patients of other groups(P＜0.05 or P＜0.01).Similarly,those biomarkers in patients of UAP group were usually higher than those in patients of CON or SAP groups(P＜0.05).There Was a positive correlation between the expression of CD40L and the serum level of VCAM-1 in paients of AMI group(P＜0.05),and likewise,a positive correlation also existed between the serum level of sCD40L and other factors,hsCRP,ICAM-1 as well as VCAM-1,in patients of AMI group(P＜0.05).Conclusions The enhanced expression of CD40L of the CD4+T cells and high serum level of sCD40L are present in patients with acute coronary syndrome.The hsCRP,ICAM-1 and VCAM-1 play roles in the pathogenesis of ACS,and they have correlation with enhanced expression of CD40L and high serum level of sCD40L.Therefore,CD40L and sCD40L may be used as indicators of risk in coronary heart disease.

[Objective] The present study was to evaluate the association of serum total cholesterol level and prognosis in patients with acute left heart failure and associated mechanisms.[Methods] Sixty-eight patients due to acute episode of left heart failure prospectively enrolled,and baseline data and biochemical parameters were collected.After discharge,patients were follow-up for 1 month and they were divided into two groups (with and without cardiovascular events).Differences between groups were evaluated and the association of serum total cholesterol level and cardiovascular events were analyzed by logistic regression analysis.[Results] The mean age was 57.3 ± 12.6 years old and 52 cases were male patients accounting for 76.5 ％.Among these patients,46 had a diagnosis of coronary heart disease (67.6 ％),10 rheumatic heart disease (14.7 ％),12 dilated cardiomyopathy (17.7％),38hypertension (55.9％) and 24 diabetes mellitus (35.3％).After 1 month's follow up,39 patients (57.4％) had experienced cardiovascular events,36 cases were re-hospitalized,and 3 died from heart failure.Compared to those with cardiovascular events,event free individuals were younger and were less likely smokers (P ＜ 0.05).In addition,event free group had lower serum levels of N-terminal pro-BNP and C-reactive protein (P ＜ 0.05) while serum levels of total cholesterol and albumin were significantly higher (P ＜ 0.05).There was no significant difference in medication between these two groups.After adjusted for age,gender,smoking,systolic blood pressure,serum albumin level,diabetes,hypertension and medications,increased total cholesterol level was independently associated with better prognosis with odds ratio of 0.91 (95 ％ confidence interval 0.80-0.96).Further adjusted for C-reactive protein,the association was attenuated to non-significance,with odds ratio of 0.97 (95 ％ confidence interval 0.87-1.09).[Conclusion] Adequate serum total cholesterol level was beneficial for improving short-term cardiovascular outcomes in patients with left heart failure and the potential mechanisms might be related to cholesterol effects on improving nutritional status and anti-inflammation.

AIM: To study the reactions of human platelet to active complement and the effects of anti-CD59 on human platelet activation induced by complement. METHODS: By applying CVF to activate complement, the platelet aggregation and release reactions induced by activated complement with or without appling anti-CD59 with different doses to block the complement modulative protein CD59 in healthy individuals, were observed. RESULTS: CVF induced platelet release and significant and lasting metamorphosis in healthy individuals, but platelet aggregation was not observed. CVF-induced platelet metamorphosis showed positive linear correlation to lg concentration of CVF (r=0 970. P

Aim To explore the best way of calculating antihypertensive effect of nifedipine GITS on trough to peak ratio (T/PR), and smoothness index (SI) of the drug from ambulatory blood pressure monitoring (ABPM). Methods 32 cases of mild to moderate essential hypertension patients were enrolled and each was given 30 mg of nifedipine GITS once daily. ABPM was repeated for four weeks. ABPM data were analyzed statistically and T/PR calculated by both individual and whole group way. Results The casual blood pressure(CBP) and ABP were lowered by (24?12)/(12?8) mmHg and ( 14.5 ? 3.9 )/( 11.2 ? 3.0) mmHg .The T/PR by individual way was 0.65 ? 0.23 for SBP and 0.66 ? 0.25 for DBP, while by whole group way 0.62 for SBP and 0.68 for DBP. The smoothness index (SI), a new method for assessing the homogeneity of 24 hour blood pressure reduction by antihypertensive therapy, was 3.74 for SBP and 3.77 for DBP after treatment. Conclusion Nifedipine GITS lowers blood pressure effectively and smoothly for 24 hours long. Antihypertensive effects can be reflected by T/PR and SI.

OBJECTIVETo investigate the effect of atorvastatin on cardiac remodeling and function after acute myocardial infarction (AMI) in rats and whether this effect is mediated by transforming growth factor-β1 (TGF-β1) signaling pathway.

METHODSAMI was induced by left coronary artery ligation in 64 male Sprague-Dawley rats, and 45 surviving rats were randomized into control group (n=15), low-dose atorvastatin group (10 mg/kg, n=15) and high-dose atorvastatin group (20 mg/kg, n=15). Similar surgical procedure was performed in sham-operated rats (n=15) without coronary ligation. Atorvastatin was given daily by gavage from the first day after AMI. Eight weeks later, the cardiac function, left ventricular weight/body mass index (LVMI), collagen volume fraction (CVF), and the expressions of TGF-β1 and Smad2 were compared between the groups.

RESULTSAMI caused significantly reduced cardiac function, increased LVMI and CVF, and upregulated expressions of TGF-β1 and Smad2 mRNA and proteins in the control group (P<0.05). The cardiac function, LVMI, and CVF were improved by atorvastatin, which also down-regulated the expressions of TGF-β1 and Smad2 (P<0.05), and the effects were more prominent in high-dose atorvastatin group (P<0.05).

CONCLUSIONAtorvastatin can dose-dependently improve cardiac remodeling and function after AMI in rats, which is mediated by regulating the activity of TGF-β1/Smad2 signaling pathway.

Animals ; Atorvastatin Calcium ; Heart ; drug effects ; physiopathology ; Heptanoic Acids ; pharmacology ; Male ; Myocardial Infarction ; physiopathology ; Pyrroles ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects ; Smad2 Protein ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Ventricular Remodeling ; drug effects