节能日光温室光照强度的分布及其变化

在充分考虑了温室结构和植株生长影响的基础上,对日光温室光照强度的变化规律进行了研究,得到的主要结论如下:冠层上部辐射强度的南北差异比东西差异大;冠层下部光照条件东西差异明显,南北差异不大。总体上讲,辐射强度上下差异比南北差异明显。     

木那格葡萄的组培快繁试验

以木那格葡萄的茎尖、单芽茎段为外植体，进行组培快繁试验。蛄果看出，适宜茎尖分化的培养基为B5 BA1．0mg／L IBA 0．1mg／L。适宜单芽茎段一次成苗生长的培养基为B3 BA0．05mg/L IBA0．2mg／L。适宜的生根培齐基为1／2MS IBA 0．2mg／L 蔗糖40g／L。健壮生根的试管苗要待4片叶以上移栽，移栽基质以蛭石较好。时间宜在4—5月份。     

Effects of FK506 on anti-glomerular basement membrane nephritis in rats

AIM:To investigate the effects of FK506 on anti-glomerular basement membrane(GBM) nephritis in rats. METHODS: Anti-GBM nephritis model was elaborated by rabbit anti-rat GBM antibody injection in SD rats in this study. The rats were divided into three groups: FK506 treated group(0.5 mg·kg^-1·d^-1, sc), untreated nephritis control group and normal control group. FK506 was administered daily six hours after injection of anti-GBM IgG. All the rats were observed urinary protein at the 4th day, the 14th day and the 21st day. At the same time, the kidney specimens were collected, and T cell transforming function was also monitored.RESULTS:Rats injected with rabbit anti-GBM Ab developed heavy proteinuria by 4 days, and serum creatinine and serum urea appeared which kept on the rising. Glmerular hypercellularity, crescents, and protein casts were observed in nephritic rats. By electron microscopy, the thickening of GBM and loss of foot processes were seen. T cell transforming function was higher than normal. But, all pathological changes obviously turned for the better in FK506 treated group. CONCLUSION:FK506 could inhibit the progression of rat anti-GBM nephritis.     

Serum contents of E-selectin,sICAM-1, sVCAM-1 in patients with acute coronary syndrome

AIM:To explore the serum levels of certain adhesion molecules and its significance in acute coronary syndrome(ACS). METHODS:The subjects included 40 patients with acute myocardial infarction(AMI) and 40 patients with unstable angina pectoris (UAP). Among the 80 patients, 60 patients accepted a follow-up 4 months. At the same time we selected 40 controls from people who attended a routine health check in the university. Serum levels of E-selectin, sICAM-1, sVCAM-1 were measured by ELISA.RESULTS:Serum levels of E-selectin, sICAM-1, sVCAM-1 were significantly higher in the ACS group(AMI or UAP) than in the control group. Four months later, the levels of E-selectin, sICAM-1 became significantly lower in the follow-up group than in the ACS group, while sVCAM-1 showed no significant difference. CONCLUSION:Serum levels of E-selectin, sICAM-1 may have certain diagnostic value for ACS, and can be a useful marker reflecting the stability of the disease.     

25s rRNA 基因部分序列比较在香菇栽培菌种鉴定上的应用

对目前中国7个主要香菇栽培品种：科，26，939，135，9311，申10和7402和25s rRNA基因中的D1／D2片段进行了DNA序列测定，根据DNA序列测定结果对它们之间的同源性进行了分析。结果表明，所测定的7个香菇栽培品种之间的亲缘关系非常近，同源性很高。通过聚类分析，根据香菇之间的亲缘关系，可以将这7个品种分为2类，即苏香，939和9311为一类，26，申10，135和7402为一类。     

SeGLP-1的分离纯化及硒活性结构分析

灵芝（Ganoderma lucidum)加硒深层培养后的菌丝（含Se1600μg/g)分别经水及碱水提取，醇析，透析，Sevage法脱蛋白，DEAE－cellulose柱层析纯化，得SeGLP-1。经SephadexG－100，聚丙烯酰胺凝胶电泳和紫外光谱分析鉴定，SeGLP-1为均一级分。GC与TLC分析表明，SeGLP-1含Gal,Glu,Xyl,Rha,Man，其单糖摩尔比为Gal:Glu:Xyl:Rha:Man=0.23:1.00:0.72:0.25:0.09。SeGLP-1硒含量1642μg/g。SeGLP-1中Se活性中心的结构可能为O＝Se=O,即Se取代了灵芝多糖GLP－1中－OCH3结构上的CH3，从而形成了硒氧双键结构。     

Metallothionein inhibits homocysteine-induced proliferation of rat vascular smooth muscle cells

AIM:To investigate the effect of metallothionein(MT) on proliferation of rat vascular smooth muscle cells (VSMCs) stimulated by homocysteine and its mechanism. METHODS:VSMCs proliferation was measured by [³-H]-TdR incorporation, mitogen-activated protein kinase(MAPK)activity were determined by immunoprecipitation method, the intracellular contents of MT and malondialdehyde (MDA)were assayed by -hemoglobin saturation method and TBA reaction, respectively, and lactate dehydrogenase (LDH) leakage was measured by NADH oxidation. RESULTS:Hcy(10^-6-10^-4 mmol/L) stimulated [³-H]-TdR incorporation by the VSMCs in a concentration-dependent manner. Compared with control, [³-H]-TdR incorporation in VSMCs treated with 0.1 mmol/L Hcy was increased by 4.2 fold (P＜0.01). Meanwhile, Hcy enhanced MAPK activity, MDA formation and LDH release (P＜0.01)in a concentration-dependent manner. Treatment of VSMCs with MT alone did not change above parameters, compared with control. However, MT (10^-6-10^-4 mol/L)attenuated significantly Hcy-stimulated proliferation of VSMCs (P＜0.01)in a concentration-dependent manner. And MT inhibited obviously Hcy-induced activation of MAPK activity, MDA formation and LDH release. Preincubation of VSMCs with 0.5 mmol/L ZnCl₂ for 6 h induced an increase cellular MT content by 5.7-fold (P＜0.01). The MT-overexpressed VSMCs resisted Hcy-stimulating action on MAPK activity, MDA formation and LDH leakage (P＜0.01). CONCLUSION:These results show that MT has an inhibitory effect on Hcy-induced VSMCs proliferation, and that MT could inhibit Hcy-stimulated MAPK activity and lipid peroxidation.     

In vitro growth inhibition effects of rhHGF/cHGF on SMMC-7721 human HCC cell line

AIM:To examine the effects of recombinant human hepatocyte growth factor(rhHGF) and native calf HGF(cHGF) on SMMC-7721 human hepatocellular carcinoma(HCC) cell line. METHODS:Human HCC cell line culture, photometric assay, and flow cytometric assay were used in this study .RESULTS:A similar type of dose-dependent cell growth inhibition effect on SMMC-7721 human HCC cells by rhHGF(5-20 μg/L) as well as by cHGF(25-100 mg/L) had been found, with the maximal effect at the highest concentration used. Approximately over 50% of the cells treated with rhHGF(5 μg/L, 10 μg/L, 20 μg/L) accumulated in the quiescent G₀/G₁ phase of the cell cycle over incubation periods for 3 d. CONCLUSION:The growth of SMMC-7721 human HCC cells was strongly inhibited by both rhHGF and cHGF. This might be because the cells exposed to HGF became arrested in the G₀/G₁ phase.     

Establishment of chronic obstructive pulmonary disease rat models by passive cigarette smoking and intratracheal instillation of lipopolysaccharide

AIM:To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS:48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group(n=12), rats were bred 4 weeks;healthy control II group(n=12), rats were bred for 3months. (2) Model group I (n=12), 200μg lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method.RESULTS:The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups(P＜0.01,P＜0.05).FEV_0.3/FVC% of two model groups, PaO₂ and SaO₂ of model I group were significantly decreased, while R_i and R_e in model I group were significantly increased than that of control I group(P＜0.05). The PaCO₂ and the counts of lymphocytes and alveolar macrophages of both model groups were significantly increased than those of the control groups (P＜0.01). Lots of alveolar macrophages had phagocyted smoke granules. The amounts of hydroxyproline of two model groups were significantly increased than those of control group((P＜0.05) and were negatively related to the FEV_0.3/FVC%, respectively (P＜0.01,P＜0.01) and positively related to airway resistance of model I group(P＜0.01). CONCLUSIONS:COPD rat models were successfully established by passive cigarette smoking plus intratracheal instillation of LPS and cigarette smoking only. The pathologic changes were similar but milder than those of COPD patients. The airway obstruction of model I group was more severe than that of model II group, but they have no significant difference.     

Effects of carvedilol,cilazapril and their combination on left ventricular remodeling after acute myocardial infarction in rats

AIM:To compare the effects of carvedilol, cilazapril and their combination on left ventricular remodeling(LVRM) after acute myocardial infarction(AMI) in rats. METHODS: Twenty-four hours after AMI operation, 100 surviving rats were randomly assigned to: ①AMI control(n= 25), ②AMI+carvedilol(1 mg·kg^-1 ·d^-1, n= 25)(C1), ③AMI+cilazapril(1 mg·kg^-1 ·d^-1, n= 25)(Z1), and ④ AMI+combination(n= 25) groups. Sham-operated group(n= 17) were selected randomly. After 4 weeks of therapy with the drugs gastric gavage, hemodynamic and pathological studies were performed. RESULTS: There were no significant differences in MI size among the four AMI groups(all P> 0.05) Left ventricular(LV) end diastolic pressure(LVEDP), volume(LVV), weight(LVW) and septal thickness(STh) were all higher and left ventricular pressure maximal rate of rise and fall(±d p /d t) were lower(all P< 0.01) in AMI group than sham-operated group. The LVEDP, LVV, LVW and STh were all lower and ±dp /dt were higher in Z1, C1, and combination groups than those in AMI group(P< 0.05, P< 0.01), with LVEDP and STh were more lower in the combination group than in the two monotherapy group(P< 0.05, P< 0.01), but there were no significant differences in other variables among the three therapy groups. CONCLUSION: Carvedilol, cilazapril and their combination all can prevent from LVRM after AMI in rats, improve hemodynamics and LV function, with the combination superior.