套袋黄冠梨黑点病与钙素营养和果实衰老的关系

为探明套袋黄冠梨果实黑点病发病原因,从采后生理、矿质营养水平、酚类物质酶促褐变和果实衰老等方面对套袋黄冠梨果实黑点病进行了研究。结果表明:套袋果呼吸强度显著高于不套袋果;套袋果Ca含量仅为不套袋果的49%-63%,果皮钙素含量未套袋果>套袋健康果>套袋病果,套袋病果与不套袋果果皮N/Ca比值分别为9.8和6.1,K/Ca比值分别为17.6和8.8;果皮和果心酚类物质含量及多酚氧化酶活性(PPO)呈套袋病果>套袋健康果>未套袋果的趋势;套袋病果果皮丙二醛(MDA)含量及电导率显著高于未套袋果;果皮钙素含量与其PPO活性、多酚及丙二醛含量、电导率呈高度负相关。初步分析黄冠梨果实黑点病病因为缺钙性生理衰老。     

苏南丘陵区秋播苜蓿适用伴生作物筛选试验

为解决苏南丘陵区苜蓿苗期的杂草问题,从保护播种入手,在多年生黑麦草、一年生黑麦草、黑麦、小黑麦四种作物共五个品种中寻找适宜的伴生作物.通过对产量、株高、杂草率等多个指标测定分析,筛选出中新830小黑麦、赣选一号黑麦草适于用作苜蓿播种的伴生作物,同时获得两个苜蓿存活率最高的处理：苜蓿（15kg/hm^2）＋中新830小黑麦（150kg/hm^2）撒播及苜蓿（18 kg/hm^2）＋中新830小黑麦（250kg/hm^2）30cm条播.试验还表明撒播方式下,苜蓿播量与其竞争力不成正比。     

Expression of peroxisome proliferator-activated receptor α in rat fatty liver

AIM:To investigate the role of expression of peroxisome proliferator-activated receptor α(PPAR α) in pathogenesis of rat fatty liver.METHODS:The rats were treated with a low dose of carbon terachloride (CCl₄) and fed a high fat diet to produce fatty liver. We determined the concentrations of triglyceride (TG), total cholesterol (TC), free fatty acid (FFA) in liver and the alanine aminotransferase (ALT) activity, tumor necrosis factor-α (TNF-α), FFA in serum and the degree of hepatocytic steatosis. Total RNA of liver was extracted, and the expression of PPAR α were analyzed by semi-quantitative RT-PCR method.RESULTS:In model group, the hepatocytic PPAR α mRNA expression decreased to 0.41±0.28, compared to 1.41±0.29 in the control group (P＜0.01). The contents of TG, TC, FFA in model rat liver were (1.88±0.20) mmol·L^-1, (11.03±1.12) mmol·L^-1 and (1 260.38±151.27) μmol·L^-1, respectively, compared to (0.53±0.10) mmol·L^-1, (1.25±0.25) mmol·L^-1 and (334.30±27.09) μmol·L^-1 in the control group (P＜0.01). The activity of ALT, concentrations of TNF-α and FFA in serum were also increased remarkably in model group.CONCLUSION:Oxidation of fatty acid and utilization of lipids in liver are affected by reducing the expression of PPAR α, which result lipid accumulation in liver.     

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.     

Changes of myocardial glycogen content and right ventricular function in hypoxia swimming rats

AIM: To investigate the changes of myocardium glycogen content and the relation ship between changes of the myocardial glycogen content and the myocardial function. METHODS: Male Wistar rats were placed in (hypoxia rats) and made to swim in (hypoxia swimming rats) a hypobaxic chamber simulating an altitude of 5 000 m above sea level. The content of myocardium glycogens was determined by colorimetry. RESULTS: The myocardium
glycogen content of rats significantly reduced along with the prolongation of hypoxic exposure and approached to control level in hypoxia swimming rats. The myocardial function of right ventricule was improved significantly compared with control group.CONCLUSION: Moderate exercise (swimming) is beneficial to hypoxic adaptation of rats under the condition of chronic hypoxia.     

纳米微粒材料生物学活性研究进展

综述了纳米微粒的生物学效应及其免疫调节、抗菌、抗肿瘤等多种生物学活性.     

甘肃东方蜜蜂的形态特征研究

通过测定甘肃2个不同样点的4群东方蜜蜂发现,甘肃蜜蜂种群内遗传变异丰富,种群中许多形态性状特征表现出较明显的地理变异性;蜜蜂个体增大、体色变深,具体是:前翅长、前翅宽、背板3,4宽;后腿长、蜡镜长、蜡镜宽、蜡镜间距、腹片3,6的长和宽逐渐增加;背板3,4、小盾片的色素度逐渐加深。这些均具有生态适应意义。     

Antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes

AIM: To observe the antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes. METHODS: Rat thymus lymphocytes were separated by Ficoll-Urografin density gradient centrifugation. Lipofectin was used to introduce antisense, sense and mismatched oligonucleotides for c-myc to rat thymus lymphocytes. The antiproliferative effect was assayed by incorporation of [³H]-TdR and MTS cell proliferation assay. TR-PCR was used to detect the expression of c-myc mRNA. RESULTS: c-myc antisense oligonucleotide inhibited ratthymus lymphocytes proliferation[(0.14±0.03)A vs(0.32±0.16)A,P<0.05],but this ef ect had no relationship with the concentration of c-myc antisense oligonucleot ide.c-myc antisense oligonucleotide decreased the expression of c-myc mRNA in rat thymus lymphocytes. CONCLUSION: c-myc antisense oligonucleotide inhibited rat thymus lymphocyte proliferation.     

Taurine reduced oxygen free radical production induced by homocysteine in electron transport chain and homocysteine inhibites taurine transporter in mitochondria membrane

AIM: To observe effects of homocysteine and antagonized effects of taurine on electronic leakage and free radical production in myocardial mitochondria. METHODS: Myocardial mitochondria of rat heart was isolated, and was broken by supersonic wave to prepare submitochondria. Recombinant of succinic acid cytochrome c reductase was prepared with mitochondria of porcine heart. They were co-incubated with homocysteine and/or taurine with various concentration. The H₂O₂ and O₂^- were determined by chemiluminescence methods. The taurine transporter of heart mitochondria and its propert, and effects of homocysteine on its function were studied with glass filter. RESULTS: Homocysteine stimulated oxygen free radical production in heart mitochondria, submitochondria, and succinic acid cytochrome c in a concentration-dependent manner. Although taurine itself did not affect oxygen free radical production, taurine did inhibit oxygen free radical production in mitochondria, submitochondria and succinic acid cytochrome c in a concentration-dependent manner. Taurine transporters of Na⁺-dependent were existed in mitochondria membrane. Homocysteine inhibited taurine transtport in mitochondria in a concentration-dependent manner. CONCLUSIONS: Taurine inhibited electronic leakage and oxygen free radical production induced by homocysteine in electron transport chain. There were taurine transporters in mitochondria membrane, and transport functions of taurine transporter were inhibited by homocysteine.     

Effects of glycine on intracellular of free calcium and tumor necrosis factor-α of cardiomyocytes during hypoxia/reoxygenation

AIM: To observe the influence of glycine on intracellular free calcium, the concentration of tumor necrosis factor-α and the survival rate of myocardial cells during hypoxia/reoxygenation (H/R). METHODS: The simulated model of myocardial ischemia-reperfusion with the primary cultured cardiomyocytes of neonatal rats was established, and the cultured cardiomyocytes were divided into seven groups, control group, hypoxia/reoxygenation group, glycine (0.5 mmol/L) plus hypoxia/reoxygenation group, glycine (1.0 mmol/L) plus hypoxia/reoxygenation group, glycine (2.0 mmol/L) plus hypoxia/reoxygenation group, glycine (4.0 mmol/L) plus hypoxia/reoxygenation group, 4.0 mmol/L glycine group. RESULTS: Within certain concentration (0.5-2.0 mmol/L), the glycine could inhibit the calcium overload resulting from hypoxia/reoxygenation injury in cells in a dose-dependent manner with the optimal inhibitory effect at 2.0 mmol/L. Glycine inhibited the secretion of tumor necrosis factor-α from myocardial cells and increased the survival rate of myocardial cells. CONCLUSION: Glycine has a protective effect on hypoxia/reoxygenation myocardial cells, which may be related to inhibiting calcium overload and decreasing the production of tumor necrosis factor-α.