不同添加物质对香烟烟雾水溶物引起的蚕豆根尖细胞微核率的影响

本课题研究了不同添加物质对香烟烟雾水溶物引起的蚕豆根尖细胞微核率的影响。结果表明亚硒酸钠、烟酰胺、绿茶浸出物和维生素C均能显著降低由香烟烟雾水溶物引起的微核率,上述物质可能具有减轻吸烟引起的遗传毒性损伤的作用。此外,本文还对上述结果的意义进行了讨论。     

重铬酸钾对蚕豆根尖细胞致畸效应的研究

以蚕豆根尖为材料,研究重铬酸钾对蚕豆根尖细胞的致畸效应。采用蚕豆根尖细胞的微核试验和染色体畸变试验方法,以不同浓度的重铬酸钾为诱变剂,测定蚕豆根尖细胞的微核率和染色体畸变率。结果表明:重铬酸钾能诱发较高频率的微核率,即在一定浓度范围内,其微核率随重铬酸钾处理浓度的升高而增加,但高于一定浓度后反而呈下降趋势;不同浓度的重铬酸钾均使蚕豆根尖细胞有丝分裂指数增大;重铬酸钾还能诱导蚕豆根尖细胞产生较高频率的染色体畸变,且产生多种类型的染色体畸变。结论是重铬酸钾对蚕豆根尖细胞具有明显的致畸效应。     

褐藻寡糖抗环磷酰胺诱导蚕豆根尖的细胞遗传毒性

采用蚕豆根尖细胞的微核试验和染色体畸变试验方法,测定不同浓度的褐藻寡糖对环磷酰胺(cyclophosphamide,CP)诱导的蚕豆根尖细胞的微核率、有丝分裂指数和染色体畸变率的影响。结果表明:褐藻寡糖能有效抑制环磷酰胺诱导的蚕豆根尖细胞微核的产生,即在一定浓度范围内,微核率随褐藻寡糖处理浓度的降低而减少,但低于一定浓度后反而呈上升趋势;不同浓度的褐藻寡糖均可使蚕豆根尖细胞有丝分裂指数增大;褐藻寡糖还能有效降低蚕豆根尖细胞染色体畸变率。因此,褐藻寡糖对蚕豆根尖细胞具有明显的诱抗活性和调节细胞分裂生长的效应。     

初生根长度对蚕豆根尖细胞微核率影响的研究

研究了不同长度蚕豆初生根微核率的差异,结果表明,初生根越短微核率越低,初生根越长微核率越高,提示蚕豆根尖细胞微核是可积累的,细胞分裂次数越多微核率越高,从而对蚕豆根尖微核测试的可靠性提供理论参考。     

SO2对蚕豆根尖和叶尖细胞遗传损伤作用的研究

采用微核实验技术,研究大气污染物SO2对蚕豆根尖和叶尖细胞的遗传损伤效应。结果表明2.80和28 mg.m-3的SO2熏气可以诱发蚕豆根尖和叶尖细胞损伤,导致根尖细胞有丝分裂指数下降,根尖和叶尖间期细胞微核率增高,并具有时间效应和浓度效应。经水恢复培养后,根尖分裂细胞数增多,微核率降低,说明恢复培养能够缓解高浓度SO2对根尖细胞的遗传损伤。用石蜡层隔断SO2在根部水中的溶解后,根尖细胞微核率低于叶尖细胞微核率,而在非隔断组中则相反,说明SO2在水中的溶解是产生毒性效应的重要原因。高浓度SO2熏气对蚕豆根尖和叶尖细胞具有遗传学毒性,由于根尖分生区具有较高的分裂指数和微核率,对环境SO2毒性的反应更灵敏,蚕豆根尖微核实验更适于对环境SO2的监测。     

乙酸铜对蚕豆根尖细胞致畸效应

采用蚕豆根尖细胞的微核试验和染色体畸变试验方法,以不同浓度的乙酸铜为诱变剂,选择不同的处理时间,测定蚕豆根尖细胞的有丝分裂指数、微核率和染色体畸变率。结果表明：乙酸铜能诱发较高频率的微核率,处理6h、12h时微核率均随着乙酸铜浓度的升高而增加,具有明显的剂量效应;处理24h时在实验浓度范围内,其微核率随乙酸铜浓度的升高而增加,但高于一定浓度后反而呈下降趋势。不同浓度的乙酸铜在不同处理时间均使蚕豆根尖细胞有丝分裂指数增大。乙酸铜还能诱导蚕豆根尖细胞产生较高频率的染色体畸变,且产生多种类型的染色体畸变。因此,乙酸铜对蚕豆根尖细胞具有明显的致畸效应。     

硫酸铜对蚕豆根尖细胞有丝分裂的影响

以蚕豆根尖为材料,研究硫酸铜对蚕豆根尖细胞的遗传毒性效应。采用蚕豆根尖细胞的微核试验方法和染色体畸变试验方法,以不同浓度的硫酸铜为诱变剂,测定蚕豆根尖细胞的有丝分裂指数、微核率和染色体畸变率。结果表明:不同浓度的硫酸铜均能使蚕豆根尖细胞有丝分裂指数明显增加,即5个实验组的分裂指数均明显高于对照组(P<0.01或P<0.001);不同浓度的硫酸铜对蚕豆根尖细胞有丝分裂各期百分数的影响有异;能诱发较高频率的微核率,即在一定浓度范围内,其微核率随硫酸铜处理浓度的升高而增加,但随着硫酸铜浓度的进一步升高而呈下降趋势;硫酸铜还能诱导染色体产生多种类型的畸变,染色体畸变率随硫酸铜处理浓度的升高而增加,随着硫酸铜浓度的进一步升高而呈下降趋势,但均明显高于对照组(P<0.001)。结论是硫酸铜对蚕豆根尖细胞具有明显的遗传毒性效应。     

四硼酸钠诱导蚕豆根尖细胞微核及染色体畸变的实验研究

本文以蚕豆为实验材料,用不同浓度的四硼酸钠处理蚕豆根尖。通过对蚕豆根尖细胞镜检观察结果表明:四硼酸钠可诱导微核的形成及染色体畸变的产生,实验组与对照组差异极为显著,即细胞微核率随处理时间的延长有所增加,50与200ppm浓度诱导细胞微核率没有明显差异。此外,本文对微核的形成与染色体畸变的相关性进行了讨论。     

甲硝唑诱导蚕豆根尖细胞微核的研究

本实验研究了甲硝唑诱导蚕豆根尖细胞微核的效应。实验表明：(1)浓度为0.1、6、12、40和500 mg/L甲硝唑均能使蚕豆根尖细胞微核率显著增加,且蚕豆根尖细胞微核率和甲硝唑浓度之间存在明显的剂量-效应关系;(2)甲硝唑能引起DNA损伤,具有分子诱变剂的性能。     

明矾对蚕豆根尖细胞遗传毒性的研究

为研究明矾的遗传毒性和潜在危害提供细胞遗传学证据。以蚕豆作为实验材料观察其根尖细胞在不同浓度明矾溶液中微核率变化情况,实验证明微核率随浓度呈先上升后下降情况,总体微核率均大于对照组,故不同浓度明矾溶液均能强烈诱发蚕豆根尖细胞产生微核。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.     

2018年中国植物科学若干领域重要研究进展

2018年中国植物科学继续呈现快速发展的态势, 我国科学家在国际植物科学主流学术刊物发表论文数量大幅增加, 取得了多项具有重要影响的成果。调控植物生长-代谢平衡实现可持续农业发展入选2018年度中国科学十大进展; 中国被子植物区系进化历史研究入选2018年度中国生命科学十大进展。以水稻为代表的农作物和果蔬等经济作物研究在国际上已呈现出明显的优势, 若干领域已从“追赶”状态跨越到“领跑”地位。该文对2018年中国科学家在植物科学若干领域取得的重要研究成果进行了概括性评述, 旨在全面追踪和报道当前中国植物科学领域的发展前沿和热点, 展示中国科学家所取得的杰出成就。     

2018年中国植物科学若干领域重要研究进展

2018年中国植物科学继续呈现快速发展的态势, 我国科学家在国际植物科学主流学术刊物发表论文数量大幅增加, 取得了多项具有重要影响的成果。调控植物生长-代谢平衡实现可持续农业发展入选2018年度中国科学十大进展; 中国被子植物区系进化历史研究入选2018年度中国生命科学十大进展。以水稻为代表的农作物和果蔬等经济作物研究在国际上已呈现出明显的优势, 若干领域已从“追赶”状态跨越到“领跑”地位。该文对2018年中国科学家在植物科学若干领域取得的重要研究成果进行了概括性评述, 旨在全面追踪和报道当前中国植物科学领域的发展前沿和热点, 展示中国科学家所取得的杰出成就。     

2017年中国植物科学若干领域重要研究进展

2017年中国植物科学继续保持高速发展态势, 重大成果频出, 具体表现在中国植物学家在国际顶级学术期刊发表的文章数量平稳上升。中国植物科学领域的研究工作者成果精彩纷呈, 如新型广谱抗病机制的发现、水稻广谱抗病遗传基础及机制和疫霉菌诱发病害成灾机制研究等。2017年中国生命科学领域十大进展评选中, 有两项植物科学领域的研究成果入选。水稻生物学、进化与基因组学和激素生物学等领域学科发展突出。另外, 值得一提的是, 长期从事高等植物与代谢途径调控分子网络研究和水稻品种设计育种的李家洋院士的研究成果“水稻高产优质性状形成的分子机理及品种设计”荣获2017年国家自然科学一等奖。这一具有重大国际影响的开创性贡献标志着中国植物科学在该领域的国际科学前沿居于引领和卓越地位。该文对2017年中国本土科学家在植物科学若干领域取得的重要研究成果进行了系统梳理, 旨在全面追踪和报道当前中国植物科学领域发展的最新前沿动态, 与广大读者共同分享我国科学家所取得的辉煌成就。     

我国葫芦科植物离体培养研究进展

葫芦科植物包括多种瓜类蔬菜,对其进行离体培养研究具有重要的理论和实践意义。综述了国内在葫芦科植物器官培养、体细胞胚胎发生、花药培养、原生质体培养和体细胞杂交及离体遗传转化等方面取得的研究进展,并对葫芦科植物离体培养、遗传转化与育种的前景作了展望。     

我国葫芦科植物离体培养研究进展

葫芦科植物包括多种瓜类蔬菜,对其进行离体培养研究具有重要的理论和实践意义.综述了国内在葫芦科植物器官培养、体细胞胚胎发生、花药培养、原生质体培养和体细胞杂交及离体遗传转化等方面取得的研究进展,并对葫芦科植物离体培养、遗传转化与育种的前景作了展望.     

Changes in aquatic vegetation in Rhine floodplain streams in Alsace in relation to disturbance

Abstract. Changes are described in aquatic vegetation in oligotrophic, groundwater-fed Rhine floodplain streams in Alsace (eastern France), resulting from disturbance. Disturbance factors include changes in nutrients, either permanent ones - effluent from a waste water treatment plant or trout hatcheries - or periodic ones: flooding. Regular inputs of high levels of phosphate and ammonia modified the macrophyte vegetation in these streams. The floristic composition, which was characteristic of oligotrophic waters upstream of the eutrophicated sector, changed to that of a eutrophic situation as originally found downstream. Periodic disturbance by floods which normally occur once a year, irregularly eutrophicates the small streams, causing the development of a mixture of eutrophic and oligotrophic species. Six macrophyte communities are distinguished, indicating different trophic levels. The aquatic vegetation is adapted to the variations of phosphate and ammonia levels. Hence, aquatic macrophytes can be used as bio-indicators of fluctuations in water nutrient levels in relation to the type of disturbance.     

Morphine-potentiated platelet aggregation in in vitro and platelet plug formation in in vivo experiments

The detailed mechanisms underlying morphine-signaling pathways in platelets remain obscure. Therefore, we systematically examined the influence of morphine on washed human platelets. In this study, washed human platelet suspensions were used for in vitro studies. Furthermore, platelet thrombus formation induced by irradiation of mesenteric venules with filtered light in mice pretreated with fluorescein sodium was used for an in vivo thrombotic study. Morphine concentration dependently (0.6, 1, and 5 microM) potentiated platelet aggregation and the ATP release reaction stimulated by agonists (i.e., collagen and U46619) in washed human platelets. Yohimbine (0.1 microM), a specific alpha(2)-adrenoceptor antagonist, markedly abolished the potentiation of morphine in platelet aggregation stimulated by agonists. Morphine also potentiated phosphoinositide breakdown and intracellular Ca(2+) mobilization in human platelets stimulated by collagen (1 microg/ml). Moreover, morphine (0.6-5 microM) markedly inhibited prostaglandin E(1) (10 microM)-induced cyclic AMP formation in human platelets, while yohimbine (0.1 microM) significantly reversed the inhibition of cyclic AMP by morphine (0.6 and 1 microM) in this study. The thrombin-evoked increase in pH(i) was markedly potentiated in the presence of morphine (1 and 5 microM). Morphine (2 and 5 mg/g) significantly shortened the time require to induce platelet plug formation in mesenteric venules. We concluded that morphine may exert its potentiation in platelet aggregation by binding to alpha(2)-adrenoceptors in human platelets, with a resulting inhibition of adenylate cyclase, thereby reducing intracellular cyclic AMP formation followed by increased activation of phospholipase C and the Na(+)/H(+) exchanger. This leads to increased intracellular Ca(2+) mobilization, and finally potentiation of platelet aggregation and of the ATP release reaction.     

Apoptosis in experimental myocardial infarction in situ and in the perfused heart in vitro

We report the appearance of apoptotic cells in experimental myocardial infarction (rabbit heart) in in situ and in vitro preparations. Apoptosis was recognized by intravital staining with Hoechst 33342 (Ho342), by nick-end labeling (TUNEL) and by DNA laddering. A steady rise in the relative number of apoptotic cardiomyocytes (apoptotic index) was noted in in situ preparations. Apoptosis was first noted 6 h after the onset of ischemia with its highest value occurring after 72 h. Apoptotic nuclei were absent in remote areas of the left and right ventricles. Apoptotic nuclei within the infarcted area showed diminished intensity of Ho342 fluorescence. Three days after ischemia, a border zone adjacent to the infarcted area consisting of apoptotic macrophages was recognized. A novel finding was the appearance of apoptotic cardiomyocytes in the isolated perfused ischemic heart. Occurring as early as 50 min after the onset of ischemia, a high apoptotic index was present adjacent to the ligature placed around the coronary artery. This observation provides the opportunity to selectively examine factors leading to apoptosis in the ischemic heart under controlled experimental conditions.