人参根及茎叶皂苷对群养及隔离孤独饲育小鼠神经精神药理作用的研究

人参根及茎叶皂苷 ５０～２００ ｍｇ／ｋｇ能使群养小鼠的自发运动量明显增加,８周隔离饲育小鼠比群养小鼠自发运动量明显增加,人参根皂苷能使其剂量依赖性降低,而人参茎叶皂苷影响不明显;对戊巴比妥钠所致睡眠试验中,隔离孤独饲育小鼠比群养小鼠睡眠时间明显缩短（ｔ＝４．３５６,Ｐ＜０．００１）。人参根皂苷 ５０～２００ ｍｇ／ｋｇ使孤独饲育小鼠的睡眠时间随剂量增加而延长,２００ ｍｇ／ｋｇ组与对照组比较,ｔ＝３． ６６５,Ｐ＜０．０１。并能使 ８周隔离饲育的小鼠 ２０ ｍｉｎ内连续攻击时间有意义地下降（ｔ＝４．５４０,Ｐ＝０．００１）,但人参茎叶皂苷效果不明显。证明人参根及茎叶皂苷具有中枢兴奋作用,同时人参根皂苷还具有中枢镇静作用。     

山苦瓜的抗癌活性成分

对葫芦科植物山苦瓜Ｍｏｍｏｒｉｄｉｃａ ｄｉｏｉｃａ干燥块根的浸膏进行了分离、提纯,用Ｌ１２１０、ＣＣＥＲ－ＣＥＭ、ＬＳ１７４５癌细胞对其成分进行了体外筛选,５个化合物具有抗癌活性,经光谱鉴定,它们是拜俄尼酸（Ⅷ）、雪胆甲素（Ⅸ）、α－菠甾醇－３Ｏ－β－Ｄ－吡喃葡萄糖苷、线石竹皂元（Ⅴ）及常春藤皂苷元（Ⅶ）。     

长春花叶片愈伤组织诱导及培养过程中生物碱合成类型的变化和调节及有关酶的分析

在４种不同培养基上诱导长春花叶片愈伤组织发生的过程中,叶片中含量较高的文多灵（ｖｉｎｄｏｌｉｎｅ）和长春质碱（ｃａｔｈａｒａｎｔｈｉｎｅ）迅速降解至极低水平,而在叶片中含量较低的阿玛碱（ａｊ－ｍａｌｉｃｉｎｅ）和蛇根碱（ｓｅｒｐｅｎｔｉｎｅ）的合成却逐渐增加,同时酸性和碱性过氧化物酶（ｐｅｒｏｘｉｄａｓｅ）活性呈上升趋势,尤其碱性过氧化物酶与蛇根碱和阿玛碱的相关性较密切。光照和黑暗中的变化趋势基本一致,但光照可提高过氧化物酶的活性,对培养物的长春质碱、文多灵和蛇根碱的合成有利。不同的培养基对生物碱的合成影响较大,２,４－Ｄ显著抑制生物碱的合成,持续光照使愈伤组织的生长受到抑制,使阿玛碱向其蛇根碱转化。     

用LDH释放法判断细胞病变程度确定干扰素生物活性

目的：应用ＬＤＨ释放法测定干扰素生物活性。方法：通过检测ＷＩＳＨ细胞裂解后释放出的ＬＤＨ活性判断细胞病变的程度,确定干扰素效价。对ＬＤＨ释放法进行改进,与结晶紫染色法和ＭＴＴ比色法进行灵敏度、重复性和相关性比较。结果和结论：该法减少了实验步骤和时间,成本低,敏感性高,重复性好,与其他方法所测结果无显著差异,简便实用,优于结晶紫染色法和ＭＴＴ比色法。     

糖尿病肾病中医分型肾脏叶间动脉彩色多普勒超声分析

借助彩色多普勒频谱图,对糖尿病肾病患者肾脏叶间动脉血流参数进行分析,探讨该病中医分型的客观指标。方法：选择糖尿病肾病３５例,将其分为气阴两虚及阴阳两虚组,于每位患者双肾叶间动脉测量：收缩期峰值血流速度（ＶＳ）、舒张期末血流速度（ＶＤ）、平均血流速度（ＭＳ）、搏动指数（ＰＩ）、阻力指数（ＲＩ）。结果：气阴两虚组ＰＩ、ＲＩ值明显高于正常组（Ｐ＜０．０１）,阴阳两虚组ＰＩ、ＲＩ明显高于气阴两虚组（Ｐ＜０．０５）;阴阳两虚组ＶＤ值高于气阴两虚组及正常组（Ｐ＜０．０１）;气阴两虚组与正常组比较无统计学差异。结论：糖尿病肾病气阴两虚及阴阳两虚组中ＰＩ及ＲＩ,可以作为糖尿病肾病中医分型的客观指标。     

伤寒杆菌耐药质粒pR_(ST98)介导血清杀菌作用抗性的研究

将ｐ Ｒ Ｓ Ｔ９８ 导入不含质粒且对抗菌药物敏感的大肠杆菌、伤寒杆菌,并用十二烷基硫酸钠（ Ｓ Ｄ Ｓ） 消除耐药菌株的ｐ Ｒ Ｓ Ｔ９８ ,计算接合子及 Ｒ 质粒消除前后菌株在人、兔及豚鼠的不同浓度、不同成份血清中的存活率。ｐ Ｒ Ｓ Ｔ９８ 介导其宿主菌对血清杀菌的抗性,但在不同宿主菌中抵抗力不同;补体经典途径及旁路途径均参与血清杀菌过程。ｐ Ｒ Ｓ Ｔ９ ８ 具有多效性,其广泛的宿主性在介导细菌多重耐药的同时,还赋予细菌抵抗血清的杀菌作用,使病原菌致病性增强。     

1,25-二羟维生素D_3抑制报导载体pGL_2荧光素酶表达的研究

通过磷酸钙沉淀法将载体DNA转染Caco－2细胞。Caeo－2细胞经不同浓度1,25一二羟维生素D3处理后,测定表达的荧光素酶活性。结果;当pSG5－VDR表达载体共转染时1,25一二羟维生素D3显著地抑制Caco－2细胞荧光素酶的表达;而未使用pSG5－VDR表达载体共转染时,则无抑制作用。说明1,25一二羟维生素D3能抑制报导载体pGL2荧光素酶的表达。类似于人类PTH基因中的潜在抑制性VDRE存在于报导载体pGL2。     

Psychomotor retardation and anhedonia in depression

Anhedonia, the inability to experience pleasure, and observed changes in psychomotor performance are frequent psychopathological phenomena in major depression with possible common neurobiological mechanisms. Interest, pleasure and reactivity to pleasurable stimuli contribute to movement generation and observable behaviour. Therefore the relationship between anhedonia and psychomotor retardation was studied in 48 depressed patients. Subjectively experienced anhedonia correlated with self-rated but not with observer-rated global severity of depression. There was a significant correlation between anhedonia and psychomotor retardation assessed with the Widlöcher Retardation Scale. The results suggest the existence of an empirical relationship between reduced ability to experience pleasure and observable psychomotor retardation in depression. Specific measures of psychomotor phenomena may provide further insights into the relationship between observable behaviour and self-experienced symptoms in depression.     

Leptin-induced increase in sympathetic nervous and cardiovascular tone is mediated by proopiomelanocortin (POMC) products

The mechanism underlying the leptin-induced increased sympathetic nerve activity and cardiovascular tone was investigated in normal rats. The melanocortin (MC) peptides and other fragments derived from proopiomelancortin (POMC) have a diverse array of biological activities and have been implicated in mediating the feeding behavioral responses to leptin. In this study we evaluated the possible involvement of two major products of POMC, alpha-melanocyte stimulating hormone (alpha-MSH) and beta-endorphin, in mediating the effects of leptin on sympathetic activity and mean arterial pressure (MAP) in normal rats. Intraventricular (i.c.v.) cannulas were implanted in normal rats and allowed to recover. On the day of the study the animals were anesthetized with urethane alpha-chloralose and instrumented for the recording of MAP, lumbar sympathetic nerve activity (LSNA), and heart rate (HR). To determine the correlation between the leptin response and the POMC products, alpha-MSH and beta-endorphins were also injected into the lateral ventricle. alpha-MSH acted to increase MAP and LSNA while beta-endorphin decreased these parameters. Leptin administration by i.c.v. cannula increased the MAP and LSNA in normal rats. The i.c.v. administration of agouti protein, an alpha-MSH receptor antagonist, prior to leptin infusion blocked this response. Likewise, pretreatment with naloxone a beta-endorphin receptor antagonist also blocked the response to leptin. From these studies we conclude that the acute increased LSNA and MAP in response to i.c.v. leptin may be mediated by increased POMC and its subsequent production of breakdown product alpha-MSH and/or beta-endorphin and it is the subsequent action of alpha-MSH that increases MAP and LSNA by activation of the MC4 receptor. The naloxone antagonism of the leptin response is likely due to the blockade of presynaptic opioid inhibition of the MC4 receptor-mediated pressor response.