大鼠鼻粘膜肽能神经末梢分布的研究

用免疫组化技术（ＡＢＣ法）系统研究了大鼠鼻粘膜９种肽能神经末梢分布的特征,这９种神经肽分别是Ｐ物质（ｓｕｂｓｔａｎｃｅＰ,ＳＰ）,神经激肽Ａ（ｎｅｕｒｏｋｉｎｉｎＡ,ＮＫＡ）,神经激肽Ｂ（ｎｅｕｒｏｋｉｎｉｎＢ,ＮＫＢ）,降钙素基因相关肽（ｃａｌｃｉｔｏｎｉｎｇｅｎｅ－ｒｅｌａｔｅｄｐｅｐｔｉｄｅ,ＣＧＲＰ）,血管活性肠多肽（ｖａｓｏａｃｔｉｖｅｉｎｔｅｓｔｉｎａｌｐｏｌｙｐｅｐｔｉｄｅ,ＶＩＰ）,神经肽Ｙ（ｎｅｕｒｏｐｅｐｔｉｄｅＹ,ＮＰＹ）,甘丙肽（ｇａｌａｎｉｎ,ＧＡＬ）,生长抑素（ｓｏｍａｔｏｓｔａｔｉｎ,ＳＯＭ）及神经降压素（ｎｅｕｒｏｔｅｎｓｉｎ,ＮＴ）,同时选择与鼻粘膜神经肽（ＮＰ）作用密切相关的三叉神经节（ＴＧ）细胞进行上述ＮＰ的定位。用重组ＰＳＰ６５质粒（４００ＳＯＭｃＤＮＡ）制备ＳＯＭｍＲＮＡ单链探针,以地高辛精标记,在鼻粘膜及ＴＧ细胞进行ＳＯＭｍＲＮＡ的原位杂交组化研究。结果提示大鼠鼻粘膜有丰富的肽能神经末梢;ＴＧ细胞含有多种ＮＰ并且可以合成ＳＯＭ。该研究结果对重新认识鼻粘膜神经分布规律有一定意义。     

神经生长因子在6－OHDA化学性去交感神经中的保护作用

本实验用６－ＯＨＤＡ造成成年小白鼠领下腺化学性去交感神经,观察了神经生长因子对该神经的保护作用。６－ＯＨＤＡ（１５ｍｇ／ｋｇｉｐ）处理后２４ｈ腺体内去甲肾上腺素（ＮＥ）含量降至正常水平的２％以下。若在６－ＯＨＤＡ处理同时开始多次给予神经生长因子（ＮＧＦ）,则ＮＥ残留量明显提高。减小６－ＯＨＤＡ剂量至１０ｍｇ／ｋｇ,ＮＥ残留量增加,同时ＮＧＦ的作用亦较用６－ＯＨＤＡ１５ｍｇ／ｋｇ时更为显著。若提前２４ｈ给予ＮＧＦ,尽管仍显著提高ＮＥ残留量,但程度却显然低于与６－ＯＨＤＡ同时给予者。以上结果表明外源性ＮＧＦ对６－ＯＨＤＡ造成交感神经化学性损毁有保护作用,此作用与神经受损的严重程度以及ＮＧＦ处理时间有关。     

神经降压素对醋氨酚引起肝损伤的保护作用及其与谷胱甘肽系统的关系

本工作观察了神经降压素对醋氨酚引起的小鼠在体肝脏和离体肝细胞损伤的保护作用及其与谷胱甘肽系统的关系,结果表明,ＮＴ在整体和离体肝细胞增能减轻醋氨酚诱导的转氨酶的漏出,且在离体肝细胞部分翻转了醋氨酚引起的ＤＮＡ合成速率的下降,在离体肝细胞醋氨酚使细胞内还原谷胱甘肽,谷胱甘肽总含量和谷胱甘肽过氧化物酶活性均降低,但氧化型谷胱甘肽含量无明显改变。ＮＴ预处理后再给予醋氨酚,则ＧＳＨ含量和谷胱甘肽过氧化物醋     

GENUS ANTROPHYUM KAULF.FROM CHINA AND NEIGHBORING REGIONS

ＧＥＮＵＳＡＮＴＲＯＰＨＹＵＭＫＡＵＬＦ．ＦＲＯＭＣＨＩＮＡＡＮＤＮＥＩＧＨＢＯＲＩＮＧＲＥＧＩＯＮＳＸ．Ｃ．ＺＨＡＮＧ（Ｔｈｅｈｅｒｂａｒｉｕｍ（ＰＥ）,ＩｎｓｔｉｔｕｔｅｏｆＢｏｔａｎｙ,ＣｈｉｎｅｓｅＡｃａｄｅｍｙｏｆＳｃｉｅｎｃｅｓ,Ｂｅｉ...     

神经生长因子在6—OHDA化学性去交感神经中的保护作用

本实验用６－ＯＨＤＡ造成成年小白鼠颌下腺化学性去交感神经,观察了神经生长因子对该神经的保护作用。６－ＯＨＤＡ处理后２４小时腺体内去甲肾上腺素（ＮＥ）含量降至正常水平的２％以下。若在６－ＯＨＤＡ处理同时开始多次给予神经生长因子（ＮＧＦ）,则ＮＥ残留量明显提高。减小６－ＯＨＤＡ剂量到１０ｍｇ／ｋｇ,ＮＥ残留量增加,同时ＮＧＦ的作用亦较用６－ＯＨＤＡ１５ｍｇ／ｋｇ时列为显著。若提前２４小时给予ＮＧＦ,尽     

肾上腺髓质素（13－52）降压机制的探讨

本工作在整体和离体大鼠模型上观察研究了肾上腺髓质素（１３－５２）［ＡｄＭ（１３－５２）］的降压机制,发现ＡｄＭ（１３－５２）的降压作用可被一氧化氮合酶（ＮＯＳ）的竟争性桔抗剂Ｌ－ＮＧ－硝基－精氨酸（ＬＮＮＡ）部分抑制;ＡｄＭ（１３－５２）的舒血管作用依赖于血管内皮并可被ＬＮＮＡ抑制,且具有剂量效应关系,ＬＮＮＡ的这种效应可被Ｌ－精氨酸（Ｌ－Ａｒｇ）逆转;用亚甲蓝（ＭＢ）阻断血管内的环－磷酸鸟苷酸（ｃＧＭＰ）,则导致ＡｄＭ（１３－５２）的舒血管作用消失;放免测定显示ＬＮＮＡ可以降低血管内ｃＧＭＰ含量,而ＡｄＭ（１３－５２）则使后者含量增加,这一现象在ＡｄＭ（１３－５２）与ＬＮＮＡ合用时消失。实验结果提示,ＡｄＭ（１３－５２）的舒血管降血压效应与ＮＯ有关,可能是通过ＮＯ介导的。     

睫状神经营养因子对NO引起海马神经元毒性反应的影响

本研究采用原代培养大鼠海马神经元,观察睫状神经营养因子（ｃｉｌｉａｒｙ ｎｅｕｒｏｔｒｏｐｈｉｃ ｆａｃｔｏｒ,ＣＮＴＦ）对ＮＯ引起细胞毒性反应的影响。ＮＯ供体硝普钠与Ｓ－亚硝基－乙酰青霉胺,ＮＯＳ底物Ｌ－Ａｒｇ及钙载体ｉｏｎｏｍｙｃｉｎ,均可引起海马神经元存活率下降,ＬＤＨ漏出增加;提前２４ｈ给予不同浓度ＣＮＴＦ,均能提高神经元的存活率,减少ＬＤＨ漏出,其作用呈剂量依赖性。     

转基因猪外源基因染色体定位的研究

转基因猪外源基因染色体定位的研究ＥＸＯＧＥＮＯＵＳＧＥＮＥＬＯＣＡＬＩＺＡＴＩＯＮＯＮＣＨＲＯＭＯＳＯＭＥＳＯＦＴＲＡＮＳＧＥＮＩＣＰＩＧ关键词基因定位染色体原位杂交转基因猪ＫｅｙｗｏｒｄｓＧｅｎｅＬｏｃａｌｉｚａｔｉｏｎ,Ｉｎｓｉｔｕｈｙｂｒｉｄ...     

国外大刊重要论文简介

ＣＯＮＳＴＡＮＳ靶基因在Ａｒａｂｉｄｏｐｓｉｓ生殖发育中的不同作用ＳａｍａｃｈＡ,ＯｎｏｕｃｈｉＨ,ＧｏｌｄＳＥ,ＤｉｔｔａＧＳ,Ｓｃｈｗａｒｚ＿ＳｏｍｍｅｒＺ,ＹａｎｏｆｓｋｙＭＦ,ＣｏｕｐｌａｎｄＧＳｃｉｅｎｃｅ,2000,288:1613～1616按照拟南芥(Ａｒａｂｉｄｏ     

生物固氮作用机理

生物固氮作用机理李佳格徐继（中国科学院植物研究所,北京１０００９３）ＭＥＣＨＡＮＩＳＭＯＦＢＩＯＬＯＧＩＣＡＬＮＩＴＲＯＧＥＮＦＩＸＡＴＩＯＮＬｉＪｉａ－ｇｅＸｕＪｉ（ＩｎｓｔｉｔｕｔｅｏｆＢｏｔａｎｙ,ＣｈｉｎｅｓｅＡｃａｄｅｍｙｏｆＳｃｉｅｎｃｅ...     

表皮生长因子对肝细胞醋氨酚急性损伤的保护作用

本工作采用无血清培养的小鼠原代肝细胞制备了醋氨急性肝损伤模型,然后利用该模型观察了表皮生长因子（ＥＧＦ）对肝细胞的保护作用。结果如下：（１）小鼠原代肝细胞无血清培养液中加入终深度度为２０ｍｍｏｌ／Ｌ的醋氨酚培养１２－１４ｈ后,培养液中ＧＰＴ和ＧＰＴ的活性明显升高,可作为一种适当的肝细胞损伤。（２）提前１ｈ加入不同剂量（５０,１００,５００,１０００ｎｇ／ｍｌ）的ＥＧＦ可减轻醋氨酚相起的肝细胞损伤。     

四氯化碳中毒对大鼠离体再生肝细胞钾离子外漏的影响

本工作用三种剂量四氯化碳(CCl_4,10,15和20mmol/L)损伤正常大鼠离体肝细胞,分别在5,10,15和20min测定细胞内K~+和GPT漏出量。实验观察到细胞内K~+和GPT漏出量与CCl_4染毒的剂量和时间有明显关系,而且K~+漏出量较GPT更能灵敏地反映细胞的损伤程度;用中等剂量CCl_4(15mmol/L)损伤离体再生肝细胞20min后,细胞内K~+漏出的变化百分数明显低于正常肝细胞。这些结果表明,大鼠离体再生肝细胞具有较强的抗CCl_4损伤作用,其机制可能与再生肝细胞膜稳定性较强有关。     

15—Mt—PGF2α对CCL4所致大鼠离体肝细胞损伤的保护作用

采用大鼠离体肝细胞原代培养２４ｈ,并利用四氯化碳ＣＣｌ４造成急性肝细胞损伤模型,检定１５－甲基－前列腺素Ｆ２α（１５－Ｍｔ－ＰＧＦ２α）对肝细胞损伤的影响。结果表明：（１）１５－Ｍｔ－ＰＧＦ２α可显著降低中毒肝细胞脂质过氧化物水平,抑制肝细胞脂质过氧化,并降低谷丙转氨酶（ＧＰＴ）和谷草转氨酶（ＧＯＴ）水平,稳定脂质膜。（２）显著促进中毒肝细胞ＲＮＡ和ＤＮＡ的合成。（３）超微结构证实１５－Ｍｔ－ＰＧＦ２α能减轻ＣＣｌ４对肝细胞脂质膜,染色质,线粒体,内质网和核蛋白体的损害。     

Effect of SIN-1 in rat ventricular myocytes: interference with beta-adrenergic stimulation

We have examined the effects of the nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on Ca(2+) transients, L-type Ca(2+) current (I(Ca,L)), and cGMP/cAMP content in electrically-stimulated rat ventricular myocytes in the absence and presence of the beta-adrenergic stimulation with isoproterenol. SIN-1 had no effect at low concentrations, but decreased the amplitude of electrically-induced Ca(2+) transients at higher concentrations. SIN-1 attenuated the increase in Ca(2+) transients induced by isoproterenol in a concentration-dependent manner. SIN-1 Also reduced the amplitude of caffeine-induced Ca(2+) transients, and the increase in I(Ca,L) induced by isoproterenol. These effects of SIN-1 were associated with an increased cGMP and a decreased cAMP content in ventricular myocytes in either the absence or presence of isoproterenol. These data suggest that the inhibitory effect of SIN-1 on basal and beta-adrenergic stimulated Ca2+ signal in ventricular myocytes could be due to the depression in the SR function and I(Ca,L), possibly mediated by a cGMP/cAMP-dependent mechanism. Taken together, the present study supports the idea that NO acts as an inhibitory modulator of the cardiac function during pathological conditions associated with an abnormal production of NO such as septic shock.     

内源性一氧化氮在高血压心肌肥厚中的作用

目的和方法：本实验用Ｌ精氨酸和一氧化氮合酶（ＮＯＳ）抑制剂ＬＮＡＭＥ观察内源性一氧化氮（ＮＯ）在高血压性心肌肥厚中的作用。结果：腹主动脉缩窄引起大鼠动脉血压显著升高,左心室重量／体重比值显著增加,左心室ＮＯ含量显著下降;Ｌ精氨酸不影响主动脉缩窄大鼠动脉血压,但减轻左心室重量／体重比值,明显升高左心室ＮＯ含量,加入ＬＮＡＭＥ可消除Ｌ精氨酸的上述作用;主动脉缩窄大鼠给予ＬＮＡＭＥ,动脉血压和左心室／体重比值并没有进一步增加;假手术大鼠给予ＬＮＡＭＥ,血压明显升高,左心室重量／体重比值轻度增加;主动脉缩窄大鼠不论是服用Ｌ精氨酸还是ＬＮＡＭＥ,左心室ｃＧＭＰ含量都明显增加。结论：口服Ｌ精氨酸可减轻主动脉缩窄大鼠心肌肥厚但不影响动脉血压,此作用可能是通过Ｌ精氨酸ＮＯ途径实现的,与ｃＧＭＰ机制无关。     

Nitric oxide attenuates H(2)O(2)-induced endothelial barrier dysfunction: mechanisms of protection

Nitric oxide (.NO) attenuates hydrogen peroxide (H(2)O(2))-mediated injury in porcine pulmonary artery endothelial cells (PAECs) and modulates intracellular levels of cGMP and cAMP. We hypothesized that.NO attenuates H(2)O(2)-induced PAEC monolayer barrier dysfunction through cyclic nucleotide-dependent signaling mechanisms. To examine this hypothesis, cultured PAEC monolayers were treated with H(2)O(2), and barrier function was measured as transmonolayer albumin clearance. H(2)O(2) caused significant PAEC barrier dysfunction that was attenuated by intracellular as well as extracellular.NO generation.NO increased PAEC cGMP and cAMP levels, but treatment with inhibitors of soluble guanylate cyclase or protein kinase G did not abrogate.NO-mediated barrier protection. In contrast, H(2)O(2) decreased protein kinase A activity, and inhibiting protein kinase A abrogated the protective effect of.NO. H(2)O(2)-induced barrier dysfunction was not associated with decreased levels of cGMP or cAMP. 3-Isobutyl-1-methylxanthine and the cGMP analog 8-bromo-cGMP had little effect on H(2)O(2)-mediated endothelial barrier dysfunction, whereas 8-bromo-cAMP plus 3-isobutyl-1-methylxanthine was protective. These results indicate that.NO modulates vascular endothelial barrier function through cAMP-dependent signaling mechanisms.     

Effects of intracellular cyclic AMP and cyclic GMP levels on DNA synthesis of young-adult rat hepatocytes in primary culture.

Possible roles of dibutyryladenosine 3',5'-cyclic monophosphate (cAMP) and dibutyryl-guanosine 3',5'-cyclic monophosphate (cGMP) in regulation of hepatocyte DNA synthesis were examined using primary cultures of young-adult rat hepatocytes maintained in arginine-free medium. Throughout the experimental period, nonparenchymal cells were hardly observed in the selective medium. When epidermal growth factor (EGF) was added to the cultures, a transient increase in the intracellular cAMP level preceded the elevation of hepatocyte DNA synthesis. EGF-stimulated hepatocyte DNA synthesis was remarkably enhanced by the elevation of the intracellular cAMP level induced by treatment with cAMP alone or a combination of cAMP and theophylline, an inhibitor of cyclic nucleotide phosphodiesterase. Furthermore, the early elevation of intracellular cAMP alone, which was induced by treatment with the combination of cAMP and theophylline, caused a remarkable increase in hepatocyte DNA synthesis. On the other hand, addition of EGF to the cultures caused a rapid decrease in the intracellular cGMP level followed by an increase in hepatocyte DNA synthesis. EGF-stimulated hepatocyte DNA synthesis was severely suppressed or completely inhibited by the elevation of the intracellular cGMP level induced by treatment with cGMP alone or a combination of cGMP and dipyridamole, a specific inhibitor of cGMP phosphodiesterase. These findings indicate that cAMP and cGMP act oppositely on the regulation of DNA synthesis of young-adult rat hepatocytes in primary culture: cAMP plays a positive role, whereas cGMP plays a negative role. Also it is strongly suggested that an early elevation of the intracellular cAMP level is essential for the onset of DNA synthesis in hepatocyte primary cultures.     

高效氯氰菊酯对欧洲鲫鱼血清谷丙转氨酶和谷草转氨酶活性的影响

Synthetic pyrethroids are considered as possible sub-stitutesfor some organophosphate carbamates or organochlo-rine insecticides,and have been used extensivelyfor morethantwo decades[1].Pyrethroids are preferred over otherinsecticides because of their easy degradation into non-toxic or less toxic metabolites under natural conditions.Consequently,there has recently beena dramatic increaseinthe use of pyrethroid pesticides to control insect pests.However,synthetic pyrethroids were also reported …