小鼠卵激活过程中胞质游离Ca~(2 )的变化及孤雌发育研究

乙醇和电刺激均可使小鼠MⅡ期卵母细胞激活并在体外孤雌发育至囊胚。小鼠卵对乙醇十分敏感。用7%—8%乙醇处理5min后95%以上的卵母细胞(卵龄为HCG注射后18—19h)内形成原核。3—4次电刺激后卵的激活率为71.58%;仅刺激1次卵的激活率为63.63%。乙醇刺激可诱导卵内游离Ca~(2 )浓度出现多次升高;单一电刺激仅能诱导卵内游离Ca~(2 )浓度出现1次升高;多次电刺激可诱导卵内游离Ca~(2 )浓度多次升高,而且电刺激次数与Ca~(2 )浓度升高成一一对应关系。对于电刺激,介质中足够量的Ca~(2 )对卵激活至关重要。在无Ca~(2 )的介质中,电刺激很难使卵激活。正常受精刺激诱导卵内游离Ca~(2 )浓度出现多次有规律的升高。实验结果表明,卵母细胞激活过程中胞质游离Ca~(2 )浓度重复多次升高可促使卵母细胞恢复成熟分裂。     

慢性缺氧对大鼠左右心室功能、心肌肌原纤维Ca~（2＋），Mg~（2＋）－ATP

模拟５０００ｍ中度缺氧时,大鼠右室功能显著加强,而左室功能加强不显著;左右心室肌原纤维Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶活性下降,肌球蛋白同功酶Ｖ２和Ｖ３百分含量增加,Ｖ１百分含量减少。８０００ｍ重度缺氧时,右室功能减弱,但无统计学意义,左室功能减弱有显著性;ＡＴＰ酶活性和同功酶的变化超过５０００ｍ组。此外,右室ＡＴＰ酶活性与ＰＡＰ呈反比且有显著性,左室ＡＴＰ酶活性与ＣＡＳＰ虽也呈反比但无显著性;右室同功酶Ｖ３百分含量与ＰＡＰ呈正比,左室同功酶Ｖ３百分含量与ＣＡＳＰ不呈比例。上述结果表明,因短期突发严重缺氧引起的心肌供氧不足对左心室心肌的直接损伤作用大于右心室心肌。     

山羊关节炎─脑炎前病毒的PCR检测

山羊关节炎─脑炎前病毒的ＰＣＲ检测相文华,丁恩雨,秦运安,吕晓玲,沈荣显（中国农业科学院哈尔滨兽医研究所哈尔滨１５０００１）关键词聚合酶链反应,山羊关节炎—脑炎病毒,整合山羊关节炎—脑炎（ＣａｐｒｉｎｅＡｒｔｈｒｉｔｉｓ－Ｅｎｃｅｐｈａｌｉｔｉｓ,Ｃ...     

霍山三种石斛与其栽培土壤中微量元素分布关系研究

本文应用灰色系统理论,对安徽霍山三种石斛与其栽培土壤中15种微量元素分布状况进行了关联分析．结果发现.其关联序为γ_根＞γ_叶＞γ_茎;γ_(-年茎)≈γ_(二年茎)≈γ_(三年茎);γ_(霍斛)＞γ_(铁斛)＞γ_(铜斛).可见霍山石斛与其栽培土壤间的微量元素相关性比其它石斛强,因而可通过增施微肥的办法来提高霍山石解中某些人体必需微量元素的含量．     

藻－菌生态系统代谢功能的生态学研究

在室内模拟条件下,研究了一些生态因子对藻－菌（Ａ＋Ｂ）生态系统代谢有机碳（Ｃ６Ｈ１２Ｏ６）、ＮＨ３－Ｎ和无机磷（ＩＰ）的影响．研究结果表明,当藻－菌生态系统中藻（Ａ）或菌（Ｂ）的起始数量一定时,其代谢Ｃ６Ｈ１２Ｏ６的速率,随与之组合的Ｂ或Ａ的起始数量增加（数量比则相应降低）而增加．在光照和黑暗条件下,Ａ＋Ｂ系统代谢上述３种营养物质的速率均有一定的差异．黑暗下Ｃ６Ｈ１２Ｏ６的平均代谢速率较光照下高１２．３％（Ｐ＜０．０５）,ＩＰ和ＮＨ３－Ｎ的平均代谢速率则分别较光照下低１４．４％（Ｐ＜０．０５）和１６．２％（Ｐ＜０．００１）．在Ａ＋Ｂ系统和Ａ、Ｂ单培养物中,３种营养物质的代谢速率均随有机负荷量增加而增加,而且Ａ＋Ｂ系统的代谢速率分别高于单培养的Ａ和Ｂ,其中ＮＨ３－Ｎ代谢尤为显著．文章还就生态系统结构与功能的关系问题进行了讨论．     

不同树种混交林及其纯林对土壤理化性质影响的研究

对针阔混交林土壤理化性质的研究表明,针阔混交林比针叶树纯林对土壤的改良作用要好,它使土壤总孔隙度增加２—１９％,水分含量增加６—３１％,枯枝落叶年凋落量增加２—２００％;土壤养分含量全Ｎ、ＮＨ４－Ｎ、代换性Ｃａ、代换性Ｍｇ和腐殖质含量分别增加４５—７５％、３３—８２％、５５—８５％、４４—８４％和３７—４６％．     

金属离子螯合剂对橙汁中L—抗坏血酸的保护及其机理探讨

本文研究了在加热过程中金属离子螯合剂植酸、聚磷酸钠和EDTANa_2对橙汁和橙汁模拟体系中L—抗坏血酸的稳定作用,并采用红外光谱和紫外差光谱对EDTANa_2的保护机理作了初步探讨。结果表明:植酸和聚磷酸钠均不能降低Cu~(2+)对橙汁模拟体系中L—抗坏血酸氧化降解的催化作用,而EDTANa_2不仅能络合Cu~(2+),减少L—抗坏血酸的催化降解损失,而且红外光谱和紫外差光谱及溶剂微扰研究还揭示出EDTANa_2可与L—抗坏血酸形成氢键保护,这种氢键保护作用受到糖和柠檬酸的不利影响。     

Overexpression of Arabidopsis COP1 results in partial suppression of light-mediated development: evidence for a light-inactivable repressor of photomorphogenesis.

Arabidopsis seedlings are genetically endowed with the capability to follow two distinct developmental programs: photomorphogenesis in the light and skotomorphogenesis in darkness. The regulatory protein CONSTITUTIVE PHOTO-MORPHOGENIC1 (COP1) has been postulated to act as a repressor of photomorphogenesis in the dark because loss-of-function mutations of COP1 result in dark-grown seedlings phenocopying the light-grown wild-type seedlings. In this study, we tested this working model by overexpressing COP1 in the plant and examining its inhibitory effects on photomorphogenic development. Stable transgenic Arabidopsis lines overexpressing COP1 were generated through Agrobacterium-mediated transformation. Overexpression was achieved using either the strong cauliflower mosaic virus 35S RNA promoter or additional copies of the wild-type gene. Analysis of these transgenic lines demonstrated that higher levels of COP1 can inhibit aspects of photomorphogenic seedling development mediated by either phytochromes or a blue light receptor, and the extent of inhibition correlated quantitatively with the vivo COP1 levels. This result provides direct evidence that COP1 acts as a molecular repressor of photomorphogenic development and that multiple photoreceptors can independently mediate the light inactivation of COP1. It also suggests that a controlled inactivation of COP1 may provide a basis for the ability of plants to respond quantitatively to changing light signals, such as fluence rate and photoperiod.     

Arabidopsis COP8, COP10, and COP11 genes are involved in repression of photomorphogenic development in darkness.

Wild-type Arabidopsis seedlings are capable of following two developmental programs: photomorphogenesis in the light and skotomorphogenesis in darkness. Screening of Arabidopsis mutants for constitutive photomorphogenic development in darkness resulted in the identification of three new loci designated COP8, COP10, and COP11. Detailed examination of the temporal morphological and cellular differentiation patterns of wild-type and mutant seedlings revealed that in darkness, seedlings homozygous for recessive mutations in COP8, COP10, and COP11 failed to suppress the photomorphogenic developmental pathway and were unable to initiate skotomorphogenesis. As a consequence, the mutant seedlings grown in the dark had short hypocotyls and open and expanded cotyledons, with characteristic photomorphogenic cellular differentiation patterns and elevated levels of light-inducible gene expression. In addition, plastids of dark-grown mutants were defective in etioplast differentiation. Similar to cop1 and cop9, and in contrast to det1 (deetiolated), these new mutants lacked dark-adaptive change of light-regulated gene expression and retained normal phytochrome control of seed germination. Epistatic analyses with the long hypocotyl hy1, hy2, hy3, hy4, and hy5 mutations suggested that these three loci, similar to COP1 and COP9, act downstream of both phytochromes and a blue light receptor, and probably HY5 as well. Further, cop8-1, cop10-1, and cop11-1 mutants accumulated higher levels of COP1, a feature similar to the cop9-1 mutant. These results suggested that COP8, COP10, and COP11, together with COP1, COP9, and DET1, function to suppress the photomorphogenic developmental program and to promote skotomorphogenesis in darkness. The identical phenotypes resulting from mutations in COP8, COP9, COP10, and COP11 imply that their encoded products function in close proximity, possibly with some of them as a complex, in the same signal transduction pathway.     

Evidence that methylation of the FMR-I locus is responsible for variable phenotypic expression of the fragile X syndrome.

DNA at the FMR-1 locus was analyzed by Southern blot using probe StB12.3 in an unusual fragile X family with six brothers, three of whom are affected with fragile X to varying degrees, two of whom are nonpenetrant carriers, and one of whom is unaffected. Fragile X chromosome studies, detailed physical examinations, and psychological testing were completed on all six. Two of the affected brothers and the two nonpenetrant brothers were found to be methylation mosaics. The three affected males spanned the phenotypic and cognitive spectrum of the fragile X syndrome. A correlation was seen between the degree of methylation and the phenotypic expression identified in the three affected males. The two males initially classified as nonpenetrant were found to have mild phenotypic expression which consisted of minor cognitive deficits and a partial physical phenotype. These two, who were negative on fragile X chromosome studies, were found on DNA analysis to have large broad smears, with approximately 97% of the DNA unmethylated. The results described here indicate that some "nonpenetrant" carrier males may have varying amounts of methylation of the FMR-1 region, which can result in mild expression of the fragile X syndrome. The apparently mild phenotypic and cognitive expression of the fragile X syndrome in the two males, initially classified as nonpenetrant, who are mosaic for hypermethylation of an expansion of the CGG repeat in the premutation range, indicates that expression of the syndrome is not confined to males with large, hypermethylated expansions (full mutation) but has instead a gradient effect with a threshold for the full expression of the phenotype.