邻二氮菲－Fe2＋氧化法检测H2O2／Fe2＋产生的羟自由基

报告检测H₂O₂/Fe^2＋所产生羟自由基的新方法. 羟自由基氧化反应后, 邻二氮菲-Fe^2＋的A₅₃₆明显下降, 且△A₅₃₆与邻二氮菲, FeSO₄及H₂O₂呈量效关系, 随反应时间延长, △A₅₃₆依幂函数规律上升. 此法试验结果表明, 甘露醇, 抗坏血酸及硫肥清除羟自由基作用呈明显的量效关系.     

固定化酵母细胞生产1,6-二磷酸果糖研究

本文研究了固定化酵母细胞制备果糖1,6二磷酸(FDP)的方法及其生产。用卡拉胶包埋方法固定化酿酒酵母(Sacchromyces cerevisae),对含葡萄糖1.0M,磷酸盐0.8M的糖磷液,pH6.5,在37℃下进行磷酸化反应。反复分批转化20天以上,可达到平均产FDPH_427.58mg/ml,最高为59.94mg/ml。用100ml固定化细胞生物反应器连续运转309h,稀释速率D=0.097h~(-1),平均产FDPH_4 21.51mg/ml。20L反应器连续运转,生产能力达到1.7g/h.L。用层析方法制备FDPNa_3结晶粉,提取收率为72.08％,制备质量达到或超过了国内外同类产品的质量要求。     

鹅掌楸雌配子体败育对生殖的影响

胚珠和雌配子体败育是限制鹅掌楸生殖成功的一个重要因素。中国东部和西部鹅掌楸种群在雌配子体发育的各阶段上的败育程度有差异,以西部种群的发育较好。西部分布区较合适的生境促进了胚囊的发育,一定温度和湿度的环境可以活化珠心细胞输送营养物质供给雌配子体发育,提高受精和结籽的能力     

水稻叶片对模拟酸雨伤害的生理反应

水稻暴露于ｐＨ２．５～４．２的模拟酸雨中２个月后测定表明：叶片叶绿素含量下降,细胞液离子外渗率增加,气孔阻抗增高,蒸腾速率降低。不同叶位的水稻叶片对模拟酸雨的敏感性不同,杂交稻（汕优６３）对模拟酸雨的敏感性较粳稻（中粳８６４）高     

不同生长期蛋鸡的体脂水平和肝脏脂肪酸合成酶活性的关系

 不同生长期蛋鸡的体脂水平和肝脏脂肪酸合成酶活性的关系田维熙,董妍,权晖,陈文峰（中国科学院研究生院生物教学部,北京１０００３９）动物体脂的控制是一个复杂过程．不同种类不同年龄的动物体脂水平有很大差异,控制机制是什么,哪些是关键的控制因素？不久前我们曾...     

GPX－abzyme对受XO／HX系统损伤的心肌线粒体的保护作用

探讨了研制的具有谷胱甘肽过氧化物酶活力的含硒抗体酶（ＧＰＸ－ａｂｚｙｍｅ）对于受损心肌线粒体的保护作用,利用牛的心肌线粒体为实验材料,通过线粒体的膨胀度、脂质过氧化物含量、ＣＣＯ活力变化及电镜观察等几个方面证明ＧＰＸ－ａｂｚｙｍｅ能抵抗ＸＯ／ＨＸ系统产生的自由基的损伤作用,ＥＳＲ研究也表明ＧＰＸ－ａｂｚｙｍｅ能明显降低ＸＯ／ＨＸ损伤系统中的自由基含量。     

木瓜蛋白酶PPAⅢ自水解作用

木瓜蛋白酶ＰＰＡⅢ自水解作用王秀艳,周慧,葛玉斌,李惟（吉林大学分子生物学系,长春１３００２３）ＰＰＡⅢ、ｐａｐａｉｎ、ｐｅｐｓｉｎｅ、ｓｔｅｍｂｒｏｍｅｌａｉｎ等都属于以Ｃｙｓ－ＳＨ为活性中心的酶,同种分子之间存在着一种相互切割的趋势,称为酶自水解...     

A NEW SPECIES OF GENUS GRYPOCENTRUS RUTHE (HYMENOPTERA: ICHNEUMONIDAE)

Abstract  One new species of Grypocentrus , namely G. kasparyani , collected in Shenyang, China, is described.     

Laminin and Neuropeptide Y Are Increased by Synapsin Transfection in Cultured NG108-15 Neuroblastoma/Glioma Hybrid Cells

Abstract: We have investigated the presence and expression of laminin and neuropeptide Y (NPY) in several NG108-15 cell lines transfected with synapsin Ib, IIa, or IIb. The content of laminin, a basal membrane glycoprotein that promotes adhesion and induces neurite outgrowth and neuronal differentiation, was increased in all transfected cell lines examined. In cells that were chemically differentiated with prostaglandin E₁ plus 3-isobutyl-1-methylxanthine, laminin levels were increased even further. The content of NPY, suggested to be a neurotransmitter/neuromodulator in peripheral sympathetic neurons as well as in central neurons, was also increased in all transfected cell lines examined. Immunohistochemical analysis combined with confocal laser microscopy showed that NPY staining was granular and very often enriched in neuritic varicosities. The distribution and the staining pattern of NPY were consistent with storage of NPY in large dense-cored vesicles. The results indicate that, in differentiated neurons, the synapsins increase the levels of a neuropeptide transmitter stored in large dense-cored vesicles and of an extracellular matrix protein associated with neuronal maturation.     

Human immunodeficiency virus type 1 envelope protein does not stimulate either prostaglandin formation or the expression of prostaglandin H synthase in THP-1 human monocytes/macrophages.

Prostaglandin E2 is observed at elevated levels during human immunodeficiency virus (HIV) infection and thus may contribute to the HIV-dependent immunosuppression. The mechanisms responsible for this increase are not understood. Evidence indicates that the viral envelope proteins perturb membrane signaling mediated by the CD4 receptor, suggesting that the free envelope protein and/or the intact virus may be responsible for the increase in prostaglandin E2 levels. In this study, we have used THP-1 human monocytes and THP-1 cells differentiated by 12-O-tetradecanoylphorbol-13-acetate treatment into macrophages to determine if the HIV envelope protein, gp120, or an anti-CD4 receptor antibody stimulates prostaglandin formation by interacting with the CD4 receptor. Incubation of THP-1 cells with OKT4A antibody greatly stimulated the CD4-p56lck receptor complex as estimated by enhanced p56lck autophosphorylation, while the gp120 gave small but significant responses. Monocytic THP-1 cells poorly metabolized arachidonic acid to prostaglandin E2 and thromboxane B2 as measured by high-pressure liquid chromatography analysis. Western blot (immunoblot) and Northern (RNA) blot analyses revealed that unstimulated monocytes expressed little prostaglandin H synthase 1 and 2 (PGHS-1 and -2). Incubation of the monocytes with lipopolysaccharide, OKT4A, or gp120 did not increase the formation of prostaglandins. The expression of PGHS-1 or PGHS-2 was also not increased. Differentiation of the monocytes to macrophages by 12-O-tetradecanoylphorbol-13-acetate treatment resulted in increased expression of PGHS-1 and increased formation of prostaglandins compared with that for the monocytes. Lipopolysaccharide stimulation of the macrophages increased the formation of prostaglandins and increased the expression of PGHS-2 in the macrophages. However, OKT4A or gp120 preparation, at concentrations that stimulated p56lck autophosphorylation, did not enhance the formation of prostaglandins or the expression of PGHS-1 or PGHS-2. OKT4A and gp120 also did not stimulate the release of arachidonic acid, indicating that phospholipase A2 was not activated by the CD4 receptor in either the THP-1 monocytes or macrophages. These results indicate that activation of the CD4-p56lck receptor signal transduction pathway by the HIV envelope protein does not increase prostaglandin formation.