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101.
Abstract One new species of Grypocentrus , namely G. kasparyani , collected in Shenyang, China, is described. 相似文献
102.
Laminin and Neuropeptide Y Are Increased by Synapsin Transfection in Cultured NG108-15 Neuroblastoma/Glioma Hybrid Cells 总被引:2,自引:0,他引:2
† Gabriel Fried Hui Quan Han ‡Björn Meister ‡Tomas Hökfelt Paul Greengard 《Journal of neurochemistry》1995,64(6):2674-2680
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. 相似文献
103.
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. 下载免费PDF全文
R Hui J F Curtis M T Sumner S B Shears W C Glasgow T E Eling 《Journal of virology》1995,69(12):8020-8026
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. 相似文献
104.
康宁木霉CP88329纤维素酶产生条件的研究 总被引:27,自引:2,他引:25
从生霉棉布上分离出的康宁木霉CP88105经诱变处理,获得一株高产纤维素酶的突变株CP88329。在固体培养基上,28℃培养72小时,所产纤维素酶固体曲,以羧甲基纤维素钠为底物酶活力为4880u/g;以脱脂棉为底物酶活力为480u/g。产酶活力水平均为出发菌的3倍。酶在脱脂棉上作用最适条件为pH4.5-5.0,45-50℃;45℃保温4h,pH稳定范围为3.5-6.5;60℃保温1h,酶活力剩余20%。酶可用于苎麻布抛光处理和牛仔服“石磨”处理。 相似文献
105.
Thermotolerance in cultures of Chlorella zofingiensis was induced by heat shock treatment at supraoptimal temperatures (40and
45 °C for 30 min). Thermotolerance was assayed by two methods: the survival of the cells at 70 °C and the growth of diluted
cultures at 35 and 45 °C. A culture without heat shock treatment was unable to grow at 45 °C. According to eletrophoretic
analyses, the synthesis of proteins of 95, 73, 60, 43 and 27 kDa was induced by heat shock treatment. The large molecular
weight proteins (95, 73, 60 and43 kDa) were present in non-heat treated cells, but the heat shock treatment increased their
quantity in cells. The synthesis of a low molecular weight protein (27 kDa) was induced by heat shock treatment. The induced
thermotolerance could be inhibited by the presence of an 80S ribosomal translation inhibitor, cycloheximide(CHI). The first
12 amino acid residues from the N-terminus of the27 kDa heat shock induced protein are Val-Glu-Trp-Try-Gly-Pro-Asn-Arg-Ala-Lys-Phe-Leu.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
106.
107.
Selective Changes in Cell Bodies and Growth Cones of Nerve Growth Factor-Differentiated PC12 Cells Induced by Chemical Hypoxia 总被引:2,自引:1,他引:1
Abstract: Cytosolic free Ca2+ concentration ([Ca2+]i) was measured in differentiated PC12 cells to test whether chemical hypoxia selectively alters intracellular Ca2+ in growth cones and cell bodies. Hypoxia increased [Ca2+]i and exaggerated its response to K+ depolarization in both parts of the cells. [Ca2+]i in the cell bodies was greater than that in the growth cones under resting conditions and in response to K+ or hypoxia. Ca2+-channel blockers selectively altered these responses. The L-channel blocker nifedipine reduced [Ca2+]i following K+ depolarization by 67% in the cell bodies but only 25% in the growth cones. In contrast, the N-channel blocker ω-conotoxin GVIA (ω-CgTX) diminished K+-induced changes in [Ca2+]i only in the growth cones. During hypoxia, nifedipine was more effective in the cell bodies than in the growth cones. During hypoxia, ω-CgTX diminished K+-induced changes by 50–75% in both parts of the cell, but only immediately after depolarization. The combination of nifedipine and ω-CgTX diminished the [Ca2+]i response to K+ with or without hypoxia by >90% in the cell body and 70% in the growth cones. Thus, the increased Ca2+ entry with K+ during hypoxia is primarily through L channels in the cell bodies, whereas in growth cones influx through L and N channels is about equal. The results show that chemical hypoxia selectively alters Ca2+ regulation in the growth cone and cell body of the same cell. 相似文献
108.
甘蔗抗逆细胞系选择及其生化特性的研究 总被引:1,自引:0,他引:1
利用脯氨酸类似物羟脯氨酸(Hyp)的生长抑制作用,筛选出抗Hyp的甘蔗(Saccha-rum sinensis Roxb)细胞变异系R932。抗性系体内游离脯氨酸含量超常积累(×3.2)。而且其体内脯氨酸合成途径中的关键酶γ-谷氨酸激酶对脯氨酸的反馈抑制较不敏感。R932抗PEG和低温能力较供体加强。实验结果表明γ-谷氨酸激酶特性的变化可能导致细胞内脯氨酸的过量积累,脯氨酸的过量积累有利于植物细胞对抗恶劣环境。 相似文献
109.
软骨血管生成抑制因子抑制血管生成的研究 总被引:14,自引:1,他引:13
小牛气管软骨经盐酸胍抽提,丙酮分级沉淀,膜超滤,柱层析等步骤得到软骨血管生成抑制因子(cartilage angiogenesis inhibiting factor,CAIF).SDS-聚丙烯酰胺凝胶电泳显示CAIF由单一组分组成,分子量为27700.通过[ 3H]-TdR掺入,活细胞检测等方法测定CAIF对内皮细胞、Hela细胞、QGY7703细胞与小鼠骨髓细胞、人皮肤成纤维细胞等的DNA合成的影响,以及细胞毒作用.采用鸡胚绒毛尿囊膜实验测定CAIF对血管生成的抑制效应.结果显示:CAIF对内皮细胞产生强的抑制作用,对Hela细胞抑制很弱,对QGY7703细胞、小鼠骨髓细胞、人皮肤成纤维细胞均无抑制作用;对鸡胚绒毛尿囊膜的血管生成产生明显的抑制作用.提示CAIF能较特异地抑制血管生成,CAIF达到电泳纯,是专一性较强的血管生成抑制因子. 相似文献