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971.
本文提取人骨骼肌α辅肌动蛋白(α-actinin)是综合了文献报导有关提取兔肌α-actinin的和提取鸡胗α-actinin的方法,稍加修改而确定的。用Hasselbach-Schneider缓冲液提取骨骼肌中的肌球蛋白后,将残余物经硼酸-缓冲液提取、匀浆及高速离心去掉肌动蛋白和肌原纤维的其它成份,上清加硫酸铵至30%,35%饱合度所得的沉淀用220mmol/LTris-乙酸溶解、透析、离心后经DE-52柱层析可得电泳纯。α-actinin。将人骨骼肌α-actinin纯化制品免疫了三只大耳白纯种家兔,两个多月后,三只兔子都产生免抗人骨骼肌α-actinin的特异抗血清,用双向免疫扩散法和酶联免疫吸附试验(ELISA)测定,产生的抗体效价较高,用双扩散法测定效价为1:32,用ELISA测定,用比率法判断结果,效价最高者为1:100,000左右,经免疫电镜观察结果证实,上述抗血清可以满足进一步实验要求。 相似文献
972.
973.
菜心(BrassicacampestrisL.ssp.chinensisvar.utilis)叶子高速捣碎后,滤液经酸碱处理,硫酸铵分步沉淀,凝胶柱层析等步骤分离纯化溶菌酶,酶比活力达3414.6U/mg,纯化倍数为197.4。菜心溶菌酶在较宽的温度或pH值范围均有活性,最适温度为60℃,最适pH值为5.8,底物Km值为87μg/mL。该酶对热和酸碱的稳定性较高,巯基和酪氨酸残基不是该酶活性中心的必需基团。 相似文献
974.
本文报导了胰腺提取物中两种可被钙/钙调素依赖性蛋白激酶磷酸化的热稳定蛋白。SDS-PAGE测定其表观分子量分别为17.7kD和6kD。经钙/钙调素依赖性蛋白激酶磷酸化后,其最大磷酸参入量为8.8μmol/g蛋白。同时磷酸化作用导致17.7kD蛋白在SDS-PAGE中迁移率发生变化。本文还进一步分析了各种阳离子对磷酸化的影响,并对此两种蛋白可能具有的生理功能进行了初步探讨。 相似文献
975.
用共振拉曼和紫外-可见吸收光谱研究了水溶金属卟啉4-N-乙酸乙酯基-吡啶基铜卟啉和镍卟啉[简称Cu(NEAE)和Ni(NEAE)]及4-N-乙腈基-吡啶基铜卟啉[简称Cu(NACN)]与小牛胸腺DNA的相互作用。分析表明Cu(NEAE)、Ni(NEAE)和Cu(NACN)分别以外部键联、部分插入和沟槽方式与DNA作用;卟啉插入DNA时吡啶基团向卟啉环平面转动但不可能转成与之共面;而以非插入方式作用时吡啶基团会向垂直于或者平行于卟啉环平面转动。吡啶取代基的大小和空间位阻是影响相互作用方式的关键因素之一。 相似文献
976.
从对照和用DEHP处理的大鼠肝脏提取核蛋白,以含酰基CoA氧化酶(AOX)基因表达调控部位的DNA片段和该基因的不同蛋白结合位点的DNA片段作为核蛋白结合反应的探针,通过凝胶电泳迁移率改变实验和Southwestern印迹分析检查了DEHP对AOX基因反式作用因子的影响。结果表明,降血脂药物DEHP可显著增加AOX基因反式作用因子的含量和(或)与基因的结合活性,在转录水平上促进基因的表达。 相似文献
977.
Y. Li M. M. Bhargava A. Joseph L. Jin E. M. Rosen I. D. Goldberg 《In vitro cellular & developmental biology. Animal》1994,30(2):105-110
Summary Using an automated cell analyzer system, the effect of hepatocyte growth factor/scatter factor (HGF/SF), epidermal growth
factor (EGF), basic fibroblast growth factor (bFGF), endothelial acidic fibroblast growth factor (a-FGF), platelet derived
growth factor (PDGF), and recombinant human insulinlike growth factor (IGF) on the motility and morphology of Madin-Darby
canine kidney (MDCK), rat hepatomas, C2, and H5–6 and murine mammary carcinoma (EMT-6) cells was investigated. Treatment of MDCK cells with HGF/SF, bFGF, EGF, and a-FGF resulted
in an increase in average cell velocity and in the fraction of moving cells. Cells treated with the PDGF and IGF did not show
significant alterations in velocity. MDCK cells treated with each growth factor were classified into groups of “fast” and
“slow” moving cells based on their average velocities, and the average morphologic features of the two groups were quantitated.
Fast-moving cells had larger average area, circularity, and flatness as compared to slow-moving cells. Factors that stimulated
cell movement also induced alterations in cell morphologic parameters including spreading, flatness, area, and circularity.
HGF/SF also scattered and stimulated motility of C2 and H5–6 hepatoma cells. In contrast to MDCK cells, there was no significant difference between the morphology of the fast moving
and slow moving C2 and H5–6 cells. These studies suggest that growth factor cytokines have specific effects on motility of normal and tumor cells. 相似文献
978.
Zhuang XC Sun YZ Cui J Zhu JM Jiang C Xiang QL Li CS 《Journal of gravitational physiology : a journal of the International Society for Gravitational Physiology》1994,1(1):P61-P63
In the environment of microgravity, the disused atrophy of skeletal muscle, especially leg's muscle, would occur. The three purposes of this study were: 1. To observe the dynamic changes of disused atrophy of skeletal muscle under simulated weightlessness; 2. To approach the mechanism of disused atrophy of muscle; 3. To approach the countermeasures for reducing the degree of atrophy of muscle. 相似文献
979.
Wen-Hsiung Li 《Journal of molecular evolution》1993,36(1):96-99
Summary The current convention in estimating the number of substitutions per synonymous site (K
S
) and per nonsynonymous site (K
A
) between two protein-coding genes is to count each twofold degenerate site as one-third synonymous and two-thirds nonsynonymous
because one of the three possible changes at such a site is synonymous and the other two are nonsynonymous. This counting
rule can considerably overestimate theK
S
value because transitional mutations tend to occur more often than transversional mutations and because most transitional
mutations at twofold degenerate sites are synonymous. A new method that gives unbiased estimates is proposed. An application
of the new and the old method to 14 pairs of mouse and rat genes shows that the new method gives aK
S
value very close to the number of substitutions per fourfold degenerate site whereas the old method gives a value 30% higher.
Both methods give aK
A
value close to the number of substitutions per nondegenerate site. 相似文献
980.
Lymphocytes protect against and are not required for reovirus-induced myocarditis. 总被引:11,自引:10,他引:1
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Many studies suggest that host lymphocytes are damaging, rather than protective, in virally induced myocarditis. We have investigated the role of lymphocyte-based immunity in murine myocarditis by using a myocarditic reovirus (reovirus serotype 3 8B), nonmyocarditic reoviruses, adoptive transfer experiments, and mice with severe combined immunodeficiency (SCID mice). Prior to infection, passive transfer of monoclonal antibodies specific for 8B capsid proteins protected neonatal mice against 8B-induced myocarditis, indicating that humoral immunity can protect against myocarditis. Some monoclonal antibodies acted by blocking viral spread to and/or replication in the heart. Passive transfer of reovirus-immune, but not naive, spleen cells prior to infection protected neonatal mice from 8B-induced myocarditis. Depletion of either CD4 or CD8 T cells resulted in increased viral titer in the heart but did not abrogate immune cell-mediated protection against myocardial injury. This shows that both CD4 and CD8 T cells can act independently to protect myocardial tissue from reovirus infection. In addition, reovirus 8B caused extensive myocarditis in SCID mice. This confirms a prior report (B. Sherry, F. J. Schoen, E. Wenske, and B. N. Fields, J. Virol. 63:4840-4849, 1989) that T cells are not required for reovirus-induced myocarditis and demonstrates for the first time that B cells are not required for reovirus-induced myocarditis. We used SCID mice and a panel of reoviruses to assess (i) the relationship between growth in the heart and myocardial damage and (ii) the possibility that nonmyocarditic reoviruses exhibit a myocarditic phenotype in the absence of functional lymphocytes. Growth in the heart was not the sole determinant of myocarditic potential in SCID mice. Although 8B induced myocarditis in SCID mice, no or minimal myocarditis was found in SCID mice infected with four reovirus strains previously shown (B. Sherry and B. N. Fields, J. Virol. 63:4850-4856, 1989) to be nonmyocarditic or poorly myocarditic in normal neonatal mice. We conclude that (i) humoral immunity and cellular immunity are protective against, and not required for, reovirus-induced myocarditis and (ii) the potential to induce cardiac damage is a property of the virus independent of lymphocyte-based immunity. 相似文献