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153.
Mitochondrial proteomic analysis of a cell line model of familial amyotrophic lateral sclerosis 总被引:3,自引:0,他引:3
Fukada K Zhang F Vien A Cashman NR Zhu H 《Molecular & cellular proteomics : MCP》2004,3(12):1211-1223
Mutations in copper-zinc superoxide dismutase (SOD1) have been linked to a subset of familial amytrophic lateral sclerosis (fALS), a fatal neurodegenerative disease characterized by progressive motor neuron death. An increasing amount of evidence supports that mitochondrial dysfunction and apoptosis activation play a critical role in the fALS etiology, but little is known about the mechanisms by which SOD1 mutants cause the mitochondrial dysfunction and apoptosis. In this study, we use proteomic approaches to identify the mitochondrial proteins that are altered in the presence of a fALS-causing mutant G93A-SOD1. A comprehensive characterization of mitochondrial proteins from NSC34 cells, a motor neuron-like cell line, was achieved by two independent proteomic approaches. Four hundred seventy unique proteins were identified in the mitochondrial fraction collectively, 75 of which are newly discovered proteins that previously had only been reported at the cDNA level. Two-dimensional gel electrophoresis was subsequently used to analyze the differences between the mitochondrial proteomes of NSC34 cells expressing wild-type and G93A-SOD1. Nine and 36 protein spots displayed elevated and suppressed abundance respectively in G93A-SOD1-expressing cells. The 45 spots were identified by MS, and they include proteins involved in mitochondrial membrane transport, apoptosis, the respiratory chain, and molecular chaperones. In particular, alterations in the post-translational modifications of voltage-dependent anion channel 2 (VDAC2) were found, and its relevance to regulating mitochondrial membrane permeability and activation of apoptotic pathways is discussed. The potential role of other proteins in the mutant SOD1-mediated fALS is also discussed. This study has produced a short list of mitochondrial proteins that may hold the key to the mechanisms by which SOD1 mutants cause mitochondrial dysfunction and neuronal death. It has laid the foundation for further detailed functional studies to elucidate the role of particular mitochondrial proteins, such as VDAC2, in the pathogenesis of familial ALS. 相似文献
154.
E K Silverman J D Mosley D C Rao L J Palmer M A Province R C Elston S T Weiss E J Campbell 《Human heredity》2001,52(4):223-232
OBJECTIVES: Severe alpha 1-antitrypsin (A1AT) deficiency is the one proven genetic risk factor for chronic obstructive pulmonary disease (COPD). Familial aggregation has been demonstrated for COPD among individuals who do not have A1AT deficiency, but linkage analysis of COPD has not been reported. To investigate the optimal phenotype definitions and analytical methods for the linkage analysis of COPD, we examined a set of 28 A1AT- deficient families containing 155 individuals. We have used the protease inhibitor (PI) type as a genetic marker rather than a disease gene, and we have performed linkage analysis between PI type and serum A1AT level and spirometry-related phenotypes. METHODS: Linkage analysis was performed on the quantitative phenotypes forced expiratory volume at 1 s (FEV(1) as % predicted), the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC as % predicted), and serum A1AT level using the variance component approach in SOLAR, the generalized estimating equation approach in RELPAL, and the model-based classical lod score method in LINKAGE. Linkage analysis with qualitative A1AT and spirometry phenotypes was performed using a model-based method (LINKAGE) and a model-free method (GENEHUNTER). Adjustments for smoking effects were investigated under each method. RESULTS: All of the methods demonstrated linkage of PI type to serum A1AT level. Interestingly, however, the other quantitative phenotypes provided only weak evidence for linkage of PI type to lung disease. Better evidence for linkage of lung disease to PI type was found using a moderate or a mild threshold for the definition of airflow obstruction. CONCLUSIONS: For linkage analysis of spirometry phenotypes in A1AT deficiency, qualitative phenotypes provided stronger evidence for linkage than quantitative phenotypes. Possible contributors to the stronger evidence for linkage to qualitative spirometry phenotypes include the ascertainment scheme and the nonnormality of the pulmonary function data in PI Z subjects. This study provides guidelines for studies of the genetics of COPD unrelated to A1AT deficiency. 相似文献
155.
二爪螨属和中(虫穴)螨属各一新种(蜱螨亚纲,前爪螨科,(虫穴)螨科) 总被引:1,自引:0,他引:1
记述尾足螨股前爪螨科二爪螨属1新种,具齿二爪螨Dinychus dentatus sp.nov.和革螨股(虫穴)螨科中(虫穴)螨属1新种,敦化中(虫穴)螨Mesozercon dunhuaensis sp.nov.,中(虫穴)螨属在中国为首次记录. 相似文献
156.
[目的]观察西药配合中成药治疗猕猴奇异变形杆菌性腹泻的疗效。[方法]将63例奇异变形杆菌性腹泻病猴随机分为两组,治疗组41例,予黄连素注射液、藿香正气水等中成药,并配合敏感抗生素治疗;对照组22例,只予抗生素治疗。[结果]治疗组有效率85.4%,对照组59.l%。两组疗效比较,差异显著(P<0.05)。[结论]中西药合治疗效优于单纯抗生素治疗。 相似文献
157.
Cross-trait familial resemblance for body fat and blood pressure: familial correlations in the Québec Family Study. 下载免费PDF全文
T. Rice M. Province L. Prusse C. Bouchard D. C. Rao 《American journal of human genetics》1994,55(5):1019-1029
Cross-trait resemblance between body fat and blood pressure (BP) was examined among families in the Québec Family Study by using a bivariate familial correlation model assessing both intraindividual (e.g., comparison of father's body fat with his own BP) and interindividual (e.g., comparison of father's body fat with son's BP) cross-trait correlations. Each of six body-fat measures-(i) percent body fat, (ii) body-mass index, (iii) the sum of six skinfolds, (iv) the ratio of the sum of six skinfolds to total fat mass, (v) the ratio of the trunk skinfold sum to the extremity skinfold sum, and (vi) the regression of the trunk-extremity skinfold ratio on the sum of six skinfolds--was analyzed separately with systolic BP and with diastolic BP. Results showed that (1) upper-body fat was the strongest interindividual correlate of BP (especially the correlation of trunk-extremity ratio with diastolic BP), suggesting shared pleiotropic genetic and/or common familial environmental effects; (2) summary body-fat measures either were inconsistent (in the case of both percent body fat and sum of six skinfolds) or gave no evidence of interindividual cross-trait resemblance with BP (in the case of body-mass index); and (3) intraindividual resemblance between the sum of six skinfolds and BP largely vanished once the skinfold sum was adjusted for fat mass, suggesting that the intraindividual association may be mediated largely by the absolute amount of subcutaneous fat rather than by the subcutaneous proportion. Finally, the magnitude of the spouse resemblance for the trunk-extremity ratio with diastolic BP suggests that a significant proportion of the resemblance may be due to environmental influences. In summary, our investigation confirms a heritable link between BP and truncal-abdominal fat as predicted by the metabolic-syndrome hypothesis. That this result is obtained in primarily normotensive, nonobese families, suggests the connection involves normal metabolic paths. 相似文献
158.
应用回春生制剂对肝硬化,各型肝炎治疗效果的观察 总被引:3,自引:1,他引:3
取从一健康成人分出的青春型双歧杆菌制成活菌制剂,观察其对肝硬化和各型肝炎的疗效。实验组患者除接受与对照组同样的常规治疗外,加服回春生。检测实验组和对照组麝香草酚浊度试验(TTT)并进行比较,结果表明,用回春生治疗后,肝硬化组34例(P<0.05),慢性活动性肝炎组39例(P<0.01),急性黄疸性肝炎组21例(P<0.05)TTT 比值均明显低于对照组相应为21,32,19例,提示:回春生影响患者肝脏内促进改善蛋白代谢具有较好的调节作用。 相似文献
159.
拟诺卡菌属(Nocardiopsis)是拟诺卡菌科(Nocardiopsaceae) 的唯一属.该属内进行物种鉴别时通常是在多相分类方法基础上,以全基 因组杂交同源性在70%以下的为不同物种,此为国际公认的定种标准;但在 进行大量菌株的比对时操作比较复杂,于是多种基于DNA的基因图谱技术发 展起来.本实验利用适宜引物,对拟诺卡菌属15株基准株基因组DNA的16S -23S rDNA 间隔区序列(ITS)和REP序列进行了扩增,获得了两种基因指 纹图谱,同时根据UPGMA聚类法构建了相应的进化距离树图.结果表明,对 于拟诺卡菌属中不同物种的区分,两种基因图谱技术的分辨力相当,均可 以较好的呈现物种间差异,可以作为拟诺卡菌属菌株多相分类的组成部分 ,应用于物种水平的分类与鉴定. 相似文献
160.
J. Kleffe M. A. Province D. C. Rao 《Biometrical journal. Biometrische Zeitschrift》1993,35(8):899-915
MINQUE (Minimum Norm Quadratic Unbiased Estimators) theory is applied to the problem of estimation of variance components in family data (siblings) with variable family size. Using this approach, the traditional iterative maximum likelihood estimators are shown to be asymptotically normal, even though the data come from non-identical parent distributions. Asymptotic expressions are also obtained for the variance of the MINQUE estimators which hold even if the data are decidedly non-normal (e.g. a mixture of normals). In the case of normal data, exact small-sample variance estimates are derived. Simulations demonstrate the fast rate of convergence to asymptotic properties as the number of families increases. These desirable qualities suggest that the easy to compute MINQUE class of estimators may provide a useful alternative method for modelling familial aggregation. 相似文献