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41.
42.
Production and Further Characterization of an Alkaline Elastase Produced by Alkalophilic Bacillus Strain Ya-B 总被引:2,自引:0,他引:2 下载免费PDF全文
Ying-Chieh Tsai Ray-Yeng Juang Sheun-Fuh Lin Shiow-Wen Chen Makari Yamasaki Gakuzo Tamura 《Applied microbiology》1988,54(12):3156-3161
The characteristics of the obligate alkalophilic Bacillus sp. strain Ya-B, which produces alkaline elastase extracellularly, were examined. This strain grew at pH 7.0 only in the presence of 1% or more NaCl. Its fatty acid distribution pattern was similar to that of other Bacillus species in which iso-C15 and anteiso-C15 were the most abundant fatty acids. About 120 mg of enzyme was recovered from 1 liter of culture broth in a medium (pH 10.1) containing mainly glucose, soymeal, and glycerol. The antiserum against this enzyme did not recognize microbial proteinases, such as subtilisins, but reacted with proteinase C, which was purified from commercial pronase. Chemical modification studies revealed that certain histidine and tyrosine residues might be involved in the enzyme activity. This enzyme underwent a partial unfolding at pHs higher than 12.0, as indicated by the circular dichroism study. 相似文献
43.
The proteinaceous noncompetitive inhibitor of starch phosphorylase isolated from the root of sweet potato (Ipomoea batatas [L.] Lam.) (TC Chang, JC Su 1986 Plant Physiol 80: 534-538) has been identified as a β-amylase. The starch phosphorylase inhibitor and β-amylase activities copurified to give a protein indistinguishable from commercial β-amylase by electrophoretic and immunological methods, and the two activities showed parallel responses in pH, temperature, and inhibitor sensitivity tests. The amylolytic pattern of the inhibitor corresponded to that of β-amylase and its inhibitory effect toward starch phosphorylase was due to neither deprivation of starch, the primer for the phosphorylase assay, nor the inhibitory effect of amylolytic products. 相似文献
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Keping Xie Suyun Huang Yunfang Wang Pedro J. Beltran Shin-Hun Juang Zhongyun Dong John C. Reed Timothy J. McDonnell David J. McConkey I. J. Fidler 《Cancer immunology, immunotherapy : CII》1996,43(2):109-115
Cytokine-mediated cell death in tumor cells can be achieved through endogenous nitric oxide (NO) from within tumor cells
or exogenous NO from either activated macrophages or endothelial cells. The purpose of this study was to determine the role
of Bcl-2 in NO-mediated apoptosis. The incubation of murine L929 and NIH3T3 cells with interleukin-1α (IL-1α) and interferon
γ (IFNγ) induced high endogenous NO production only in the L929 cells that also underwent apoptosis. NIH3T3 cells were not
resistant to NO-mediated apoptosis. In fact, the incubation of L929 and NIH3T3 cells with exogenous NO derived from NO donors,
sodium nitroprusside, or S-nitroso-N-acetyl-DL-penicillamine (SNAP) induced death, characterized by typical apoptotic morphology and DNA fragmentation, in both cell types,
but to a higher degree in NIH3T3 cells than in the L929 cells. We then measured the effect of Bcl-2 expression on exogenous
NO-induced apoptosis. At both the mRNA and protein levels, L929 fibroblasts expressed higher levels of endogenous mouse Bcl-2
than did NIH3T3 cells. At the same time, L929 cells were much more resistant to exogenous NO-induced cell death than were
NIH3T3 cells. The inverse correlation between mouse Bcl-2 expression and sensitivity to exogenous NO-mediated cell death was
also found in the murine K-1735 melanoma C-23 and X-21 clonal populations. Transfection of both NIH3T3 cells and L929 cells
with the human bcl-2 gene led to resistance to both exogenous and endogenous NO-mediated apoptosis. These data demonstrate that NO-mediated apoptosis
can be suppressed by expression of Bcl-2, suggesting that abnormal expression of Bcl-2 may influence the efficacy of tumor
immunotherapy.
Received: 28 June 1998 / Accepted: 23 August 1996 相似文献
46.
Themistocles L. Assimes I. -T. Lee Jyh-Ming Juang Xiuqing Guo Tzung-Dau Wang Eric T. Kim Wen-Jane Lee Devin Absher Yen-Feng Chiu Chih-Cheng Hsu Lee-Ming Chuang Thomas Quertermous Chao A. Hsiung Jerome I. Rotter Wayne H.-H. Sheu Yii-Der Ida Chen Kent D. Taylor 《PloS one》2016,11(3)
By means of a combination of genome-wide and follow-up studies, recent large-scale association studies of populations of European descent have now identified over 46 loci associated with coronary artery disease (CAD). As part of the TAICHI Consortium, we have collected and genotyped 8556 subjects from Taiwan, comprising 5423 controls and 3133 cases with coronary artery disease, for 9087 CAD SNPs using the CardioMetaboChip. We applied penalized logistic regression to ascertain the top SNPs that contribute together to CAD susceptibility in Taiwan. We observed that the 9p21 locus contributes to CAD at the level of genome-wide significance (rs1537372, with the presence of C, the major allele, the effect estimate is -0.216, standard error 0.033, p value 5.8x10-10). In contrast to a previous report, we propose that the 9p21 locus is a single genetic contribution to CAD in Taiwan because: 1) the penalized logistic regression and the follow-up conditional analysis suggested that rs1537372 accounts for all of the CAD association in 9p21, and 2) the high linkage disequilibrium observed for all associated SNPs in 9p21. We also observed evidence for the following loci at a false discovery rate >5%: SH2B3, ADAMTS7, PHACTR1, GGCX, HTRA1, COL4A1, and LARP6-LRRC49. We also took advantage of the fact that penalized methods are an efficient approach to search for gene-by-gene interactions, and observed that two-way interactions between the PHACTR1 and ADAMTS7 loci and between the SH2B3 and COL4A1 loci contribute to CAD risk. Both the similarities and differences between the significance of these loci when compared with significance of loci in studies of populations of European descent underscore the fact that further genetic association of studies in additional populations will provide clues to identify the genetic architecture of CAD across all populations worldwide. 相似文献
47.
Restriction-map variation associated with the G6PD polymorphism in natural populations of Drosophila melanogaster 总被引:10,自引:0,他引:10
Restriction-map variation was studied in 126 copies of the G6pd region in X
chromosome lines of Drosophila melanogaster from North America, Europe, and
Africa. Special attention was focused on the distribution of variation
relative to the geographically variable polymorphism for two
electrophoretic variants. Nucleotide heterozygosity as determined by eight
six-cutter restriction enzymes for the 13-kb region is estimated, on the
basis of the worldwide sample, to be 0.065%, which is the lowest value
reported for any comparable region in the D. melanogaster genome.
Significant linkage disequilibrium between electrophoretic alleles and
restriction-site variation is observed for several sites. In contrast to
published studies of other genetic regions, there are large insertions that
reach significant frequencies and are found across considerable geographic
distances. There is a clustering of this variation inside the first large
intervening sequence of the G6PD gene.
相似文献
48.
49.
Polyacrylamide gel slabs can be dried quickly without elaborate tools and the results are similar or even better than those obtained with a commercial drying apparatus. The discontinuous, sodium dodecyl sulfate, and gradient polyacrylamide gel slabs yielded similar results regardless of the staining methods, e.g., Coomassie blue, periodate-Schiff's reagent, or ammoniacal silver. 相似文献
50.
Although Abl functions in mature neurons, work to date has not addressed Abl's role on Cdk5 in neurodegeneration. We found that beta-amyloid (Abeta42) initiated Abl kinase activity and that blockade of Abl kinase rescued both Drosophila and mammalian neuronal cells from cell death. We also found activated Abl kinase to be necessary for the binding, activation, and translocalization of Cdk5 in Drosophila neuronal cells. Conversion of p35 into p25 was not observed in Abeta42-triggered Drosophila neurodegeneration, suggesting that Cdk5 activation and protein translocalization can be p25-independent. Our genetic studies also showed that abl mutations repressed Abeta42-induced Cdk5 activity and neurodegeneration in Drosophila eyes. Although Abeta42 induced conversion of p35 to p25 in mammalian cells, it did not sufficiently induce Cdk5 activation when c-Abl kinase activity was suppressed. Therefore, we propose that Abl and p35/p25 cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration. 相似文献