全文获取类型
收费全文 | 14485篇 |
免费 | 843篇 |
国内免费 | 717篇 |
出版年
2023年 | 198篇 |
2022年 | 313篇 |
2021年 | 421篇 |
2020年 | 431篇 |
2019年 | 636篇 |
2018年 | 540篇 |
2017年 | 339篇 |
2016年 | 354篇 |
2015年 | 481篇 |
2014年 | 933篇 |
2013年 | 1122篇 |
2012年 | 700篇 |
2011年 | 977篇 |
2010年 | 685篇 |
2009年 | 689篇 |
2008年 | 744篇 |
2007年 | 748篇 |
2006年 | 659篇 |
2005年 | 609篇 |
2004年 | 521篇 |
2003年 | 474篇 |
2002年 | 414篇 |
2001年 | 259篇 |
2000年 | 243篇 |
1999年 | 205篇 |
1998年 | 188篇 |
1997年 | 143篇 |
1996年 | 148篇 |
1995年 | 126篇 |
1994年 | 150篇 |
1993年 | 108篇 |
1992年 | 120篇 |
1991年 | 116篇 |
1990年 | 81篇 |
1989年 | 78篇 |
1988年 | 62篇 |
1987年 | 72篇 |
1986年 | 67篇 |
1985年 | 118篇 |
1984年 | 114篇 |
1983年 | 79篇 |
1982年 | 93篇 |
1981年 | 97篇 |
1980年 | 89篇 |
1979年 | 62篇 |
1978年 | 58篇 |
1977年 | 42篇 |
1976年 | 45篇 |
1975年 | 21篇 |
1974年 | 26篇 |
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
131.
T cells in murine lupus: propagation and regulation of disease 总被引:4,自引:0,他引:4
MRL/Mp-lpr/lpr mice develop a spontaneous lupus syndrome, including hypergammaglobulinemia, autoantibodies, glomerulonephritis, and lymphadenopathy. To investigate the role of lymphocyte subsets in the pathogenesis of disease, lupus-prone MRL mice deficient in T cells, T cells, or both were generated. Mice deficient in T cells developed a partially penetrant lupus syndrome, characterized by lymphadenopathy, elevated levels of class-switched immunoglobulins, an increased incidence of antinuclear antibodies, and immune deposits in kidneys which progressed to renal insufficiency over time. In comparison to wild type animals, T cell-deficient animals developed an accelerated and exacerbated disease phenotype, characterized by accelerated hypergammaglobulinemia and enhanced autoantibody production and mortality. Repertoire analysis of these latter animals identified polyclonal expansion (V) of CD4+B220-cells. Mice lacking both and T cells failed to generate class-switched autoantibodies and immune complex renal disease. First, these findings demonstrate that murine lupus in the setting of Fas-deficiency does not absolutely require the presence of T cells, and they also suggest that a significant basis for MRL/lpr disease, including renal disease, involves T cell-independent, T cell dependent, polyreactive B cell autoimmunity, upon which T cell-dependent mechanisms aggravate specific autoimmune responses. Second, these data indicate that T cells partake in the regulation of systemic autoimmunity, presumably via their effects on CD4+B220-T cells that provide B cell help. Finally, these results demonstrate that MRL/lpr B cells, despite their intrinsic abnormalities, cannot per se cause tissue injury without T cell help.Abbreviations snRNPs
small nuclear ribonucleoprotein particles 相似文献
132.
Some novel transcription attenuation mechanisms used by bacteria 总被引:2,自引:0,他引:2
133.
Isolation of a gene essential for biosynthesis of the lipopeptide antibiotics plipastatin B1 and surfactin in Bacillus subtilis YB8 总被引:12,自引:0,他引:12
Bacillus subtilis YB8 was found to produce the lipopeptide antibiotics surfactin and plipastatin B1. A gene, lpa-8, required for the production of both lipopeptides was cloned from strain YB8. When this gene was inactivated in strain YB8,
neither surfactin nor plipastatin B1 was produced. However, the defective strain transformed with an intact lpa-8 gene had restored ability to produce both peptides. Nucleotide sequence analysis of the region essential for the production
of the peptides revealed the presence of a large open reading frame. The deduced amino acid sequence of lpa-8 (224 amino acid residues) showed sequence similarity to that of sfp (from surfactin-producing B. subtilis), lpa-14 (from iturin A- and surfactin-producing B. subtilis), psf-1 (from surfactin-producing Bacillus pumilus), gsp (from gramicidin-S-producing Bacillus brevis), and entD (from siderophore-enterobactin-producing Escherichia coli), which are able to complement a defect in the sfp gene and promote production of the lipopeptide antibiotic surfactin. The sequence similarity among these proteins and the
product similarity of cyclic peptides suggests that they might be involved in the biosynthesis or secretion of the peptides.
Received: 14 July 1995 / Accepted: 22 December 1995 相似文献
134.
The content of reduced glutathione and of glutathione disulfide as well as the activities of glutathione reductase, glutathione peroxidase, glutathione S-transferases, catalase and superoxide dismutases were determined in human hepatoma Hep 3B cells in relation to free-radical toxicity in order to appreciate the defense capacities of these cells compared to data on normal hepatocytes. When Hep 3B cells were exposed to lindane, a known inducer of free-radical production, superoxide dismutase activity appeared as the best-adapted cellular parameter for early detection of the resulting free-radical toxicity.Abbreviations AAS
atomic absorption spectrometry
- CDNB
1-chloro-2,4-dinitrobenzene
- DMEM
Dulbecco's modified Eagle medium
- GPx
glutathione peroxidase
- G.Red
glutathione reductase
- GSH
reduced glutathione
- GSSG
glutathione disulfide
- GST
glutathione S-transferases
- Prot
proteins
- SOD
superoxide dismutase 相似文献
135.
乙肝病毒PreSl片段与乙肝表面抗原羧端的融合表达 总被引:4,自引:0,他引:4
我们利用聚合酶链反应法(PCR)得到了编码乙肝病毒肝细胞受体结合位点PreSl(21 ̄47)的基因片段,并将它分别融合到S基因中相应于第175,188和223位氨基酸残基处。所得到的融合基因插入痘苗病毒表达载体pGJP-5后,在哺乳动物细胞CV-1中进行了暂时表达,对融合蛋白的表达、分泌和抗原性的研究表明,3种融合基因均能表达具有S和PreSl双重抗原性的融合蛋白,但融合位点对表达水平和分泌性质有 相似文献
136.
牛肝提取物提高仔鸡免疫力的研究 总被引:15,自引:0,他引:15
将牛肝提取物注射到第13日龄和第15日龄鸡胚中能显著提高孵出后仔鸡的抗SRBC血清抗体的效价,促进脾和法氏囊淋巴细胞增殖、分化。同时,牛肝提取物与雏鸡法氏囊粗提取液,抗鸡法氏囊病毒抗体均有增强仔鸡抵抗传染性法氏囊病的能力。实验结果表明牛肝提取物中可能含有类似法氏囊素的物质。 相似文献
137.
应用PCR技术扩增出HBVDNAC基因片段并与pAT153质粒重组,转化到E.coliRRI中,经体内扩增,提纯,用光生物素标记,制备了C基因的重组质粒探针。该探针检测灵敏度在Southern印迹中达1pg,在点印迹中为5pg。用此探针以Southern印迹方式配合PCR技术检测乙肝病人血清中的HBVDNA,在53例PCR产物电泳检测阴性的样品中,Southern杂交又检出18例阳性。 相似文献
138.
本文比较了用HSV-1(IEA)和B病毒(IFA)的方法检查猴B病毒相关抗体和B病毒抗体的结果:IEA检查出的B病毒相关抗体阴性猴,经IFA检查,全部为B病毒抗体阴性。用IFA检查了B病毒相关抗体阴性的恒河猴,在单笼隔离饲养六个月后,有98.3%的动物B病毒相关抗体仍为阴性,表明IRA的阴性结果有较好的一致性。本文讨论了建立无B病毒感染猴群的可行性。 相似文献
139.
D. M. Stresser G. S. Bailey D. E. Williams L. F. Bjeldanes 《Journal of biochemical and molecular toxicology》1995,10(4):191-201
Dietary indole-3-carbinol inhibits carcinogenesis in rodents and trout. Several mechanisms of inhibition may exist. We reported previously that 3,3′-diindolylmethane, an in vivo derivative of indole-3-carbinol, is a potent noncompetitive inhibitor of trout cytochrome P450 (CYP) 1A-dependent ethoxyresorufin O-deethylase with Ki values in the low micromolar range. We now report a similar potent inhibition by 3,3′-diindolylmethane of rat and human CYP1A1, human CYP1A2, and rat CYP2B1 using various CYP-specific or preferential activity assays. 3,3′-Diindolylmethane also inhibited in vitro CYP-mediated metabolism of the ubiquitous food contaminant and potent hepatocarcinogen, aflatoxin B1. There was no inhibition of cytochrome c reductase. In addition, we found 3,3′-diindolylmethane to be a substrate for rat hepatic microsomal monooxygenase(s) and tentatively identified a monohydroxylated metabolite. These observations indicate that 3,3′-diindolylmethane can inhibit the catalytic activities of a range of CYP isoforms from lower and higher vertebrates in vitro. This broadly based inhibition of CYP-mediated activation of procarcinogens may be an indole-3-carbinol anticarcinogenic mechanism applicable to all species, including humans. © 1995 John Wiley & Sons, Inc. 相似文献
140.
Richard Wales Hazel C. Gorham Khalid Hussain Lynne M. Roberts J. Michael Lord 《Glycoconjugate journal》1994,11(4):274-281
Deleted forms of ricin B chain (RTB) containing only one of the two galactose binding sites were produced inE. coli and targeted to the periplasm by fusion to theompA orompF signal sequences. The proteins were then isolated from the periplasm and their sugar binding properties assessed. Previous studies investigating the properties of such proteins produced inXenopus laevis oocytes suggested that deleted forms of RTB, when not glycosylated, retain their ability to bind simple sugars, unlike the full-length unglycosylated proteins. When produced inE. coli however we found that only one, EB733, of a number of deleted forms of RTB closely related to those previously produced inXenopus laevis oocytes, bound to simple sugars. All of the deletion forms of RTB were found to bind in the asialofetuin binding assay; an assay which has been previously utilized to measure binding of lectins to the terminal galactose residues of glycoprotein oligosaccharides. However, in contrast to glycosylated RTB, binding of the deletion mutants could be competed to only a small degree or not at all with galactose. The only deletion mutant observed to bind to free galactose when produced inE. coli corresponded closely to the complete domain 2 of RTB. It is assumed that this mutant forms a stable structure similar to that of the C-terminal domain in the full-length protein. The structural integrity of EB733 was not only suggested by its sugar binding properties and solubility but also by its consistently higher level of expression and the absence of any apparent susceptibility toE. coli proteases.Abbreviations RTA
ricin toxin A chain
- RTB
ricin toxin B chain
- ER
endoplasmic reticulum
- SDS-PAGE
sodium dodecyl sulphate-polyacrylamide gel electrophoresis
- IPTG
isopropyl -d-thiogalactopyranoside 相似文献