全文获取类型
收费全文 | 2509篇 |
免费 | 6篇 |
国内免费 | 3篇 |
专业分类
电工技术 | 5篇 |
综合类 | 1篇 |
化学工业 | 23篇 |
金属工艺 | 5篇 |
机械仪表 | 5篇 |
建筑科学 | 9篇 |
能源动力 | 4篇 |
轻工业 | 12篇 |
水利工程 | 1篇 |
无线电 | 7篇 |
一般工业技术 | 35篇 |
冶金工业 | 2387篇 |
原子能技术 | 11篇 |
自动化技术 | 13篇 |
出版年
2021年 | 2篇 |
2019年 | 2篇 |
2017年 | 4篇 |
2016年 | 2篇 |
2015年 | 4篇 |
2014年 | 1篇 |
2013年 | 8篇 |
2012年 | 5篇 |
2011年 | 5篇 |
2010年 | 8篇 |
2009年 | 5篇 |
2008年 | 2篇 |
2007年 | 5篇 |
2006年 | 5篇 |
2005年 | 2篇 |
2004年 | 9篇 |
2003年 | 6篇 |
2002年 | 2篇 |
2001年 | 5篇 |
2000年 | 3篇 |
1999年 | 85篇 |
1998年 | 745篇 |
1997年 | 459篇 |
1996年 | 280篇 |
1995年 | 161篇 |
1994年 | 117篇 |
1993年 | 165篇 |
1992年 | 23篇 |
1991年 | 21篇 |
1990年 | 26篇 |
1989年 | 18篇 |
1988年 | 17篇 |
1987年 | 19篇 |
1986年 | 26篇 |
1985年 | 16篇 |
1984年 | 1篇 |
1983年 | 4篇 |
1982年 | 13篇 |
1981年 | 15篇 |
1980年 | 24篇 |
1979年 | 4篇 |
1978年 | 6篇 |
1977年 | 55篇 |
1976年 | 121篇 |
1975年 | 2篇 |
1974年 | 2篇 |
1973年 | 2篇 |
1971年 | 1篇 |
1969年 | 1篇 |
1955年 | 4篇 |
排序方式: 共有2518条查询结果,搜索用时 156 毫秒
231.
GW Muller MG Shire LM Wong LG Corral RT Patterson Y Chen DI Stirling 《Canadian Metallurgical Quarterly》1998,8(19):2669-2674
N-Phthaloyl 3-amino-3-arylpropionic acid analogs of thalidomide that are potent inhibitors of tumor necrosis factor-alpha are reported. These compounds were found to be potent inhibitors of phosphodiesterase 4. 相似文献
232.
PR Romano F Zhang SL Tan MT Garcia-Barrio MG Katze TE Dever AG Hinnebusch 《Canadian Metallurgical Quarterly》1998,18(12):7304-7316
The human double-stranded RNA (dsRNA)-dependent protein kinase PKR inhibits protein synthesis by phosphorylating translation initiation factor 2alpha (eIF2alpha). Vaccinia virus E3L encodes a dsRNA binding protein that inhibits PKR in virus-infected cells, presumably by sequestering dsRNA activators. Expression of PKR in Saccharomyces cerevisiae inhibits protein synthesis by phosphorylation of eIF2alpha, dependent on its two dsRNA binding motifs (DRBMs). We found that expression of E3 in yeast overcomes the lethal effect of PKR in a manner requiring key residues (Lys-167 and Arg-168) needed for dsRNA binding by E3 in vitro. Unexpectedly, the N-terminal half of E3, and residue Trp-66 in particular, also is required for anti-PKR function. Because the E3 N-terminal region does not contribute to dsRNA binding in vitro, it appears that sequestering dsRNA is not the sole function of E3 needed for inhibition of PKR. This conclusion was supported by the fact that E3 activity was antagonized, not augmented, by overexpressing the catalytically defective PKR-K296R protein containing functional DRBMs. Coimmunoprecipitation experiments showed that a majority of PKR in yeast extracts was in a complex with E3, whose formation was completely dependent on the dsRNA binding activity of E3 and enhanced by the N-terminal half of E3. In yeast two-hybrid assays and in vitro protein binding experiments, segments of E3 and PKR containing their respective DRBMs interacted in a manner requiring E3 residues Lys-167 and Arg-168. We also detected interactions between PKR and the N-terminal half of E3 in the yeast two-hybrid and lambda repressor dimerization assays. In the latter case, the N-terminal half of E3 interacted with the kinase domain of PKR, dependent on E3 residue Trp-66. We propose that effective inhibition of PKR in yeast requires formation of an E3-PKR-dsRNA complex, in which the N-terminal half of E3 physically interacts with the protein kinase domain of PKR. 相似文献
233.
A Di Chiacchio MG Rimoli L Avallone F Arena E Abignente W Filippelli A Filippelli G Falcone 《Canadian Metallurgical Quarterly》1998,331(9):273-278
A series of 2-phenylimidazo[1,2-a]pyridine-3-carboxylic esters, acids, and amides were synthesized and pharmacologically tested in order to evaluate their antiinflammatory and analgesic activity and their ulcerogenic action on the gastro-intestinal tract. The most active member of this series of compounds was found to be 6-methyl-2-phenylimidazo[1,2-a]pyridine-3-carboxylic acid (5c). 相似文献
234.
AM Leone LE Gustafsson PL Francis MG Persson NP Wiklund S Moncada 《Canadian Metallurgical Quarterly》1994,201(2):883-887
The physiological role of nitric oxide (NO) is being investigated in many experimental and clinical settings. There is considerable evidence that NO is involved in the regulation of lung vascular function. In addition there are many studies reporting the beneficial effect of NO inhalation. NO formed from L-Arginine has been detected in exhaled breath using indirect mass spectrometry and chemiluminescence. Both methods provided good evidence for the presence of NO in breath samples but were not unequivocal. We therefore developed a method using gas-chromatography-mass spectrometry which allowed us to measure trace levels of NO in air and breath. Eight healthy volunteers supplied numerous breath samples for analysis. A clear peak for nitric oxide was observed in seven volunteers. The mean level was 13ppb (n = 7, range < 2 to 19ppb). This data is in good agreement with our previous data and unequivocally confirms the presence of nitric oxide in human breath. 相似文献
235.
236.
A Schwingshackl I Blasko E Steiner P Pozzilli MG Cavallo P Berger B Grubeck-Loebenstein 《Canadian Metallurgical Quarterly》1998,241(1):265-268
Formation of amylin-containing islet amyloid deposits may contribute to the progressive deterioration of beta cell function in non-insulin-dependent diabetes mellitus. As diabetes mellitus occurs in male, but rarely in female transgenic mice expressing human amylin in their pancreatic beta cells, it is of interest to study the influence of estradiol (E2) and testosterone (T) on amylin-induced cytotoxicity in human cells. The insulinoma cell line CM, thyroid epithelial cells (TEC) in primary culture, and nontransformed fibroblast lines were used. The occurrence of apoptotic cell death was assessed by nuclear labeling with propidium iodide. Amylin was cytotoxic on all cell types tested, but had the most pronounced effect on TEC and the weakest on the CM cell line. Although both E2 and T decreased the proportion of apoptotic cells in cultures kept in the absence of amylin, neither of the two hormones was able to counteract amylin-induced cytotoxicity. beta cell death and hyperglycemia can thus presumably not be prevented by the neutralization of amylin effects by sex steroids. 相似文献
237.
238.
Plasma apolipoprotein AI (apoAI) and lecithin-cholesterol acyltransferase (LCAT) play important roles in reverse cholesterol transport, promoting the removal of excess cholesterol from peripheral cells and reducing formation of atherosclerotic lesions. Gene augmentation of either apoAI or LCAT, or both, are thus attractive targets for prevention or treatment of atherosclerosis. With the eventual aim of safe and efficient gene delivery to skeletal muscle, our chosen secretory platform for systemic delivery of anti-atherogenic proteins, we have constructed conventional and AAV-based plasmid vectors containing human apoAI or LCAT cDNAs; their efficacy was tested by lipoplex transfection of mouse C2C12 muscle cells or human 293 cells. The secretion of apoAI or LCAT by transduced cultures was two- to five-fold higher using AAV-based plasmid vectors than conventional plasmid vectors. Additionally, cells transfected with a bicistronic AAV-based vector containing an internal ribosome entry site (IRES) efficiently expressed both apoAI and LCAT simultaneously. Furthermore, AAV-based vector sequences were retained by host cells, whereas those of conventional plasmid vectors were lost. These studies indicate that ectopic overexpression of apoAI and LCAT in muscle tissue using AAV-based plasmid vectors might provide a feasible anti-atherogenic strategy in vivo. 相似文献
239.
MG Volovik EG Gabdullina AV Zeveke IIa Kle?nbok SN Kolesov SA Polevaia IV Snezhnitskaia 《Canadian Metallurgical Quarterly》1998,84(3):256-259
The ETV6 (TEL) locus at chromosome band 12p 13 is a major site of translocations in acute leukemia, particularly in childhood acute lymphoblastic leukemia (ALL). In cases with translocations involving ETV6, the normal ETV6 allele is often deleted. In addition, loss of heterozygosity of ETV6 is frequently observed in childhood'ALL. Thus, it has been suggested that ETV6 may have an anti-oncogenic role to play, in addition to its oncogenic role. We have described an unusual case of ALL in which ETV6 is found fused to the ABL gene; ABL is normally activated by fusion to the BCR gene in the 9:22 translocation. We expanded the primary cells from this ETV6/ABL rearranged case of ALL in SCID animals and analyzed them for expression of both ETV6/ABL and the normal ETV6 mRNA. We found that both the rearranged and normal ETV6 mRNAs are expressed in the expanded cell population. Furthermore, sequence analysis of the ETV6 PCR product revealed no point mutations which would influence the amino acid sequence. Thus, deletion of the second ETV6 allele is not necessary for the transformation to leukemia by ETV6/ABL. 相似文献
240.