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101.
Rasmussen's encephalitis is a rare progressive pediatric epileptic syndrome. Recent evidence from experimental animals and patients with the disease suggests an important role for both humoral and cell-mediated immune mechanisms in the pathogenesis of this disease. The glutamate receptor subunit GluR3 may be an important autoantigen in the disease. (This review has been modified from a review published in Current Opinion in Neurology 1996, 9:141-145.) 相似文献
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Ataxia-telangiectasia (A-T) is a rare hereditary syndrome involving cerebellar degeneration, immunodeficiency, cancer risk, and radiosensitivity. Since the cloning of the A-T gene, ATM, in 1995, research on this pleiotropic disease and its molecular basis has expanded tremendously. ATM is a large protein kinase that appears to be one of the primary sensors of DNA strand-break damage. The vast majority of mutations in ATM result in truncation and destabilization of the protein, but certain missense and splicing errors have been shown to result in a less severe phenotype. A-T heterozygotes have been shown to have a slightly increased risk of cancer, but their increased in vitro radiosensitivity does not seem to result in any in vivo sensitivity. ATM does seem to act as a classic tumor suppressor gene in T-prolymphocytic leukemia, and LOH at the ATM locus is a common event in some tumor types, suggesting a general role for ATM in cancer. Recent work has shown the interaction of ATM with proteins involved in cell cycle control, and the direct phosphorylation of some of these interactors by ATM. ATM knockout mice have been created by several groups, and recapitulate the immunodeficiency, radiosensitivity, cancer risk, and fertility defects of A-T, although the effect on the cerebellum is slight. These diverse topics, and their integration into a global understanding of A-T, were the basis of the 7th International A-T Workshop. 相似文献
104.
Although the product of the UL12 gene of herpes simplex virus type 1 (HSV-1) has been shown to possess both exonuclease and endonuclease activities in vitro, and deletion of most of the gene within the viral genome results in inefficient production and maturation of infectious virions, the function of the deoxyribonuclease (DNase) activity per se in virus replication remains unclear. In order to correlate the in vitro and in vivo activities of the protein encoded by UL12, mutant proteins were tested for nuclease activity in vitro by a novel hypersensitivity cleavage assay and for their ability to complement the replication of a DNase null mutant, AN-1. Rabbit reticulocyte lysates programmed with wild-type UL12 RNA cleaved at the same sites cleaved by purified HSV-1 DNase, but distinct from those cleaved by DNase 1 or micrococcal nuclease. All mutants which lacked DNase activity in vitro also failed to complement the replication of AN-1 in nonpermissive cells. Likewise, all mutants which contained HSV-1 DNase activity, as detected by the hypersensitivity cleavage assay, were capable of complementing the replication of the DNase null mutant, though to varying extents. Of particular note was the d1-126 mutant protein, which, despite having the same specific activity as the wild-type enzyme in vitro, complemented the replication of AN-1 significantly less than the wild-type protein. The results suggest that DNase activity per se is required for efficient replication of HSV-1 in vivo. However, residues, including the N-terminal 126 amino acids, which are dispensable for enzymatic activity in vitro may facilitate the accessibility or activity of the protein in vivo. 相似文献
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BB de Vries AM Wiegers E de Graaff AJ Verkerk JO Van Hemel DJ Halley JP Fryns LM Curfs MF Niermeijer BA Oostra 《Canadian Metallurgical Quarterly》1993,1(1):72-79
The fragile X mental retardation syndrome is caused by unstable expansion of a CGG repeat in the FMR-1 gene. Clinical expression is associated with a large expansion of the CGG repeat. The mutation in the FMR-1 gene and the cytogenetic expression of the fragile site at Xq27.3 have been studied in 52 fragile X male patients. The percentage of the cytogenetic expression of the fragile site at Xq27.3 positively correlates with the mean size of the full mutation in the FMR-1 gene (p < 0.0001) irrespective of the presence of additional premutation alleles. We noted a less frequent occurrence of additional premutation alleles in adult patients compared with juveniles, suggesting a continued mitotic instability in life. Additionally, the level of mental retardation has been ascertained in 35 patients using the Stanford-Binet or Terman-Merrill test of general intelligence. The presence of a full mutation in the FMR-1 gene seemed decisive for the occurrence of mental impairment in the patient. No correlation is observed between the degree of mental retardation and the size of the full mutation. The degree of mental retardation seemed not to be influenced by the presence of premutation alleles in part of the cells in addition to a full mutation. One patient is described with the 'Prader-Willi-like' subphenotype of the fragile X syndrome, showing a deletion in the FMR-1 gene in a part of his cells in addition to a full mutation. 相似文献
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S. Juanto J.O. Zerbino M.I. Miguez J.R. Vilche A.J. Arvia 《Electrochimica acta》1987,32(12):1743-1749
The ellipsometric and voltammetric responses of iron in 0.04 M NaOH + xM NaCl (0 x 0.3) are investigated. Three main processes, barrier layer formation, outer layer formation and pitting corrosion which depend differently on the presence of NaCl can be distinguished. The first process becomes practically independent of NaCl concentration. Otherwise, under certain conditions NaCl increases the charge associated with the outer layer formation through pitting. The dependence of the latter on NaCl concentration is in agreement with data earlier reported in the literature. A relation among the three processes is discussed in terms of competitive anion adsorption on iron specimen and formation of redox couples within the hydrous oxide layer produced on iron. 相似文献
110.
AM Mulichak JO Hui AG Tomasselli RL Heinrikson KA Curry CS Tomich S Thaisrivongs TK Sawyer KD Watenpaugh 《Canadian Metallurgical Quarterly》1993,268(18):13103-13109
The crystal structure of human immunodeficiency virus (HIV) type 2 protease has been determined in complexes with peptidic inhibitors Noa-His-Cha psi [CH(OH)CH(OH)]Val-Ile-Amp (U75875) and Qnc-Asn-Cha psi [CH(OH)CH2]Val-Npt(U92163) (where Noa is naphthyloxyacetyl, Cha is cyclohexylalanine, Amp is 2-aminomethylpyridine, Qnc is quinoline-2-carbonyl, and Npt is neopentylamine), which have dihydroxyethylene and hydroxyethylene moieties, respectively, in place of the normal scissile bond of the natural ligand. The complexes crystallize in space group P2(1)2(1)2(1), with one dimer-inhibitor complex per asymmetric unit and average cell dimensions of a = 33.28 A, b = 45.35 A, c = 135.84 A. Data were collected to approximately 2.5-A resolution. The model structures were refined with resulting R-factors of around 0.19. As expected, the HIV-2 protease structure is approximately C2-symmetric with a gross structure very similar to that of the HIV-1 enzyme. The inhibitors bind in an extended conformation positioned lengthwise in the binding cleft in a manner similar to that found in the HIV-1 protease-inhibitor complexes previously reported. The substitution of the bulkier Ile82 side chain in the HIV-2 protease may help explain the better ability of HIV-2 protease to bind and hydrolyze ligands with small P1 and P1' side groups. It appears that differences in specificity between the proteases of HIV-1 and HIV-2 are not merely a result of simple side chain substitutions, but may be complicated by differences in main chain flexibility as well. 相似文献