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31.
Antibiotic therapy plays a central role in the medical management of patients with cystic fibrosis. While totally convincing efficacy data are lacking, antibiotics probably have a pronounced beneficial effect on both morbidity and mortality. Much has been learned in the past 20 years about antibiotic use in this population. At the same time, new antimicrobial agents with the potential to treat this condition have become available for use. The pharmacokinetics of a number of antibiotic classes, including beta-lactams, aminoglycosides and quinolones, are altered in this patient population. Increased total body clearance is a common occurrence but is not always changed enough to warrant altered dosages. Nonetheless, in light of altered pharmacokinetics in the cystic fibrosis population, appropriate dosage and monitoring parameters for a number of antibiotics have been determined. 相似文献
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Common region of ALL-1 gene disrupted in epipodophyllotoxin-related secondary acute myeloid leukemia
CA Felix NJ Winick M Negrini WP Bowman CM Croce BJ Lange 《Canadian Metallurgical Quarterly》1993,53(13):2954-2956
Translocations at chromosomal band 11q23 characterize most de novo acute lymphoblastic leukemias (ALL) of infants, acute myeloid leukemias (AML) of infants and young children, and secondary AMLs following epipodophyllotoxin exposure. The chromosomal breakpoints at 11q23 have been cloned from isolated cases of de novo ALL and AML. Using an 859-base pair BamHI fragment of human ALL-1 complementary DNA that recognizes the genomic breakpoint region for de novo ALL and AML, we investigated two cases of secondary AML that followed etoposide-treated primary B-lineage ALL. In the first case, the translocation occurred between chromosomes 9 and 11 and the breakpoint at 11q23 localized to the same 9-kilobase region of the ALL-1 gene that is disrupted in most of the de novo leukemias. In the second case the translocation was between chromosomes 11 and 19. The breakpoint occurred outside of the ALL-1 breakpoint cluster region. 相似文献
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MD Cohen ST Auringer JL Grosfeld CA Galliani NA Heerema 《Canadian Metallurgical Quarterly》1993,23(6):463-466
The purpose of this study is to present three patients with multifocal primary neuroblastoma, to review the literature, and describe the radiographic findings. SUBJECTS AND METHODS: Three children with multifocal neuroblastoma have been identified. The case histories and imaging findings in these patients are reviewed. RESULTS: Two children had synchronous and one child had metachronous multifocal primary neuroblastoma. The primary tumors were both in the abdomen in one patient, both in the chest in another patient, and in the chest and abdomen in the third patient. Evidence for multifocal origin of these tumors, rather than metastatic spread, is presented. CONCLUSION: Multifocal primary neuroblastomas can occur. The tumors maybe synchronous or metachronous. Awareness of this disorder may prevent errors in diagnosis and staging. Although not identified in our patients there is a strong familial incidence of neuroblastomas in those patients with multifocal tumors. 相似文献
35.
We demonstrated recently that dominant negative mutants of rat DNA polymerase beta (Pol beta) interfere with repair of alkylation damage in Saccharomyces cerevisiae. To identify the alkylation repair pathway that is disrupted by the Pol beta dominant negative mutants, we studied the epistatic relationship of the dominant negative Pol beta mutants to genes known to be involved in repair of DNA alkylation damage in S. cerevisiae. We demonstrate that the rat Pol beta mutants interfere with the base excision repair pathway in S. cerevisiae. In addition, expression of one of the Pol beta dominant negative mutants, Pol beta-14, increases the spontaneous mutation rate of S. cerevisiae whereas expression of another Pol beta dominant negative mutant, Pol beta-TR, does not. Expression of the Pol beta-14 mutant in cells lacking APN1 activity does not result in an increase in the spontaneous mutation rate. These results suggest that gaps are required for mutagenesis to occur in the presence of Pol beta-14 but that it is not merely the presence of a gap that results in mutagenesis. Our results suggest that mutagenesis can occur during the gap-filling step of base excision repair in vivo. 相似文献
37.
基于PSOS的TM1300应用系统中的BSP研究 总被引:1,自引:0,他引:1
通过在应用软件与板级支持包BSP之间加一层库函数的方法较好地解决了应用程序与板级支持包函数间的通信问题,减少了板级支持包函数的维护复杂度,从而为嵌入式系统板级支持包的实现提供了一个有价值的思路。 相似文献
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Dystrophin is a plasma membrane-associated cytoskeletal protein of the spectrin superfamily. The dystrophin cytoskeleton has been first characterized in muscle. Muscular 427 kDa dystrophin binds to subplasmalemmal actin filaments via its amino-terminal domain. The carboxy-terminus of dystrophin binds to a plasma membrane anchor, beta-dystroglycan, which is associated on the external side with the extracellular matrix receptor, alpha-dystroglycan, that binds to the basal lamina proteins laminin-1, laminin-2, and agrin. In the muscle, the dystroglycan complex is associated with the sarcoglycan complex that consists of several glycosylated, integral membrane proteins. The absence or functional deficiency of the dystrophin cytoskeleton is the cause of several types of muscular dystrophies including the lethal Duchenne muscular dystrophy (DMD), one of the most severe and most common genetic disorders of man. The dystrophin complex is believed to stabilize the plasma membrane during cycles of contraction and relaxation. Muscular dystrophin and several types of dystrophin variants are also present in extramuscular tissues, e.g. in distinct regions of the central nervous systems including the retina. Absence of dystrophin from these sites is believed to be responsible for some extramuscular symptoms of DMD, e.g. mental retardation and disturbances in retinal electrophysiology (reduced b-wave in electroretinograms). The reduced b-wave in electroretinograms indicated a disturbance of neurotransmission between photoreceptors and ON-bipolar cells. At least two different dystrophin variants are present in photoreceptor synaptic complexes. One of these dystrophins (Dp260) is virtually exclusively expressed in the retina. In the neuroretina, dystrophin is found in significant amounts in the invaginated photoreceptor synaptic complexes. At this location dystrophin colocalizes with dystroglycan. Agrin, an extracellular ligand of alpha-dystroglycan, is also present at this location whereas the proteins of the sarcoglycan complex appear to be absent in photoreceptor synaptic complexes. Dystrophin and dystroglycan are located distal from the ribbon-containing active synaptic zones where both proteins are restricted to the photoreceptor plasma membrane bordering on the lateral sides of the synaptic invagination. In addition, some neuronal profiles of the postsynaptic complex also contain dystrophin and beta-dystroglycan. These profiles appear to belong at least in part to projections of the photoreceptor terminals into the postsynaptic dendritic complex. In view of the abnormal neurotransmission between photoreceptors and ON-bipolar cells in DMD patients the dystrophin/beta-dystroglycan-containing projections of photoreceptor presynaptic terminals into the postsynaptic dendritic plexus might somehow modify the ON-bipolar pathway. Another retinal site associated with dystrophin/beta-dystropglycan is the plasma membrane of Müller cells where dystrophin/beta-dystroglycan appear to be present at particular high concentrations. At this location the dystrophin/dystroglycan complex may play a role in the attachment of the retina to the vitreous, and, under pathological conditions, in traction-induced retinal detachment. 相似文献