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181.
Superoxide dismutase activity of the captopril-iron complex 总被引:2,自引:0,他引:2
With an assay that generates superoxide anion radicals without the intervention of metal ions we investigated the antioxidant properties of captopril, an angiotensin-converting enzyme inhibitor with a sulfhydryl group. Under these conditions, increasing concentrations of the drug were seen not to scavenge O·
2
–
directly. However, a combination of captopril and iron could bring about the breakdown of the superoxide anion; a result that may help to understand the free radical-scavenging properties of captopril. 相似文献
182.
Qinghong Xu Elizabeth A. Ottinger Nuria A. Solé George Barany 《Letters in Peptide Science》1997,3(6):333-342
Summary In the course of solid-phase synthesis of phosphopeptides by a post-assembly global phosphorylation strategy, the corresponding H-phosphonate peptides form as byproducts. We describe model studies to investigate this side reaction as a function of reaction conditions, and use this information to develop conditions that minimize the problem, i.e., use of dibenzyl N,N-di-isopropyl phosphoramidite for phosphitylation, followed immediately by oxidation with anhydrous tert-butyl hydroperoxide in dry tetrahydrofuran under argon, and final acidolytic cleavage.This work was taken in part from the Ph.D. Theses of E.A. Ottinger (1994) and Q. Xu (1996), University of Minnesota, Minneapolis, MN, U.S.A. Preliminary presentations of portions of this work were made at the Twenty-Second European Peptide Symposium, Interlaken, Switzerland, September 13–19, 1992, see Ref. 1, at the 14th American Peptide Symposium, Columbus, OH, U.S.A., June 18–23, 1995, and at the Fourth International Symposium on Solid Phase Synthesis & Combinatorial Chemical Libraries, Edinburgh, Scotland, U.K., September 12–16, 1995, see Ref. 2. The title side reaction was first discussed for tyrosine (see Refs 1 and 3), but all of the mechanism studies discussed herein are for serine and threonine.Amino acid symbols denote the l-configuration, and abbreviations for amino acids and peptides follow rules of the IUPAC-IUB Commission of Biochemical Nomenclature [J. Biol. Chem., 247 (1972) 977]. 相似文献
183.
184.
Annalisa Botta Elizabeth A. Lindsay Vesna Jurecic Antonio Baldini 《Mammalian genome》1997,8(12):890-895
We have constructed a comparative map in mouse of the critical region of human 22q11 deleted in DiGeorge (DGS) and Velocardiofacial
(VCFS) syndromes. The map includes 11 genes potentially haploinsufficient in these deletion syndromes. We have localized all
the conserved genes to mouse Chromosome (Chr) 16, bands B1-B3. The determination of gene order shows the presence of two regions
(distal and proximal), containing two groups of conserved genes. The gene order in the two regions is not completely conserved;
only in the proximal group is the gene order identical to human. In the distal group the gene order is inverted. These two
regions are separated by a DNA segment containing at least one gene which, in the human DGS region, is the most proximal of
the known deleted genes. In addition, the gene order within the distal group of genes is inverted relative to the human gene
order. Furthermore, a clathrin heavy chain-like gene was not found in the mouse genome by DNA hybridization, indicating that
there is an inconsistent level of gene conservation in the region. These and other independent data obtained in our laboratory
clearly show a complex evolutionary history of the DGS-VCFS region. Our data provide a framework for the development of a
mouse model for the 22q11 deletion with chromosome engineering technologies.
Received: 8 July 1997 / Accepted 11 August 1997 相似文献
185.
186.
Metastasis formation is a major clinical problem in cancer treatment, and no significant progress in the treatment of metastatic
spread has been made. This apparent lack of progress is partly caused by the absence of clinically relevant animal models
of meta stases. The binding of the lectin Helix pomatia agglutinin (HPA) has been associated with a poor prognosis in breast
and colon cancer patients. HPA-positive and -negative human breast and colon cancer cell lines were transplanted into severe
combined immunodeficient (SCID) mice. HPA-positive breast cancer cell lines (MCF-7 and T47D) metastasized in SCID mice, whereas
the HPA-negative ones (BT20, HS578T and HBL100) did not. The HPA-positive colon cancer cell line HT29 metastasized, while
the HPA-negative ones (COLO320DM, SW480 and SW620) did not. However, in two of eight SCID mice inoculated with the HPA-negative
colon cancer cell line, CACO2 metastatic deposits were found. Despite this exception, HPA binding is a good indicator of the
metastasis of human breast and colon cancer cells in SCID mice: 23 out of 26 HPA-positive cancers metastasized, as opposed
to only two out of 38 HPA-negative cancers. This experimental model is well suited for investigating the functional role of
carbohydrate residues recognized by HPA in breast and colon cancer metastasis.
This revised version was published online in November 2006 with corrections to the Cover Date. 相似文献
187.
Connexin46 Is Retained as Monomers in a trans-Golgi Compartment of Osteoblastic Cells 总被引:5,自引:1,他引:4 下载免费PDF全文
Michael Koval James E. Harley Elizabeth Hick Thomas H. Steinberg 《The Journal of cell biology》1997,137(4):847-857
Connexins are gap junction proteins that form aqueous channels to interconnect adjacent cells. Rat osteoblasts express connexin43 (Cx43), which forms functional gap junctions at the cell surface. We have found that ROS 17/2.8 osteosarcoma cells, UMR 106-01 osteosarcoma cells, and primary rat calvarial osteoblastic cells also express another gap junction protein, Cx46. Cx46 is a major component of plasma membrane gap junctions in lens. In contrast, Cx46 expressed by osteoblastic cells was predominantly localized to an intracellular perinuclear compartment, which appeared to be an aspect of the TGN as determined by immunofluorescence colocalization. Hela cells transfected with rat Cx46 cDNA (Hela/Cx46) assembled Cx46 into functional gap junction channels at the cell surface. Both rat lens and Hela/Cx46 cells expressed 53-kD (nonphosphorylated) and 68-kD (phosphorylated) forms of Cx46; however, only the 53-kD form was produced by osteoblasts. To examine connexin assembly, monomers were resolved from oligomers by sucrose gradient velocity sedimentation analysis of 1% Triton X-100–solubilized extracts. While Cx43 was assembled into multimeric complexes, ROS cells contained only the monomer form of Cx46. In contrast, Cx46 expressed by rat lens and Hela/Cx46 cells was assembled into multimers. These studies suggest that assembly and cell surface expression of two closely related connexins were differentially regulated in the same cell. Furthermore, oligomerization may be required for connexin transport from the TGN to the cell surface. 相似文献
188.
189.
Role of inhibition of nitric oxide production in monocrotaline-induced pulmonary hypertension 总被引:1,自引:0,他引:1
Mathew Rajamma; Gloster Elizabeth S.; Sundararajan T.; Thompson Carl I.; Zeballos Guillermo A.; Gewitz Michael H. 《Journal of applied physiology》1997,82(5):1493-1498
Mathew, Rajamma, Elizabeth S. Gloster, T. Sundararajan, Carl I. Thompson, Guillermo A. Zeballos, andMichael H. Gewitz. Role of inhibition of nitric oxide productionin monocrotaline-induced pulmonary hypertension. J. Appl. Physiol. 82(5): 1493-1498, 1997.Monocrotaline (MCT)-induced pulmonary hypertension (PH) isassociated with impaired endothelium-dependent nitric oxide(NO)-mediated relaxation. To examine the role of NO in PH,Sprague-Dawley rats were given a single subcutaneous injection ofnormal saline [control (C)], 80 mg/kg MCT, or the same doseof MCT and a continuous subcutaneous infusion of 2 mg · kg1 · day1of molsidomine, a NO prodrug (MCT+MD). Two weeks later, plasma NO3 levels, pulmonary arterialpressure (Ppa), ratio of right-to-left ventricular weights (RV/LV) toassess right ventricular hypertrophy, and pulmonary histology wereevaluated. The plasma NO3 level inthe MCT group was reduced to 9.2 ± 1.5 µM(n = 12) vs. C level of 17.7 ± 1.8 µM (n = 8; P < 0.02). In the MCT+MD group,plasma NO3 level was 12.3 ± 2.0 µM (n = 8). Ppa and RV/LV in theMCT group were increased compared with C [Ppa, 34 ± 3.4 mmHg(n = 6) vs. 19 ± 0.8 mmHg(n = 8) and 0.41 ± 0.01 (n = 9) vs. 0.25 ± 0.008 (n = 8), respectively;P < 0.001]. In the MCT+MDgroup, Ppa and RV/LV were not different when compared with C [19 ± 0.5 mmHg (n = 5) and 0.27 ± 0.01 (n = 9), respectively;P < 0.001 vs. MCT]. Medial wall thickness of lung vessels in the MCT group was increased comparedwith C [31 ± 1.5% (n = 9)vs. 13 ± 0.66% (n = 9);P < 0.001], and MDpartially prevented MCT-induced pulmonary vascular remodeling [22 ± 1.2% (n = 11);P < 0.001 vs. MCT and C].These results indicate that a defect in the availability of bioactive NO may play an important role in the pathogenesis of MCT-induced PH. 相似文献
190.
Brown Robert H.; Mitzner Wayne; Wagner Elizabeth M. 《Journal of applied physiology》1997,83(2):366-370
Brown, Robert H., Wayne Mitzner, and Elizabeth M. Wagner.Interaction between airway edema and lung inflation onresponsiveness of individual airways in vivo. J. Appl.Physiol. 83(2): 366-370, 1997.Inflammatorychanges and airway wall thickening are suggested to cause increasedairway responsiveness in patients with asthma. In fivesheep, the dose-response relationships of individual airways weremeasured at different lung volumes to methacholine (MCh) before andafter wall thickening caused by the inflammatory mediator bradykininvia the bronchial artery. At 4 cmH2O transpulmonary pressure(Ptp), 5 µg/ml MCh constricted the airways to a maximum of 18 ± 3%. At 30 cmH2O Ptp, MCh resultedin less constriction (to 31 ± 5%). Bradykinin increased airwaywall area at 4 and 30 cmH2O Ptp(159 ± 6 and 152 ± 4%, respectively;P < 0.0001). At 4 cmH2O Ptp, bradykinin decreasedairway luminal area (13 ± 2%; P < 0.01), and the dose-response curve was significantly lower (P = 0.02). At 30 cmH2O, postbradykinin, the maximalairway narrowing was not significantly different (26 ± 5%;P = 0.76). Bradykinin produced substantial airway wall thickening and slight potentiation ofthe MCh-induced airway constriction at low lung volume. At high lung volume, bradykinin increased wall thickness but had no effecton the MCh-induced airway constriction. We conclude that inflammatoryfluid leakage in the airways cannot be a primary cause of airwayhyperresponsiveness. 相似文献