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61.
62.
63.
Coding haplotype analysis supports HCR as the putative susceptibility gene for psoriasis at the MHC PSORS1 locus 总被引:13,自引:0,他引:13
Asumalahti K Veal C Laitinen T Suomela S Allen M Elomaa O Moser M de Cid R Ripatti S Vorechovsky I Marcusson JA Nakagawa H Lazaro C Estivill X Capon F Novelli G Saarialho-Kere U Barker J Trembath R Kere J;Psoriasis Consortium 《Human molecular genetics》2002,11(5):589-597
PSORS1, near HLA-C, is the major genetic determinant of psoriasis. We present genetic and structural evidence suggesting a major role for the HCR gene at the PSORS1 locus. Genotyping of 419 families from six populations revealed that coding single-nucleotide polymorphisms of HCR formed a conserved allele HCR*WWCC that associated highly significantly with psoriasis and with the HLA-Cw6 allele in all populations. Because of strong linkage disequilibrium between HLA-Cw6 and HCR*WWCC, the two genes could not be genetically distinguished by this sample size. However, the variant HCR allele was predicted to differ in secondary structure from the wild-type protein. HCR protein expression in lesional psoriatic skin differed considerably from that observed in normal skin. These results provide strong evidence for the HCR*WWCC allele as a major genetic determinant for psoriasis, probably by a mechanism impacting on keratinocyte proliferation. 相似文献
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65.
Baldomero Lara Luis Gandía Rafael Martínez-Sierra Andrés Torres A. G. García 《Pflügers Archiv : European journal of physiology》1998,435(4):472-478
This study uses a new strategy to investigate the hypothesis that, of the various Ca2+ channels expressed by a neurosecretory cell, a given channel subtype is coupled more tightly to the exocytotic apparatus
than others. The approach is based on the prediction that the degree of inhibition of the secretory response by various Ca2+ channel blockers will differ at low (0.5 mM) and high (5 mM) extracellular Ca2+ concentrations ([Ca2+]o). So, at low [Ca2+]o the K+-evoked catecholamine release from superfused bovine chromaffin cells was depressed 60–70% by 2 μM ω-agatoxin IVA (P/Q-type
Ca2+ channel blockade), by 3 μM ω-conotoxin MVIIC (N/P/Q-type Ca2+ channel blockade), or by 3 μM lubeluzole (N/P/Q-type Ca2+ channel blockade); in high [Ca2+]o these blockers inhibited the responses by only 20–35%. At 1–3 μM ω-conotoxin GVIA (N-type Ca2+ channel blockade) or 3 μM furnidipine (L-type Ca2+ channel blockade), secretion was inhibited by 30 and 50%, respectively; such inhibitory effects were similar in low or high
[Ca2+]o. Combined furnidipine plus ω-conotoxin MVIIC, ω-agatoxin IVA or ω-conotoxin GVIA exhibited additive blocking effects at
both Ca2+ concentrations. The results suggest that Q-type Ca2+ channels are coupled more tightly to exocytotic active sites, as compared to L-type channels. This hypothesis if founded
in the fact that external Ca2+ that enters the cell through a Ca2+ channel located near to chromaffin vesicles will saturate the K+ secretory response at both [Ca2+]o, i.e. 0.5 mM and 5 mM. In contrast, Ca2+ ions entering through more distant channels will be sequestered by intracellular buffers and, thus, will not saturate the
secretory machinery at lower [Ca2+]o.
Received: 23 September 1997 / Received after revision: 29 October 1997 / Accepted: 30 October 1997 相似文献
66.
67.
Laboratory detection of Haemophilus influenzae with decreased susceptibility to nalidixic acid, ciprofloxacin, levofloxacin, and moxifloxacin due to GyrA and ParC mutations 下载免费PDF全文
Pérez-Vázquez M Román F Aracil B Cantón R Campos J 《Journal of clinical microbiology》2004,42(3):1185-1191
The detection of clinical isolates with decreased fluoroquinolone susceptibilities and a resistance mechanism is of epidemiological and clinical interest. We studied the susceptibilities of 62 clinical isolates and 2 American Type Culture Collection reference strains of Haemophilus influenzae to ciprofloxacin, levofloxacin, moxifloxacin, and nalidixic acid by the microdilution and disk diffusion methods. The ciprofloxacin MICs for 34 of the isolates were >/=0.12 micro g/ml (range, 0.12 to 32 micro g/ml), and the ciprofloxacin MICs for 28 matched control isolates were =0.06 micro g/ml. In addition, we sequenced the quinolone resistance-determining regions (QRDRs) of gyrA and parC of all strains. The log(2) MICs of all quinolones were plotted against the inhibition zone diameters. The MICs and inhibition zone diameters selected to screen for the resistance mechanism were based on the susceptibility distribution data and the presence or absence of amino acid changes in the QRDRs of GyrA and ParC. Strains for which ciprofloxacin MICs were =0.06 micro g/ml, levofloxacin and moxifloxacin MICs were =0.03 micro g/ml, and nalidixic acid MICs were =2.0 micro g/ml lacked modifications in the QRDR of GyrA. In contrast, all strains for which ciprofloxacin, levofloxacin, and moxifloxacin MICs were >/=0.5 micro g/ml and the vast majority of those for which nalidixic acid MICs were >/=32 micro g/ml exhibited amino acid changes in GyrA and ParC. Nalidixic acid and the other three fluoroquinolones studied could be used to screen H. influenzae isolates for the detection of decreased susceptibilities to quinolones due to the acquisition of two amino acid changes in the QRDRs of GyrA and ParC (sensitivity, >95%; specificity, >80%). 相似文献
68.
Kurtz R 《Journal of neurophysiology》2004,92(1):458-467
In motion-sensitive visual neurons of the fly, excitatory visual stimulation elicits Ca(2+) accumulation in dendrites and presynaptic arborizations. Following the cessation of motion stimuli, decay time courses of the cytosolic Ca(2+) concentration signals measured with fluorescent dyes were faster in fine arborizations compared with the main branches. When indicators with low Ca(2+) affinity were used, the decay of the Ca(2+) signals appeared slightly faster than with high affinity dyes, but the dependence of decay kinetics on branch size was preserved. The most parsimonious explanation for faster Ca(2+) concentration decline in thin branches compared with thick ones is that the velocity of Ca(2+) clearance is limited by transport mechanisms located in the outer membrane and is thus dependent on the neurite's surface-to-volume ratio. This interpretation was corroborated by UV flash photolysis of caged Ca(2+) to systematically elicit spatially homogeneous step-like Ca(2+) concentration increases of varying amplitude. Clearance of Ca(2+) liberated by this method depended on branch size in the same way as Ca(2+) accumulated during visual stimulation. Furthermore, the decay time courses of Ca(2+) signals were only little affected by the amount of Ca(2+) released by photolysis. Thus Ca(2+) efflux via the outer membrane is likely to be the main reason for the spatial differences in Ca(2+) clearance in visual motion-sensitive neurons of the fly. 相似文献
69.
Farhi J; Homburg R; Ferber A; Orvieto R; Ben Rafael Z 《Human reproduction (Oxford, England)》1997,12(2):241-243
The most important aspect of diminished ovarian reserve is the associated
decline in reproductive potential. Assessment of ovarian reserve is mainly
based on measurement of early follicular phase follicle stimulating hormone
(FSH) concentration. The objective of this study was to report the
identification of a group of 12 infertile women initially diagnosed as
having unexplained or anovulatory infertility, who had a normal baseline
hormonal profile and did not respond to repeated ovarian stimulation with
gonadotrophins. All developed ovarian failure within a relatively short
time span. Non-response to ovarian stimulation was defined by failure to
achieve development of follicles >12 mm and failure to raise oestradiol
concentration >350 pmol/l in two successive cycles of human menopausal
gonadotrophin (HMG) doses of up to five ampoules per day for 5-8 days.
Within a mean of 9 months following the failed attempts of ovarian
stimulation the mean day 3 FSH concentrations rose from 5.4 +/- 2.7 IU/l to
53.5 +/- 19.7 IU/l. In these patients, day 3 FSH concentration failed to
indicate the low ovarian reserve manifested only by lack of clinical
response to treatment with gonadotrophins which was the first sign of
impending ovarian failure. We conclude that women with normal early
follicular phase serum FSH concentrations who do not respond to ovarian
stimulation by HMG are at risk of developing ovarian failure within several
months.
相似文献
70.
Immunohistochemical characterization of fibroblast subpopulations in normal peritoneal tissue and in peritoneal dialysis-induced fibrosis 总被引:7,自引:0,他引:7
Jiménez-Heffernan JA Aguilera A Aroeira LS Lara-Pezzi E Bajo MA del Peso G Ramírez M Gamallo C Sánchez-Tomero JA Alvarez V López-Cabrera M Selgas R 《Virchows Archiv : an international journal of pathology》2004,444(3):247-256
Peritoneal fibrosis is one of the most common morphological changes observed in continuous ambulatory peritoneal dialysis (CAPD) patients. Both resident fibroblasts and new fibroblast-like cells derived from the mesothelium by epithelial-to-mesenchymal transition are the main cells involved fibrogenesis. In order to establish markers of peritoneal impairment and pathogenic clues to explain the fibrogenic process, we conducted an immunohistochemical study focused on peritoneal fibroblasts. Parietal peritoneal biopsies were collected from four patient groups: normal controls (n=15), non-CAPD uremic patients (n=17), uremic patients on CAPD (n=27) and non-renal patients with inguinal hernia (n=12). To study myofibroblastic conversion of mesothelial cells, -smooth muscle actin (SMA), desmin, cytokeratins and E-cadherin were analyzed. The expression of CD34 by fibroblasts was also analyzed. Fibroblasts from controls and non-CAPD uremic patients showed expression of CD34, but no myofibroblastic or mesothelial markers. The opposite pattern was present during CAPD-related fibrosis. Expression of cytokeratins and E-cadherin by fibroblast-like cells and -SMA by mesothelial and stromal cells supports that mesothelial-to-myofibroblast transition occurs during CAPD. Loss of CD34 expression correlated with the degree of peritoneal fibrosis. The immunophenotype of fibroblasts varies during the progression of fibrosis. Myofibroblasts seem to derive from both activation of resident fibroblasts and local conversion of mesothelial cells.Manuel López-Cabrera and Rafael Selgas contributed equally to the article. 相似文献