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Ryo Fukuda M.D. Naruaki Kohge Shuji Akagi Nguten Thanh Xuan Alejandro Tokuda Shiro Fukumoto 《Journal of gastroenterology》1993,28(2):254-258
To investigate whether hepatitis causes mutation in the viral genome, DNA sequences in the pre-core region of duck hepatitis
B virus (DHBV) DNA were analyzed in both ducks with hepatitis and without hepatitis. Five DHBV carrier ducks were injected
with DHBV particle proteins purified from duck serum with Freund’s complete adjuvant (FCA) intrahepatically from 14 day posthatch
for 9 weeks (immunized group). Serum was drawn at the end of the 1st and 4th week after the 1st injection of DHBV particle
protein and ducks were killed at the end of the 9th week to obtain the liver. Another five ducks without treatment were used
as controls. All ducks of the immunized group showed moderate to severe hepatitis at the 9th week. All ducks in the immunized
group showed one mutation except one duck that showed two mutations only at the 9th week. Mutations were observed in the 5th,
13th, 21st, 22nd, and 28th codon of the precore region. All of them were point mutation at the 3rd base in the triplets. The
frequency of mutation was different in each duck from 20% to 60% but not 100%. There was no mutations in ducks in control
group. These results suggest that hepatitis causes mutation in the pre-core lesion genome of duck hepatitis B virus. 相似文献
173.
Erythromycin ameliorates renal injury via anti-inflammatory effects in experimental diabetic rats 总被引:7,自引:0,他引:7
Tone A Shikata K Sasaki M Ohga S Yozai K Nishishita S Usui H Nagase R Ogawa D Okada S Shikata Y Wada J Makino H 《Diabetologia》2005,48(11):2402-2411
Aims/hypothesis Recent studies have shown that the inflammatory process is involved in the pathogenesis of diabetic nephropathy. Fourteen-membered ring macrolides, including erythromycin, have anti-inflammatory, as well as antibacterial effects. The aim of this study was to investigate the renoprotective effects of erythromycin in streptozotocin (STZ)-induced diabetic rats.Methods STZ-induced diabetic rats were treated orally with erythromycin (5 mg/kg body weight) or vehicle every day for 8 weeks. To evaluate the effect of erythromycin treatment, we measured urinary albumin excretion, and examined the following in the kidney: histological changes, the expression of intercellular adhesion molecule-1 (ICAM-1), macrophage infiltration, and nuclear factor-kappa B (NF-B) activity.Results Erythromycin significantly reduced urinary albumin excretion without affecting blood glucose levels and blood pressure. Erythromycin also attenuated glomerular hypertrophy, mesangial expansion, macrophage infiltration and ICAM-1 expression in renal tissues. The expression of the gene encoding TGFB1 (also known as TGF-1), type IV collagen protein production and NF-B activity in renal tissues were increased in diabetic rats and reduced by erythromycin treatment.Conclusions/interpretation Erythromycin prevented renal injuries without changes of blood glucose levels and blood pressure in experimental diabetic rats. These results suggest that the renoprotective effects of erythromycin are based on its anti-inflammatory effect via suppression of NF-B activation. Modulation of microinflammation with erythromycin may provide a new approach for diabetic nephropathy. 相似文献
174.
175.
Value of thyroid specific peroxidase and Ki‐67 stains in preoperative cytology for thyroid follicular tumors
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178.
Functional engraftment of human peripheral T and B cells and sustained production of autoantibodies in NOD/LtSzscid/IL‐2Rγ−/− mice
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Yuki Ishikawa Takashi Usui Aoi Shiomi Masakazu Shimizu Kosaku Murakami Tsuneyo Mimori 《European journal of immunology》2014,44(11):3453-3463
NOD/LtSzscid/IL‐2Rγ?/? (NSG) mice have advantages in establishing humanized mouse models. However, transferring human PBMCs into these mice often causes lethal GVH disease. In this study, we discovered an improved method for the engraftment of normal or pathological human PBMCs into NSG mice and examined the subsequent induction of specific immune responses. We sequentially transferred human CD4+ memory T (Tm) and B cells obtained from PBMCs of healthy adults or patients with autoimmune diseases into NSG mice. Removing naïve CD4+ T cells from the transferred PBMCs allowed successful engraftment without lethal GVH disease. The transferred Tm cells were found to reside mainly in the spleen and the lymphoid nodules, where they expressed MHC class II molecules and produced cytokines, including IL‐21. Surprisingly, the transferred B cells were also well maintained in the lymphoid organs, underwent de novo class‐switch recombination, and secreted all isotypes of human Igs at significant levels. Moreover, transferring patient‐derived Tm and B cells resulted in sustained production of IgM‐rheumatoid factor and antiaminoacyl transfer RNA synthetase Abs in these mice. These results suggest that transfer of Tm and B cells derived from human PBMCs into NSG mice could be a useful method for the study of human autoimmune mechanisms. 相似文献
179.
Influence of PD‐L1 cross‐linking on cell death in PD‐L1‐expressing cell lines and bovine lymphocytes
Ryoyo Ikebuchi Satoru Konnai Tomohiro Okagawa Kazumasa Yokoyama Chie Nakajima Yasuhiko Suzuki Shiro Murata Kazuhiko Ohashi 《Immunology》2014,142(4):551-561
Programmed death‐ligand 1 (PD‐L1) blockade is accepted as a novel strategy for the reactivation of exhausted T cells that express programmed death‐1 (PD‐1). However, the mechanism of PD‐L1‐mediated inhibitory signalling after PD‐L1 cross‐linking by anti‐PD‐L1 monoclonal antibody (mAb) or PD‐1–immunogloblin fusion protein (PD‐1‐Ig) is still unknown, although it may induce cell death of PD‐L1+ cells required for regular immune reactions. In this study, PD‐1‐Ig or anti‐PD‐L1 mAb treatment was tested in cell lines that expressed PD‐L1 and bovine lymphocytes to investigate whether the treatment induces immune reactivation or PD‐L1‐mediated cell death. PD‐L1 cross‐linking by PD‐1‐Ig or anti‐PD‐L1 mAb primarily increased the number of dead cells in PD‐L1high cells, but not in PD‐L1low cells; these cells were prepared from Cos‐7 cells in which bovine PD‐L1 expression was induced by transfection. The PD‐L1‐mediated cell death also occurred in Cos‐7 and HeLa cells transfected with vectors only encoding the extracellular region of PD‐L1. In bovine lymphocytes, the anti‐PD‐L1 mAb treatment up‐regulated interferon‐γ (IFN‐γ) production, whereas PD‐1‐Ig treatment decreased this cytokine production and cell proliferation. The IFN‐γ production in B‐cell‐depleted peripheral blood mononuclear cells was not reduced by PD‐1‐Ig treatment and the percentages of dead cells in PD‐L1+ B cells were increased by PD‐1‐Ig treatment, indicating that PD‐1‐Ig‐induced immunosuppression in bovine lymphocytes could be caused by PD‐L1‐mediated B‐cell death. This study provides novel information for the understanding of signalling through PD‐L1. 相似文献
180.