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排序方式: 共有332条查询结果,搜索用时 187 毫秒
41.
42.
Inhibition of calcineurin phosphatase activity in adult bone marrow transplant patients treated with cyclosporine A 总被引:2,自引:1,他引:1
Pai SY; Fruman DA; Leong T; Neuberg D; Rosano TG; McGarigle C; Antin JH; Bierer BE 《Blood》1994,84(11):3974-3979
In vitro studies have demonstrated that cyclosporine A (CsA) acts by inhibiting the phosphatase activity of calcineurin, an important mediator of T-cell activation. The relationship of CsA administration in vivo, calcineurin activity, and graft-versus-host disease (GVHD) has yet to be studied. The calcineurin activities of mononuclear cells isolated from 62 bone marrow transplant recipients and 12 normal volunteers were determined and analyzed with respect to administration of CsA, presence or absence of CsA in plasma, and presence or absence of GVHD. Of 62 patients, 33 were taking CsA and 29 were not. Early posttransplant (< 100 days), the calcineurin activity of patients on CsA was significantly lower than that of patients not on CsA (P = .0004) and than that of normal volunteers (P < .0001). Similarly, late posttransplant (> 100 days), the calcineurin activity of patients taking CsA was inhibited compared with normal volunteers (P < .05). The calcineurin activity of patients with acute GVHD who were taking CsA was lower than that of patients on CsA without acute GVHD matched for time posttransplant (P = .02). Calcineurin activity in patients on CsA with chronic GVHD was similar to those without chronic GVHD on drug. In conclusion, calcineurin activity is significantly suppressed by in vivo administration of CsA. The lower calcineurin activity of patients on CsA with acute GVHD suggests that CsA-resistant GVHD is not the result of inadequate suppression of calcineurin activity. These data suggest that if inhibition of calcineurin is the only physiologic target of CsA administration, simply increasing doses of CsA or treatment with other inhibitors of calcineurin, such as FK506, would not be expected to ameliorate GVHD. 相似文献
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Ruel M Al-Faleh H Kulik A Chan KL Mesana TG Burwash IG 《The Journal of thoracic and cardiovascular surgery》2006,131(5):1036-1044
46.
SNAP-25 deficit and hippocampal connectivity in schizophrenia 总被引:3,自引:2,他引:1
Young CE; Arima K; Xie J; Hu L; Beach TG; Falkai P; Honer WG 《Cerebral cortex (New York, N.Y. : 1991)》1998,8(3):261-268
Regional abnormalities of brain connectivity may be an important substrate
for the expression of schizophrenia, a severe form of mental illness. Brain
imaging and postmortem morphometric studies indicate hippocampal structure
is abnormal in schizophrenia. To study molecular components of hippocampal
connectivity the presynaptic proteins SNAP-25 and synaptophysin were
assayed in postmortem samples. Immunocytochemical studies indicated reduced
SNAP-25 immunoreactivity in schizophrenia compared to controls,
particularly in the terminal fields of entorhinal cortex projections.
Although there were no overall changes in synaptophysin immunoreactivity,
in the granule cell layer of the dentate gyrus synaptophysin
immunoreactivity was increased in schizophrenia. These results indicate
that disconnection of a subset of hippocampal circuitry from the entorhinal
cortex, as well as intrinsic changes in hippocampal connectivity, may
contribute to the mechanism of illness in schizophrenia.
相似文献
47.
Peter R. Mitoff Thierry G. Mesana Lisa M. Mielniczuk Jackie Grenon John P. Veinot Leslie T. Cooper Jr. Ross A. Davies 《The Canadian journal of cardiology》2013
A young woman thought to have seronegative rheumatoid arthritis developed Stevens-Johnson syndrome after treatment with sulfasalazine; this resolved with prednisone. Later she was found to be HLA-B27-positive in keeping with a spondyloarthropathy. Soon afterward, she developed clinical myopericarditis and cardiogenic shock that responded initially to methylprednisolone and intravenous immunoglobulin, but recurred. An endomyocardial biopsy demonstrated active myocarditis with a mixed cell composition including rare giant cells, but not enough to classify it as giant cell myocarditis. Heart failure symptoms returned and she eventually required a heart transplant; the explanted heart showed giant cell myocarditis. 相似文献
48.
TG Bird L Boutler A Cole S Lorenzini WY Lu T Hay R Ridgway M Williams B Knight S Gordon Keylock D Wjotacha T Jamieson JP Iredale AR Clarke OJ Sansom SJ Forbes 《Lancet》2013
Insufficient regeneration of the adult liver is believed to cause failure to recover from severe liver disease. An undifferentiated cell population with stem-cell-like qualities known as hepatic progenitor cells (HPCs) is hypothesised to have a central role in regeneration of the adult liver during massive or chronic liver disease. Stem cells in other organ systems are believed to reside in a specialised microenvironment or niche that supports their maintenance and function. The existence of a hepatic stem cell niche might provide a means of therapeutically manipulating endogenous HPCs in vivo as a regenerative therapy.To investigate the physiological potential of HPCs to regenerate the mammalian liver, we have established a novel model of hepatocellular injury and HPC activation using genetic manipulation of hepatocytes. After hepatocyte senescence and death in this model (AhCre Mdm2flox), HPCs expand and bring about the complete regeneration of the liver parenchyma.We demonstrate that a stereotypical niche, consisting partly of macrophages, exists in both animal models and correlating human disease. Using cell tracking, we show active recruitment of extrahepatic macrophages into this niche during injury. In health, intravenous injection of macrophages results in macrophage engraftment to the liver niche, with subsequent HPC activation and changes to liver structure and function.Within the niche, macrophages use paracrine signalling to control both HPC proliferation and cell fate via TWEAK (tumour-necrosis-factor-like weak inducer of apoptosis) and the Wnt signalling pathway, respectively. After hepatocellular injury, macrophages ingest hepatocyte debris, and release Wnt which promotes HPC differentiation into hepatocytes. TWEAK is vital for HPC proliferation in the AhCre Mdm2flox model of regeneration. Here, the absence of TWEAK signalling results in liver failure and mortality.This work has demonstrated for the first time the ability of a solid organ to fully regenerate in the adult mammal from progenitor cells, and additionally highlights mechanisms by which this process can be modulated by either small molecule or cell therapy.FundingUniversity of Edinburgh. 相似文献
49.
Luc M Beauchesne John P Veinot Lyall A Higginson Thierry Mesana 《Cardiovascular pathology》2004,13(3):165-167
A patient with a 10-year-old Medtronic Hancock II porcine aortic bioprosthesis developed severe aortic insufficiency. A transesophageal echocardiogram showed a long and mobile mass attached to the bioprosthesis which was consistent with a torn cusp. The patient underwent replacement of the prosthesis with a mechanical valve. Pathological examination showed two subacute tears arising from the same suture buttressing site. These two tears allowed a portion of the valve apparatus to prolapse. 相似文献
50.
Pavel Drevinek Matthew TG Holden Zhaoping Ge Andrew M Jones Ian Ketchell Ryan T Gill Eshwar Mahenthiralingam 《BMC infectious diseases》2008,8(1):1-16