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81.
Mayne M Moffatt T Kong H McLaren PJ Fowke KR Becker KG Namaka M Schenck A Bardoni B Bernstein CN Melanson M 《European journal of immunology》2004,34(4):1217-1227
DNA microarray profiling of CD4(+) and CD8(+) cells from non-treated relapsing and remitting multiple sclerosis (MS) patients determined that the cytoplasmic binding partner of fragile X protein (CYFIP2, also called PIR121) was increased significantly compared to healthy controls. Western analysis confirmed that CYFIP2 protein was increased approximately fourfold in CD4(+) cells from MS compared to inflammatory bowel disorder (IBD) patients or healthy controls. Because CYFIP2 acts as part of a tetrameric complex that regulates WAVE1 activation we hypothesized that high levels of CYFIP2 facilitate T cell adhesion, which is elevated in MS patients. Several findings indicated that increased levels of CYFIP2 facilitated adhesion. First, adenoviral-mediated overexpression of CYFIP2 in Jurkat cells increased fibronectin-mediated adhesion. Secondly, CYFIP2 knock-down experiments using antisense oligodeoxynucleotides reduced fibronectin-mediated binding in Jurkat and CD4(+) cells. Thirdly, inhibition of Rac-1, a physical partner with CYFIP2 and regulator of WAVE1 activity, reduced fibronectin-mediated adhesion in Jurkat and CD4(+) cells. Finally, inhibition of Rac-1 or reduction of CYFIP2 protein decreased fibronectin-mediated adhesion in CD4(+) cells from MS patients to levels similar to controls. These studies suggest that overabundance of CYFIP2 protein facilitates increased adhesion properties of T cells from MS patients. 相似文献
82.
Congenital insensitivity to pain with anhidrosis is a syndrome characterized by loss of pain and sensation. The condition frequently evolves into deep wounds and prolonged healing times. Anhidrosis is another prominent component of the disorder. Often associated with recurrent episodes of unexplained fever, it can result in patient mortality. Recent investigations point to Trk A, the high affinity receptor for nerve growth factor (NGF), as a candidate for the site of the mutation that causes the disorder. Functional NGF receptors, such as Trk A and the Trk family of tyrosine kinases, are essential for NGF signaling of human lymphocytes. In this study, we demonstrated that the presence of a trk A mutation in patient B cells results in a novel lymphocyte signaling defect. In these B cells, NGF failed to induce Trk A phosphorylation, cytoskeleton assembly, or MAP kinase activation. These abnormalities may explain some of the clinical features of the disease. 相似文献
83.
目的:从基因水平研究肝移植急性排斥反应中T淋巴细胞信号传导途径。方法:利用4096条大鼠cDNA克隆的基因芯片对从急性排斥组Wistar→SD(n=5)和对照组SD→SD(n=5)两组肝移植大鼠T细胞中抽提、纯化mRNA,扩增、逆转录成cDNA,荧光标记后与芯片杂交,扫描后筛选出差异表达的基因。结果:在4096个基因中共发现差异表达基因190条,其中ll条与细胞信号传导有关的基因差异表达明显:MHC(3条)、CD3抗原(1条)相关基因;蛋白酶类:蛋白激酶C结合蛋白、蛋白酪氨酸磷酸酯酶D型受体、磷脂酰肌醇二磷酸酶基因各l条;涉及核酸信号传导、激活、转录、翻译的基因3条。结论:T细胞在肝移植术后排斥反应中信号传导机制涉及多个基因,基因芯片技术的大规模筛选为进一步研究T细胞在排斥反应中的信号传导途径提供了客观依据和目标。 相似文献
84.
Induction of NO synthesis in macrophages by Newcastle disease virus is associated with activation of nuclear factor-{kappa}B 总被引:3,自引:0,他引:3
Umansky Victor; Shatrov Vladimir A.; Lehmann Volker; Schirrmacher Volker 《International immunology》1996,8(4):491-498
Newcastle disease virus (NDV) has received much attention recentlybecause of its non-specific immune stimulating potential andits various anti-tumor activities. Here we describe that NDVinduces synthesis of NO and causes an activation of nuclearfactor-kB (NF-kB) In murine macrophages. These reactions werepart of an activation process which included also stimulationof adenosine deaminase and inhibition of 5'-nucleotidase. NDV-mediatedNO synthesis and NF-kB activation were blocked by an antioxidant(butylated hydroxyanisole), by an inhibitor of protein tyrosinekinase (genistein) and of protein kinase A (H-89), but not byan inhibitor of protein kinase C (staurosporin). These datasuggest that signalling requirements of NF-kB activation andNO production in NDV-treated macrophages are similar. 相似文献
85.
《Immunity》2020,52(4):683-699.e11
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86.
87.
Protein kinase mediators of integrin signal transduction 总被引:6,自引:0,他引:6
Protein kinases are important mediators of signal transduction initiated by soluble growth factors and cytokines. Cellular
interactions with the extracellular matrix are mediated largely by members of the integrin class of cell adhesion molecules,
which also subsume signal transduction functions required for cell growth, differentiation, and survival. Here we review the
involvement of protein kinases in mediating integrin intracellular signal transduction and the possible role for these molecules
in regulating integrin adhesion. Although in most cases mechanistic details are incomplete, the emerging theme of protein
kinases mediating cross-talk between growth factor receptor and integrin signalling systems provides a timely backdrop against
which to present new developments in this area. The contribution of the actin cytoskeleton to integrin signal transduction
is discussed, with respect to the concept of ’solid-state’ signalling providing a mechanism for imposing order on the protein-protein
interactions which underlie signal discrimination. Moreover, we review evidence that dysregulated integrin signalling contributes
to pathological processes including arthritis, thrombasthenia, leucocyte adhesion deficiencies, and tumour angiogenesis and
invasion.
Received: 14 May 1996 / Accepted: 2 July 1996 相似文献
88.
This study is aimed at detecting gastrointestinal sounds (GIS) and correlating their characteristics with gastrointestinal
(GI) conditions. The central hypotheses are that GIS generation depends on the motility patterns and the mechanical properties
of the gut, and that changes in those result in measurable differences in GIS. An animal model which included both healthy
rats and those with small bowel obstruction (SBO) was developed. The acoustic bursts, of GIS were detected by amplitude thresholding
the signal envelope. Three methods of envelope estimation were proposed and evaluated. Envelope estimation using a Hilbert
transform was found to produce the best results in the current application. The duration and dominant frequency of each detected
GIS event was estimated and clear differences between healthy and diseased rats were discovered. In the control state, GIS
events were found to consistently be of relatively short duration (3–65ms). Although the majority of events in the SBO state
had similar short duration, infrequent longer events were also detected and appeared to be pathognomonic. Long duration events
(>100 ms) occurred in each of seven obstructed, but in none of 14 non-obstructed, cases (p<0.001). It is concluded that GIS
analysis may prove useful in the non-invasive, rapid, and accurate diagnosis of SBO. 相似文献
89.
钙离子载体在诱导人外周血单核细胞分化为树突状细胞中的作用 总被引:2,自引:0,他引:2
目的研究钙离子载体(CI)能否诱导人外周血单核细胞(PBMC)分化为树突状细胞(DC),并初步探讨其信号转导途径。方法分离健康献血者的PBMC,在体外用CI(A23187)或人重组粒细胞/巨噬细胞集落刺激因子(rhGM—CSF)和CI培养40h,或rhGM-CSF和白细胞介素4(IL-4)培养7d,部分PBMC预先用W-7或CsA或K35926处理30min后,再加入上述细胞因子或CI。相差显微镜下观察细胞形态,流式细胞仪检测细胞表面CD14、CD80、CD86、CD83等分子的表达,MTT比色法检测其对同种异体混合T淋巴细胞的刺激增殖作用。结果健康献血者的PBMC经CI培养40h,或rhGM—CSF与CI培养40h,或rhGM-CSF与IL-4培养7d,均可获得DC的典型形态和表面分子的表达,包括CD14表达下调、共刺激分子(CD80、CD86)表达上调,以及较强刺激同种异体混合T淋巴细胞增殖的作用;CI诱导的DC其CD14分子的下调及CD83分子的上调更明显,刺激混合T淋巴细胞的增殖能力更强;rhGM-CSF可协同CI诱导PBMC向DC的分化。经rhGM—CSF及CI处理的PBMC,其形态、表面标志物及对T细胞的刺激增殖能力,均受到W-7或CsA或KT5926不同程度的抑制;而rhGM-CSF及IL-4所诱导的PBMC其形态、表面分子的表达以及刺激T细胞增殖的作用却不受上述抑制剂的影响。结论CI可快速诱导PBMC向DC分化,其分化过程可能受控于Ca^2 /钙调蛋白及其下游的多个细胞信号转导途径的调节。 相似文献
90.
Jack M. Rogers Masahiro Usui Bruce H. KenKnight Raymond E. Ideker William M. Smith 《Annals of biomedical engineering》1997,25(5):761-768
We have developed a method for quantifying the complexity of activation patterns observed during ventricular fibrillation
(VF) that is based on our previously reported methodology for decomposing epicardial mapping data into a set of isolated wavefronts.
One-half second datasets are acquired from a 21×24 array of unipolar electrodes (1 mm spacing), and the wavefronts are isolated.
A correlation technique is used to compute the similarity between all possible pairs of the isolated wavefronts. From these
data, the wavefronts are sorted into clusters, each of which represents a recurring wavefront morphology. We define multiplicity
(M) as the number of clusters needed to account for 90% of the total activations in the VF episode.M measures the complexity of the rhythm. In repetitive patterns (e.g., sinus rhythm),M=1, indicating that the same morphology repeatedly activates the mapped region. Typically, in VF,M>1, with larger numbers representing more complex, disorganized patterns. As an example, we computedM at 5, 10, 15, and 20 sec after electrical induction of VF in six pigs.M decreased significantly (p<0.001), suggesting increasing organization during this period. 相似文献