全文获取类型
收费全文 | 669篇 |
免费 | 81篇 |
国内免费 | 8篇 |
专业分类
耳鼻咽喉 | 3篇 |
儿科学 | 66篇 |
妇产科学 | 6篇 |
基础医学 | 96篇 |
口腔科学 | 30篇 |
临床医学 | 73篇 |
内科学 | 139篇 |
皮肤病学 | 19篇 |
神经病学 | 24篇 |
特种医学 | 128篇 |
外科学 | 41篇 |
综合类 | 42篇 |
预防医学 | 24篇 |
眼科学 | 29篇 |
药学 | 13篇 |
肿瘤学 | 25篇 |
出版年
2023年 | 1篇 |
2022年 | 2篇 |
2021年 | 4篇 |
2020年 | 6篇 |
2019年 | 7篇 |
2018年 | 21篇 |
2017年 | 8篇 |
2016年 | 21篇 |
2015年 | 23篇 |
2014年 | 26篇 |
2013年 | 40篇 |
2012年 | 20篇 |
2011年 | 12篇 |
2010年 | 43篇 |
2009年 | 45篇 |
2008年 | 15篇 |
2007年 | 26篇 |
2006年 | 12篇 |
2005年 | 17篇 |
2004年 | 7篇 |
2003年 | 11篇 |
2002年 | 6篇 |
2001年 | 7篇 |
2000年 | 4篇 |
1999年 | 6篇 |
1998年 | 40篇 |
1997年 | 42篇 |
1996年 | 42篇 |
1995年 | 36篇 |
1994年 | 22篇 |
1993年 | 28篇 |
1992年 | 4篇 |
1991年 | 6篇 |
1990年 | 6篇 |
1989年 | 18篇 |
1988年 | 15篇 |
1987年 | 10篇 |
1986年 | 13篇 |
1985年 | 14篇 |
1984年 | 7篇 |
1983年 | 12篇 |
1982年 | 5篇 |
1981年 | 13篇 |
1980年 | 7篇 |
1979年 | 4篇 |
1978年 | 4篇 |
1977年 | 8篇 |
1976年 | 9篇 |
1975年 | 2篇 |
1884年 | 1篇 |
排序方式: 共有758条查询结果,搜索用时 15 毫秒
81.
Pre‐therapy inflammation and coagulation activation and long‐term CD4 count responses to the initiation of antiretroviral therapy
下载免费PDF全文
![点击此处可从《HIV medicine》网站下载免费的PDF全文](/ch/ext_images/free.gif)
82.
83.
Williams MA; Kouroumoussis I; Syndercombe-Court D; Hendry L; Newland AC; Kelsey SM 《Blood》1995,86(11):4234-4242
Monocyte expression and secretion of tumor necrosis factor (TNF) and TNF receptors (TNF-R) p55 and p75 was studied in patients receiving granulocyte-macrophage colony-stimulating factor (GM-CSF) after intensive chemotherapy. TNF expression and secretion of biologically active TNF was increased at regeneration compared with that of patients who had received chemotherapy alone. This effect persisted for several weeks after cessation of growth factor therapy. GM-CSF restored the responsiveness of monocytes to bacterial lipopolysaccharide (LPS), which appeared to be diminished after chemotherapy alone. Expression and secretion of TNF-R p55 and p75 by monocytes was augmented by GM-CSF therapy in association with the increase in TNF protein. We propose that GM-CSF administration after chemotherapy restores the normal responsiveness of monocytes to a secondary stimulus such as LPS and primes monocytes to respond to LPS with increased expression and secretion of TNF and TNF-R. 相似文献
84.
Activation of human platelets by immune complexes prepared with cationized human IgG 总被引:1,自引:0,他引:1
Schattner M; Lazzari M; Trevani AS; Malchiodi E; Kempfer AC; Isturiz MA; Geffner JR 《Blood》1993,82(10):3045-3051
The present study shows that the ability of soluble immune complexes (IC), prepared with human IgG and rabbit IgG antibodies against human IgG, to trigger platelet activation was markedly higher for IC prepared with cationized human IgG (catIC) compared with those prepared with untreated human IgG (cIC). CatIC induced platelet aggregation and adenosine triphosphate release in washed platelets (WP), gel-filtered platelets (GFP), or platelet-rich plasma (PRP) at physiologic concentrations of platelets (3 x 10(8)/mL) and at low concentrations of catIC (1 to 30 micrograms/mL). On the contrary, under similar experimental conditions, cIC did not induce aggregation in PRP, WP, or GFP. Low aggregation responses were only observed using high concentrations of both WP (9 x 10(8)/mL) and cIC (500 micrograms/mL). Interestingly, catIC were also able to induce platelet activation under nonaggregating conditions, as evidenced by P-selectin expression. Cationized human IgG alone did not induce platelet aggregation in PRP but triggered either WP or GFP aggregation. However, the concentration needed to induce these responses, was about eightfold higher than those required for catIC. The responses induced either by catIC or cationized human IgG were completely inhibited by treatment with heparin, dextran sulphate, EDTA, prostaglandin E1, or IV3, a monoclonal antibody against the receptor II for the Fc portion of IgG (Fc gamma RII). The data presented in this study suggest that IgG charge constitutes a critical property that conditions the ability of IC to trigger platelet activation. 相似文献
85.
86.
In vivo behavior of human radioiodinated antithrombin III: distribution among three physiologic pools 总被引:3,自引:0,他引:3
It has recently been shown that antithrombin III (AT) distributes between plasma, a noncirculating vascular-associated pool and an extravascular pool in rabbit. Study of the in vivo behavior of autologous human 131I-AT demonstrates that in humans AT also distributes among three pools that are analogous to those found in rabbit. From the in vivo kinetic behavior of the 131I-labeled AT, the fractions of total-body AT in the plasma, noncirculating vascular- associated, and extravascular pools were calculated to be 0.393 +/- 0.015, 0.109 +/- 0.016, and 0.496 +/- 0.014, respectively. From three- exponential plasma radioactivity disappearance curves, an average plasma fractional catabolic rate, j3, of 0.576 +/- 0.034 day-1 was obtained for five healthy young men. This is almost identical to the result obtained if plasma 131I-AT disappearance is assumed to fit a two- exponential curve (0.546 +/- 0.038), where the constant C2 from *Ap(t) = C1e-a1t + C2e-a2t is assumed to be equal to 1 - C1. The fraction of the total vascular AT catabolized daily, j3.5, was calculated to be 0.457 +/- 0.034, and the fractional catabolic rate of total-body AT, jT, averaged 0.2271 +/- 0.0176. The results give further support to a model of in vivo behavior in which the vascular AT distributes between plasma and an endothelial receptor. Thus, the latter may serve to mediate activation of AT for its reaction with coagulation proteases and to mediate its entrance into the endothelial cell, where it is either transported to the extravascular fluids or is catabolized. 相似文献
87.
We have previously reported the isolation of a monoclonal antibody (NHL- 30.5) that reacts with an antigen expressed on a substantial proportion of marrow and blood cells of most patients with newly diagnosed or relapsing acute myeloid leukemia. This antigen is also found on several cell lines derived from myeloid malignancies of human origin. It is not present on mature hemopoietic cells or on the majority of differentiating bone marrow cells. In order to determine whether the NHL-30.5 antigen may, nevertheless, be expressed on low-frequency primitive normal hemopoietic cells, not detected in standard antibody screening procedures, its expression was studied on clonogenic erythropoietic and granulopoietic cells. Light-density (less than 1.077 g/mL) suspensions of normal or chronic myelogenous leukemia bone marrow and peripheral blood cells were stained with NHL-30.5 and fluorescein isothiocyanate labeled second antibody and then sorted into two fractions using the fluorescence-activated cell sorter. The first contained the top 5% of cells with the highest fluorescence intensity. The remainder were collected in the second fraction. Colony assays of both fractions showed the first to be enriched in CFU-E, BFU-E, and CFU- C content (fourfold to 17-fold). The second fraction was correspondingly depleted of these progenitors. These findings reveal NHL-30.5 antigen expression to be a transient event during normal hemopoiesis that characterizes primitive hemopoietic cells on several pathways. Subsequent experiments showed that the presence of up to 10 micrograms/mL of purified NHL-30.5 antibody in colony assay cultures neither inhibited nor stimulated colony formation. Marrow fibroblasts (subcultured marrow adherent cells) were NHL-30.5 negative. Immunoprecipitation studies showed that the antigen detected by NHL- 30.5 is clearly distinct from that identified by My-10, another monoclonal antibody that has previously shown some similarities to NHL- 30.5. It thus appears that the NHL-30.5 antibody reacts with a new myeloid differentiation antigen of as yet unidentified function that is normally restricted in its expression to early stages of hemopoiesis. 相似文献
88.
BACKGROUND: Cyclooxygenase (COX) is the rate-limiting enzyme in the synthesis of prostaglandins. It exists in two isoforms: COX-1 which is constitutively expressed and COX-2 which is an inducible form activated by a variety of cytokines during inflammation. DISCUSSION: Interest in this enzyme arose in the early 1990s when, following epidemiological studies, aspirin (which is a COX inhibitor) was found to reduce the risk of colorectal cancer. Since then various studies to decipher the mechanisms by which COX reduces the development of colorectal cancer have been undertaken. One of the mechanisms being studied is its role in the angiogenesis of colorectal cancer. Angiogenesis of its own has been well established as a key factor in the development of tumours. Agents that specifically inhibit COX-2 are now in clinical development and have been licensed to be used in patients with familial adenomatosis polyposis. CONCLUSION: What needs to be determined is whether the antiangiogenic effects of COX-2 inhibitors can be used in the prevention and/or treatment of colorectal cancer and its metastases. 相似文献
89.