全文获取类型
收费全文 | 807篇 |
免费 | 68篇 |
国内免费 | 11篇 |
专业分类
耳鼻咽喉 | 1篇 |
儿科学 | 26篇 |
妇产科学 | 4篇 |
基础医学 | 90篇 |
口腔科学 | 17篇 |
临床医学 | 151篇 |
内科学 | 144篇 |
皮肤病学 | 15篇 |
神经病学 | 19篇 |
特种医学 | 119篇 |
外科学 | 132篇 |
综合类 | 51篇 |
预防医学 | 54篇 |
眼科学 | 4篇 |
药学 | 35篇 |
1篇 | |
中国医学 | 2篇 |
肿瘤学 | 21篇 |
出版年
2022年 | 2篇 |
2021年 | 10篇 |
2020年 | 4篇 |
2019年 | 3篇 |
2018年 | 5篇 |
2017年 | 8篇 |
2016年 | 3篇 |
2015年 | 41篇 |
2014年 | 46篇 |
2013年 | 41篇 |
2012年 | 27篇 |
2011年 | 49篇 |
2010年 | 32篇 |
2009年 | 32篇 |
2008年 | 30篇 |
2007年 | 40篇 |
2006年 | 38篇 |
2005年 | 26篇 |
2004年 | 24篇 |
2003年 | 14篇 |
2002年 | 23篇 |
2001年 | 18篇 |
2000年 | 18篇 |
1999年 | 21篇 |
1998年 | 19篇 |
1997年 | 24篇 |
1996年 | 23篇 |
1995年 | 24篇 |
1994年 | 27篇 |
1993年 | 14篇 |
1992年 | 13篇 |
1991年 | 7篇 |
1990年 | 15篇 |
1989年 | 20篇 |
1988年 | 17篇 |
1987年 | 13篇 |
1986年 | 17篇 |
1985年 | 28篇 |
1984年 | 11篇 |
1983年 | 8篇 |
1982年 | 4篇 |
1981年 | 16篇 |
1980年 | 9篇 |
1979年 | 2篇 |
1978年 | 6篇 |
1977年 | 8篇 |
1976年 | 4篇 |
1969年 | 1篇 |
1957年 | 1篇 |
排序方式: 共有886条查询结果,搜索用时 15 毫秒
1.
2.
J M Debets R Kampmeijer M P van der Linden W A Buurman C J van der Linden 《Critical care medicine》1989,17(6):489-494
Tumor necrosis factor (TNF) cachectin has been implicated as an important host mediator responsible for shock and multiple organ failure (MOF) observed during sepsis. Using a sensitive enzyme-linked immunosorbent assay, we measured plasma TNF levels in 43 septic patients suffering from a broad range of diseases. Measurements were taken on the day that sepsis was diagnosed. Eleven patients had detectable TNF plasma levels ranging from 10 to 100 pg/ml (TNF-positive group); in 32 patients circulating TNF could not be detected (TNF-negative group). The groups did not differ significantly as to age, underlying disease, percentage positive bacteremia and bacteriologic profile, sepsis score, and extent of MOF. Eight (73%) of 11 TNF-positive patients died from sepsis during ICU stay, vs. 11 (34%) of 32 TNF-negative patients (p less than .05). This study demonstrates that sepsis is accompanied by detectable circulating TNF in 25% of the cases, and for these patients mortality is twice that for comparable TNF-negative patients. 相似文献
3.
4.
5.
6.
R.M.H. Wijnen B.-G. Ericzon A.T.M.G. Tiebosch W.A. Buurman C.G. Groth G. Kootstra 《Transplant international》1992,5(Z1):S454-S458
We investigated clinical, biochemical, and histopathological parameters in FK506-treated cynomolgus monkeys. Eight monkeys given oral FK506, 1 (n = 4) or 10 (n = 4) mg/kg daily, survived the 90 days of treatment apparently in good health and without significant changes in biochemical and histopathological parameters, as did 2 control monkeys except one monkey on 10 mg/kg/day FK506 orally, who was found to have a malignant lymphoma. In contrast, monkeys given intramuscular FK506 1 mg/kg daily (n = 4) had to be sacrificed at day 20, 25, 32, and 47 because of severe illness. They showed abnormal biochemical parameters (increased serum urea and aspartate aminotransferase activity) and major histopathological changes in the kidney (mesangial cell proliferation and acute tubular necrosis), pancreas (depletion of beta cells), liver (steatosis), and heart (cardiomyopathy). Intramuscular administration of 1 mg/kg daily resulted in serum levels ranging from 10 to 15 ng/ml, while oral administration at a dose of 1 or 10 mg/kg daily resulted in equal or even higher serum levels (range 2–70 ng/ml). Thus, the height of the serum trough level of FK506 using the enzyme immunoassay is not related to the toxicity of FK506 in cynomolgus monkeys. 相似文献
7.
I Engelberts S K Samyo J F Leeuwenberg C J van der Linden W A Buurman 《The Journal of surgical research》1992,53(2):136-144
As a model for septic shock, LPS was infused into anesthetized Cynomolgus monkeys. Hematologic and metabolic parameters proved the induced shock response. The data presented show that administration of LPS to Cynomolgus monkeys induced a generalized inflammatory status, which was characterized by systemic release of the cytokines TNF and IL-6. Further it was demonstrated, using immune-histological methods, that a generalized expression in vivo of the endothelial leukocyte adhesion molecule (ELAM)-1 was induced on endothelial cells by LPS infusion. ELAM-1 expression was most pronounced on vasculature of lung tissue and skin. As shown in serial skin biopsies, ELAM-1 expression was induced rapidly: at 2 hr after the onset of LPS infusion, reaching maximum after 4 hr. The expression of ELAM-1 is considered to be of relevance for the mechanism which underlies the stasis of PMN in the tissues during septic shock. 相似文献
8.
9.
Previously we have described the properties of store-operated channel currents (SOCs) in freshly dispersed rabbit portal vein smooth muscle cells. In addition to Ca2+ store depletion these SOCs could also be activated by α-adrenoceptor stimulation and diacylglycerol (DAG) via a protein kinase C (PKC)-dependent mechanism. In the present study we have investigated the effect of β-adrenoceptor stimulation on SOCs in rabbit portal vein myocytes. With whole-cell recording the selective β-adrenoceptor agonist isoprenaline reduced the current evoked by cyclopiazonic acid (CPA, sarcoplasmic/endoplasmic reticulum ATPase inhibitor) by over 85%. With cell-attached patch recording, bath application of isoprenaline produced a pronounced inhibition of SOC activity evoked by either CPA or the acetoxymethyl ester form of BAPTA (BAPTA-AM). SOC activity evoked by CPA, the DAG analogue, 1-oleoyl-acetyl- sn -glycerol (OAG) or the phorbol ester, phorbol-12,13-dibutyrate (PDBu) was also markedly inhibited by the adenylate cyclase activator, forskolin, and the cell-permeable non-hydrolysable analogue of cyclic adenosine monophosphate (cAMP), 8-Br-cAMP. With inside-out patches, bath application of PDBu evoked channel currents with similar properties to SOCs which were inhibited by over 90% by a catalytic subunit of protein kinase A (PKA) and by 8-Br-cAMP. Moreover bath application of PKA inhibitors, H-89, KT5720 and an inhibitory peptide to quiescent cell-attached or inside-out patches, activated channel currents with similar properties to SOCs. These data suggest that in rabbit portal vein myocytes, stimulation of β-adrenoceptors inhibits SOC activity via a cAMP-dependent protein kinase signal transduction cascade. In addition it is concluded that constitutive PKA activity has a profound inhibitory effect on SOC activity in this vascular preparation. 相似文献
10.
Healthy subjects express differences in clinical responses to inhaled lipopolysaccharide that are related with inflammation and with atopy 总被引:2,自引:0,他引:2
Michel O Dentener M Corazza F Buurman W Rylander R 《The Journal of allergy and clinical immunology》2001,107(5):797-804
BACKGROUND: Endotoxin and its purified derivative LPS are important contaminants of both domestic and occupational environments that have been related to airway diseases. A body of data suggests that there is considerable interindividual variability in LPS sensitivity. OBJECTIVE: The aim of the study was to relate the individual clinical responses to inhaled LPS with the inflammatory process and the atopic status. METHODS: Fifteen healthy subjects were challenged each week by inhalation with saline solution or LPS (0.5, 5, or 50 microg). The systemic response was defined by the increase in body temperature, blood neutrophilia, acute-phase proteins (C-reactive protein and LPS-binding protein [LBP]), and E-selectin. The LPS-induced airway response was defined as the increase in airway responsiveness and related to the cell count and concentration of TNF-alpha, myeloperoxidase, and eosinophil cationic protein in induced sputum. The atopic status was defined as an increase in IgE or a positive skin prick test result. RESULTS: Subjects (n = 7) with a significant increase in body temperature had a larger increase in the systemic inflammatory response (blood neutrophilia; P <.01) and in blood concentrations of C-reactive protein (P <.02) and LBP (P <.01). Subjects with a significant increase in airway responsiveness (n = 8) had an increase in the sputum concentration of eosinophil cationic protein (P <.01). The amplitude of the systemic response (increase in body temperature [P <.001], blood neutrophilia [P <.02], and rise in LBP [P <.05] and decrease in FEV(1) [P <.01]) were inversely associated with the atopic status, suggesting a link between atopy and LPS responsiveness. CONCLUSIONS: The clinical response to LPS occurs systemically or locally and is associated with inflammation. The atopic status was inversely related to the systemic inflammation. 相似文献