全文获取类型
收费全文 | 1507篇 |
免费 | 56篇 |
国内免费 | 5篇 |
专业分类
耳鼻咽喉 | 9篇 |
儿科学 | 13篇 |
妇产科学 | 13篇 |
基础医学 | 181篇 |
口腔科学 | 25篇 |
临床医学 | 112篇 |
内科学 | 597篇 |
皮肤病学 | 6篇 |
神经病学 | 64篇 |
特种医学 | 46篇 |
外科学 | 133篇 |
综合类 | 5篇 |
预防医学 | 27篇 |
眼科学 | 7篇 |
药学 | 189篇 |
中国医学 | 9篇 |
肿瘤学 | 132篇 |
出版年
2023年 | 8篇 |
2022年 | 24篇 |
2021年 | 40篇 |
2020年 | 13篇 |
2019年 | 19篇 |
2018年 | 26篇 |
2017年 | 14篇 |
2016年 | 21篇 |
2015年 | 32篇 |
2014年 | 43篇 |
2013年 | 52篇 |
2012年 | 91篇 |
2011年 | 94篇 |
2010年 | 52篇 |
2009年 | 49篇 |
2008年 | 93篇 |
2007年 | 103篇 |
2006年 | 119篇 |
2005年 | 81篇 |
2004年 | 106篇 |
2003年 | 83篇 |
2002年 | 82篇 |
2001年 | 31篇 |
2000年 | 39篇 |
1999年 | 34篇 |
1998年 | 16篇 |
1997年 | 15篇 |
1996年 | 12篇 |
1995年 | 8篇 |
1994年 | 3篇 |
1993年 | 10篇 |
1992年 | 18篇 |
1991年 | 16篇 |
1990年 | 11篇 |
1989年 | 11篇 |
1988年 | 7篇 |
1987年 | 17篇 |
1986年 | 7篇 |
1985年 | 4篇 |
1984年 | 7篇 |
1983年 | 10篇 |
1982年 | 4篇 |
1981年 | 3篇 |
1979年 | 12篇 |
1977年 | 4篇 |
1976年 | 4篇 |
1973年 | 4篇 |
1972年 | 3篇 |
1971年 | 2篇 |
1970年 | 2篇 |
排序方式: 共有1568条查询结果,搜索用时 31 毫秒
41.
42.
Kujiraoka T Hattori H Ito M Nanjee MN Ishihara M Nagano M Iwasaki T Cooke CJ Olszewski WL Stepanova IP Egashira T Miller NE 《Atherosclerosis》2004,176(1):57-62
We have previously shown that intravenous apolipoprotein (apo) A-I/phosphatidylcholine (apo A-I/PC) discs increase plasma high-density lipoprotein (HDL) concentration in humans. We have now studied the associated changes in two enzymes, paraoxonase (PON) and platelet-activating factor acetylhydrolase (PAF-AH) that are carried in whole or in part by HDLs, and are thought to influence atherogenesis by hydrolyzing oxidized phospholipids in lipoproteins. Apo A-I/PC discs (40 mg/kg over 4 h) were infused into eight healthy males. Although plasma apo A-I and HDL cholesterol increased on average by 178 and 158%, respectively, plasma total PON and total PAF-AH concentrations did not rise. By the end of the infusion, HDL-associated PAF-AH had increased by 0.56 +/- 0.14 microg/mL (mean +/- S.D., P < 0.01), and nonHDL-associated PAF-AH had decreased by 0.84 +/- 0.11 microg/mL (P < 0.05). These changes were accompanied by an increase in the HDL-associated PAF-AH/apo A-I ratio from 0.19 to 0.35 (P < 0.05), and by a decrease in the nonHDL-associated PAF-AH/apo B ratio from 2.1 to 1.4 (P < 0.05). No changes in PON or PAF-AH concentrations were detected in prenodal lymph (tissue fluid), collected continuously from the leg. Our results show that the total concentrations of PON and PAF-AH in plasma are uninfluenced by plasma HDL concentration. PAF-AH transfers readily between HDLs and LDLs in vivo, and its distribution between them is determined partly by their relative concentrations and partly by HDL composition. 相似文献
43.
Ishibashi M Hiasa K Zhao Q Inoue S Ohtani K Kitamoto S Tsuchihashi M Sugaya T Charo IF Kura S Tsuzuki T Ishibashi T Takeshita A Egashira K 《Circulation research》2004,94(9):1203-1210
Activated monocytes are present in the arterial walls of hypertensive patients and animals. Monocyte chemoattractant protein-1 (MCP-1), which controls monocyte function through its receptor (CCR2), is implicated in hypertensive inflammatory changes in the arterial wall. The role of CCR2 expression on monocytes in hypertension-induced vascular remodeling, however, has not been addressed. We hypothesized that CCR2 on monocytes is critical in hypertension-induced vascular inflammation and remodeling. Hypertension was induced by infusion of angiotensin II (Ang II) into wild-type mice, CCR2-deficient (CCR2-/-) mice, and bone marrow-transferred mice with a leukocyte-selective CCR2 deficiency (BMT-CCR2-/-). In wild-type mice, Ang II increased CCR2 intensity in circulating monocytes, which was prevented by an Ang II type-1 (AT1) receptor blocker or blunted in AT1 receptor-deficient mice. Enhanced CCR2 intensity on monocytes was observed in hypertensive patients and rats, and was reduced by treatment with the Ang II receptor blocker, supporting the clinical relevance of the observation in mice. In CCR2-/- and BMT-CCR2-/- mice, Ang II-induced vascular inflammation and vascular remodeling (aortic wall thickening and fibrosis) were blunted as compared with control mice. In contrast, Ang II-induced left ventricular hypertrophy developed in CCR2-/- and BMT-CCR2-/- mice. The present study suggests that CCR2 expression in monocytes has a critical role in vascular inflammation and remodeling in Ang II-induced hypertension, and possibly in other forms of hypertension. 相似文献
44.
45.
46.
Rie Yamamoto Hiroshi Akazawa Kaoru Ito Haruhiro Toko Masanori Sano Noritaka Yasuda Yingjie Qin Yoko Kudo Takeshi Sugaya Kenneth R Chien Issei Komuro 《Circulation journal》2007,71(12):1958-1964
BACKGROUND: Angiotensin II (AT) is implicated in the development of cardiac remodeling, which leads to heart failure, and pharmacological inhibition of the AT type 1 (AT1) receptor has improved mortality and morbidity in patients of heart failure. The aim of this study was to elucidate the role of the AT1 receptor in disease progression in muscle LIM protein (MLP)-deficient mice, which are susceptible to heart failure because of defective function of mechanosensors in cardiomyocytes. METHOD AND RESULTS: Hearts from MLP knockout (MLPKO) mice and MLP-AT1a receptor double knockout (DKO) mice were analyzed. MLPKO hearts showed marked chamber dilatation with cardiac fibrosis and reactivation of the fetal gene program. All of these changes were significantly milder in the DKO hearts. Impaired left ventricular (LV) contractility and filling were alleviated in DKO hearts. However, the impaired relaxation and downregulated expression of sarcoplasmic reticulum calcium-ATPase 2 were unchanged in DKO hearts. CONCLUSIONS: The AT1a receptor is involved in progression of LV remodeling and deterioration of cardiac function in the hearts of MLPKO mice. These results suggest that blockade of the receptor is effective in preventing progression of heart failure in dilated cardiomyopathy. 相似文献
47.
48.
N. Kubo M. Morita Y. Nakashima H. Kitao A. Egashira H. Saeki E. Oki Y. Kakeji Y. Oda Y. Maehara 《Diseases of the esophagus》2014,27(3):285-293
Both internal and external oxidative stresses act on DNA and can induce carcinogenesis. 8‐hydroxydeoxyguanosine (8‐OHdG) is an indicator of oxidative stress and it leads to transversion mutations and carcinogenesis. 8‐OHdG is excision‐repaired by 8‐OHdG DNA glycosylase (OGG1). The purpose of this study is to clarify the effect of oxidative DNA damage and repair enzymes on esophageal carcinogenesis. The levels of 8‐OHdG and OGG1 were immunohistochemically evaluated in resected specimens, including squamous cell carcinoma (SCC) in 97 patients with esophageal cancer. Higher levels of 8‐OHdG in normal esophageal epithelium were associated with a higher smoking index (P = 0.0464). The 8‐OHdG level was higher in cancerous areas than in normal epithelia (P = 0.0061), whereas OGG1 expression was weaker in cancerous areas than in normal epithelia (P < 0.0001). An increase of OGG1 expression in normal epithelium was observed as 8‐OHdG levels increased (P = 0.0011). However, this correlation was not observed in cancerous areas. High OGG1 expression in the cytoplasm was related to deeper tumors (P = 0.0023), node metastasis (P = 0.0065) and stage (P = 0.0019). Oxidative DNA damage, which is attributable to smoking as well as disturbances in DNA repair systems, appears to be closely related to esophageal carcinogenesis and its progression. 相似文献
49.
Yosuke Omori Toshiaki Mano Tomohito Ohtani Yasushi Sakata Yasuharu Takeda Shunsuke Tamaki Yasumasa Tsukamoto Takeshi Miwa Kazuhiro Yamamoto Issei Komuro 《Yonago acta medica》2014,57(3):109-116
Background
Cardiac fibrosis is considered to be a crucial factor in the development of heart failure. Blockade of the mineralocorticoid receptor (MR) attenuated cardiac fibrosis and improved the prognosis of patients with chronic heart failure but the ligand for MR and the regulatory mechanism of MR pathway in the diseased heart are unclear. Here, we investigated whether glucocorticoids can promote cardiac fibrosis through MR in oxidative stress and the involvement of elongation factor eleven-nineteen lysine-rich leukemia (ELL), a co-activator of MR, in this pathway.Methods and Results
The MR antagonist eplerenone attenuated corticosterone-induced collagen synthesis assessed by [3H]proline incorporation in rat neonatal cultured cardiac fibroblasts in the presence of H2O2, as an oxidative stress but not in the absence of H2O2. H2O2 increased the ELL expression levels and MR-bound ELL. ELL expression levels and MR-bound ELL were also increased in the left ventricle of heart failure model rats with significant fibrosis and enhanced oxidative stress. Eplerenone did not attenuate corticosterone-induced increase of [3H]proline incorporation in the presence of H2O2 after knockdown of ELL expression using small interfering RNA in cardiac fibroblasts.Conclusion
Glucocorticoids can promote cardiac fibrosis via MR in oxidative stress, and oxidative stress modulates MR response to glucocorticoids through the interaction with ELL. Preventing cardiac fibrosis by modulating glucocorticoid-MR-ELL pathway may become a new therapeutic strategy for heart failure. 相似文献50.
Go Kuwata Terumi Kamisawa Koichi Koizumi Taku Tabata Seiichi Hara Sawako Kuruma Takashi Fujiwara Kazuro Chiba Hideto Egashira Junko Fujiwara Takeo Arakawa Kumiko Momma Shinichiro Horiguchi 《Gut and liver》2014,8(1):29-34