全文获取类型
收费全文 | 213493篇 |
免费 | 36656篇 |
国内免费 | 5989篇 |
专业分类
耳鼻咽喉 | 5679篇 |
儿科学 | 6217篇 |
妇产科学 | 3375篇 |
基础医学 | 10331篇 |
口腔科学 | 2631篇 |
临床医学 | 33875篇 |
内科学 | 56786篇 |
皮肤病学 | 8119篇 |
神经病学 | 17590篇 |
特种医学 | 8968篇 |
外国民族医学 | 37篇 |
外科学 | 48230篇 |
综合类 | 10271篇 |
现状与发展 | 92篇 |
一般理论 | 16篇 |
预防医学 | 11145篇 |
眼科学 | 4814篇 |
药学 | 7838篇 |
64篇 | |
中国医学 | 3334篇 |
肿瘤学 | 16726篇 |
出版年
2024年 | 870篇 |
2023年 | 5598篇 |
2022年 | 3371篇 |
2021年 | 6062篇 |
2020年 | 8153篇 |
2019年 | 4082篇 |
2018年 | 9388篇 |
2017年 | 9156篇 |
2016年 | 10165篇 |
2015年 | 10920篇 |
2014年 | 18719篇 |
2013年 | 18760篇 |
2012年 | 9970篇 |
2011年 | 10275篇 |
2010年 | 13472篇 |
2009年 | 16809篇 |
2008年 | 9214篇 |
2007年 | 7513篇 |
2006年 | 9698篇 |
2005年 | 6752篇 |
2004年 | 5442篇 |
2003年 | 4273篇 |
2002年 | 4128篇 |
2001年 | 5546篇 |
2000年 | 4680篇 |
1999年 | 4750篇 |
1998年 | 4455篇 |
1997年 | 4303篇 |
1996年 | 4043篇 |
1995年 | 3787篇 |
1994年 | 2437篇 |
1993年 | 1902篇 |
1992年 | 1890篇 |
1991年 | 1830篇 |
1990年 | 1463篇 |
1989年 | 1530篇 |
1988年 | 1292篇 |
1987年 | 1112篇 |
1986年 | 1085篇 |
1985年 | 871篇 |
1984年 | 663篇 |
1983年 | 601篇 |
1982年 | 571篇 |
1981年 | 472篇 |
1980年 | 397篇 |
1979年 | 378篇 |
1978年 | 365篇 |
1977年 | 423篇 |
1975年 | 304篇 |
1972年 | 341篇 |
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
1.
2.
3.
4.
5.
6.
Two Janus-associated kinase inhibitors (JAKi) (initially ruxolitinib and, more recently, fedratinib) have been approved as treatment options for patients who have intermediate-risk and high-risk myelofibrosis (MF), with pivotal trials demonstrating improvements in spleen volume, disease symptoms, and quality of life. At the same time, however, clinical trial experiences with JAKi agents in MF have demonstrated a high frequency of discontinuations because of adverse events or progressive disease. In addition, overall survival benefits and clinical and molecular predictors of response have not been established in this population, for which the disease burden is high and treatment options are limited. Consistently poor outcomes have been documented after JAKi discontinuation, with survival durations after ruxolitinib ranging from 11 to 16 months across several studies. To address such a high unmet therapeutic need, various non-JAKi agents are being actively explored (in combination with ruxolitinib in first-line or salvage settings and/or as monotherapy in JAKi-pretreated patients) in phase 3 clinical trials, including pelabresib (a bromodomain and extraterminal domain inhibitor), navitoclax (a B-cell lymphoma 2/B-cell lymphoma 2-xL inhibitor), parsaclisib (a phosphoinositide 3-kinase inhibitor), navtemadlin (formerly KRT-232; a murine double-minute chromosome 2 inhibitor), and imetelstat (a telomerase inhibitor). The breadth of data expected from these trials will provide insight into the ability of non-JAKi treatments to modify the natural history of MF. 相似文献
7.
Weina Cheng Yazhi Wang Jingxian Liu Xiaofei Li Ming Yu Cancan Duan Liu Liu Jianyong Zhang 《Journal of applied toxicology : JAT》2022,42(6):970-980
Cantharidin (CTD) is an effective antitumor agent. However, it exhibits significant hepatotoxicity, the mechanism of which remains unclear. In this study, biochemical and histopathological analyses complemented with ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS)-based targeted metabolomic analysis of bile acids (BAs) were employed to investigate CTD-induced hepatotoxicity in rats. Sixteen male and female Sprague–Dawley rats were randomly divided into two groups: control and CTD (1.0 mg/kg) groups. Serum and liver samples were collected after 28 days of intervention. Biochemical, histopathological, and BA metabolomic analyses were performed for all samples. Further, the key biomarkers of CTD-induced hepatotoxicity were identified via multivariate and metabolic pathway analyses. In addition, metabolite–gene–enzyme network and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to identify the signaling pathways related to CTD-induced hepatotoxicity. The results revealed significantly increased levels of biochemical indices (alanine aminotransferase, aspartate aminotransferase, and total bile acid). Histopathological analysis revealed that the hepatocytes were damaged. Further, 20 endogenous BAs were quantitated via UHPLC-MS/MS, and multivariate and metabolic pathway analyses of BAs revealed that hyocholic acid, cholic acid, and chenodeoxycholic acid were the key biomarkers of CTD-induced hepatotoxicity. Meanwhile, primary and secondary BA biosynthesis and taurine and hypotaurine metabolism were found to be associated with the mechanism by which CTD induced hepatotoxicity in rats. This study provides useful insights for research on the mechanism of CTD-induced hepatotoxicity. 相似文献
8.
9.
10.