全文获取类型
收费全文 | 9486篇 |
免费 | 590篇 |
国内免费 | 43篇 |
专业分类
耳鼻咽喉 | 47篇 |
儿科学 | 262篇 |
妇产科学 | 159篇 |
基础医学 | 1842篇 |
口腔科学 | 250篇 |
临床医学 | 771篇 |
内科学 | 1931篇 |
皮肤病学 | 293篇 |
神经病学 | 1201篇 |
特种医学 | 309篇 |
外科学 | 816篇 |
综合类 | 43篇 |
一般理论 | 6篇 |
预防医学 | 523篇 |
眼科学 | 142篇 |
药学 | 573篇 |
中国医学 | 19篇 |
肿瘤学 | 932篇 |
出版年
2024年 | 6篇 |
2023年 | 61篇 |
2022年 | 136篇 |
2021年 | 234篇 |
2020年 | 183篇 |
2019年 | 249篇 |
2018年 | 285篇 |
2017年 | 183篇 |
2016年 | 280篇 |
2015年 | 300篇 |
2014年 | 383篇 |
2013年 | 496篇 |
2012年 | 723篇 |
2011年 | 778篇 |
2010年 | 405篇 |
2009年 | 425篇 |
2008年 | 633篇 |
2007年 | 668篇 |
2006年 | 626篇 |
2005年 | 631篇 |
2004年 | 594篇 |
2003年 | 543篇 |
2002年 | 453篇 |
2001年 | 81篇 |
2000年 | 73篇 |
1999年 | 88篇 |
1998年 | 124篇 |
1997年 | 74篇 |
1996年 | 66篇 |
1995年 | 60篇 |
1994年 | 43篇 |
1993年 | 36篇 |
1992年 | 18篇 |
1991年 | 22篇 |
1990年 | 16篇 |
1989年 | 19篇 |
1988年 | 8篇 |
1987年 | 8篇 |
1986年 | 12篇 |
1985年 | 10篇 |
1984年 | 6篇 |
1983年 | 10篇 |
1981年 | 4篇 |
1979年 | 9篇 |
1978年 | 4篇 |
1977年 | 4篇 |
1975年 | 4篇 |
1973年 | 5篇 |
1972年 | 5篇 |
1963年 | 3篇 |
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
101.
Loss of beta-catenin expression in metastatic gastric cancer. 总被引:10,自引:0,他引:10
Matthias P A Ebert Jun Yu Juliane Hoffmann Alba Rocco Christoph R?cken Sabine Kahmann Oliver Müller Murray Korc Joseph J Sung Peter Malfertheiner 《Journal of clinical oncology》2003,21(9):1708-1714
PURPOSE: Beta-catenin (beta-catenin) participates in intercellular adhesion and is an integral part of the Wnt signaling pathway. The role of beta-catenin in the pathogenesis of gastric cancer and its metastasis is largely unknown. PATIENTS AND METHODS: Immunohistochemistry and Western blot analysis were used to analyze the expression of beta-catenin in 87 human gastric cancers, in metastasis and cancer cell lines. The beta-catenin and the adenomatous polyposis coli (APC) genes were analyzed for gene mutations. Furthermore, methylation of the beta-catenin promoter in cell lines was assessed by treatment with 5'-azadeoxycytidine and sodium bisulfite genomic sequencing. RESULTS: beta-Catenin expression was present at either the cell membrane or the cytoplasm in 34 of 75 primary gastric cancers. Expression of beta-catenin was significantly more frequent in intestinal-type (P =.0049) and well-differentiated gastric cancers (P <.001). There were no quantitative differences between gastric cancers and the nonmalignant gastric tissues, as determined by Western blot analysis. One of 18 metastatic cancer lesions and four of five gastric cancer cell lines expressed beta-catenin protein. N87 cells, derived from the liver metastasis of a gastric cancer, did not express beta-catenin. Treatment with 5'-azadeoxycytidine restored beta-catenin protein levels in this cell line, which exhibited significantly more 5-methylcytosines in the beta-catenin promoter compared with the other cell lines. CONCLUSION: beta-Catenin expression is lost in a subgroup of primary gastric cancers, is frequently absent in metastases, and exhibits nuclear localization in cancers with either beta-catenin or APC gene mutations. Interestingly, the loss of beta-catenin expression in metastatic gastric cancers may result from hypermethylation of the beta-catenin promoter. 相似文献
102.
Peter Albers Roswitha Siener Sabine Kliesch Lothar Weissbach Susanne Krege Christoph Sparwasser Harald Schulze Axel Heidenreich Werner de Riese Volker Loy Erhard Bierhoff Christian Wittekind Rolf Fimmers Michael Hartmann 《Journal of clinical oncology》2003,21(8):1505-1512
PURPOSE: To prospectively assess potential risk factors for relapse in clinical stage I nonseminomatous germ cell tumors of the testis (CS I NSGCT). PATIENTS AND METHODS: From September 1996 to May 2002, 200 patients with CS I NSGCT were prospectively assigned to retroperitoneal lymph node dissection (RPLND), and risk factor assessment was performed within a multicenter protocol. One hundred sixty-five patients had an adequate minimum follow-up of 12 months (mean, 34.5 months) or had pathologic stage II. RESULTS: Pathologic stage II disease was found in 27.9% of patients. Only 0.6% of patients relapsed in the retroperitoneum after confirmation of pathologic stage I disease. With reference pathology, vascular invasion (VI) was most predictive of stage in multifactorial analysis (accuracy, 65.1%). However, the positive predictive value (PPV) of VI to predict patients who have metastatic disease or relapse during follow-up was only 52.7%. With absent VI, low-risk patients had a negative predictive value (NPV) of 76.9%. With a combination of several risk factors, the PPV increased to 63.6% and the negative predictive value increased to 86.5%. CONCLUSION: Even with an optimal combination of prognostic factors and reference pathology, more than one third of patients predicted to have pathologic stage II or relapse during follow-up will not harbor metastatic disease and, therefore, would be overtreated with adjuvant therapy. However, patients at low risk may be predicted at an 86.5% level, and thus, surveillance in highly compliant patients would be a valuable option. For high-risk patients, further reduction of adjuvant treatment is necessary. 相似文献
103.
104.
Colocalization of the tetraspanins, CO-029 and CD151, with integrins in human pancreatic adenocarcinoma: impact on cell motility. 总被引:6,自引:0,他引:6
Sabine Gesierich Claudia Paret Dagmar Hildebrand Jürgen Weitz Kaspar Zgraggen Friedrich H Schmitz-Winnenthal Vaclav Horejsi Osamu Yoshie Dorothee Herlyn Leonie K Ashman Margot Z?ller 《Clinical cancer research》2005,11(8):2840-2852
PURPOSE: Patients with pancreatic adenocarcinoma have a poor prognosis due to the extraordinary high invasive capacity of this tumor. Altered integrin and tetraspanin expression is suggested to be an important factor. We recently reported that after protein kinase C activation, colocalization of alpha6beta4 with the tetraspanin CO-029 strongly supports migration of a rat pancreatic adenocarcinoma. The finding led us to explore whether and which integrin-tetraspanin complexes influence the motility of human pancreatic tumors. EXPERIMENTAL DESIGN: Integrin and tetraspanin expression of pancreatic and colorectal adenocarcinoma was evaluated with emphasis on colocalization and the impact of integrin-tetraspanin associations on tumor cell motility. RESULTS: The majority of pancreatic and colorectal tumors expressed the alpha2, alpha3, alpha6, beta1, and beta4 integrins and the tetraspanins CD9, CD63, CD81, CD151, and CO-029. Expression of alpha6beta4 and CO-029 was restricted to tumor cells, whereas alpha1, alpha2, alpha3, alpha6, beta1, and CD9, CD81, CD151 were also expressed by the surrounding stroma. CD63, CD81, and beta1 expression was observed at comparably high levels in healthy pancreatic tissue. alpha3beta1 frequently colocalized and coimmunoprecipitated with CD9, CD81, and CD151, whereas alpha6beta4 colocalized and coimmunoprecipitated mostly with CD151 and CO-029. Notably, protein kinase C activation strengthened only the colocalization of CD151 and CO-029 with beta4 and was accompanied by internalization of the integrin-tetraspanin complex, decreased laminin 5 adhesion, and increased cell migration. CONCLUSION: alpha6beta4 is selectively up-regulated in pancreatic and colorectal cancer. The association of alpha6beta4 with CD151 and CO-029 correlates with increased tumor cell motility. 相似文献
105.
106.
107.
Svjetlana Mohrmann Anna Maier-Bode Frederic Dietzel Petra Reinecke Natalia Krawczyk Thomas Kaleta Ulrike Kreimer Gerald Antoch Tanja N. Fehm Katrin Sabine Roth 《Breast care (Basel, Switzerland)》2022,17(2):159
BackgroundThe question of how to deal with B3 lesions is of emerging interest.MethodsIn the breast diagnostics of 192 patients between 2009 and 2016, a minimally invasive biopsy revealed a B3 lesion with subsequent resection. This study investigates the malignancy rate of different B3 subgroups and the risk factors that play a role in obtaining a malignant finding.ResultsThe distribution of B3 lesions after minimally invasive biopsy was as follows: atypical ductal hyperplasia (ADH), 7.3%; flat epithelial atypia (FEA), 7.8%; lobular neoplasia (LN), 7.8%; papilloma (Pa), 49.5%; phylloidal tumour (PT), 8.9%; radial sclerosing scar (RS), 3.1%; mixed findings, 10.4%; and other B3 lesions, 5.2%. Most B3 lesions were detected by stereotactic vacuum-assisted biopsy (44.3%), 36.5% by ultrasound-assisted biopsy, and 19.3% by magnetic resonance imaging-assisted biopsy. Most B3 lesions (55.2%) were verified by surgical resection, whereas 30.7% were downgraded to a benign lesion. About 14.1% of the cases were upgraded to malignant lesions, 9.4% to ductal carcinoma in situ and 4.7% to invasive carcinoma. In relation to individual B3 lesions, the following malignancy rates were found: 28.6% (ADH), 13.3% (FEA), 33.3% (LN), 12.6% (Pa), 5.9% (PT), and 0% (RS). The most important risk factor was increasing age. Postmenopausal status was considered an increased risk for an upgrade (p = 0.015). A known malignancy in the ipsilateral breast was a significant risk factor for a malignant upgrade (p = 0.003).ConclusionIncreasing knowledge about B3 lesions allows us to develop a “lesion-specific” therapy approach in the heterogeneous group of B3 lesions, with follow-up imaging for some lesions with less malignant potential and concordance with imaging or further surgical resection in cases of disconcordance with imaging or higher malignant potential. 相似文献
108.
Rita K. Schmutzler Bjrn Schmitz-Luhn Bettina Borisch Peter Devilee Diana Eccles Per Hall Judith Balmaa Stefania Boccia Peter Dabrock Günter Emons Wolfgang Gaissmaier Jacek Gronwald Stefanie Houwaart Stefan Huster Karin Kast Alexander Katalinic Sabine C. Linn Sowmiya Moorthie Paul Pharoah Kerstin Rhiem Tade Spranger Dominique Stoppa-Lyonnet Johannes Jozef Marten van Delden Marc van den Bulcke Christiane Woopen 《Breast care (Basel, Switzerland)》2022,17(2):208
BackgroundRisk-adjusted cancer screening and prevention is a promising and continuously emerging option for improving cancer prevention. It is driven by increasing knowledge of risk factors and the ability to determine them for individual risk prediction. However, there is a knowledge gap between evidence of increased risk and evidence of the effectiveness and efficiency of clinical preventive interventions based on increased risk. This gap is, in particular, aggravated by the extensive availability of genetic risk factor diagnostics, since the question of appropriate preventive measures immediately arises when an increased risk is identified. However, collecting proof of effective preventive measures, ideally by prospective randomized preventive studies, typically requires very long periods of time, while the knowledge about an increased risk immediately creates a high demand for action.SummaryTherefore, we propose a risk-adjusted prevention concept that is based on the best current evidence making needed and appropriate preventive measures available, and which is constantly evaluated through outcome evaluation, and continuously improved based on these results. We further discuss the structural and procedural requirements as well as legal and socioeconomical aspects relevant for the implementation of this concept. 相似文献
109.
110.
Martin Ganssauge Helmut Wilhelm Karl-Ulrich Bartz-Schmidt Sabine Aisenbrey 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2009,247(12):1707-1710