全文获取类型
收费全文 | 2142篇 |
免费 | 206篇 |
国内免费 | 7篇 |
专业分类
耳鼻咽喉 | 45篇 |
儿科学 | 60篇 |
妇产科学 | 27篇 |
基础医学 | 333篇 |
口腔科学 | 24篇 |
临床医学 | 173篇 |
内科学 | 531篇 |
皮肤病学 | 59篇 |
神经病学 | 213篇 |
特种医学 | 75篇 |
外科学 | 286篇 |
综合类 | 3篇 |
预防医学 | 120篇 |
眼科学 | 62篇 |
药学 | 132篇 |
中国医学 | 3篇 |
肿瘤学 | 209篇 |
出版年
2024年 | 2篇 |
2023年 | 30篇 |
2022年 | 32篇 |
2021年 | 79篇 |
2020年 | 52篇 |
2019年 | 113篇 |
2018年 | 121篇 |
2017年 | 65篇 |
2016年 | 78篇 |
2015年 | 90篇 |
2014年 | 106篇 |
2013年 | 127篇 |
2012年 | 215篇 |
2011年 | 190篇 |
2010年 | 124篇 |
2009年 | 81篇 |
2008年 | 149篇 |
2007年 | 147篇 |
2006年 | 101篇 |
2005年 | 99篇 |
2004年 | 76篇 |
2003年 | 75篇 |
2002年 | 67篇 |
2001年 | 7篇 |
2000年 | 8篇 |
1999年 | 7篇 |
1998年 | 11篇 |
1997年 | 13篇 |
1996年 | 5篇 |
1995年 | 6篇 |
1994年 | 6篇 |
1993年 | 4篇 |
1992年 | 8篇 |
1991年 | 6篇 |
1990年 | 5篇 |
1988年 | 7篇 |
1987年 | 6篇 |
1986年 | 4篇 |
1984年 | 5篇 |
1983年 | 6篇 |
1981年 | 2篇 |
1979年 | 2篇 |
1976年 | 2篇 |
1973年 | 1篇 |
1972年 | 1篇 |
1971年 | 1篇 |
1970年 | 1篇 |
1968年 | 1篇 |
1967年 | 2篇 |
1966年 | 3篇 |
排序方式: 共有2355条查询结果,搜索用时 15 毫秒
31.
Katherine R. Amato Marie-Claire Arrieta Meghan B. Azad Michael T. Bailey Josiane L. Broussard Carlijn E. Bruggeling Erika C. Claud Elizabeth K. Costello Emily R. Davenport Bas E. Dutilh Holly A. Swain Ewald Paul Ewald Erin C. Hanlon Wrenetha Julion Ali Keshavarzian Corinne F. Maurice Gregory E. Miller Geoffrey A. Preidis Laure Segurel Burton Singer Sathish Subramanian Liping Zhao Christopher W. Kuzawa 《Proceedings of the National Academy of Sciences of the United States of America》2021,118(25)
Individuals who are minoritized as a result of race, sexual identity, gender, or socioeconomic status experience a higher prevalence of many diseases. Understanding the biological processes that cause and maintain these socially driven health inequities is essential for addressing them. The gut microbiome is strongly shaped by host environments and affects host metabolic, immune, and neuroendocrine functions, making it an important pathway by which differences in experiences caused by social, political, and economic forces could contribute to health inequities. Nevertheless, few studies have directly integrated the gut microbiome into investigations of health inequities. Here, we argue that accounting for host–gut microbe interactions will improve understanding and management of health inequities, and that health policy must begin to consider the microbiome as an important pathway linking environments to population health. 相似文献
32.
Human chronic lymphocytic leukemia B cells can escape DNA damage-induced apoptosis through the nonhomologous end-joining DNA repair pathway 总被引:2,自引:1,他引:2 下载免费PDF全文
Deriano L Guipaud O Merle-Béral H Binet JL Ricoul M Potocki-Veronese G Favaudon V Maciorowski Z Muller C Salles B Sabatier L Delic J 《Blood》2005,105(12):4776-4783
Nonhomologous end-joining (NHEJ) DNA factors maintain genomic stability through their DNA double-strand break (DSB) repair and telomere-associated activities. Unrepaired or misrepaired DSBs can lead to apoptotic death or chromosomal damage. The B cells of some B-chronic lymphocytic leukemia (B-CLL) patients are resistant to radiation-induced apoptosis in vitro. We show here that the novel DNA-dependent protein kinase (DNA-PK) inhibitor, NU7026 (2-(morpholin-4-yl)-benzo[h]chomen-4-one), and the phosphatidylinositol 3 (PI-3) kinase inhibitor, wortmannin, restored sensitivity to DNA damage-induced apoptosis of otherwise resistant cells. These resistant malignant B cells also escaped DSB-induced apoptosis following exposure to etoposide or neocarzinostatin. We found that at 15 minutes after irradiation, the levels of NHEJ (as measured by an in vitro DSB end-ligation assay) and DNA-PK catalytic subunit (DNA-PKcs) activity were, respectively, 2-fold and 4-fold higher in radio-resistant than in radio-sensitive B-CLL cells or Epstein-Barr virus (EBV)-transformed B cells. Ku70/Ku80 heterodimer DNA end-binding activity was also 2- to 3-fold higher in the resistant B-CLL cell subset compared with the sensitive B-CLL cell subset. Our results provide the first evidence that overactivating the NHEJ DNA repair pathway impairs DNA damage-induced apoptosis in malignant B cells and that this may contribute to their resistance to current chemotherapy. 相似文献
33.
Hidden Genetic Variation in LCA9‐Associated Congenital Blindness Explained by 5′UTR Mutations and Copy‐Number Variations of NMNAT1 下载免费PDF全文
Frauke Coppieters Anne Laure Todeschini Takuro Fujimaki Annelot Baert Marieke De Bruyne Caroline Van Cauwenbergh Hannah Verdin Miriam Bauwens Maté Ongenaert Mineo Kondo Françoise Meire Akira Murakami Reiner A. Veitia Bart P. Leroy Elfride De Baere 《Human mutation》2015,36(12):1188-1196
Leber congenital amaurosis (LCA) is a severe autosomal‐recessive retinal dystrophy leading to congenital blindness. A recently identified LCA gene is NMNAT1, located in the LCA9 locus. Although most mutations in blindness genes are coding variations, there is accumulating evidence for hidden noncoding defects or structural variations (SVs). The starting point of this study was an LCA9‐associated consanguineous family in which no coding mutations were found in the LCA9 region. Exploring the untranslated regions of NMNAT1 revealed a novel homozygous 5′UTR variant, c.‐70A>T. Moreover, an adjacent 5′UTR variant, c.‐69C>T, was identified in a second consanguineous family displaying a similar phenotype. Both 5′UTR variants resulted in decreased NMNAT1 mRNA abundance in patients’ lymphocytes, and caused decreased luciferase activity in human retinal pigment epithelial RPE‐1 cells. Second, we unraveled pseudohomozygosity of a coding NMNAT1 mutation in two unrelated LCA patients by the identification of two distinct heterozygous partial NMNAT1 deletions. Molecular characterization of the breakpoint junctions revealed a complex Alu‐rich genomic architecture. Our study uncovered hidden genetic variation in NMNAT1‐associated LCA and emphasized a shift from coding to noncoding regulatory mutations and repeat‐mediated SVs in the molecular pathogenesis of heterogeneous recessive disorders such as hereditary blindness. 相似文献
34.
35.
36.
Pierre Ollitrault MD MSc Laure Champ-Rigot MD PhD Virginie Ferchaud MD MSc Arnaud Pellissier MD Olivier Coffin MD Paul Milliez MD PhD 《Journal of cardiovascular electrophysiology》2021,32(2):545-546
The IntellaMap OrionTM (Boston Scientific) is a 64-electrode basket catheter allowing for ultrahigh-density mapping of complex cardiac arrhythmias. We report the case of a basket catheter vascular entrapment, requiring surgical removal. 相似文献
37.
Flt3-ligand induces adhesion of haematopoietic progenitor cells via a very late antigen (VLA)-4- and VLA-5-dependent mechanism 总被引:4,自引:0,他引:4
Solanilla A Grosset C Duchez P Legembre P Pitard V Dupouy M Belloc F Viallard JF Reiffers J Boiron JM Coulombel L Ripoche J 《British journal of haematology》2003,120(5):782-786
The adhesion of haematopoietic progenitor cells (HPC) to the bone marrow microenvironment is a process regulated by cytokines. In this study, we have shown that flt3-ligand (FL), a growth factor that controls early haematopoiesis, regulated the function and expression of the beta-1 integrins, very late antigen (VLA)-4 and VLA-5 on HPC. The modulation of the adhesiveness of HPC by FL was studied by adhesion assays on umbilical vein endothelial cells (HUVEC). Stimulation by FL induced two peaks of increased adhesiveness of HPC. The first peak was at around 30 min and was mechanistically related to an activation of the beta-1 integrins, mainly VLA-4 and VLA-5. The second peak was at around 12 h and was related to increased expression of VLA-4 and VLA-5. The control of HPC adhesiveness by FL is a previously unreported property of FL that may be important for the homing and the retention of flt3-expressing HPC within the bone marrow microenvironment. 相似文献
38.
39.
40.
Laure Verret Alice Krezymon Hélène Halley Stéphanie Trouche Meike Zerwas Marine Lazouret Jean-Michel Lassalle Claire Rampon 《Neurobiology of aging》2013
Levels of educational and occupational attainment, as components of cognitive reserve, may modify the relationship between the pathological hallmarks and cognition in Alzheimer's disease (AD). We examined whether exposure of a Tg2576 transgenic mouse model of AD to environmental enrichment (EE) at a specific period during the amyloidogenic process favored the establishment of a cognitive reserve. We found that exposure to EE during early adulthood of Tg2576 mice—before amyloidogenesis has started—reduced the severity of AD-related cognitive deficits more efficiently than exposure later in life, when the pathology is already present. Interestingly, early-life exposure to EE, while slightly reducing forebrain surface covered by amyloid plaques, did not significantly impact aberrant inhibitory remodeling in the hippocampus of Tg2576 mice. Thus, transient early-life exposure to EE exerts long-lasting protection against cognitive impairment during AD pathology. In addition, these data define the existence of a specific life time frame during which stimulatory activity most efficiently builds a cognitive reserve, limiting AD progression and favoring successful aging. 相似文献