全文获取类型
收费全文 | 940篇 |
免费 | 33篇 |
国内免费 | 3篇 |
专业分类
儿科学 | 72篇 |
妇产科学 | 11篇 |
基础医学 | 82篇 |
口腔科学 | 25篇 |
临床医学 | 84篇 |
内科学 | 242篇 |
皮肤病学 | 21篇 |
神经病学 | 33篇 |
特种医学 | 250篇 |
外科学 | 40篇 |
综合类 | 10篇 |
预防医学 | 35篇 |
眼科学 | 4篇 |
药学 | 28篇 |
中国医学 | 1篇 |
肿瘤学 | 38篇 |
出版年
2023年 | 2篇 |
2022年 | 3篇 |
2021年 | 4篇 |
2020年 | 2篇 |
2019年 | 5篇 |
2018年 | 13篇 |
2017年 | 10篇 |
2016年 | 8篇 |
2015年 | 11篇 |
2014年 | 17篇 |
2013年 | 18篇 |
2012年 | 16篇 |
2011年 | 9篇 |
2010年 | 35篇 |
2009年 | 42篇 |
2008年 | 27篇 |
2007年 | 20篇 |
2006年 | 19篇 |
2005年 | 13篇 |
2004年 | 14篇 |
2003年 | 14篇 |
2002年 | 8篇 |
2001年 | 10篇 |
2000年 | 5篇 |
1999年 | 11篇 |
1998年 | 50篇 |
1997年 | 66篇 |
1996年 | 50篇 |
1995年 | 41篇 |
1994年 | 51篇 |
1993年 | 51篇 |
1992年 | 12篇 |
1991年 | 10篇 |
1990年 | 10篇 |
1989年 | 38篇 |
1988年 | 39篇 |
1987年 | 28篇 |
1986年 | 28篇 |
1985年 | 26篇 |
1984年 | 11篇 |
1983年 | 21篇 |
1982年 | 18篇 |
1981年 | 18篇 |
1980年 | 21篇 |
1979年 | 3篇 |
1978年 | 8篇 |
1977年 | 12篇 |
1976年 | 9篇 |
1975年 | 17篇 |
1948年 | 1篇 |
排序方式: 共有976条查询结果,搜索用时 15 毫秒
61.
The effects of a novel cytokine FLK2/FLT3 ligand (FL) on human fetal bone marrow-derived CD34+CD19+ pro-B cells were analyzed in a stromal- cell-independent, serum-deprived culture system. FL, like interleukin-3 (IL-3), synergized with IL-7 in promoting pro-B cell growth, and differentiation of these cells into CD34-CD19+clgM+slgM- pre-B cells, whereas a small proportion of these cells even differentiate into more mature slgM+ B cells. In contrast, KIT ligand (KL) and granulocyte- macrophage colony-stimulating factor (GM-CSF) were ineffective in promoting IL-7-dependent pro-B cell growth and differentiation. Maximal levels of pro-B cell expansion, generally resulting in 15- to 30-fold increases in cellularity, were obtained in cultures supplemented with optimal doses of FL + IL-7 + IL-3. The addition of mouse bone marrow stromal cells further enhanced the proliferation and differentiation of pro-B cells obtained in the presence of these three cytokines. Under these conditions, cultures could be maintained for more than 4 weeks, and in general 40- to 50-fold increases in cell numbers were observed by 3 weeks of culture. The percentages of clgM+ and slgM+ B cells increased 1.5- to 3-fold and 2-fold, respectively, suggesting that stromal cells may provide additional costimulatory signals for human B- cell growth and differentiation that are different from IL-7, IL-3, and FL. Collectively, our results indicate that FL, in contrast to KL, strongly promotes long-term expansion and differentiation of human pro- B cells in the presence of IL-7 or in combination of IL-7 and IL-3, which is a novel property of this hematopoietic growth factor. 相似文献
62.
CJ Stewart ECL Marrs S Magorrian A Nelson C Lanyon JD Perry ND Embleton SP Cummings JE Berrington 《Acta paediatrica (Oslo, Norway : 1992)》2012,101(11):1121-1127
Aim: To describe gut colonization in preterm infants using standard culture and 16S gene rRNA profiling, exploring differences in healthy infants and those who developed NEC/late onset sepsis (LOS). Methods: Ninety‐nine stools from 38 infants of median 27‐week gestation were cultured; 44 stools from 27 infants had their microbial profiles determined by 16S. Ordination analyses explored effects of patient variables on gut communities. Results: Standard microbiological culture identified a mean of two organisms (range 0–7), DGGE 12 (range 3–18) per patient. Enterococcus faecalis and coagulase negative staphylococci (CONS) were most common by culture (40% and 39% of specimens). Meconium was not sterile. No fungi were cultured. Bacterial community structures in infants with NEC and LOS differed from healthy infants. Infants who developed NEC carried more CONS (45% vs 30%) and less Enterococcus faecalis (31% vs 57%). 16S identified Enterobacter and Staphylococcus presence associated with NEC/LOS, respectively. Conclusions: Important differences were found in the gut microbiota of preterm infants who develop NEC/LOS. The relationship of these changes to current practices in neonatal intensive care requires further exploration. 相似文献
63.
64.
65.
Background
Genetic polymorphisms of the TCF7L2 gene are strongly associated with large increments in type 2 diabetes risk in different populations worldwide. In this study, we aimed to confirm the effect of the TCF7L2 polymorphism rs7903146 on diabetes risk in a Brazilian population and to assess the use of this genetic marker in improving diabetes risk prediction in the general population. 相似文献66.
Deeg HJ; Storb R; Thomas ED; Appelbaum F; Buckner CD; Clift RA; Doney K; Johnson L; Sanders JE; Stewart P; Sullivan KM; Witherspoon RP 《Blood》1983,61(5):954-959
Eight patients with Fanconi's anemia were given cyclophosphamide alone (seven patients) or combined with procarbazine and antithymocyte globulin (one patient) followed by marrow grafts from HLA-identical siblings. All patients had engraftment. Seven developed acute and three chronic graft-versus-host disease (GVHD). Three patients died with GVHD and infectious complications (days 19, 56, and 82) and one with an intracerebral hemorrhage (day 540). Four patients are surviving 647- 3435 days after grafting, two are well, and two have chronic GVHD that is improving. These results show that Fanconi's anemia can be treated successfully by allogeneic marrow transplantation. 相似文献
67.
Preliminary evidence for a role of apolipoprotein E alleles in identifying haemodialysis patients at high vascular risk 总被引:1,自引:0,他引:1
Olmer M; Renucci JE; Planells R; Bouchouareb D; Purgus R 《Nephrology, dialysis, transplantation》1997,12(4):691-693
Conventional risk factors have very low predictive power in identifying
haemodialysis patients at high risk of vascular accidents. A role for
apolipoprotein E isotypes was looked for in a small, but rigorously
defined, cohort of longterm haemodialysis patients. In individuals with
high vascular risk, as identified by higher common carotid intima/media
thickness, we found an excess of apolipoprotein E4 alleles. This
preliminary result requires confirmation in large patient cohorts.
相似文献
68.
69.
70.
A Nørremølle E Budtz-Jørgensen K Fenger JE Nielsen SA Sørensen and L Hasholt 《Clinical genetics》2009,75(3):244-250
Huntington disease (HD) is caused by an expanded CAG repeat sequence in the HD gene. Although the age at onset is correlated to the CAG repeat length, this correlation only explains approximately half of the variation in onset age. Less variation between siblings indicates that the variation is, in part, explained by genetic modifiers. We analyzed polymorphic loci within or close to the HD gene on the HD chromosome in Danish HD patients. We found one specific haplotype segregating with later age at onset, compared with patients with similar CAG repeat length and another haplotype. The nine Danish families in the study carrying this haplotype most likely have a common founder. Several of the polymorphic loci displayed alleles that may be specific to the late-onset haplotype, implicating that from this study we cannot determine which of the loci tested (or other polymorphic loci in this chromosomal area) do in fact contain genetic modifiers of age at onset. 相似文献