全文获取类型
收费全文 | 269篇 |
免费 | 42篇 |
出版年
2021年 | 3篇 |
2019年 | 4篇 |
2017年 | 2篇 |
2016年 | 7篇 |
2015年 | 11篇 |
2014年 | 14篇 |
2013年 | 5篇 |
2012年 | 14篇 |
2011年 | 15篇 |
2010年 | 9篇 |
2009年 | 7篇 |
2008年 | 12篇 |
2007年 | 7篇 |
2006年 | 7篇 |
2005年 | 5篇 |
2004年 | 22篇 |
2003年 | 6篇 |
2002年 | 3篇 |
2001年 | 13篇 |
2000年 | 11篇 |
1999年 | 7篇 |
1998年 | 5篇 |
1997年 | 4篇 |
1996年 | 3篇 |
1995年 | 2篇 |
1994年 | 3篇 |
1993年 | 3篇 |
1992年 | 4篇 |
1991年 | 10篇 |
1990年 | 6篇 |
1989年 | 5篇 |
1988年 | 6篇 |
1987年 | 4篇 |
1986年 | 3篇 |
1985年 | 4篇 |
1983年 | 6篇 |
1982年 | 4篇 |
1981年 | 4篇 |
1978年 | 4篇 |
1977年 | 8篇 |
1976年 | 2篇 |
1974年 | 4篇 |
1973年 | 3篇 |
1972年 | 3篇 |
1970年 | 2篇 |
1969年 | 2篇 |
1968年 | 3篇 |
1967年 | 4篇 |
1966年 | 3篇 |
1915年 | 1篇 |
排序方式: 共有311条查询结果,搜索用时 15 毫秒
41.
42.
43.
DNA rearrangements on both homologues of chromosome 17 in a mildly delayed individual with a family history of autosomal dominant carpal tunnel syndrome. 总被引:7,自引:2,他引:5 下载免费PDF全文
L Potocki K S Chen T Koeuth J Killian S T Iannaccone S K Shapira C D Kashork A S Spikes L G Shaffer J R Lupski 《American journal of human genetics》1999,64(2):471-478
Disorders known to be caused by molecular and cytogenetic abnormalities of the proximal short arm of chromosome 17 include Charcot-Marie-Tooth disease type 1A (CMT1A), hereditary neuropathy with liability to pressure palsies (HNPP), Smith-Magenis syndrome (SMS), and mental retardation and congenital anomalies associated with partial duplication of 17p. We identified a patient with multifocal mononeuropathies and mild distal neuropathy, growth hormone deficiency, and mild mental retardation who was found to have a duplication of the SMS region of 17p11.2 and a deletion of the peripheral myelin protein 22 (PMP22) gene within 17p12 on the homologous chromosome. Further molecular analyses reveal that the dup(17)(p11.2p11.2) is a de novo event but that the PMP22 deletion is familial. The family members with deletions of PMP22 have abnormalities indicative of carpal tunnel syndrome, documented by electrophysiological studies prior to molecular analysis. The chromosomal duplication was shown by interphase FISH analysis to be a tandem duplication. These data indicate that familial entrapment neuropathies, such as carpal tunnel syndrome and focal ulnar neuropathy syndrome, can occur because of deletions of the PMP22 gene. The co-occurrence of the 17p11.2 duplication and the PMP22 deletion in this patient likely reflects the relatively high frequency at which these abnormalities arise and the underlying molecular characteristics of the genome in this region. 相似文献
44.
Human Osteogenesis Involves Differentiation-Dependent Increases in the Morphogenically Active 3′ Alternative Splicing Variant of Acetylcholinesterase 下载免费PDF全文
45.
46.
47.
48.
Elke EM Brouwers Alwin DR Huitema Jos H Beijnen Jan HM Schellens 《BMC clinical pharmacology》2008,8(1):7
Background
The aim of this study was to evaluate long-term platinum retention in patients treated with cisplatin and oxaliplatin. 相似文献49.
Dorit Samocha‐Bonet Dov Lichtenberg Aaron Tomer Varda Deutsch Tamar Mardi Yelena Goldin Subchi Abu‐Abeid Galina Shenkerman Hana Patshornik Itzhak Shapira Shlomo Berliner 《Obesity (Silver Spring, Md.)》2003,11(3):403-407
Objective: Previous studies have suggested that obesity enhances the inflammatory response, producing macromolecules involved in the induction and/or maintenance of increased erythrocyte aggregation. The objectives of this study were to evaluate the correlation between inflammation markers, erythrocyte adhesiveness/aggregation, and the degree of obesity and to assess phosphatidylserine expression on erythrocyte surface membrane of obese vs. nonobese individuals. Research Methods and Procedures: Erythrocyte adhesiveness/aggregation in the peripheral venous blood was evaluated by using a new biomarker, phosphatidylserine expression was assessed by means of flow cytometry, and markers of inflammation were measured in 65 subjects: 30 obese [body mass index (BMI) = 41 ± 7.7 kg/m2] and 35 nonobese (BMI = 24 ± 2.7 kg/m2) individuals. Pearson correlations and Student's t test were performed. Results: A highly significant difference was noted in the degree of erythrocyte adhesiveness/aggregation and markers of inflammation between the study groups. BMI correlated with erythrocyte adhesiveness/aggregation (r = 0.42, p = 0.001), erythrocyte sedimentation rate (r = 0.42, p = 0.001), high‐sensitive C‐reactive protein (r = 0.55, p < 10?4), fibrinogen (r = 0.37, p = 0.004), and white blood cell count (r = 0.45, p < 10?4). The degree of erythrocyte adhesiveness/aggregation correlated with erythrocyte sedimentation rate (r = 0.5, p < 10?4), high‐sensitive C‐reactive protein (r = 0.56, p < 10?4), fibrinogen (r = 0.54, p < 10?4), and white blood cell count (r = 0.32, p = 0.01). Discussion: Our results suggest that obesity‐related erythrocyte adhesiveness/aggregation is probably mediated through increased concentrations of adhesive macromolecules in the circulation and not necessarily through hyperlipidemia or phosphatidylserine exposure on erythrocyte's membrane. 相似文献
50.