全文获取类型
收费全文 | 3148篇 |
免费 | 185篇 |
国内免费 | 10篇 |
专业分类
耳鼻咽喉 | 16篇 |
儿科学 | 72篇 |
妇产科学 | 54篇 |
基础医学 | 531篇 |
口腔科学 | 83篇 |
临床医学 | 235篇 |
内科学 | 699篇 |
皮肤病学 | 79篇 |
神经病学 | 443篇 |
特种医学 | 82篇 |
外科学 | 280篇 |
综合类 | 15篇 |
一般理论 | 1篇 |
预防医学 | 216篇 |
眼科学 | 35篇 |
药学 | 214篇 |
中国医学 | 8篇 |
肿瘤学 | 280篇 |
出版年
2024年 | 11篇 |
2023年 | 56篇 |
2022年 | 103篇 |
2021年 | 152篇 |
2020年 | 91篇 |
2019年 | 97篇 |
2018年 | 122篇 |
2017年 | 90篇 |
2016年 | 100篇 |
2015年 | 113篇 |
2014年 | 143篇 |
2013年 | 192篇 |
2012年 | 259篇 |
2011年 | 239篇 |
2010年 | 141篇 |
2009年 | 128篇 |
2008年 | 196篇 |
2007年 | 212篇 |
2006年 | 166篇 |
2005年 | 162篇 |
2004年 | 134篇 |
2003年 | 110篇 |
2002年 | 120篇 |
2001年 | 16篇 |
2000年 | 10篇 |
1999年 | 13篇 |
1998年 | 20篇 |
1997年 | 23篇 |
1996年 | 10篇 |
1995年 | 21篇 |
1994年 | 6篇 |
1993年 | 11篇 |
1992年 | 7篇 |
1991年 | 8篇 |
1990年 | 5篇 |
1989年 | 10篇 |
1988年 | 6篇 |
1987年 | 4篇 |
1986年 | 2篇 |
1985年 | 3篇 |
1984年 | 5篇 |
1983年 | 2篇 |
1982年 | 4篇 |
1978年 | 2篇 |
1976年 | 2篇 |
1971年 | 2篇 |
1964年 | 2篇 |
1960年 | 2篇 |
1931年 | 1篇 |
1922年 | 1篇 |
排序方式: 共有3343条查询结果,搜索用时 15 毫秒
51.
Araujo VP Aguiar-Oliveira MH Oliveira JL Rocha HM Oliveira CR Rodrigues TM Nunes MA Britto IM Ximenes R Barreto-Filho JA Meneguz-Moreno RA Pereira RM Valença EH Oliveira-Neto LA Vicente TA Blackford A Salvatori R 《European journal of endocrinology / European Federation of Endocrine Societies》2012,166(6):977-982
52.
53.
Adolfo Pisanu Isabella Reccia Giulia Porceddu Alessandro Uccheddu 《Journal of gastrointestinal surgery》2013,17(11):2029-2030
54.
55.
Tatsuro Misu Romana Höftberger Kazuo Fujihara Isabella Wimmer Yoshiki Takai Shuhei Nishiyama Ichiro Nakashima Hidehiko Konno Monika Bradl Ferenc Garzuly Yasuto Itoyama Masashi Aoki Hans Lassmann 《Acta neuropathologica》2013,125(6):815-827
Neuromyelitis optica (NMO) is an autoimmune disease targeting aquaporin 4 (AQP4), localized mainly at the astrocytic foot processes. Loss of AQP4 and glial fibrillary acidic protein (GFAP) was reported, but the pathological significance of astrocytopathy is still controversial. Here we show that active lesions in NMO display a wide spectrum of pathology even within a single tissue block of an individual patient. We have distinguished six different lesion types. The first reflects complement deposition at the surface of astrocytes, associated with granulocyte infiltration and astrocyte necrosis and followed by demyelination, global tissue destruction and the formation of cystic, necrotic lesions (lesion type 2). Such destructive lesions lead to Wallerian degeneration in lesion-related tracts (lesion type 3). Around active NMO lesions AQP4 may selectively be lost in the absence of aquaporin 1 (AQP1) loss or other structural damage (lesion type 4). Another pattern is characterized by clasmatodendrosis of astrocytes, defined by cytoplasmic swelling and vacuolation, beading and dissolution of their processes and nuclear alterations resembling apoptosis, which was associated with internalization of AQP4 and AQP1 and astrocyte apoptosis in the absence of complement activation. Such lesions give rise to extensive astrocyte loss, which may occur in part in the absence of any other tissue injury, such as demyelination or axonal degeneration (lesion type 5). Finally, lesions with a variable degree of astrocyte clasmatodendrosis are found, which show plaque-like primary demyelination that is associated with oligodendrocyte apoptosis, but with preservation of axons (lesion type 6). In active multiple sclerosis (MS) lesions astrocytes reveal changes of reactive protoplasmatic or fibrillary gliosis. Only in a subset of lesions, in patients with aggressive disease, loss of AQP4 is observed in the initial stage of their formation, which is associated with retraction of astrocyte processes in the absence of complement deposition, granulocyte infiltration or loss of AQP1 or astrocytes. Our data underline the primary assault of astrocytes in NMO lesions, but also indicate that different mechanisms of tissue injury operate in parallel in the same patient and even within the same lesion. 相似文献
56.
Friedrich M. Wurst Hans-Jürgen Rumpf Gregory E. Skipper John P. Allen Isabella Kunz Petra Beschoner Natasha Thon 《General hospital psychiatry》2013
Objective
Surveys assessing alcohol use among physicians have most commonly employed the Alcohol Use Disorders Identification Test (AUDIT) or the AUDIT-C, the most common short version of the AUDIT. As with other screeners, prevalence estimation is dependent on the accuracy of the test as well as choice of the cutoff value. The aim of the current study is to derive more precise prevalence estimates of alcohol problems in physicians by correcting for false-positive and false-negative results.Method
In the context of a survey, the AUDIT was sent out via email or standard postal service to all 2484 physicians in Salzburg, Austria. A total of 456 physicians participated. A published correction formula was used to estimate the real prevalence of alcohol use problems.Results
Applying a cutoff of 5 points for the AUDIT-C, 15.7% of female and 37.7% of male physicians screened positive. Use of a correction based on general population data and the sensitivity and specificity of the AUDIT-C resulted in much lower prevalence rates: 4.0% for female and 9.5% for male physicians. Using the full AUDIT, 19.6% of the female physicians and 48% of the male physicians were screened positive. Using the correction, the estimated prevalence rates for females and males were 6.3% and 15.5%, respectively.Conclusions
Our findings demonstrate that uncorrected screening results may markedly overestimate the prevalence of physicians drinking problems. 相似文献57.
58.
Miryam Carecchio MD Monia Magliozzi BSc Massimiliano Copetti PhD Alessandro Ferraris MD PhD Laura Bernardini PhD Monica Bonetti BSc Giovanni Defazio MD Mark J. Edwards PhD Isabella Torrente BSc Fabio Pellegrini MSc Cristoforo Comi MD PhD Kailash P. Bhatia MD FRCP Enza Maria Valente MD PhD 《Movement disorders》2013,28(6):787-794
Mutations or exon deletions of the epsilon‐sarcoglycan (SGCE) gene cause myoclonus‐dystonia (M‐D), but a subset of M‐D patients are mutation‐negative and the sensitivity and specificity of current genetic testing criteria are unknown. We screened 46 newly enrolled M‐D patients for SGCE mutations and deletions; moreover, 24 subjects previously testing negative for SGCE mutations underwent gene dosage analysis. In our combined cohorts, we calculated sensitivity, specificity, positive and negative predictive values, and area under the curve of 2 published sets of M‐D diagnostic criteria. A stepwise logistic regression was used to assess which patients' characteristics best discriminated mutation carriers and to calculate a new mutation predictive score (“new score”), which we validated in previously published cohorts. Nine of 46 (19.5%) patients of the new cohort carried SCGE mutations, including 5 novel point mutations and 1 whole‐gene deletion; in the old cohort, 1 patient with a complex phenotype carried a 5.9‐Mb deletion encompassing SGCE. Current diagnostic criteria had a poor ability to discriminate SGCE‐positive from SGCE‐negative patients in our cohort; conversely, age of onset, especially if associated with psychiatric features (as included in the new score), showed the best discriminatory power to individuate SGCE mutation carriers, both in our cohort and in the validation cohort. Our results suggest that young age at onset of motor symptoms, especially in association with psychiatric disturbance, are strongly predictive for SGCE positivity. We suggest performing gene dosage analysis by multiple ligation‐dependent probe amplification (MLPA) to individuate large SGCE deletions that can be responsible for complex phenotypes. © 2013 Movement Disorder Society 相似文献
59.
Richard Musil Peter Zill Florian Seemüller Brigitta Bondy Michael Obermeier Ilja Spellmann Wolfram Bender Mazda Adli Isabella Heuser Joachim Zeiler Wolfgang Gaebel Wolfgang Maier Marcella Rietschel Dan Rujescu Rebecca Schennach Hans-Jürgen Möller Michael Riedel 《European archives of psychiatry and clinical neuroscience》2013,263(5):405-412
The role of the brain-derived neurotrophic factor (BDNF) in the pathophysiology of major depressive disorder (MDD) remains to be elucidated. Recent post hoc analyses indicated a potential association of three polymorphisms in the BDNF gene with worse treatment outcome in patients with the subtype of melancholic depression. We aimed at replicating these findings in a German naturalistic multicenter follow-up. Three polymorphisms in the BDNF gene (rs7103411, rs6265 (Val66Met) and rs7124442) were genotyped in 324 patients with MDD and 470 healthy controls. We applied univariate tests and logistic regression models stratifying for depression subtype and gender. The three polymorphisms were not associated with MDD as diagnosis. Further, no associations were found in univariate tests. With logistic regression, we only found a tendency towards an association of the rs6265 (Val66Met) polymorphism with overall response to treatment (response rates: GG (val/val) < GA (val/met) < AA (met/met); p = 0.0129) and some gender differences for the rs6265 (Val66Met) and rs7103411 polymorphisms. Treatment outcome stratified for subtypes of depression did not differ significantly between the investigated polymorphisms or using haplotype analyses. However, results showed a tendency towards significance. At this stage, we cannot support an influence of these three polymorphisms. Further studies in larger patient samples to increase sample sizes of subgroups are warranted. 相似文献
60.