全文获取类型
收费全文 | 836篇 |
免费 | 48篇 |
国内免费 | 8篇 |
专业分类
耳鼻咽喉 | 3篇 |
儿科学 | 22篇 |
妇产科学 | 13篇 |
基础医学 | 88篇 |
口腔科学 | 9篇 |
临床医学 | 90篇 |
内科学 | 165篇 |
皮肤病学 | 23篇 |
神经病学 | 68篇 |
特种医学 | 18篇 |
外科学 | 162篇 |
综合类 | 4篇 |
预防医学 | 143篇 |
眼科学 | 28篇 |
药学 | 33篇 |
中国医学 | 1篇 |
肿瘤学 | 22篇 |
出版年
2023年 | 4篇 |
2022年 | 9篇 |
2021年 | 26篇 |
2020年 | 14篇 |
2019年 | 18篇 |
2018年 | 22篇 |
2017年 | 16篇 |
2016年 | 15篇 |
2015年 | 38篇 |
2014年 | 32篇 |
2013年 | 45篇 |
2012年 | 58篇 |
2011年 | 60篇 |
2010年 | 40篇 |
2009年 | 33篇 |
2008年 | 56篇 |
2007年 | 79篇 |
2006年 | 39篇 |
2005年 | 55篇 |
2004年 | 41篇 |
2003年 | 41篇 |
2002年 | 25篇 |
2001年 | 9篇 |
2000年 | 22篇 |
1999年 | 13篇 |
1998年 | 4篇 |
1997年 | 2篇 |
1995年 | 5篇 |
1993年 | 5篇 |
1992年 | 5篇 |
1991年 | 2篇 |
1990年 | 4篇 |
1989年 | 2篇 |
1988年 | 4篇 |
1987年 | 5篇 |
1986年 | 2篇 |
1985年 | 5篇 |
1984年 | 3篇 |
1983年 | 3篇 |
1982年 | 2篇 |
1979年 | 5篇 |
1976年 | 2篇 |
1974年 | 2篇 |
1973年 | 4篇 |
1972年 | 2篇 |
1971年 | 3篇 |
1970年 | 1篇 |
1969年 | 1篇 |
1968年 | 1篇 |
1959年 | 1篇 |
排序方式: 共有892条查询结果,搜索用时 390 毫秒
11.
Chinn S Jarvis D Melotti R Luczynska C Ackermann-Liebrich U Antó JM Cerveri I de Marco R Gislason T Heinrich J Janson C Künzli N Leynaert B Neukirch F Schouten J Sunyer J Svanes C Vermeire P Wjst M Burney P 《Lancet》2005,365(9471):1629-35; discussion 1600-1
12.
Gobejishvili Nino Gogilashvili Tamar Khechuashvili Sofio Nikoladze Sopio Shanava Zita Tserodze Ana Kukuladze Tea Bakradze Marika Makaridze Lali 《Clinical rheumatology》2022,41(3):935-937
Clinical Rheumatology - The program’s goal is to launch the platform of positive perspectives for people who are suffering from/working in rheumatic and musculoskeletal diseases through the... 相似文献
13.
Bone marrow‐on‐a‐chip: Long‐term culture of human haematopoietic stem cells in a three‐dimensional microfluidic environment
下载免费PDF全文
![点击此处可从《Journal of tissue engineering and regenerative medicine》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Stefan Sieber Lorenz Wirth Nino Cavak Marielle Koenigsmark Uwe Marx Roland Lauster Mark Rosowski 《Journal of tissue engineering and regenerative medicine》2018,12(2):479-489
Multipotent haematopoietic stem and progenitor cells (HSPCs) are the source for all blood cell types. The bone marrow stem cell niche in which the HSPCs are maintained is known to be vital for their maintenance. Unfortunately, to date, no in vitro model exists that accurately mimics the aspects of the bone marrow niche and simultaneously allows the long‐term culture of HSPCs. In this study, a novel three‐dimensional coculture model is presented, based on a hydroxyapatite coated zirconium oxide scaffold, comprising of human mesenchymal stromal cells (MSCs) and cord blood derived HSPCs, enabling successful HSPC culture for a time span of 28 days within the microfluidic multiorgan chip. The HSPCs were found to stay in their primitive state (CD34+CD38?) and capable of granulocyte, erythrocyte, macrophage, megakaryocyte colony formation. Furthermore, a microenvironment was formed bearing molecular and structural similarity to the in vivo bone marrow niche containing extracellular matrix and signalling molecules known to play an important role in HSPC homeostasis. Here, a novel human in vitro bone marrow model is presented for the first time, capable of long‐term culture of primitive HSPCs in a microfluidic environment. 相似文献
14.
15.
16.
17.
18.
Amy L. Schneider Candace T. Myers Alison M. Muir Sophie Calvert Alice Basinger M. Scott Perry Lance Rodan Katherine L. Helbig Chelsea Chambers Kathleen M. Gorman Mary D. King Sandra Donkervoort Ariane Soldatos Carsten G. Bnnemann Nino Spataro Elisabeth Gabau Montserrat Arellano Gerarda Cappuccio Nicola Brunetti‐Pierri Elsa Rossignol Fadi F. Hamdan Jacques L. Michaud Christopher Balak Heather C. Mefford Ingrid E. Scheffer 《Epilepsia》2021,62(1):e13-e21
Chromosome 1q41‐q42 deletion syndrome is a rare cause of intellectual disability, seizures, dysmorphology, and multiple anomalies. Two genes in the 1q41‐q42 microdeletion, WDR26 and FBXO28, have been implicated in monogenic disease. Patients with WDR26 encephalopathy overlap clinically with those with 1q41‐q42 deletion syndrome, whereas only one patient with FBXO28 encephalopathy has been described. Seizures are a prominent feature of 1q41‐q42 deletion syndrome; therefore, we hypothesized that pathogenic FBXO28 variants cause developmental and epileptic encephalopathies (DEEs). We describe nine new patients with FBXO28 pathogenic variants (four missense, including one recurrent, three nonsense, and one frameshift) and analyze all 10 known cases to delineate the phenotypic spectrum. All patients had epilepsy and 9 of 10 had DEE, including infantile spasms (3) and a progressive myoclonic epilepsy (1). Median age at seizure onset was 22.5 months (range 8 months to 5 years). Nine of 10 patients had intellectual disability, which was profound in six of nine and severe in three of nine. Movement disorders occurred in eight of 10 patients, six of 10 had hypotonia, four of 10 had acquired microcephaly, and five of 10 had dysmorphic features, albeit different to those typically seen in 1q41‐q42 deletion syndrome and WDR26 encephalopathy. We distinguish FBXO28 encephalopathy from both of these disorders with more severe intellectual impairment, drug‐resistant epilepsy, and hyperkinetic movement disorders. 相似文献
19.
Lee AW Kyrozis A Chevaleyre V Kow LM Devidze N Zhang Q Etgen AM Pfaff DW 《Proceedings of the National Academy of Sciences of the United States of America》2008,105(20):7333-7338
Estrogens act within the ventromedial nucleus of the hypothalamus (VMN) to facilitate lordosis behavior. Estradiol treatment in vivo induces alpha(1b)-adrenoreceptor mRNA and increases the density of alpha(1B)-adrenoreceptor binding in the hypothalamus. Activation of hypothalamic alpha(1)-adrenoceptors also facilitates estrogen-dependent lordosis. To investigate the cellular mechanisms of adrenergic effects on VMN neurons, whole-cell patch-clamp recordings were carried out on hypothalamic slices from control and estradiol-treated female rats. In control slices, bath application of the alpha(1)-agonist phenylephrine (PHE; 10 microM) depolarized 10 of 25 neurons (40%), hyperpolarized three neurons (12%), and had no effect on 12 neurons (48%). The depolarization was associated with decreased membrane conductance, and this current had a reversal potential close to the K(+) equilibrium potential. The alpha(1b)-receptor antagonist chloroethylclonidine (10 microM) blocked the depolarization produced by PHE in all cells. From estradiol-treated rats, significantly more neurons in slices depolarized (71%) and fewer neurons showed no response (17%) to PHE. PHE-induced depolarizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na(+) and Ca(2+) channels. These data indicate that alpha(1)-adrenoceptors depolarize VMN neurons by reducing membrane conductance for K(+). Estradiol amplifies alpha(1b)-adrenergic signaling by increasing the proportion of VMN neurons that respond to stimulation of alpha(1b)-adrenergic receptors, which is expected in turn to promote lordosis. 相似文献
20.
Alberto Facchini Sandra Magnoni Vittorio Civelli Fabio Triulzi Mario Nosotti Nino Stocchetti 《Neurocritical care》2013,19(3):376-380