全文获取类型
收费全文 | 49931篇 |
免费 | 3245篇 |
国内免费 | 192篇 |
专业分类
耳鼻咽喉 | 532篇 |
儿科学 | 1274篇 |
妇产科学 | 881篇 |
基础医学 | 6498篇 |
口腔科学 | 1260篇 |
临床医学 | 4862篇 |
内科学 | 10155篇 |
皮肤病学 | 787篇 |
神经病学 | 4878篇 |
特种医学 | 2568篇 |
外国民族医学 | 6篇 |
外科学 | 7270篇 |
综合类 | 604篇 |
一般理论 | 42篇 |
预防医学 | 4194篇 |
眼科学 | 1205篇 |
药学 | 3003篇 |
中国医学 | 70篇 |
肿瘤学 | 3279篇 |
出版年
2023年 | 228篇 |
2022年 | 367篇 |
2021年 | 851篇 |
2020年 | 646篇 |
2019年 | 846篇 |
2018年 | 997篇 |
2017年 | 804篇 |
2016年 | 949篇 |
2015年 | 1083篇 |
2014年 | 1521篇 |
2013年 | 2118篇 |
2012年 | 3180篇 |
2011年 | 3376篇 |
2010年 | 1890篇 |
2009年 | 1745篇 |
2008年 | 3125篇 |
2007年 | 3205篇 |
2006年 | 3155篇 |
2005年 | 3078篇 |
2004年 | 2882篇 |
2003年 | 2798篇 |
2002年 | 2694篇 |
2001年 | 617篇 |
2000年 | 570篇 |
1999年 | 639篇 |
1998年 | 607篇 |
1997年 | 473篇 |
1996年 | 425篇 |
1995年 | 405篇 |
1994年 | 326篇 |
1993年 | 296篇 |
1992年 | 373篇 |
1991年 | 340篇 |
1990年 | 308篇 |
1989年 | 325篇 |
1988年 | 293篇 |
1987年 | 309篇 |
1986年 | 281篇 |
1985年 | 303篇 |
1984年 | 310篇 |
1983年 | 293篇 |
1982年 | 319篇 |
1981年 | 300篇 |
1980年 | 263篇 |
1979年 | 227篇 |
1978年 | 235篇 |
1977年 | 196篇 |
1976年 | 168篇 |
1975年 | 177篇 |
1974年 | 183篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
992.
993.
994.
O'Sullivan RP Greenberger JS Goff J Cao S Kingston KA Zhou S Dixon T Houghton FD Epperly MW Wang H Glowacki J 《Experimental hematology》2012,40(6):499-509
The senescence accelerated-prone mouse variant 6 (SAMP6) shows normal growth followed by rapid aging, development of osteopenia, and shortened lifespan, compared with control R1 mice. Because oxidative stress is a fundamental mechanism of tissue aging, we tested whether cellular parameters that are associated with oxidative stress are impaired with marrow from SAMP6 mice. We compared in vitro hematopoiesis, irradiation sensitivity, proliferative potential, and osteoblastogenesis with marrow cells from SAMP6 and R1 mice. Marrow cells from SAMP6 mice showed shortened in vitro hematopoiesis; their stromal cells showed greater radiation sensitivity and decreased proliferation. Consistent with those properties, there was constitutive upregulation of transforming growth factor-β(1), an inhibitor of hematopoiesis, and of cell cycle inhibitory genes, p16(INK4A) and p19(ARF). Paradoxically, there was constitutive expression of osteoblast genes in stromal cells from SAMP6 mice, but in vitro matrix mineralization was impaired. These studies and data included in other reports indicate that impaired proliferation of osteoblast progenitors in SAMP6 marrow may be a major factor contributing to accelerated loss of bone mass. In sum, marrow from SAMP6 mice had diminished capacity for long-term hematopoiesis, increased radiosensitivity, and reduced proliferative capacity. 相似文献
995.
996.
For eutherian mammals a continuum of maternal support insures that development of progeny follows an optimal program. Beginning in utero, such support extends into the early neonatal period when bioactive factors are communicated from mother to offspring in colostrum/milk. Defined as lactocrine signaling, communication of milk-borne bioactive factors from mother to offspring as a consequence of nursing is important for development of somatic tissues, including the female reproductive tract (FRT). Data for the domestic pig indicate that lactocrine signaling contributes to the maternal continuum of factors that define the developmental program and determine the developmental trajectory of FRT tissues during early neonatal life. Both naturally occurring and manmade factors of environmental origin can be communicated to neonates in milk and affect development with lasting consequences. Here, evidence for lactocrine programming of FRT development and the potential for environmental endocrine disruption of this process are reviewed. 相似文献
997.
Percy MJ Chung YJ Harrison C Mercieca J Hoffbrand AV Dinardo CL Santos PC Fonseca GH Gualandro SF Pereira AC Lappin TR McMullin MF Lee FS 《American journal of hematology》2012,87(4):439-442
Congenital or familial erythrocytosis/polycythemia can have many causes, and an emerging cause is genetic disruption of the oxygen‐sensing pathway that regulates the Erythropoietin (EPO) gene. More specifically, recent studies have identified erythrocytosis‐associated mutations in the HIF2A gene, which encodes for Hypoxia Inducible Factor‐2α (HIF‐2α), as well as in two genes that encode for proteins that regulate it, Prolyl Hydroxylase Domain protein 2 (PHD2) and the von Hippel Lindau tumor suppressor protein (VHL). We report here the identification of two new heterozygous HIF2A missense mutations, M535T, and F540L, both associated with erythrocytosis. Met‐535 has previously been identified as a residue mutated in other patients with erythrocytosis; although, the mutation of this particular residue to Thr has not been reported. In contrast, Phe‐540 has not been reported as a residue mutated in erythrocytosis, and we present evidence here that this mutation impairs interaction of HIF‐2α with both VHL and PHD2. Am. J. Hematol. 2012. © 2012 Wiley Periodicals, Inc. 相似文献
998.
Ladan Kobari Frank Yates Noufissa Oudrhiri Alain Francina Laurent Kiger Christelle Mazurier Shaghayegh Rouzbeh Wassim El-Nemer Nicolas Hebert Marie-Catherine Giarratana Sabine Fran?ois Alain Chapel Hélène Lapillonne Dominique Luton Annelise Bennaceur-Griscelli Luc Douay 《Haematologica》2012,97(12):1795-1803
Background
Human induced pluripotent stem cells offer perspectives for cell therapy and research models for diseases. We applied this approach to the normal and pathological erythroid differentiation model by establishing induced pluripotent stem cells from normal and homozygous sickle cell disease donors.Design and Methods
We addressed the question as to whether these cells can reach complete erythroid terminal maturation notably with a complete switch from fetal to adult hemoglobin. Sickle cell disease induced pluripotent stem cells were differentiated in vitro into red blood cells and characterized for their terminal maturation in terms of hemoglobin content, oxygen transport capacity, deformability, sickling and adherence. Nucleated erythroblast populations generated from normal and pathological induced pluripotent stem cells were then injected into non-obese diabetic severe combined immunodeficiency mice to follow the in vivo hemoglobin maturation.Results
We observed that in vitro erythroid differentiation results in predominance of fetal hemoglobin which rescues the functionality of red blood cells in the pathological model of sickle cell disease. We observed, in vivo, the switch from fetal to adult hemoglobin after infusion of nucleated erythroid precursors derived from either normal or pathological induced pluripotent stem cells into mice.Conclusions
These results demonstrate that human induced pluripotent stem cells: i) can achieve complete terminal erythroid maturation, in vitro in terms of nucleus expulsion and in vivo in terms of hemoglobin maturation; and ii) open the way to generation of functionally corrected red blood cells from sickle cell disease induced pluripotent stem cells, without any genetic modification or drug treatment.Key words: human induced pluripotent stem cells, terminal maturation, erythropoietic differentiation 相似文献999.