全文获取类型
收费全文 | 7054篇 |
免费 | 506篇 |
国内免费 | 12篇 |
专业分类
耳鼻咽喉 | 63篇 |
儿科学 | 239篇 |
妇产科学 | 166篇 |
基础医学 | 877篇 |
口腔科学 | 51篇 |
临床医学 | 763篇 |
内科学 | 1264篇 |
皮肤病学 | 162篇 |
神经病学 | 751篇 |
特种医学 | 157篇 |
外科学 | 1003篇 |
综合类 | 46篇 |
一般理论 | 3篇 |
预防医学 | 848篇 |
眼科学 | 255篇 |
药学 | 474篇 |
中国医学 | 1篇 |
肿瘤学 | 449篇 |
出版年
2023年 | 80篇 |
2022年 | 131篇 |
2021年 | 275篇 |
2020年 | 182篇 |
2019年 | 230篇 |
2018年 | 306篇 |
2017年 | 215篇 |
2016年 | 197篇 |
2015年 | 240篇 |
2014年 | 324篇 |
2013年 | 410篇 |
2012年 | 607篇 |
2011年 | 544篇 |
2010年 | 303篇 |
2009年 | 233篇 |
2008年 | 357篇 |
2007年 | 382篇 |
2006年 | 364篇 |
2005年 | 365篇 |
2004年 | 305篇 |
2003年 | 302篇 |
2002年 | 238篇 |
2001年 | 81篇 |
2000年 | 86篇 |
1999年 | 58篇 |
1998年 | 54篇 |
1997年 | 45篇 |
1996年 | 30篇 |
1995年 | 29篇 |
1994年 | 28篇 |
1993年 | 25篇 |
1992年 | 46篇 |
1991年 | 52篇 |
1990年 | 36篇 |
1989年 | 25篇 |
1988年 | 23篇 |
1987年 | 36篇 |
1986年 | 23篇 |
1985年 | 29篇 |
1984年 | 15篇 |
1983年 | 25篇 |
1981年 | 13篇 |
1979年 | 28篇 |
1978年 | 18篇 |
1976年 | 18篇 |
1975年 | 13篇 |
1974年 | 20篇 |
1973年 | 16篇 |
1972年 | 12篇 |
1969年 | 13篇 |
排序方式: 共有7572条查询结果,搜索用时 0 毫秒
91.
Radcliff K Tang TB Lim J Zhang Z Abedin M Demer LL Tintut Y 《Circulation research》2005,96(4):398-400
Vascular calcification develops within atherosclerotic lesions and results from a process similar to osteogenesis. One of the paracrine regulators of bone-derived osteoblasts, insulin-like growth factor-I (IGF-I), is also present in atherosclerotic lesions. To evaluate its possible role in vascular calcification, we assessed its in vitro effects on proliferation and differentiation in calcifying vascular cells (CVCs), a subpopulation of bovine aortic medial cells. Results showed that IGF-I inhibited spontaneous CVC differentiation and mineralization as evidenced by decreased alkaline phosphatase (AP) activity and decreased matrix calcium incorporation, respectively. Furthermore, IGF-I inhibited the AP activity induced by bacterial lipopolysaccharide, TNF-alpha, or H2O2. It also induced CVC proliferation based on 3H-thymidine incorporation. Results from Northern analysis and tests using IGF-I analogs suggest that IGF-I effects are mediated through the IGF-I receptor. IGF-I also activated both the extracellular signal-regulated protein kinase (ERK) and phosphatidylinositol 3-kinase (PI3K) pathways. Inhibition of either the ERK or PI3K pathway reversed IGF-I effects on CVC proliferation and AP activity, suggesting a common downstream target. Overexpression of ERK activator also mimicked IGF-I inhibition of lipopolysaccharide-induced AP activity. These results suggest that IGF-I promotes proliferation and inhibits osteoblastic differentiation and mineralization of vascular cells via both ERK and PI3K pathways. 相似文献
92.
93.
Solomon Aragie Sintayehu Gebresillasie Ambahun Chernet Ayalew Shiferaw Zerihun Tadesse Mulat Zerihun Nicole E. Varnado Sun Y. Cotter Dionna M. Wittberg Zhaoxia Zhou Elizabeth Kelly Callahan Scott D. Nash Kristen Aiemjoy Jeremy D. Keenan 《The American journal of tropical medicine and hygiene》2021,104(4):1271
94.
95.
Hallak H Seiler AE Green JS Henderson A Ross BN Rubin R 《Alcoholism, clinical and experimental research》2001,25(7):1058-1064
BACKGROUND: Ethanol inhibits insulin-like growth factor-I receptor (IGF-IR) activation. However, the potency of ethanol for inhibition of the IGF-IR and other receptor tyrosine kinases varies considerably among different cell types. We investigated the effect of ethanol on IGF-I signaling in several neuronal cell types. METHODS: IGF-I signaling was examined in SH-SY5Y neuroblastoma cells, primary cultured rat cerebellar granule neurons, and rat NG-108 neuroblastoma x glioma hybrids. The tyrosine phosphorylation of IGF-IR, IRS-2, Shc, and p42/p44 MAP kinase (MAPK), and the association of Grb-2 with Shc, were examined by immunoprecipitations and Western blotting. RESULTS: IGF-I-mediated tyrosine phosphorylation of MAPK was inhibited by ethanol in all cell lines. IGF-IR autophosphorylation was markedly inhibited by ethanol in SH-SY5Y cells, was only mildly inhibited in cerebellar granule neurons, and was unaffected in rat NG-108 cells. In vitro tyrosine autophosphorylation of immunopurified IGF-IR obtained from all cell lines was inhibited by ethanol. There was also differential ethanol sensitivity of IRS-2 and Shc phosphorylation, and the association of Shc with IRS-2, among the different cell types. CONCLUSIONS: The findings demonstrate that IGF-I-mediated MAPK activation is a sensitive target of ethanol in diverse neuronal cell types. The data are consistent with ethanol-induced inhibition of IGF-IR activity, although the extent of IGF-IR tyrosine autophosphorylation per se is a poor marker of the inhibitory action of ethanol on this receptor. Furthermore, despite uniform inhibition of MAPK in the different neuronal cell types, tyrosine phosphorylation of proximal mediators of the IGF-IR are differentially inhibited by ethanol. 相似文献
96.
97.
A strategy to improve treatment‐related mortality and abandonment of therapy for childhood ALL in a developing country reveals the impact of treatment delays 下载免费PDF全文
Amaranto Suarez MD Martha Piña MD Diana X. Nichols‐Vinueza MD John Lopera MD Lyda Rengifo MD Mauricio Mesa MD Marcela Cardenas RN Lisa Morrissey RN Galo Veintemilla MD Martha Vizcaino MD Ligia Del Toro MD Victor Vicuna PhD Jorge Fernandez LICSW Donna Neuberg ScD Kristen Stevenson MS Alejandro Gutierrez MD 《Pediatric blood & cancer》2015,62(8):1395-1402
Background
Treatment‐related mortality and abandonment of therapy are major barriers to successful treatment of childhood acute lymphoblastic leukemia (ALL) in the developing world.Procedure
A collaboration was undertaken between Instituto Nacional de Cancerologia (Bogota, Colombia), which serves a poor patient population in an upper‐middle income country, and Dana‐Farber/Boston Children's Cancer and Blood Disorders Center (Boston, USA). Several interventions aimed at reducing toxic deaths and abandonment were implemented, including a reduced‐intensity treatment regimen and a psychosocial effort targeting abandonment. We performed a cohort study to assess impact.Results
The Study Population comprised 99 children with ALL diagnosed between 2007 and 2010, and the Historic Cohort comprised 181 children treated prior to the study interventions (1995–2004). Significant improvements were achieved in the rate of deaths in complete remission (13% to 3%; P = 0.005), abandonment (32% to 9%; P < 0.001), and event‐free survival with abandonment considered an event (47% to 65% at 2 years; P = 0.016). However, relapse rate did not improve. Medically unnecessary treatment delays were common, and landmark analysis revealed that initiating the PIII phase of therapy ≥4 weeks delayed predicted markedly inferior disease‐free survival (P = 0.016). Conversely, patients who received therapy without excessive delays had outcomes approaching those achieved in high‐income countries.Conclusions
Implementation of a twinning program was followed by reductions in abandonment and toxic deaths, but relapse rate did not improve. Inappropriate treatment delays were common and strongly predicted treatment failure. These findings highlight the importance of adherence to treatment schedule for effective therapy of ALL. Pediatr Blood Cancer 2015;62:1395–1402. © 2015 Wiley Periodicals, Inc. 相似文献98.
Enteroviruses and humans have long co‐existed. Although recognized in ancient times, poliomyelitis and type 1 diabetes (T1D) were exceptionally rare and not epidemic, due in large part to poor sanitation and personal hygiene which resulted in repeated exposure to fecal–oral transmitted viruses and other infectious agents and viruses and the generation of a broad protective immunity. As a function of a growing acceptance of the benefits of hygienic practices and microbiologically clean(er) water supplies, the likelihood of exposure to diverse infectious agents and viruses declined. The effort to vaccinate against poliomyelitis demonstrated that enteroviral diseases are preventable by vaccination and led to understanding how to successfully attenuate enteroviruses. Type 1 diabetes onset has been convincingly linked to infection by numerous enteroviruses including the group B coxsackieviruses (CVB), while studies of CVB infections in NOD mice have demonstrated not only a clear link between disease onset but an ability to reduce the incidence of T1D as well: CVB infections can suppress naturally occurring autoimmune T1D. We propose here that if we can harness and develop the capacity to use attenuated enteroviral strains to induce regulatory T cell populations in the host through vaccination, then a vaccine could be considered that should function to protect against both autoimmune as well as virus‐triggered T1D. Such a vaccine would not only specifically protect from certain enterovirus types but more importantly, also reset the organism's regulatory rheostat making the further development of pathogenic autoimmunity less likely. Copyright © 2014 John Wiley & Sons, Ltd. 相似文献
99.
Human dental stem cell derived transgene‐free iPSCs generate functional neurons via embryoid body‐mediated and direct induction methods 下载免费PDF全文
100.