全文获取类型
收费全文 | 2595篇 |
免费 | 469篇 |
国内免费 | 14篇 |
专业分类
耳鼻咽喉 | 7篇 |
儿科学 | 55篇 |
妇产科学 | 182篇 |
基础医学 | 238篇 |
口腔科学 | 24篇 |
临床医学 | 916篇 |
内科学 | 400篇 |
皮肤病学 | 21篇 |
神经病学 | 184篇 |
特种医学 | 78篇 |
外科学 | 283篇 |
综合类 | 56篇 |
一般理论 | 2篇 |
预防医学 | 335篇 |
眼科学 | 34篇 |
药学 | 141篇 |
中国医学 | 1篇 |
肿瘤学 | 121篇 |
出版年
2021年 | 26篇 |
2020年 | 18篇 |
2019年 | 22篇 |
2018年 | 91篇 |
2017年 | 109篇 |
2016年 | 128篇 |
2015年 | 118篇 |
2014年 | 124篇 |
2013年 | 161篇 |
2012年 | 123篇 |
2011年 | 118篇 |
2010年 | 106篇 |
2009年 | 134篇 |
2008年 | 125篇 |
2007年 | 112篇 |
2006年 | 101篇 |
2005年 | 108篇 |
2004年 | 99篇 |
2003年 | 73篇 |
2002年 | 73篇 |
2001年 | 63篇 |
2000年 | 72篇 |
1999年 | 51篇 |
1998年 | 32篇 |
1997年 | 28篇 |
1996年 | 27篇 |
1995年 | 27篇 |
1994年 | 30篇 |
1993年 | 22篇 |
1992年 | 38篇 |
1991年 | 45篇 |
1990年 | 47篇 |
1989年 | 51篇 |
1988年 | 43篇 |
1987年 | 31篇 |
1986年 | 41篇 |
1985年 | 38篇 |
1984年 | 22篇 |
1983年 | 22篇 |
1980年 | 19篇 |
1979年 | 22篇 |
1978年 | 27篇 |
1977年 | 19篇 |
1975年 | 19篇 |
1974年 | 19篇 |
1971年 | 20篇 |
1970年 | 25篇 |
1969年 | 19篇 |
1968年 | 19篇 |
1967年 | 23篇 |
排序方式: 共有3078条查询结果,搜索用时 15 毫秒
81.
82.
Sameer H. Halani Austin S. Hembd Xingchen Li Ben Kirby Courtney C. Beard Nicholas T. Haddock Thomas M. Suszynski 《Journal of hand and microsurgery》2022,14(1):10
Free tissue transfer is a cornerstone of complex reconstruction. In many cases, it represents the last option available for a patient and their reconstruction. At high-volume centers, the risk of free flap failure is low but its occurrence can be devastating. Currently, the mainstay for flap monitoring is the clinical examination. Though reliable when performed by experienced clinicians, the flap exam is largely subjective, is performed discontinuously, and often results in significant time delay between detection of flap compromise and intervention. Among emerging flap monitoring technologies, the most promising appear to be those that rely on noninvasive transcutaneous oxygen and carbon dioxide measurements, which provide information regarding flap perfusion. In this article, we review and summarize the literature on various techniques but primarily emphasizing those technologies that rely on transcutaneous gas measurements. We also define characteristics for the ideal flap monitoring tool and discuss critical barriers, predominantly cost, preventing more widespread utilization of adjunct monitoring technologies, and their implications. 相似文献
83.
84.
85.
86.
A diaper bank and home visiting partnership: Initial exploration of research and policy questions 下载免费PDF全文
87.
Colorectal cancer is the second leading cause of cancer mortality in the United States. Substantial human and animal data support the ability of nonsteroidal anti-inflammatory drugs to cause regression of existing colon tumors and prevent new tumor formation. The mechanism by which the nonsteroidal anti-inflammatory drug sulindac prevents tumor growth is poorly understood and seems complex as sulindac can modulate several growth-related signaling pathways. Sulindac metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate cyclic GMP-dependent protein kinase (PKG); (b) activate c-jun NH2-terminal kinase (JNK); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease beta-catenin protein expression at times and doses consistent with apoptosis. The purpose of this study was to determine if PKG, ERK1/2, JNK, and beta-catenin are independent targets for sulindac in vitro. Pharmacologic activation of PKG with YC-1 increases JNK phosphorylation and induces apoptosis in colon cancer cells without modulating ERK1/2 phosphorylation or beta-catenin protein expression. Inhibition of ERK1/2 with U0126 induces apoptosis but fails to activate JNK phosphorylation or down-regulate beta-catenin protein expression. Cotreatment with U0126 and YC-1 synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of sulindac treatment on ERK1/2, JNK, and beta-catenin. These results indicate that sulindac metabolites modulate ERK1/2 and PKG pathways independently in colon cancer cells and suggest that the full apoptotic effect of sulindac is mediated by more than one pathway. Using similar combinatorial approaches in vivo may provide more effective, less toxic chemopreventive and chemotherapeutic strategies. Such therapies could dramatically reduce the incidence and death rate from colorectal cancer. 相似文献
88.
89.
90.
Lucy A Murtha Damian D McLeod Debbie Pepperall Sarah K McCann Daniel J Beard Amelia J Tomkins William M Holmes Christopher McCabe I Mhairi Macrae Neil J Spratt 《Journal of cerebral blood flow and metabolism》2015,35(4):592-600
In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35 °C) or moderate (32.5 °C) hypothermia, or normothermia (37 °C) was induced after stroke onset. Edema was measured in three studies, using wet–dry weight calculations, T2-weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ΔICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset. 相似文献