全文获取类型
收费全文 | 5706篇 |
免费 | 485篇 |
国内免费 | 9篇 |
专业分类
耳鼻咽喉 | 45篇 |
儿科学 | 125篇 |
妇产科学 | 216篇 |
基础医学 | 848篇 |
口腔科学 | 95篇 |
临床医学 | 551篇 |
内科学 | 1285篇 |
皮肤病学 | 154篇 |
神经病学 | 413篇 |
特种医学 | 266篇 |
外国民族医学 | 5篇 |
外科学 | 795篇 |
综合类 | 61篇 |
一般理论 | 6篇 |
预防医学 | 505篇 |
眼科学 | 52篇 |
药学 | 330篇 |
中国医学 | 11篇 |
肿瘤学 | 437篇 |
出版年
2022年 | 39篇 |
2021年 | 81篇 |
2020年 | 41篇 |
2019年 | 71篇 |
2018年 | 82篇 |
2017年 | 68篇 |
2016年 | 73篇 |
2015年 | 76篇 |
2014年 | 117篇 |
2013年 | 163篇 |
2012年 | 255篇 |
2011年 | 283篇 |
2010年 | 154篇 |
2009年 | 140篇 |
2008年 | 267篇 |
2007年 | 270篇 |
2006年 | 224篇 |
2005年 | 243篇 |
2004年 | 247篇 |
2003年 | 239篇 |
2002年 | 213篇 |
2001年 | 216篇 |
2000年 | 224篇 |
1999年 | 162篇 |
1998年 | 103篇 |
1997年 | 85篇 |
1996年 | 67篇 |
1995年 | 52篇 |
1994年 | 64篇 |
1993年 | 49篇 |
1992年 | 143篇 |
1991年 | 110篇 |
1990年 | 120篇 |
1989年 | 116篇 |
1988年 | 115篇 |
1987年 | 120篇 |
1986年 | 88篇 |
1985年 | 94篇 |
1984年 | 79篇 |
1983年 | 65篇 |
1981年 | 40篇 |
1979年 | 59篇 |
1978年 | 45篇 |
1974年 | 50篇 |
1973年 | 50篇 |
1972年 | 42篇 |
1971年 | 47篇 |
1969年 | 38篇 |
1968年 | 35篇 |
1967年 | 45篇 |
排序方式: 共有6200条查询结果,搜索用时 0 毫秒
81.
Jonas N. Muller MD 《Archives of environmental & occupational health》2013,68(6):705-713
Biological parameters known to be affected in lead poisoning were measured in rats following ingestion of graded dosages of lead. Intranuclear inclusion bodies are formed in renal tubular lining cells with smaller doses of lead than produce other changes. Decreased body weight is the next most sensitive abnormality. This is followed by increased delta-aminolevulinic acid (ALA) excretion, reticulocytosis, renal edema, and aminoaciduria. Anemia only occurs at the highest lead dosage. Over a wide range of lead ingestion, urinary lead excretion remains constant, although renal lead content increases. Quantitative lead analyses of cell organelles show that lead is concentrated within the inclusion bodies. Relatively small amounts of lead are present in the cytoplasm and mitochondria. It is suggested that soft-tissue lead accumulates in the intranuclear inclusion body, thereby sparing toxic injury to cytoplasmic organelles. 相似文献
82.
Marlon E. Cerf Charna S. Chapman Christo J. Muller Johan Louw 《Metabolism: clinical and experimental》2009,58(12):1787-1792
Hyperglycemia and compromised β-cell development were demonstrated in neonatal rats programmed with a gestational high-fat diet. The aim of this study was to determine whether these changes were attributed to impaired insulin release and altered immunoreactivity of Pdx-1, glucokinase (GK), and glucose transporter (GLUT)–2 in high-fat–programmed neonates. Fetuses were maintained, via maternal nutrition, on either a standard laboratory diet (control) or a high-fat diet throughout gestation (HFG). Pancreata from 1-day–old neonates were excised for islet isolation and the subsequent measurement of insulin release at 2.8, 6.5, 13, and 22 mmol/L glucose. Other pancreata were either snap frozen for quantitative polymerase chain reaction or formalin fixed for immunohistochemistry followed by image analysis. The HFG neonates had reduced insulin release at 13- and 22-mmol/L glucose concentrations. No significant differences were found in Pdx-1, GK, or GLUT-2 messenger RNA expression. In HFG neonates, immunoreactivity of both Pdx-1 and GK was significantly reduced, with a nonsignificant reduction in GLUT-2. Gestational high-fat programming impairs insulin release and reduces Pdx-1 and GK immunoreactivity. 相似文献
83.
84.
85.
Heparin inhibits bovine testicular hyaluronidase activity in myocardium of dogs with coronary artery occlusion 总被引:1,自引:0,他引:1
R A Wolf D Glogar L Y Chaung P E Garrett G Ertl J Tumas E Braunwald R A Kloner M L Feldstein J E Muller 《The American journal of cardiology》1984,53(7):941-944
Bovine testicular hyaluronidase (BTH) reduces experimental myocardial infarct size and ameliorates electrocardiographic signs of ischemia. This study was done to determine if heparin, an in vitro inhibitor of hyaluronidase activity, blocks the action of BTH in the myocardium of dogs after coronary artery occlusion. BTH was administered intravenously as 5,000 NF units/kg at 0.5 and 2.5 hours after coronary occlusion. Heparin was administered intravenously as a 150-unit/kg loading dose, followed by 10 units/kg per hour i.v., beginning 15 minutes before coronary occlusion. The area of myocardial ischemia at risk was assessed by a radiolabeled microsphere technique; the area that developed necrosis was assessed by a histochemical technique. In vivo activity of BTH was assessed by a colorimetric analysis of the BTH substrate, i.e., hyaluronic acid (HA), extracted from myocardial tissue. For biochemical analysis of HA, the heart was divided into anterior myocardium, which included ischemic tissue and posterior nonischemic myocardium. The myocardial HA content of dogs treated with BTH plus heparin (anterior, 3.44 +/- 0.40 micrograms HA/mg protein; posterior, 3.69 +/- 0.33 micrograms HA/mg protein) was not significantly different from control (anterior, 3.61 +/- 0.29 micrograms HA/mg protein; posterior, 3.55 +/- 0.23 micrograms HA/mg protein). In contrast, BTH lowered myocardial HA content (anterior, 2.16 +/- 0.21 micrograms HA/mg protein; posterior, 2.08 +/- 0.14 micrograms HA/mg protein) compared with either BTH plus heparin or control groups in both anterior myocardium (p = 0.006) and posterior myocardium (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
86.
Maxence Meyer MD Lidia Calabrese MD Anita Meyer MD Florentin Constancias PhD Louise F. Porter MD PhD Marion Muller Manon Leitner Amandine Leitner Antonin Michaud Georges Kaltenbach MD PhD Elise Schmitt MD PhD Patrick Karcher MD Erik Sauleau MD PhD Saïd Chayer PhD HDR Floriane Zeyons MD Marianne Riou MD Soraya El Ghannudi Abdo MD Frédéric Blanc MD PhD Samira Fafi-Kremer PharmD PhD Aurélie Velay PharmD PhD Thomas Vogel MD PhD 《Journal of the American Geriatrics Society》2021,69(5):1167-1170
87.
88.
Corticotropin-releasing activity of the renin-angiotensin system peptides in rat and in man 总被引:1,自引:0,他引:1
In this study we investigated in the rat the binding and corticotropin-releasing factor (CRF) activity of various constituents of the renin-angiotensin system and the possible angiotensin II receptor changes following procedures known to alter plasma renin activity. We investigated also the CRF activity of angiotensin II in vitro and in vivo in humans. The CRF activity of peptides was studied by their ability to stimulate ACTH release from pituitary cells. Deleting amino acids from the N-terminus of angiotensin II resulted in decreased CRF activity; while the ED50 for angiotensin II was 2 nM, it increased to about 10 nM for the (2-8)-heptapeptide. Angiotensin I had a weak CRF activity, whereas the substrate angiotensinogen had no stimulatory effect even at a concentration of 100 nM. There was a strong correlation between the activation and binding properties of all peptides tested. Dietary salt load or depletion as well as dexamethasone treatment did not affect the number nor the affinity of pituitary angiotensin II receptors. Angiotensin II had a CRF activity on human pituitary cells in vitro. However, peripherally injected agiotensin II at a pressive dose of 7 ng/kg/min did not produce any ACTH release in normal male volunteers. These data suggest that angiotensin II may play a modulatory role in the physiological regulation of ACTH secretion, but this role might be attributed to the endogenous brain angiotensin II as it is not closely dependent on the angiotensin II plasma levels. 相似文献
89.
90.
Jan D. Marshall Jean Muller Gayle B. Collin Gabriella Milan Stephen F. Kingsmore Darrell Dinwiddie Emily G. Farrow Neil A. Miller Francesca Favaretto Pietro Maffei Hélène Dollfus Roberto Vettor Jürgen K. Naggert 《Human mutation》2015,36(7):660-668
Alström Syndrome (ALMS), a recessive, monogenic ciliopathy caused by mutations in ALMS1, is typically characterized by multisystem involvement including early cone‐rod retinal dystrophy and blindness, hearing loss, childhood obesity, type 2 diabetes mellitus, cardiomyopathy, fibrosis, and multiple organ failure. The precise function of ALMS1 remains elusive, but roles in endosomal and ciliary transport and cell cycle regulation have been shown. The aim of our study was to further define the spectrum of ALMS1 mutations in patients with clinical features of ALMS. Mutational analysis in a world‐wide cohort of 204 families identified 109 novel mutations, extending the number of known ALMS1 mutations to 239 and highlighting the allelic heterogeneity of this disorder. This study represents the most comprehensive mutation analysis in patients with ALMS, identifying the largest number of novel mutations in a single study worldwide. Here, we also provide an overview of all ALMS1 mutations identified to date. 相似文献