全文获取类型
收费全文 | 285篇 |
免费 | 13篇 |
国内免费 | 26篇 |
专业分类
儿科学 | 19篇 |
妇产科学 | 1篇 |
基础医学 | 22篇 |
口腔科学 | 1篇 |
临床医学 | 27篇 |
内科学 | 91篇 |
皮肤病学 | 2篇 |
神经病学 | 3篇 |
特种医学 | 60篇 |
外科学 | 31篇 |
综合类 | 14篇 |
预防医学 | 8篇 |
眼科学 | 1篇 |
药学 | 29篇 |
中国医学 | 1篇 |
肿瘤学 | 14篇 |
出版年
2023年 | 1篇 |
2022年 | 4篇 |
2021年 | 1篇 |
2020年 | 2篇 |
2019年 | 1篇 |
2018年 | 6篇 |
2016年 | 1篇 |
2015年 | 6篇 |
2014年 | 1篇 |
2013年 | 5篇 |
2012年 | 3篇 |
2011年 | 4篇 |
2010年 | 6篇 |
2009年 | 10篇 |
2008年 | 7篇 |
2007年 | 16篇 |
2006年 | 16篇 |
2005年 | 12篇 |
2004年 | 4篇 |
2003年 | 2篇 |
2002年 | 10篇 |
2001年 | 4篇 |
2000年 | 7篇 |
1999年 | 8篇 |
1998年 | 18篇 |
1997年 | 13篇 |
1996年 | 12篇 |
1995年 | 10篇 |
1994年 | 13篇 |
1993年 | 10篇 |
1992年 | 5篇 |
1991年 | 3篇 |
1990年 | 11篇 |
1989年 | 16篇 |
1988年 | 16篇 |
1987年 | 14篇 |
1986年 | 4篇 |
1985年 | 3篇 |
1984年 | 4篇 |
1983年 | 3篇 |
1982年 | 11篇 |
1981年 | 5篇 |
1980年 | 3篇 |
1979年 | 4篇 |
1978年 | 1篇 |
1977年 | 3篇 |
1976年 | 3篇 |
1975年 | 1篇 |
1973年 | 1篇 |
排序方式: 共有324条查询结果,搜索用时 15 毫秒
101.
Syngeneic bone marrow transplantation reduces the hearing loss associated with murine mucopolysaccharidosis type VII 总被引:4,自引:0,他引:4
MPS VII mice are deficient in beta-glucuronidase and share many clinical, biochemical, and pathologic characteristics with human mucopolysaccharidosis type VII (MPS VII). We have shown that syngeneic bone marrow transplantation (BMT) prolongs survival and reduces lysosomal storage in many organs of the MPS VII mouse. In this report, we quantify the hearing loss and determine the impact of syngeneic BMT on the development of deafness and the associated pathology in the MPS VII mouse. Eleven weeks after syngeneic BMT performed at birth, treated MPS VII mice had normal auditory-evoked brainstem responses (ABR), whereas untreated MPS VII mice had ABR thresholds 43 dB higher than normal. Treated MPS VII mice had beta-glucuronidase-positive cells in the temporal bone and in the subepithelial connective tissue of the external auditory canal. There was less thickening of the tympanic membrane and middle ear mucosa and decreased distortion of the ossicles and the cochlear bone. Although transplanted MPS VII mice had increased ABR thresholds by 33 weeks of age, four of the six had thresholds 12 to 32 dB lower than untreated mutants. These data indicate that syngeneic BMT in newborn MPS VII mice prevents early hearing loss and, in some animals, results in long-term improved auditory function. 相似文献
102.
Dexamethasone suppresses phospholipase C activation and insulin secretion from isolated rat islets 总被引:3,自引:0,他引:3
Zawalich WS Tesz GJ Yamazaki H Zawalich KC Philbrick W 《Metabolism: clinical and experimental》2006,55(1):35-42
Dexamethasone inhibits insulin secretion from isolated islets. In the present experiments, possible underlying biochemical mechanisms responsible for defective secretion were explored. Dexamethasone (1 micromol/L) had no immediate deleterious effect on 15 mmol/L glucose-induced insulin release from perifused rat islets. However, a 3-hour preincubation period with 1 micromol/L dexamethasone resulted in parallel reductions in both the first (64%) and second phases (74%) of 15 mmol/L glucose-induced insulin secretion monitored during a dynamic perifusion. When measured after the perifusion, there were no differences in insulin content or in the capacity of control or dexamethasone-treated islets to use glucose. Dexamethasone (1 micromol/L) preexposure also reduced phorbol ester- and potassium-induced secretion. In additional experiments, islets were labeled for 3 hours with 3H-inositol in the presence or absence of 1 micromol/L dexamethasone. The steroid did not affect total 3H-inositol incorporation during the labeling period. However, the capacity of 15 mmol/L glucose, 30 mmol/L KCl, and 100 micromol/L carbachol to activate phospholipase C (PLC), monitored by the accumulation of labeled inositol phosphates, was significantly reduced in dexamethasone-pretreated islets. Inclusion of the nuclear glucocorticoid receptor antagonist RU486 (mifepristone, 10 micromol/L) abolished the adverse effects of dexamethasone on both glucose-induced inositol phosphate accumulation and insulin secretion. Quantitative Western blot analyses revealed that the islet contents of PLCdelta1, PLCbeta1, beta2, beta3, and protein kinase C alpha were unaffected by dexamethasone pretreatment. These findings demonstrate that dexamethasone pretreatment impairs insulin secretion via a genomic action and that impaired activation of the PLC/protein kinase C signaling system is involved in the evolution of its inhibitory effect on secretion. 相似文献
103.
104.
105.
106.
107.
MR imaging and scintigraphy of gene expression through melanin induction 总被引:15,自引:0,他引:15
Weissleder R; Simonova M; Bogdanova A; Bredow S; Enochs WS; Bogdanov A Jr 《Radiology》1997,204(2):425
108.
109.
Prior exposure of isolated perifused rat islets to the sulfated gut hormone cholecystokinin-8 (CCK-8S) dramatically increased their insulin secretory response to 7.5 mM glucose, 10 mM arginine, and 10 mM alpha-ketoisocaproate. In the case of glucose, the heightened secretory response was still apparent 60-80 min after CCK-8S removal from the perifusion medium. Prior exposure of perifused islets to arginine (10 mM), tolbutamide (25 microM), or forskolin (1.0 microM) did not sensitize them to 7.5 mM glucose. CCK-8S exposure increased 3H efflux from islets prelabeled with [3H]inositol, and the increase in 3H efflux was sustained after CCK-8S removal from the perifusion medium. The duration of this increase in 3H efflux paralleled the temporal characteristics of this sensitization process and was significantly attenuated by 25 microM asperlicin, a competitive antagonist of CCK binding to its membrane receptor. Arginine, tolbutamide, or forskolin treatment of islets did not increase 3H efflux from [3H]inositol-prelabeled islets. The results suggest that the turnover of membrane phosphoinositides induced by CCK-8S is largely responsible for this heightened state of secretory responsiveness to various stimulants. Second-messenger molecules generated during phosphoinositide turnover may be responsible for the phenomenon of sensitization displayed by islet tissue to CCK-8S addition. 相似文献
110.