全文获取类型
收费全文 | 601篇 |
免费 | 46篇 |
国内免费 | 1篇 |
专业分类
耳鼻咽喉 | 1篇 |
儿科学 | 78篇 |
妇产科学 | 7篇 |
基础医学 | 64篇 |
口腔科学 | 11篇 |
临床医学 | 86篇 |
内科学 | 149篇 |
皮肤病学 | 18篇 |
神经病学 | 36篇 |
特种医学 | 94篇 |
外科学 | 27篇 |
综合类 | 10篇 |
预防医学 | 23篇 |
眼科学 | 1篇 |
药学 | 27篇 |
中国医学 | 1篇 |
肿瘤学 | 15篇 |
出版年
2023年 | 2篇 |
2022年 | 6篇 |
2021年 | 2篇 |
2020年 | 5篇 |
2019年 | 5篇 |
2018年 | 12篇 |
2017年 | 11篇 |
2016年 | 10篇 |
2015年 | 20篇 |
2014年 | 16篇 |
2013年 | 32篇 |
2012年 | 17篇 |
2011年 | 14篇 |
2010年 | 36篇 |
2009年 | 20篇 |
2008年 | 23篇 |
2007年 | 10篇 |
2006年 | 12篇 |
2005年 | 11篇 |
2004年 | 9篇 |
2003年 | 6篇 |
2002年 | 10篇 |
2001年 | 10篇 |
2000年 | 5篇 |
1999年 | 9篇 |
1998年 | 24篇 |
1997年 | 31篇 |
1996年 | 27篇 |
1995年 | 31篇 |
1994年 | 23篇 |
1993年 | 37篇 |
1992年 | 5篇 |
1991年 | 7篇 |
1990年 | 15篇 |
1989年 | 16篇 |
1988年 | 17篇 |
1987年 | 11篇 |
1986年 | 13篇 |
1985年 | 13篇 |
1984年 | 3篇 |
1983年 | 4篇 |
1982年 | 6篇 |
1981年 | 14篇 |
1980年 | 6篇 |
1979年 | 2篇 |
1978年 | 5篇 |
1977年 | 7篇 |
1976年 | 12篇 |
1975年 | 4篇 |
1957年 | 1篇 |
排序方式: 共有648条查询结果,搜索用时 15 毫秒
581.
PS Teirstein V Massullo S Jani RJ Russo DA Cloutier RA Schatz EM Guarneri S Steuterman K Sirkin S Norman P Tripuraneni 《Circulation》1999,99(2):243-247
BACKGROUND: Although early trials indicate the treatment of restenosis with radiation therapy is safe and effective, the long-term impact of this new technology has been questioned. The possibility of late untoward consequences, such as aneurysm formation, perforation, and accelerated vascular disease, is of significant concern. Furthermore, it is not known whether the beneficial effects of radiation therapy will be durable or whether radiation will only delay restenosis. METHODS AND RESULTS: A double-blind, randomized trial was undertaken to compare 192Ir with placebo sources in patients with previous restenosis after coronary angioplasty. Patients were randomly assigned to receive a 0.76-mm (0. 03-in) ribbon containing sealed sources of either 192Ir or placebo. All patients underwent repeat coronary angiography at 6 months. All living patients were contacted 24 months after their index study procedure. Patients were assessed with respect to the need for target-lesion revascularization or nontarget-lesion revascularization, occurrence of myocardial infarction, or death. Over a 9-month period, 55 patients were enrolled; 26 were randomized to 192Ir and 29 to placebo. Follow-up was obtained in 100% of living patients at a minimum of 24 months. Target-lesion revascularization was significantly lower in the 192Ir group (15.4% versus 44.8%; P<0. 01). Nontarget-lesion revascularization was similar in 192Ir and placebo patients (19.2% versus 20.7%; P=NS). There were 2 deaths in each group. The composite end point of death, myocardial infarction, or target-lesion revascularization was significantly lower in 192Ir-treated versus placebo-treated patients (23.1% versus 51.7%; P=0.03). No patient in the 192Ir group sustained a target-lesion revascularization later than 10 months. CONCLUSIONS: At 2-year clinical follow-up, treatment with 192Ir demonstrates significant clinical benefit. Although further follow-up (including late angiography) will be necessary, no clinical events have occurred to date in the 192Ir group to suggest major untoward effects of vascular radiotherapy. At the intermediate follow-up time point, vascular radiotherapy continues to be a promising new treatment for restenosis. 相似文献
582.
羟考酮对左旋氧氟沙星在人体内药物动力学的影响 总被引:1,自引:1,他引:0
目的研究羟考酮对左旋氧氟沙星(LVFX)在人体内药物动力学的影响。方法8名健康志愿者,单用LVFX或合用羟考酮,用HPLC法测定血药浓度。结果单用LVFX500mg后的药物动力学参数分别为tmax(1.562±1.050)h,cmax(6.6419±0.15860)μg/ml,AUC(47.65±11.29)h*μg/ml,T1/2(β)(7.034±0.941)h;合用羟考酮时,LVFX的药物动力学参数分别为tmax(1.125±0.641)h,cmax(7.652±2.594)μg/ml,AUC(48.74±10.58)h*μg/ml,T1/2(β)(6.275±0.588)h。两者除T1/2ka和cmax外,无显著性差异。结论羟考酮对LVFX在人体内药物动力学参数无影响。 相似文献
583.
584.
585.
586.
AC Lindgren U Grandell EM Ritzén M Anvret 《Acta paediatrica (Oslo, Norway : 1992)》1996,85(2):195-198
The Prader-Willi syndrome (PWS) is a genetic disorder which is difficult to diagnose from clinical symptoms in newborns and young children. However, it is known that in PWS a fragment within the q11-13 region of the paternally derived chromosome 15 is deleted. Recently it has been observed that the D15S63 (PW71) locus in chromosome 15q11-13 is methylated on the maternally derived chromosome, but unmethylated on the paternally derived chromosome. Based on this observation a rapid diagnostic test (the PW71 methylation test) using methylation-sensitive restriction enzymes has been developed for patients presumed to have PWS. We have studied 56 patients; 30 patients with classical features of PWS and 26 patients with only psychomotor retardation and obesity, referred to us from different parts of Sweden. Twenty-nine of the 30 classical PWS patients were found to have an absence of the unmethylated paternally derived PW71(D15S63) locus in chromosome 15q11-13. None of the patients with only obesity and psychomotor retardation had this "absence" pattern on chromosome 15q11-13. Using the PW71 methylation test on patients with PWS, a concordance of 96% was found. The PW71 methylation test is presently the method of choice for rapid diagnostic testing of patients suspected of having PWS. 相似文献
587.
Fast gradient field-echo imaging is becoming more common in morphologic studies but is not as widespread as might be hoped because of its susceptibility to local field inhomogeneities that lead to spin dephasing (reducing T2 to T2*) and geometric distortion (frequency misregistration). These problems are manifested in both the in-plane and section-select directions. The authors show that reversal of many of these adverse effects is possible through the acquisition of the gradient field echo in a three- and four-dimensional mode for a fixed echo time (TE), since phase-encoding leads to the capture of the echo within the sampling window. This echo centering is shown to be equivalent to the reduction of dephasing across a pixel. Improvements are also obtained by reducing TE to as short a value as possible. 相似文献
588.
Murine myeloid cells can be transformed in vitro by infection with recombinant retroviruses carrying activated myb genes. While these myb- transformed hematopoietic cells (MTHCs) can proliferate continuously in culture, they exhibit several characteristics of progenitor cells of the granulocyte-macrophage (GM) lineage, including an absolute dependence on hematopoietic growth factors (HGFs) such as GM colony- stimulating factor (GM-CSF) for survival and growth. Whereas we have previously shown that MTHCs respond synergistically to certain combinations of HGFs, we report here that MTHCs apparently require two HGFs for proliferation, because GM-CSF alone appears insufficient to promote growth when MTHCs are cultured at very low densities. However, proliferation can be stimulated by either increasing the density at which MTHCs are cultured (implying the production of an autocrine growth factor) or by the presence of a feeder layer of irradiated fibroblasts. We find that the activity of such feeder layers is greatest when the MTHCs are allowed to contact them directly; and by using mutant fibroblast lines, that it depends on the production of CSF- 1, but not Steel factor (SLF). In contrast, the autocrine factor appears not to be either CSF-1 or SLF, and the possibility is raised that it may represent a novel HGF activity. Potential implications of these results for normal and leukemic hematopoiesis are discussed. 相似文献
589.
Chedin M; Filhol O; Duminy C; Bolla M; Benistant C; Roche S; Chambaz EM; Cochet C 《Carcinogenesis》1997,18(8):1463-1472
Two different protein tyrosine kinases were detected in the cytosolic
fraction of different human tumor tissues. After partial purification, the
two enzymes, which were highly active in breast tumor tissues, were
characterized. One of them, soluble tyrosine kinase-1 (STK-1), represents a
soluble form of the c-Src protein, which is apparently underphosphorylated
on its C-terminal tyrosine residue whereas the other (STK-2) is a 48-kDa
protein tyrosine kinase (PTK), which is molecularly and functionally
related to the C-terminal Src kinase (Csk). These two protein tyrosine
kinases clearly exhibit a different substrate specificity, and are
responsible for the high tyrosine kinase activity present in the cytosolic
fraction of human breast cancer. In addition, it was observed that STK-1
and STK-2 are also expressed in the breast cancer cell line, CAL-51.
相似文献
590.
Walder RY; Shalev H; Brennan TM; Carmi R; Elbedour K; Scott DA; Hanauer A; Mark AL; Patil S; Stone EM; Sheffield VC 《Human molecular genetics》1997,6(9):1491-1497
Familial hypomagnesemia with secondary hypocalcemia (HSH) (MIM 307600) was
studied in three inbred Bedouin kindreds from Israel. The three kindreds,
one extended and two nuclear families, contained 13 affected individuals,
11 males and two females. Assuming that the individuals affected with
hypomagnesemia shared a chromosomal region inherited from a common
ancestor, we used a DNA pooling strategy in a genome-wide search for loci
which show homozygosity for shared alleles in affected individuals. DNA
samples from affected individuals within a single kindred were pooled and
used as the template for PCR amplification of short tandem repeat
polymorphic markers (STRPs). Pooled DNA from unaffected siblings and
parents were used as controls. A shift towards homozygosity was observed in
the affected DNA pool compared with the control pools with D9S301
(GATA7D12). Genotyping of individual DNA samples with D9S301 and several
flanking markers confirmed linkage to chromosome 9 with maximum LOD scores
of 3.4 (theta = 0.05), 3.7 (theta = 0) and 2.3 (theta = 0) for the three
families. We have identified a 14 cM interval on chromosome 9
(9q12-9q22.2), flanked by proximal marker D9S1874 and distal marker
D9S1807, within which all affected individuals from the three kindreds are
homozygous for a shared haplotype. The disease segregates with a common
affected haplotype in the three families, suggesting that hypomagnesemia is
caused by a common ancestral mutation in these families. Although HSH has
been previously reported to be X linked, these linkage data demonstrate
that the disorder is an autosomal recessive disease in these kindreds.
Mapping of a chromosomal breakpoint in a somatic cell line established from
a patient with HSH and a balanced X;9 translocation placed the chromosomal
breakpoint in a 500 kb region flanked by D9S1844 and D9S273. Identification
of the gene responsible for hypomagnesemia will provide insight into the
regulation of this essential cation.
相似文献