全文获取类型
收费全文 | 92篇 |
免费 | 5篇 |
专业分类
儿科学 | 6篇 |
妇产科学 | 1篇 |
基础医学 | 12篇 |
口腔科学 | 4篇 |
临床医学 | 10篇 |
内科学 | 8篇 |
神经病学 | 2篇 |
特种医学 | 4篇 |
外科学 | 8篇 |
综合类 | 3篇 |
预防医学 | 2篇 |
眼科学 | 1篇 |
药学 | 7篇 |
肿瘤学 | 29篇 |
出版年
2023年 | 1篇 |
2020年 | 1篇 |
2019年 | 1篇 |
2018年 | 1篇 |
2017年 | 2篇 |
2016年 | 3篇 |
2015年 | 3篇 |
2014年 | 1篇 |
2013年 | 3篇 |
2012年 | 2篇 |
2011年 | 6篇 |
2010年 | 4篇 |
2009年 | 1篇 |
2008年 | 3篇 |
2007年 | 5篇 |
2006年 | 3篇 |
2005年 | 5篇 |
2004年 | 5篇 |
2003年 | 2篇 |
2002年 | 2篇 |
2001年 | 1篇 |
2000年 | 1篇 |
1999年 | 2篇 |
1998年 | 9篇 |
1997年 | 3篇 |
1996年 | 3篇 |
1995年 | 1篇 |
1994年 | 1篇 |
1993年 | 2篇 |
1991年 | 4篇 |
1990年 | 1篇 |
1989年 | 1篇 |
1988年 | 2篇 |
1986年 | 2篇 |
1985年 | 2篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1980年 | 1篇 |
1976年 | 1篇 |
1973年 | 1篇 |
1967年 | 2篇 |
1966年 | 1篇 |
排序方式: 共有97条查询结果,搜索用时 0 毫秒
21.
Melvin George Amrita Jena Varsha Srivatsan Rajaram Muthukumar VE Dhandapani 《Current Cardiology Reviews》2016,12(1):37-46
Background:
Several diagnostic and prognostic biomarkers are being explored in heart failure. GDF-15 belongs to the transforming growth factor β (TGF-β) cytokine family that is highly up regulated in inflammatory conditions. We undertook this systematic review to summarize the current evidence on the utility of GDF-15 as a biomarker in heart failure.Design and Methods:
Multiple electronic databases for studies that reported the association between GDF- 15 and heart failure were searched using different electronic databases such as MEDLINE, Science Direct, Springer Link, Scopus, Cochrane Reviews, and Google Scholar using pre-defined inclusion- exclusion criteria.Results:
Twenty one original studies were identified that included data from 20,920 study participants. GDF 15 was found to be a strong prognosticator of all-cause mortality in heart failure patients. Several studies found the benefit of using GDF-15 as a component of a multi-biomarker strategy in prognosticating patients with heart failure.Conclusion:
More studies are warranted to elucidate the molecular pathways involving GDF-15 and to see how knowledge about GDF-15 can be used to make therapeutic decisions in the clinic. 相似文献22.
The toxic and antitumor effects of cisplatin were shown to depend upon the activity of microsomal oxidation system enzymes. Administration of the drug in combination with K-2-9 enterosorbent was followed by an increase in its antitumor effect and amelioration of toxicity. 相似文献
23.
24.
Murine L1210 leukemia cells possessing an increased resistance to cisplatin were found to be refractory to transforming growth factor (TGF)-beta1-induced growth inhibition, while the parental L1210 cells were strongly inhibited by this cytokine. Growth inhibition was estimated on the basis of [3H]thymidine incorporation, cell counting and colony-forming assay. Cisplatin-resistant L1210 cells were also shown to be much more resistant than the parental cells to both cisplatin- and TGF-beta1-induced apoptosis. These results suggest the existence of cross-resistance to cisplatin and TGF-beta1 in the studied leukemia cells. 相似文献
25.
Simon Craig Andis Graudins Stuart R Dalziel Colin VE Powell Franz E Babl 《Emergency medicine Australasia : EMA》2019,31(1):29-34
In this series we address important topics for clinicians who participate in research as part of their work in the ED. The overarching goal of clinical research is to improve care and determine which treatment is best. Yet, defining and measuring outcomes – what is ‘best’ – can be one of the most difficult steps in the design of a study, in particular when answers to research questions cannot be captured in simple binary results. This article addresses how to choose outcome measures and highlights the increasingly important concept of core outcome sets. 相似文献
26.
27.
28.
29.
30.
Lubet RA; Steele VE; DeCoster R; Bowden C; You M; Juliana MM; Eto I; Kelloff GJ; Grubbs CJ 《Carcinogenesis》1998,19(8):1345-1351
The chemopreventive activity of the highly specific nonsteroidal aromatase
inhibitor, vorozole, was examined in the methylnitrosourea (MNU)-induced
rat model of mammary carcinogenesis. Various doses of vorozole (0.08-1.25
mg/kg body wt/day) were administered daily (by gavage) to female
Sprague-Dawley rats starting at 43 days of age. Seven days later, the rats
were given a single i.v. dose of MNU (50 mg/kg body wt). Rats were
continually treated with vorozole until the end of the experiment (120 days
post-MNU). Vorozole caused a dose dependent inhibition of mammary cancer
multiplicity. The highest dose of vorozole (1.25 mg/kg body wt/day)
decreased cancer multiplicity by approximately 90%, and simultaneously
decreased cancer incidence from 100 to 44%. The next two highest doses of
vorozole (0.63 and 0.31 mg/kg body wt/day) inhibited MNU-induced mammary
cancer multiplicity by 70-80%. Even the two lowest doses of vorozole (0.16
and 0.08 mg/kg body wt/ day) decreased cancer multiplicity -50%. Serum
level determinations were performed on a variety of endpoints at either 4
or 24 h following the last dose of vorozole. Insulin-like growth factor
(IGF)-1 levels were slightly, but significantly, increased by vorozole
treatment. Vorozole induced striking increases in serum testosterone levels
at 4 h at all the dose levels employed. Testosterone levels were
significantly elevated over controls at 24 h in rats given the lower doses
of vorozole (0.08-0.31 mg/kg body wt/day), but were significantly lower
than in rats administered the higher doses of vorozole (0.63 or 1.25 mg/kg
body wt/ day). This result presumably reflects the limited half- life of
vorozole in rats. In a second series of experiments, the effects of limited
duration of dosing with vorozole (2.5 mg/kg body wt/day) or intermittent
dosing with vorozole were determined. Treatment of rats with vorozole for
limited time periods, from 3 days post-MNU administration until 30 or 60
days post-MNU treatment, resulted in significant delays in the time to
appearance of palpable cancers. However, these limited treatments did not
greatly affect the overall incidence or multiplicity of mammary cancers
when compared with the MNU controls at the end of the study (150 days
post-MNU). Finally, the effects of intermittent dosing with vorozole (2.5
mg/kg body wt/day) were examined. Rats were administered cycles of vorozole
daily for a period of 3 weeks followed by treatment with the vorozole
vehicle for the next 3 weeks (total of four cycles). Although this
intermittent treatment did inhibit the appearance of new tumors during each
of the periods that vorozole was administered, it did not cause regression
of palpable cancers.
相似文献