全文获取类型
收费全文 | 192篇 |
免费 | 16篇 |
出版年
2022年 | 1篇 |
2021年 | 2篇 |
2020年 | 1篇 |
2019年 | 2篇 |
2018年 | 2篇 |
2017年 | 4篇 |
2015年 | 4篇 |
2014年 | 9篇 |
2013年 | 10篇 |
2012年 | 10篇 |
2011年 | 10篇 |
2010年 | 9篇 |
2009年 | 7篇 |
2008年 | 3篇 |
2007年 | 2篇 |
2006年 | 4篇 |
2005年 | 5篇 |
2004年 | 2篇 |
2003年 | 3篇 |
2002年 | 2篇 |
2001年 | 9篇 |
2000年 | 4篇 |
1999年 | 8篇 |
1998年 | 3篇 |
1996年 | 4篇 |
1995年 | 3篇 |
1994年 | 2篇 |
1993年 | 3篇 |
1992年 | 5篇 |
1991年 | 5篇 |
1990年 | 2篇 |
1989年 | 4篇 |
1988年 | 3篇 |
1987年 | 2篇 |
1986年 | 7篇 |
1985年 | 3篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1982年 | 2篇 |
1981年 | 7篇 |
1980年 | 1篇 |
1979年 | 10篇 |
1978年 | 13篇 |
1977年 | 5篇 |
1975年 | 1篇 |
1974年 | 5篇 |
1973年 | 2篇 |
1969年 | 1篇 |
排序方式: 共有208条查询结果,搜索用时 15 毫秒
1.
Defects in both insulin secretion and action have been documented in patients with noninsulin-dependent diabetes mellitus (NIDDM), leading to the suggestion that both fasting hyperglycemia and insulin resistance in NIDDM are secondary to insulin deficiency. In order to test this hypothesis, insulin secretion (plasma insulin response to oral glucose) and insulin action (insulin clamp) were determined in 25 patients with NIDDM. The results documented relationships between incremental plasma insulin response to glucose and degree of fasting hyperglycemia (r = -.045, P less than 0.05) and insulin-stimulated glucose utilization (r = 0.25, P = NS). These data indicate that differences in insulin secretory response accounted for only approximately 20% of the variance in fasting plasma glucose level and 6% of the variance in insulin resistance in NIDDM. Thus, differences in insulin-secretory response contribute modestly to magnitude of glycemia, and not at all to variations in insulin resistance in NIDDM, permitting rejection of the hypothesis that insulin resistance is secondary to insulin deficiency. 相似文献
2.
3.
4.
5.
Peter J. Hollenbeck 《Journal of neurochemistry》1993,60(6):2265-2275
Abstract: The microtubule-based motor protein kinesin is thought to drive anterograde organelle transport in axons, but nothing is known about how its force-generating activity or organelle-binding properties are regulated. Studies in other motility systems suggest that protein phosphorylation is a reasonable candidate for this function. I report here that the kinesin heavy chain (HC) and light chain (LC), as well as the 160-kDa kinesin-associated protein kinectin, are phosphorylated in vivo in cultures of chick sympathetic neurons and PC12 cells labeled metabolically with 32 P. In neurons, both kinesin chains are phosphorylated exclusively on serine residues, and limiting tryptic digestion demonstrated that the phosphorylation sites are clustered in a region of ˜5 kDa for the HC and ˜14 kDa for the LC. Partial tryptic digestion of 32 P-labeled HC followed by immunoblotting with SUK4 monoclonal anti-HC and fluorography showed that the sites of HC phosphorylation are outside the globular N-terminal head region where kinesin's microtubulebinding and mechanochemical activities reside. Treatment of metabolically labeled neurons with forskolin, phorbol esters, or calcium ionophore did not alter the extent of phosphorylation, the phosphoamino acid composition, or the V8 protease phosphopeptide maps of the HC, LC, and 160-kDa protein, with one exception: treatment with calcium ionophore reduced the specific activity of the LC. In addition, when kinesin from PC12 cells was compared with that from PC12-derived cell lines lacking protein kinase A activity, neither the extent of phosphorylation nor the phosphopeptide maps were altered for either chain. Phosphopeptide mapping experiments also showed that postlysis kinase activity can phosphorylate both the neuronal HC and LC at sites not phosphorylated in vivo. 相似文献
6.
7.
8.
C Crone J Frokjaer-Jensen JJ Friedman O Christensen 《The Journal of general physiology》1978,71(2):195-220
9.
The present studies demonstrate that the removal rate of exogenously labelled 125I-VLDL-protein is prolonged when total serum from insulin-deficient rats combined with isolated 125I-VLDL is injected into normal recipient rats (6.8 +/- 0.7 vs 4.2 +/- 0.4 min; p < 0.01), but not when 125I-VLDL-protein is isolated and injected alone (4.2 +/- 0.8 vs 4.3 +/- 0.8 min). Furthermore, the present studies demonstrate that when isolated 125I-VLDL-protein is recombined with either VLDL-free (d > 1.006 g/ml), or lipoprotein-free serum (d > 1.215 g/ml) from insulin-deficient rats, the defect in removal rate of VLDL-protein observed in total serum is reestablished (125I-VLDL + VLDL-free serum from insulin-deficient rat vs that from normal rat: 7.6 +/- 1.2 vs 4.6 +/- 0.7 min, p < 0.05; and 125I-VLDL + lipoprotein-free serum from insulin-deficient rat vs that from normal rat: 6.4 +/- 0.7 vs 4.1 +/- 0.4 min, p < 0.01). These data suggest that a factor or factors exist in lipoprotein-free serum of insulin-deficient rats which interfere with the normal removal of 125I-VLDL. Since we have previously demonstrated a prolongation in the removal rate of endogenously labeled VLDL-3H-TG, the defect in removal of VLDL from the plasma of insulin-deficient rats appears to include both the lipid and protein moieties of the VLDL particles. 相似文献
10.
Rui Liu Xuguang Guo Yikyung Park Jian Wang Xuemei Huang Albert Hollenbeck Aaron Blair Honglei Chen 《PloS one》2013,8(6)