全文获取类型
收费全文 | 443篇 |
免费 | 37篇 |
出版年
2022年 | 6篇 |
2021年 | 9篇 |
2020年 | 3篇 |
2018年 | 8篇 |
2017年 | 9篇 |
2016年 | 9篇 |
2015年 | 10篇 |
2014年 | 15篇 |
2013年 | 13篇 |
2012年 | 15篇 |
2011年 | 25篇 |
2010年 | 15篇 |
2009年 | 11篇 |
2008年 | 12篇 |
2007年 | 18篇 |
2006年 | 14篇 |
2005年 | 16篇 |
2004年 | 18篇 |
2003年 | 14篇 |
2002年 | 14篇 |
2001年 | 10篇 |
2000年 | 12篇 |
1999年 | 14篇 |
1998年 | 9篇 |
1997年 | 4篇 |
1996年 | 6篇 |
1995年 | 4篇 |
1993年 | 5篇 |
1992年 | 11篇 |
1991年 | 13篇 |
1990年 | 9篇 |
1989年 | 16篇 |
1988年 | 4篇 |
1987年 | 12篇 |
1985年 | 7篇 |
1984年 | 6篇 |
1983年 | 8篇 |
1982年 | 3篇 |
1981年 | 9篇 |
1980年 | 3篇 |
1979年 | 7篇 |
1977年 | 4篇 |
1976年 | 4篇 |
1974年 | 7篇 |
1973年 | 7篇 |
1972年 | 6篇 |
1970年 | 3篇 |
1969年 | 4篇 |
1967年 | 3篇 |
1966年 | 2篇 |
排序方式: 共有480条查询结果,搜索用时 31 毫秒
21.
Summary A procedure is described for the preparation of a membrane fraction enriched in basal-lateral plasma membranes from gastric mucosa. Gastric glands isolated from rabbit were employed as starting material, greatly reducing contamination from nonglandular cell types. The distribution of cellular components during the fractionation procedure was monitored with specific marker enzymes. (Na++K+)-ATPase, ouabain-sensitive K+-stimulatedp-nitrophenyl-phosphatase and histamine-stimulated adenylate cyclase were used as markers for basal-lateral membranes. These three markers were similarly distributed during both differential and equilibrium density gradient centrifugation. The enriched membrane fraction contained more than 30% of the total initial activities of the three basal-lateral membrane markers which were purified better than 11-fold with respect to protein. (Na++K+)-ATPase activity was resolved from the activities of acid phosphatase, pepsin, Mg2+-ATPase, cytochromec oxidase, NADPH-cytochromec reductase, glucose-6-phosphatase, (K++H+)-ATPase, DNA and RNA. 相似文献
22.
Julia Bell-Quint Trudy Forte Paul Graham 《Biochemical and biophysical research communications》1981,99(2):700-706
Cultured rat hepatocytes were used to demonstrate that the liver can synthesize two forms of apolipoprotein B. Separation of apolipoprotein B by disc gel electrophoresis indicated that hepatocyte low density lipoprotein contains predominantly apolipoprotein B with an apparent molecular weight of 345,000 ± 5,055. In contrast, the major apolipoprotein B component of hepatocyte very low density lipoprotein is a variant form with a molecular weight of 242,000 ± 2,720. Hepatocyte high density lipoprotein, unlike plasma HDL, also contains apolipoprotein B with an apparent molecular weight of 244,000 ± 2,742. Incorporation of [3H] leucine into hepatocyte apolipoprotein B components suggested de novo synthesis. 相似文献
23.
I Weinstein L R Forte H V Werner M Heimberg 《Biochemical and biophysical research communications》1979,86(2):454-459
The effects of glucagon on the concentration and output of cAMP were studied in liver slices and in perfused livers from female rats and from animals treated with ethynyl estradiol (15 μg/kg daily for 14 days). The basal content of cAMP in liver slices, or of cAMP released into the perfusion medium in the absence of glucagon, was unaffected by prior treatment of the animal with estrogen. When glucagon was added to the medium, the concentration of cAMP in liver slices was 2.29 ± 0.32 and 1.10 ± 0.11 pmol cAMP/mg wet weight from control and ethynyl estradiol treated rats, respectively. When glucagon was added, the output of cAMP by perfused livers was maximal at 20 minutes with livers from either control or ethynyl estradiol treated rats. Output of cAMP by the perfused liver, when glucagon was added to the medium, was 8.76 ± 0.69 and 1.84 ± 0.08 nmol/g by livers from control and ethynyl estradiol treated rats, respectively. This effect was the same whether animals had been fasted for 12 hours previously, or were allowed free access to food until sacrifice. Clearly, as measured by cAMP accumulation, prior treatment of the rat with ethynyl estradiol reduced the sensitivity of the hepatic cAMP response to glucagon. 相似文献
24.
25.
26.
Stefano Forte Alfredo Pagliuca Eugenia T. Maniscalchi Rosario Gulino Giovanna Calabrese Lucia Ricci-Vitiani Roberto Pallini Michele Signore Rosalba Parenti Ruggero De Maria Massimo Gulisano 《PloS one》2013,8(12)
The term astrocytoma defines a quite heterogeneous group of neoplastic diseases that collectively represent the most frequent brain tumors in humans. Among them, glioblastoma multiforme represents the most malignant form and its associated prognosis is one of the poorest among tumors of the central nervous system. It has been demonstrated that a small population of tumor cells, isolated from the brain neoplastic tissue, can reproduce the parental tumor when transplanted in immunodeficient mouse. These tumor initiating cells are supposed to be involved in cancer development and progression and possess stem cell-like features; like their normal counterpart, these cells remain quiescent until they are committed to differentiation. Many studies have shown that the role of the tumor suppressor protein PTEN in cell cycle progression is fundamental for tumor dynamics: in low grade gliomas, PTEN contributes to maintain cells in G1 while the loss of its activity is frequently observed in high grade gliomas. The mechanisms underlying the above described PTEN activity have been studied in many tumors, but those involved in the maintenance of tumor initiating cells quiescence remain to be investigated in more detail. The aim of the present study is to shed light on the role of PTEN pathway on cell cycle regulation in Glioblastoma stem cells, through a cell differentiation model. Our results suggest the existence of a molecular mechanism, that involves DUB3 and WEE1 gene products in the regulation of Cdc25a, as functional effector of the PTEN/Akt pathway. 相似文献
27.
Giovanni Forte Beatrice Bocca Angela Peruzzu Francesco Tolu Yolande Asara Cristiano Farace Riccardo Oggiano Roberto Madeddu 《Biological trace element research》2013,156(1-3):79-90
Mechanisms for the onset of diabetes and the development of diabetic complications remain under extensive investigations. One of these mechanisms is abnormal homeostasis of metals, as either deficiency or excess of metals, can contribute to certain diabetic outcomes. Therefore, this paper will report the blood levels of chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), mercury (Hg), nickel (Ni), lead (Pb), selenium (Se), and zinc (Zn) in subjects with type 1 diabetes (n?=?192, mean age 48.8 years, mean disease duration 20.6 years), type 2 diabetes (n?=?68, mean age 68.4 years, mean disease duration 10.2 years), and in control subjects (n?=?59, mean age 57.2 years), and discuss the results indicating their possible role in diabetes. The metal concentrations were measured by sector field inductively coupled plasma mass spectrometry after microwave-induced acid digestion of blood samples. The accuracy was checked using a blood-based certified reference material, and recoveries of all elements were in the range of 92–101 % of certified values. Type 1 diabetes was found to be associated with Cr (p?=?0.02), Mn (p?<?0.001), Ni (p?<?0.001), Pb (p?=?0.02), and Zn (p?<?0.001) deficiency, and type 2 diabetes with Cr (p?=?0.014), Mn (p?<?0.001), and Ni (p?<?0.001) deficiency. These deficiencies were appreciated also subdividing the understudied patients for gender and age groups. Furthermore, in type 1 diabetes, there was a positive correlation between Pb and age (p?<?0.001, ρ?=?0.400) and Pb and BMI (p?<?0.001, ρ?=?0.309), while a negative correlation between Fe and age (p?=?0.002, ρ?=??0.218). In type 2 diabetes, there was a negative correlation between Fe and age (p?=?0.017, ρ?=??0.294) and Fe and BMI (p?=?0.026, ρ?=??0.301). Thus, these elements may play a role in both forms of diabetes and combined mineral supplementations could have beneficial effects. 相似文献
28.
Cell proliferation, metabolism, migration and survival are coordinated through the tight control of two target of rapamycin (TOR) kinase complexes: TORC1 and TORC2. Here, we show that a novel phosphorylation of fission yeast Gad8 (AGC kinase) on the evolutionarily conserved threonine 6 (Thr6) prevents the physical association between Gad8 and TORC2. Accordingly, this block to protein interactions by Gad8 Thr6 phosphorylation decreases TORC2-controlled activation of Gad8. Likewise, phosphorylation of Gad8 Thr6, possibly by PKC, prevents the association of Gad8 with TORC2 thereby increasing TORC2 activity, because it reduces Gad8-mediated feedback inhibition of TORC2. Consistently, the introduction of a Gad8 T6D mutant, that mimics phosphorylation, increased TORC2 activity. Increased PKCPck2 expression prevented Gad8–TORC2 binding and so reduced the TORC2-mediated phosphorylation of Gad8 serine 546 that activates Gad8. Interestingly, independent of the Ser546 phosphorylation status, Gad8 Thr6 phosphorylation is important for remodelling the actin cytoskeleton and survival upon potassium ion and heat stresses. In contrast, Ser546 phosphorylation is required for the control of G1 arrest, mating, cell length at division and vascular size. Finally, these findings reveal a novel mode of TORC2 activation that is essential for cell survival following stress. 相似文献
29.
Endothelial progenitor cells (EPC) participate in revascularization and angiogenesis. EPC can be cultured in vitro from mononuclear cells of peripheral blood, umbilical cord blood or bone marrow; they also can be transdifferentiated from mesenchymal stem cells (MSC). We isolated EPCs from Wharton's jelly (WJ) using two methods. The first method was by obtaining MSC from WJ and characterizing them by flow cytometry and their adipogenic and osteogenic differentiation, then applying endothelial growth differentiating media. The second method was by direct culture of cells derived from WJ into endothelial differentiating media. EPCs were characterized by morphology, Dil-LDL uptake/UEA-1 immunostaining and testing the expression of endothelial markers by flow cytometry and RT-PCR. We found that MSC derived from WJ differentiated into endothelial-like cells using simple culture conditions with endothelium induction agents in the medium. 相似文献
30.