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1.
2.
K. Watanabe S. Hakomori M.E. Powell M. Yokota 《Biochemical and biophysical research communications》1980,92(2):638-646
Two amphipathic protein fractions soluble in organic solvents as well as in water have been isolated from the ganglioside fraction of bovine erythrocyte membranes by successive chromatography in chloroform-methanol mixture on DEAE-Sephadex, silicic acid, and α-hydroxypropylated Sephadex G50 (LH60) columns. These two fractions contained a similar low molecular weight protein but with distinctively different amino acid composition. One of these proteins has been characterized by having a strong Paul-Bunnell antigen activity and had a binding affinity to ganglioside. A similar protein without Paul-Bunnell antigen activity was isolated as the major ganglioside-associated protein. 相似文献
3.
盐度和CO2倍增环境下碱蓬幼苗呼吸酶活性的变化 总被引:3,自引:0,他引:3
研究了生长在正常大气CO2和CO2倍增环境中的盐生植物碱蓬(Suaedasalsa)幼苗呼吸酶活性对KCl和NaCl的反应.结果表明,在CO2倍增(700μl·L-1)和正常大气CO2(350μl·L-1)下,300mmol·L-1KCl和NaCl均能抑制琥珀酸脱氢酶(SDH)和苹果酸脱氢酶(MDH)活性,而异柠檬酸脱氢酶(IDH)活性为NaCl抑制、KCl促进;NaCl和KCl明显抑制细胞色素氧化酶(CO)和光呼吸中乙醇酸氧化酶(GO)、羟基丙酮酸还原酶(HPR)活性;并指出在KCl胁迫下,CO2使三羧酸循环(TCAC)的运行变慢,NaCl胁迫下使其加快,TCAC运行限速步骤与MDH无关,CO为盐对呼吸代谢影响的重要位点.另外,K+、Na+对蛋白表达的影响有差异,CO2可使盐胁迫下的碱蓬幼苗蛋白表达降低. 相似文献
4.
The (13)C NMR spectra of methyl beta-d-glucopyranoside, methyl beta-d-galactopyranoside, methyl beta-d-xylopyranoside, and methyl beta-l-arabinopyranoside were recorded in CaCl(2)/KCl+D(2)O mixtures and in D(2)O. The chemical shifts of C-1, C-3, and C-5 in the methyl beta-d-glucopyranoside and methyl beta-d-galactopyranoside decrease rapidly as molalities of CaCl(2)/KCl increase, while those of C-1, C-2, and C-3 in the methyl beta-d-xylopyranoside and methyl beta-l-arabinopyranoside decrease rapidly as molalities of CaCl(2)/KCl increase. Cations (Ca(2+)/K(+)) can weakly complex with O in OMe of the pyranosides studied. Results are discussed in terms of the stereochemistry of the pyranoside molecules and the structural properties of the ions. 相似文献
5.
《Bioorganic & medicinal chemistry》2019,27(16):3546-3550
Previously we have reported on a series of pyridine-3-carboxamide inhibitors of DNA gyrase and DNA topoisomerase IV that were designed using a computational de novo design approach and which showed promising antibacterial properties. Herein we describe the synthesis of additional examples from this series aimed specifically at DNA gyrase, along with crystal structures confirming the predicted mode of binding and in vitro ADME data which describe the drug-likeness of these compounds. 相似文献
6.
Eva Xepapadaki Giuseppe Maulucci Caterina Constantinou Eleni A. Karavia Evangelia Zvintzou Bareket Daniel Shlomo Sasson Kyriakos E. Kypreos 《生物化学与生物物理学报:疾病的分子基础》2019,1865(6):1351-1360
High density lipoprotein (HDL) has attracted the attention of biomedical community due to its well-documented role in atheroprotection. HDL has also been recently implicated in the regulation of islets of Langerhans secretory function and in the etiology of peripheral insulin sensitivity. Indeed, data from numerous studies strongly indicate that the functions of pancreatic β-cells, skeletal muscles and adipose tissue could benefit from improved HDL functionality. To better understand how changes in HDL structure may affect diet-induced obesity and type 2 diabetes we aimed at investigating the impact of Apoa1 or Lcat deficiency, two key proteins of peripheral HDL metabolic pathway, on these pathological conditions in mouse models. We report that universal deletion of apoa1 or lcat expression in mice fed western-type diet results in increased sensitivity to body-weight gain compared to control C57BL/6 group. These changes in mouse genome correlate with discrete effects on white adipose tissue (WAT) metabolic activation and plasma glucose homeostasis. Apoa1-deficiency results in reduced WAT mitochondrial non-shivering thermogenesis. Lcat-deficiency causes a concerted reduction in both WAT oxidative phosphorylation and non-shivering thermogenesis, rendering lcat?/? mice the most sensitive to weight gain out of the three strains tested, followed by apoa1?/? mice. Nevertheless, only apoa1?/? mice show disturbed plasma glucose homeostasis due to dysfunctional glucose-stimulated insulin secretion in pancreatic β-islets and insulin resistant skeletal muscles. Our analyses show that both apoa1?/? and lcat?/? mice fed high-fat diet have no measurable Apoa1 levels in their plasma, suggesting no direct involvement of Apoa1 in the observed phenotypic differences among groups. 相似文献
7.
Xu J Kurup P Bartos JA Patriarchi T Hell JW Lombroso PJ 《The Journal of biological chemistry》2012,287(25):20942-20956
Proline-rich tyrosine kinase 2 (Pyk2) is a member of the focal adhesion kinase family and is highly expressed in brain and hematopoietic cells. Pyk2 plays diverse functions in cells, including the regulation of cell adhesion, migration, and cytoskeletal reorganization. In the brain, it is involved in the induction of long term potentiation through regulation of N-methyl-d-aspartate receptor trafficking. This occurs through the phosphorylation and activation of Src family tyrosine kinase members, such as Fyn, that phosphorylate GluN2B at Tyr(1472). Phosphorylation at this site leads to exocytosis of GluN1-GluN2B receptors to synaptic membranes. Pyk2 activity is modulated by phosphorylation at several critical tyrosine sites, including Tyr(402). In this study, we report that Pyk2 is a substrate of striatal-enriched protein-tyrosine phosphatase (STEP). STEP binds to and dephosphorylates Pyk2 at Tyr(402). STEP KO mice showed enhanced phosphorylation of Pyk2 at Tyr(402) and of the Pyk2 substrates paxillin and ASAP1. Functional studies indicated that STEP opposes Pyk2 activation after KCl depolarization of cortical slices and blocks Pyk2 translocation to postsynaptic densities, a key step required for Pyk2 activation and function. This is the first study to identify Pyk2 as a substrate for STEP. 相似文献
8.
Alexander K Nikodémová M Mária N Kucerová J Jana K Strbák V Vladimír S 《Cellular and molecular neurobiology》2005,25(3-4):681-695
1. Hypophysiotropic thyrotropin-releasing hormone (TRH) is synthesized in the hypothalamic paraventricular nucleus (PVN) and
transported to the median eminence (ME) where it enters the hypophyseal portal blood. TRH in the ME is situated exclusively
in nerve terminals, whereas TRH in the PVN and septum is of extrinsic (nerve terminals) as well as intrinsic (perikarya) origin.
2. To determine the source and possible differential regulation of TRH release from these structures, we blocked TRH axonal
delivery by i.c.v. administration of colchicine into the lateral cerebral ventricle of euthyroid or hypothyroid rats in doses
of 7.5 μg or 7.5, 75 and 100 μg, respectively, two days prior to the evaluation of the TRH secretion from the PVN, ME and
the septum in vitro.
3. In euthyroid rats a low dose of colchicine did not significantly affect plasma TSH. The secretory response to both ethanol
in an isosmolar medium and a high K+ in the ME as well as the PVN explants was well preserved. However, colchicine treatment resulted in the significant increase
of basal secretion of TRH from the PVN.
4. Hypothyroidism induced by 200 mg/l methimazole in drinking water for two weeks resulted in growth arrest, elevated plasma
thyrotropin and decreased TRH content in the PVN and the ME. Colchicine partially decreased elevated plasma thyrotropin and
increased the TRH content in the PVN and its basal release in vitro which was independent of extracellular Ca2+. Interestingly, a TRH release from the PVN could not be further stimulated either by K+ membrane depolarization or by ethanol. TRH responsiveness to the stimulation remained unaffected in the ME. The effect of
colchicine on the septal TRH secretion was intermediate between the effect observed in the PVN and the ME.
5. In conclusion, the absence of a TRH secretory response to stimuli in the PVN after colchicine disruption of the microtubules and Golgi
system suggests that stimulated TRH release observed from the PVN explants in vitro occurs from nerve terminals projecting to the PVN from other brain regions. The independence from extracellular calcium implies
that TRH released under the non-stimulating conditions occurs most likely via the constitutive secretory pathway from dendrites
and/or perikarya. Regulation of septal TRH is markedly different from the hypophysiotropic one.
An erratum to this article is available at . 相似文献
9.
Abstract Interactions between landscape position and the acidifying effect of trees planted into loess‐derived grassland soils were studied in the Ventana region of Argentina. Forests of Pinus radiata planted at the end of 1940, were selected in two different positions from the landscape, plains and slopes. Samples of the soil surface mineral horizon were taken from landscape positions at four distances from the trees and compared with grassland soils. The values of the main soil chemical properties changed significantly with distance from trees, with a decrease in pH, base saturation, exchangeable Ca2+, Mg2+ and K+, and increase in Na+, Al3+ and particularly H+ closer to the trees. This pattern confirms the prominent role of vegetation in bringing about changes in soil properties. Regression models showed high levels of explanation (r2 > 0.85) indicating that a high percentage of the spatial variability of soil chemical properties is systematic and predictable with distance from the trees. The pH in KCl proved an excellent tool for predicting the cationic composition of soils. Organic carbon and total nitrogen were significantly higher in the plains positions than in the slopes under the trees, whereas there was no difference under grassland. The slopes of the regression lines indicated that acidification is more intense in soils on the plains. Vegetation was the main factor influencing acidification of the studied soils. The landscape position regulates the bio‐hydrological factor and thus the speed of acidification process. 相似文献
10.