全文获取类型
收费全文 | 109篇 |
免费 | 14篇 |
国内免费 | 1篇 |
出版年
2023年 | 1篇 |
2020年 | 1篇 |
2019年 | 3篇 |
2018年 | 4篇 |
2016年 | 5篇 |
2015年 | 1篇 |
2013年 | 1篇 |
2012年 | 4篇 |
2011年 | 1篇 |
2010年 | 4篇 |
2009年 | 1篇 |
2008年 | 6篇 |
2007年 | 3篇 |
2006年 | 3篇 |
2005年 | 5篇 |
2004年 | 1篇 |
2003年 | 2篇 |
2002年 | 7篇 |
2001年 | 5篇 |
2000年 | 5篇 |
1999年 | 4篇 |
1998年 | 2篇 |
1997年 | 2篇 |
1996年 | 2篇 |
1995年 | 2篇 |
1994年 | 2篇 |
1990年 | 1篇 |
1989年 | 3篇 |
1986年 | 4篇 |
1985年 | 3篇 |
1984年 | 4篇 |
1983年 | 1篇 |
1982年 | 3篇 |
1981年 | 2篇 |
1980年 | 2篇 |
1979年 | 1篇 |
1978年 | 3篇 |
1977年 | 2篇 |
1976年 | 5篇 |
1975年 | 3篇 |
1973年 | 2篇 |
1972年 | 1篇 |
1970年 | 2篇 |
1969年 | 2篇 |
1960年 | 1篇 |
1959年 | 1篇 |
1954年 | 1篇 |
排序方式: 共有124条查询结果,搜索用时 937 毫秒
1.
A method is described to measure directly in rat brain the activity of pyruvate dehydrogenase kinase (PDHa kinase; EC 2.7.1.99), which catalyzes the inactivation of pyruvate dehydrogenase complex (PDHC, EC 1.2.4.1, EC 2.3.1.12, and EC 1.6.4.3). The activity showed the expected dependence on added ATP and divalent cation, and the expected inhibition by dichloroacetate, pyruvate, and thiamin pyrophosphate. These results, and the properties of pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43), indicate that the mechanisms of control of phosphorylation of PDHC seem qualitatively similar in brain to those in other tissues. Regionally, PDHa kinase is more active in cerebral cortex and hippocampus, and less active in hypothalamus, pons and medulla, and olfactory bulbs. Indeed, the PDHa kinase activity in olfactory bulbs is uniquely low, and is more sensitive to inhibition by pyruvate and dichloroacetate than that in the cerebral cortex. Thus, there are significant quantitative differences in the enzymatic apparatus for controlling PDHC activity in different parts of the brain. 相似文献
2.
3.
Gary Gibson Pamela Nielsen Victoria Mykytyn Ken Carlson John Blass 《Neurochemical research》1989,14(1):17-24
To further elucidate the molecular basis of the selective damage to various brain regions by thiamin deficiency, changes in enzymatic activities were compared to carbohydrate flux through various pathways from vulnerable (mammillary bodies and inferior colliculi) and nonvulnerable (cochlear nuclei) regions after 11 or 14 days of pyrithiamin-induced thiamin deficiency. After 11 days,large decreases (–43 to –59%) in transketolase (TK) occurred in all 3 regions; 2-ketoglutarate dehydrogenase (KGDHC) declined (–45%), but only in mammillary bodies; pyruvate dehydrogenase (PDHC) was unaffected. By day 14, TK remained reduced by 58%–66%; KGDHC was now reduced in all regions (–48 to –55%); PDHC was also reduced (–32%), but only in the mammillary bodies. Thus, the enzyme changes did not parallel the pathological vulnerability of these regions to thiamin deficiency.14CO2 production from14C-glucose labeled in various positions was utilized to assess metabolic flux. After 14 days, CO2 production in the vulnerable regions declined severely (–46 to 70%) and approximately twice as much as those in the cochlear nucleus. Also by day 14, the ratio of enzymatic activity to metabolic flux increased as much as 56% in the vulnerable regions, but decreased 18 to 30% in the cochlear nuclei. These differences reflect a greater decrease in flux than enzyme activities in the two vulnerable regions. Thus, selective cellular responses to thiamin deficiency can be demonstrated ex vivo, and these changes can be directly related to alterations in metabolic flux. Since they cannot be related to enzymatic alterations in the three regions, factors other than decreases in the activity of these TPP-dependent enzymes must underlie selective vulnerability in this model of thiamin deficiency.Abbreviations KGDHC
2-ketoglutarate dehydrogenase complex EC 1.2.4.2., EC 2.3.1.61, EC 1.6.4.3.
- PDHC
pyruvate dehydrogenase complex EC 1.2.4.2., EC 2.3.1.12, EC 1.6.4.3
- TK
transketolase (EC 2.2.1.1)
- TPP
thiamin pyrophosphate 相似文献
4.
Tapas K. Makar Dr. Arthur J. L. Cooper Beth Tofel-Grehl Howard T. Thaler John P. Blass 《Neurochemical research》1995,20(6):705-711
Glutathione and total carnitine (i.e., free carnitine plus acid-soluble carnitine esters) were measured in an affected (superior frontal gyrus; SFG) and unaffected (cerebellum: CBL) region of Alzheimer disease (AD) and control brains. Average glutathione content in AD SFG (n=13) and AD CBL (n=7) (7.9±2.1 and 11.9±4.0 nmol/mg protein, respectively (mean ±S.D.)) was similar to that in control SFG (n=13) and CBL (n=6) (7.7±2.0 and 11.6±2.6 nmol/mg protein, respectively). However, glutathione increased significantly with age in AD brain (p=0.003) but not in control brain. Average total carnitine in AD SFG (84±47 pmol/mg protein; n=10) and AD CBL (108±86 pmol/mg protein; n=7) was not significantly different from that in the corresponding regions of control brain (148±97 (n=10) and 144±107 (n=6) pmol/mg protein, respectively). However, a significant decline of total carnitine with age in both regions was noted for AD brain, but not for control brain. Carnitine acetyltransferase activity in the AD SFG (n=13) was not significantly different from that of control SFG (n=13) (1.83±1.05 and 2.04±0.82 nmol/min/mg protein, respectively). However, carnitine acetyltransferase activity of AD CBL (n=7) was significantly lower than that of control CBL (n=6) (1.33±0.88 versus 2.26±0.66 nmol/min/mg protein; p=0.05). 相似文献
5.
Correlation of enzymatic,metabolic, and behavioral deficits in thiamin deficiency and its reversal 总被引:5,自引:0,他引:5
Gary E. Gibson Hanna Ksiezak-Reding Kwan-Fu Rex Sheu Victoria Mykytyn John P. Blass 《Neurochemical research》1984,9(6):803-814
To clarify the enzymatic mechanisms of brain damage inthiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced14CO2 and14C-acetylcholine from [U-14C]glucose at rates similar to controls under resting conditions, their K+-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60–65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3.) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30–32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals.Thus, changes in the neurological signs during pyrithiamin-induced thiamin deficiency and in recovery paralleled the reversible damage to a mitochondrial enzyme and impairment of glucose oxidation and acetylcholine synthesis. A more sustained deficit in the pentose pathway enzyme, transketolase, may relate to the anatomical abnormalities that accompany thiamin deficiency.Dedicated to Henry McIlwain. 相似文献
6.
A spectrophotometric assay for the pyruvate dehydrogenase complex (PDHC) has been adapted for use with cultured human firbroblasts. It is a coupled enzyme assay utilizing pigeon liver arylamine acetyltransferase to measure the acetyl-CoA produced by PDHC. Activity is proportional to fibroblasts protein and to tine and depends completely on added pyruvate, CoA and NAD. In extracts in which PDHC had been activated (dephosphorylated) by the method of Sheu et al. (Sheu, R.K.-F., Hu, C.C. and Utter, M.F. (1981) J. Clin. Invest. 67, 1463–1471), activities in control cell lines are 5–50 fold higher than in earlier reports. Low activity has been demonstrated in a line previously eported to be PDHC-deficient. 相似文献
7.
P Szabo K F Sheu R M Robinson K H Grzeschik J P Blass 《American journal of human genetics》1990,46(5):874-878
The chromosomal location of the gene for the alpha polypeptide of the pyruvate dehydrogenase (alpha E1), a major component of the pyruvate dehydrogenase complex, was determined by using a cloned cDNA for alpha E1. This 1-kb cDNA was isolated from a human liver lambda gt11 expression library with specific antibodies and included the coding (from amino acid 144 to the carboxy terminus) and the 3' untranslated regions. Southern blot analysis of the DNA from a panel of rodent-human hybrid cells showed that the absence or the presence of the major EcoRI fragment that hybridized with this cDNA probe was concordant with the presence of the Xq24-p22 region of the human X chromosome. The result of in situ hybridization with human metaphase chromosomes further mapped the alpha E1 gene to the Xp arm. 相似文献
8.
K.G. Blass R.L. Briand D.S. Ng S. Harold 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》1980,182(3):311-316
A miniature two-dimensional thin-layer chromatographic procedure employing silica gel impregnated glass-microfiber chromatography sheets (commercial product, ITLC-type SG sheets) has been developed for the separation of lecithin (L) and sphingomyelin (S) from a standard lipid mixture containing L, S, lysolecithin, phosphatidyl inositol (PI), phosphatidyl serine (PS), phosphatidyl ethanolamine, phosphatidyl glycerol, and diphosphatidyl glycerol. The newly developed procedure eliminates possible interference from PI and PS. Complete separation of L and S was easily achieved with chromatographic solvent migration times of approximately 3 and 2 min for the first and second dimensions, respectively. The lipids were visualized by charring and fluorescent staining techniques. The procedure has been adapted for the separation of L and S from amniotic fluid samples. 相似文献
9.
THE REGULATION OF PYRUVATE DEHYDROGENASE IN BRAIN IN VIVO 总被引:9,自引:9,他引:0
—The activity of pyruvate dehydrogenase in the brains of mice frozen in liquid nitrogen was 14·0 nmol/min per mg protein. It rose to 23·8 nmol/min per mg protein after incubation of the brain homogenate with 10mm -MgCl2 to activate (dephosphorylate) the enzyme, indicating that approx 60% of the enzyme was originally in the active form. Treatment with amobarbital or pentobarbital halved the proportion of pyruvate dehydrogenase in the active form. The proportion of pyruvate dehydrogenase in the active form increased during ischemia, activation being complete within one min. Anesthesia with amobarbital slowed the activation during ischemia but did not alter the total amount of pyruvate dehydrogenase activity. The concentration of ATP, the ATP/ADP ratio and the adenylate energy charge increased as the proportion of pyruvate dehydrogenase in the active form decreased during barbiturate anesthesia, and they decreased as the proportion of pyruvate dehydrogenase in the active form increased during ischemia. After treatment with insulin, the proportion of pyruvate dehydrogenase in the active form increased by 30%. but the energy charge did not change. Treatment of mice with ether, morphine, ethanol, or diazepam did not change the proportion of pyruvate dehydrogenase in the active form although these treatments have been reported to alter pyruvate oxidation in brain in vivo. Treatments which altered pyruvate oxidation in the brain did not consistently alter the proportion of pyruvate dehydrogenase in the active form, unless they also altered energy charge. 相似文献
10.
Wang-Sattler R Blandin S Ning Y Blass C Dolo G Touré YT delle Torre A Lanzaro GC Steinmetz LM Kafatos FC Zheng L 《PloS one》2007,2(11):e1249