全文获取类型
收费全文 | 535篇 |
免费 | 17篇 |
出版年
2020年 | 3篇 |
2018年 | 6篇 |
2017年 | 3篇 |
2015年 | 9篇 |
2014年 | 13篇 |
2013年 | 7篇 |
2012年 | 19篇 |
2011年 | 17篇 |
2010年 | 10篇 |
2009年 | 11篇 |
2008年 | 17篇 |
2007年 | 16篇 |
2006年 | 15篇 |
2005年 | 10篇 |
2004年 | 15篇 |
2003年 | 15篇 |
2002年 | 12篇 |
2001年 | 6篇 |
2000年 | 15篇 |
1999年 | 7篇 |
1997年 | 4篇 |
1995年 | 3篇 |
1992年 | 14篇 |
1991年 | 14篇 |
1990年 | 19篇 |
1989年 | 13篇 |
1988年 | 8篇 |
1987年 | 11篇 |
1986年 | 19篇 |
1985年 | 13篇 |
1984年 | 15篇 |
1983年 | 13篇 |
1981年 | 6篇 |
1980年 | 8篇 |
1979年 | 16篇 |
1978年 | 11篇 |
1977年 | 5篇 |
1976年 | 9篇 |
1975年 | 8篇 |
1974年 | 14篇 |
1973年 | 12篇 |
1972年 | 16篇 |
1971年 | 9篇 |
1970年 | 7篇 |
1969年 | 15篇 |
1968年 | 8篇 |
1967年 | 7篇 |
1966年 | 5篇 |
1965年 | 7篇 |
1964年 | 2篇 |
排序方式: 共有552条查询结果,搜索用时 15 毫秒
1.
Eric S. Goetzman John F. Alcorn Sivakama S. Bharathi Radha Uppala Kevin J. McHugh Beata Kosmider Rimei Chen Yi Y. Zuo Megan E. Beck Richard W. McKinney Helen Skilling Kristen R. Suhrie Anuradha Karunanidhi Renita Yeasted Chikara Otsubo Bryon Ellis Yulia Y. Tyurina Valerian E. Kagan Rama K. Mallampalli Jerry Vockley 《The Journal of biological chemistry》2014,289(15):10668-10679
Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial fatty acid oxidation enzyme whose expression in humans is low or absent in organs known to utilize fatty acids for energy such as heart, muscle, and liver. This study demonstrates localization of LCAD to human alveolar type II pneumocytes, which synthesize and secrete pulmonary surfactant. The physiological role of LCAD and the fatty acid oxidation pathway in lung was subsequently studied using LCAD knock-out mice. Lung fatty acid oxidation was reduced in LCAD−/− mice. LCAD−/− mice demonstrated reduced pulmonary compliance, but histological examination of lung tissue revealed no obvious signs of inflammation or pathology. The changes in lung mechanics were found to be due to pulmonary surfactant dysfunction. Large aggregate surfactant isolated from LCAD−/− mouse lavage fluid had significantly reduced phospholipid content as well as alterations in the acyl chain composition of phosphatidylcholine and phosphatidylglycerol. LCAD−/− surfactant demonstrated functional abnormalities when subjected to dynamic compression-expansion cycling on a constrained drop surfactometer. Serum albumin, which has been shown to degrade and inactivate pulmonary surfactant, was significantly increased in LCAD−/− lavage fluid, suggesting increased epithelial permeability. Finally, we identified two cases of sudden unexplained infant death where no lung LCAD antigen was detectable. Both infants were homozygous for an amino acid changing polymorphism (K333Q). These findings for the first time identify the fatty acid oxidation pathway and LCAD in particular as factors contributing to the pathophysiology of pulmonary disease. 相似文献
2.
G M Ka?nova D Markovska D Staneva V E Kagan 《Biulleten' eksperimental'no? biologii i meditsiny》1990,109(1):35-37
Looking for an appropriate model of accelerated aging in vivo we investigated the content of endogenous products of lipid peroxidation (LP) in the rat brain after single or 4 day-lasting intramuscular injection of complex-bind iron (ferum Hausman, 50 mg/kg body weight) like promoter of LP. We found that the single administration of this iron complex fails to induce endogenous LP; after 4 day-application of iron we observed significant increase in content of primary (lipid peroxides) and final (fluorescent) products of LP. Iron-promoted activation of endogenous LP could be abolished by animal pretreatment with the natural antioxidant alpha-tocopherol. The calcium antagonist nifedipine didn't affect the content of endogenous LP products neither alone nor in combination with alpha-tocopherol. 相似文献
3.
4.
V A Tiurin V E Kagan E A Serbinova N V Gorbunov A N Erin 《Biulleten' eksperimental'no? biologii i meditsiny》1986,102(12):689-692
The interaction of alpha-tocopherol with liposomes obtained from saturated and unsaturated phospholipids and the rate of its flip-flop were studied using fluorescent technique. It was found that the amount of alpha-tocopherol introduced into outer and inner monolayers remained unchanged for many hours. No migration from the outer to the inner monolayers and vice versa was observed. The effect did not depend on the fatty acid phospholipid composition. The results obtained are considered in view of the optimal conditions of membrane tissue saturation with liposome-incorporated tocopherol. 相似文献
5.
V M Savov M A Babizhaev V E Kagan 《Biulleten' eksperimental'no? biologii i meditsiny》1986,101(6):693-695
Mechanisms underlying Ca2+ effects on lipid peroxidation (LPO) induced in liposomes (from egg yolk lecithin) and UFsomes (from linolenic acid, methyl linolenate) with the aid of O2- -system (Fe2+ + ascorbate) were studied. It was shown that stimulation of lipid peroxidation by low Ca2+ concentrations (10(-6)-10(-5) M) was due to its ability to release Fe2+-ions bound to negatively charged (phosphate, carboxylic) lipid groups (of licethin, linolenic acid), thus increasing the concentration of catalytically active Fe2+. The inhibitory effect of high Ca2+ concentrations was caused by its interaction with superoxide anion-radicals and was not observed in LPO-systems, independent of O2- generation (e. g. Fe2+ + cumol hydroperoxide). 相似文献
6.
E A Serbinova R A Bakalova Ts S Sto?chev V E Kagan 《Biulleten' eksperimental'no? biologii i meditsiny》1986,102(10):419-421
The efficacy of lipid peroxidation inhibition by the natural antioxidant alpha-tocopherol and 2,2,5,7,8-pentamethyl-6-hydroxy-chromane (PMC), a derivative without hydrocarbon tail, as well as by the synthetic antioxidant 4-methyl-2,6-diterbutyl phenol (BHT) and its phospholipid derivative was studied in the membranes of rat liver microsomes and mitochondria. The presence of hydrocarbon tail in the antioxidant molecule determines the decrease of antioxidant efficiency in biomembranes. PMC and BHT exert a destructive effect on biomembranes, leading to an increase in their permeability to ions. This evidence suggests that the presence of hydrocarbon tail in the molecules of natural antioxidants provides not only for a relatively high antioxidant efficiency but also for a structural stability of biomembranes. 相似文献
7.
Mechanism of stabilization of synaptosomes with alpha-tocopherol during exposure to phospholipase A2
A N Erin V I Skrypin L L Prilipko V E Kagan 《Biulleten' eksperimental'no? biologii i meditsiny》1986,102(7):25-28
Changes in potential-dependent fluorescence were studied, using fluorescent probe di-S-C3-(5), in synaptosome suspensions exposed to phospholipase A2, alpha-tocopherol and its derivatives. Phospholipase A2 increased potential-dependent fluorescence, i.e. depolarization of synaptosome membranes. The damaging phospholipase A2 effect was prevented and/or abolished by alpha-tocopherol added to synaptosome suspensions before and after phospholipase A2. Alpha-tocopherol derivatives (2,2,5,7,8-pentamethyl-6-hydroxychromane and alpha-tocopheryl-acetate as well as 4-methyl-2,6-di-tert-butylphenol) failed to exert a protective effect on synaptosome membranes modified by phospholipase A2. It is suggested that alpha-tocopherol effect is determined by its interaction with fatty acids, with 6-hydroxy groups of chromanol nucleus and phytol chain being essential for the complex formation. 相似文献
8.
N B Polianski? L D Smirnov A A Shvedova V E Kagan 《Nauchnye doklady vysshe? shkoly. Biologicheskie nauki》1984,(1):27-31
The influence of 8 analogues of 3-hydroxypyridine upon the phosphodiesterase of rod outer segments of frog retinae has been investigated. It has been shown that the analogues of 3-hydroxypyridine inhibit the enzeme reversely and noncompetitively in case of hydrolysis towards the cAMP and cGMP. The natural analogues of 3-hydroxypyridine (pyridoxol, pyridoxale, pyridoxale-phosphate) do not exert the inhibiting effect. It is suggested that the inhibition of phosphodiesterase from rod outer segments of retinae is caused by the interaction of 3-hydroxypyridines with the hydrophobic microenvironment of the active site of the enzyme. 相似文献
9.
V E Kagan E A Serbinova A A Minin V M Savov K N Novikov 《Biokhimii?a (Moscow, Russia)》1985,50(6):986-991
The localization and mechanism of generation of active oxygen species in the enzymatic NADPH-dependent lipid peroxidation system in liver microsomes were studied. Using the spin-trapping method, the key role of active oxygen species in the initiation of NADPH-dependent enzymatic lipid peroxidation was confirmed. It was shown that active oxygen species are generated via consecutive one-electron reduction of the oxygen molecule by NADPH-cytochrome P-450 reductase. 相似文献
10.
V E Kagan R A Kopaladze L L Prilipko V M Savov 《Biulleten' eksperimental'no? biologii i meditsiny》1983,96(12):16-18
Hyperoxia brought about substantial accumulation of primary and end products of lipid peroxidation (LPO) and a significant lowering of alpha-tocopherol content in rat brain tissues. Preinjection of animals with synthetic and natural antioxidants (4-methyl-2,6-ditretbutylphenol and alpha-tocopherol) prevented LPO activation and decreased the frequency of epileptiform seizures induced by hyperoxia. Administration of a mixture of unsaturated fatty acids led to an opposite effect. The changes in the properties of serotonin receptors were found to be dependent on the hyperoxia-induced LPO. These changes were marked by the reduced specific binding of serotonin with neuronal membranes of the rat brain cortex. The data obtained allowed the conclusion about the key role played by LPO activation in toxic action of hyperbaric activation on the brain. 相似文献