|1.||Maegele, Marc: 3 articles (01/2007 - 05/2005)|
|2.||Lippert-Gruener, Marcela: 3 articles (01/2007 - 05/2005)|
|3.||Angelov, Doychin N: 3 articles (01/2007 - 05/2005)|
|4.||Garbe, Janika: 2 articles (01/2007 - 05/2005)|
|5.||Ester-Bode, Thorsten: 2 articles (07/2005 - 05/2005)|
|6.||Neiss, Wolfram F: 2 articles (07/2005 - 05/2005)|
|7.||Bouillon, Bertil: 2 articles (07/2005 - 05/2005)|
|8.||Lefering, Rolf: 2 articles (07/2005 - 05/2005)|
|9.||Diblik, Pavel: 1 article (02/2015)|
|10.||Fenclova, Zdenka: 1 article (02/2015)|
|1.||Brain Injuries (Brain Injury)
07/01/2005 - "This study was designed to investigate the additional benefits of a multimodal early onset stimulation (MEOS) paradigm when combined with enriched environment (EE) versus EE only and standard housing (SH) on the recovery after experimental traumatic brain injury (TBI). "
05/01/2005 - "This study was designed to determine whether exposure to multimodal early onset stimulation (MEOS) combined with environmental enrichment (EE) after traumatic brain injury (TBI) would improve neurological recovery and to elucidate its morphological correlates. "
01/01/2007 - "Recently we showed that the combination between MEOS and EE applied to rats for 7-15 days after traumatic brain injury (TBI) was associated with reduced CNS lesion volume and enhanced reversal of neuromotor dysfunction. "
01/01/2007 - "Late effects of enriched environment (EE) plus multimodal early onset stimulation (MEOS) after traumatic brain injury in rats: Ongoing improvement of neuromotor function despite sustained volume of the CNS lesion."
06/01/2000 - "Multimodal early onset stimulation (MEOS) in rehabilitation after brain injury."
|2.||Alcoholism (Alcohol Abuse)
09/01/1997 - "Patients with alcoholism showed an increased REE over predicted values and a preferential lipid oxidation with respect to controls; these findings could be related to induction of microsomal ethanol oxidizing system and to mitochondrial function adaptation secondary to chronic alcohol abuse. "
01/01/1993 - "Acute ethanol intake inhibits MEOS, as MEOS gives preference to ethanol as a substrate, however, chronic alcoholism induces MEOS.(ABSTRACT TRUNCATED AT 250 WORDS)"
11/01/1994 - "Cytochrome P450 2E1 (CYP 2E1), the principal component of MEOS, is ethanol inducible and has been implicated in hepatotoxicity associated with alcohol abuse and exposure to organic solvents. "
09/01/1987 - "It was shown that the rate of ethanol elimination from the rats' blood at all stages of experimental alcoholism was determined by alcohol dehydrogenase, while catalase and microsomal ethanol-oxidizing system activities did not play an important role."
09/01/1987 - "Using head space chromatography, the pharmacological analysis of changes in the activity of ethanol-oxidizing enzymatic systems: alcohol dehydrogenase, catalase, microsomal ethanol-oxidizing system under the effect of pyrazole and aminotriazole, has been performed on the model of experimental alcoholism in rats. "
|3.||Alcoholic Liver Diseases (Alcoholic Liver Disease)
07/01/2005 - "The role of the hepatic microsomal ethanol oxidizing system in the metabolism of alcohol in alcoholic liver disease was summarized by R. "
05/01/2008 - "Besides, ethanol metabolic pathways themselves (through the ADH and the MEOS system) generate toxic intermediate products (acetaldehyde, free radicals) interfering with normal metabolism of essential elements, mainly lipids, leading to cellular damage through lipid peroxidation mechanisms and impairment of the membrane fluidity, fat deposits (hepatocellular steatosis), inflammation secondary to oxidative stress and proinflammatory cytokines, activation of stellate cells, fibrogenesis, etc. Nutritional supports may be effective to improve alcoholic liver disease. "
01/01/1995 - "Antioxidants and supernutrients are special "modern" aspects of nutritional therapy in alcoholic liver disease generally related to the MEOS activation in chronic alcoholism, the excessive production of free radicals, and the depletion of glutathione, membrane phospholipids (specially phosphatidycholine), and vitamin A, E, and C. "
05/01/1992 - "We studied the effects of dietary fat composition on the activities of the microsomal ethanol oxidizing system (MEOS), paranitrophenol hydroxylase (PH) activity and ethanol-inducible cytochrome P450 isozymes (CYP2E1 and CYP2B1) in the liver of rats to determine the role of this ethanol metabolizing pathway in the pathogenesis of alcoholic liver disease (ALD). "
|4.||Body Weight (Weight, Body)
10/01/1983 - "By contrast, it was found that the activity of the microsomal ethanol-oxidizing system increased significantly after chronic alcohol consumption (by 22% expressed per gram of liver and by 54% expressed per kilogram of body weight). "
01/01/1981 - "Moreover, a hyperthyroid hepatic state achieved following the daily administration of L-thyroxine (150 micrograms/100 g of body weight) or L-3,3', 5-triiodothyronine (10 micrograms/100 g body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol-oxidizing system. "
06/01/1983 - "Concomitantly, the activities of the hepatic microsomal ethanol oxidizing system (MEOS) were strikingly augmented by 213% (P less than 0.05) and 177% (P less than 0.01) when expressed per g of liver wet weight or per 100 g of body weight, respectively, whereas hepatic alcohol dehydrogenase activities remained virtually unchanged. "
|5.||Weight Loss (Weight Reduction)
12/01/1991 - "It was also determined that ethanol can be oxidized by a microsomal ethanol oxidizing system (MEOS) involving cytochrome P-450: the newly discovered ethanol-inducible cytochrome P-450 (P-450IIE1) contributes to ethanol metabolism, tolerance, energy wastage (with associated weight loss), and the selective hepatic perivenular toxicity of various xenobiotics. "
01/01/1991 - "It was also determined that ethanol can be oxidized by a microsomal ethanol oxidizing system (MEOS) involving a specific cytochrome P-450; this newly discovered ethanol-inducible cytochrome P-450 (P-450 IIEi) contributes to ethanol metabolism, tolerance, energy wastage (with associated weight loss), and the selective hepatic perivenular toxicity of various xenobiotics. "
|1.||Ethanol (Ethyl Alcohol)
|2.||microsomal ethanol-oxidizing system (MEOS)
|3.||Alcohol Dehydrogenase (Alcohol Dehydrogenase (NAD+))
|4.||Cytochrome P-450 CYP2E1 (CYP2E1)
|5.||Cytochrome P-450 Enzyme System (Cytochrome P450)
|10.||Hypoxia-Inducible Factor 1