Disease relevance of Etohd1

• Exposure to 20% ethanol decreased fetal weight by 9-13% in the three groups [1].
• Ethanol decreased maternal weight gain and pup body and brain weight; it also retarded both sensory and motor development in the pups and impeded reversal learning in a water maze [2].
• Ethanol decreased birth weight (both studies), postweaning body weight (study 2), and brain weight (study 1), while the enriched animals in both studies were heavier [3].
• 5. Chronic administration with ethanol decreased the toxicity due to methaqualone [4].

High impact information on Etohd1

• Additionally, ethanol decreased several osteoblastic parameters including osteoblast perimeter and osteoblast culture calcium retention in both il6(+/+) and il6(-/-) mice [5].
• Ethanol decreased the affinity of the high affinity form of the receptor for isoproterenol but had no effect on the affinity of the low affinity form of the receptor, the proportion of high and low affinity forms of the receptor, the total number of agonist-binding sites, or antagonist binding [6].
• These results indicate that chronic ingestion of ethanol decreased the fluidity and the ethanol sensitivity of the synaptic membranes [7].
• In a previous study in ob/ob mice, breath ethanol decreased with a course of non-absorbable antibiotics, suggesting that the ethanol is derived from intestinal bacterial flora [8].
• 3. Concentration-response analysis of NMDA- and glycine-activated current revealed that ethanol decreased the maximal response to both agonists without affecting their EC50 values [9].

Anatomical context of Etohd1

• Furthermore, it was found that ethanol decreased the number of Fos-li neurons in the ventral tegmental area of the SLOW but not FAST mice [10].
• Self-administration of ethanol decreased bromodeoxyuridine immunoreactivity by approximately 60% (P <.01) in dentate gyrus; 70% (P <.001), in forebrain; and 80% (P <.001), in corpus callosum [11].

Associations of Etohd1 with chemical compounds

• In vitro addition of pentobarbital or ethanol decreased the fluorescence polarization of DPH in SPM [12].
• When compared to saline-treated controls, PKC activity was increased significantly (P < 0.0005) in procaine- and tetracaine-treated groups whereas ethanol decreased PKC activity [13].
• Ethanol decreased glutathione (GSH) levels and the S-adenosylmethionine (SAMe) to S-adenosylhomocysteine (SAH) ratio by 53% and 22%, respectively [14].

Other interactions of Etohd1

• Activation of striatal adenylate cyclase by guanyl-5'-yl-imidodiphosphate occurred after a characteristic lag and inclusion of ethanol decreased the T1/2 of activation by guanyl-5'-yl-imidodiphosphate from 16.9 to 11.2 min [15].
• In mice 4-12 weeks ingestion of ethanol decreased the concentration of a metallothionein-like protein fraction in the liver but not in the kidneys [16].

References