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Reports on gene reporter assays using PC12 pheochromocytoma cells transiently transfected with luciferase reporter plasmids to investigate the effect of this variant on the transcriptional activity of the hNR2B gene. Involvement of N-methyl-D-aspartate (NMDA) receptor dysfunction in the pathogenesis of schizophrenia; Nucleotide sequence of the 5'- upstream region of the human NMDA receptor 2B subunit gene.

The relationships between the individual (and racial) differences in alcohol metabolism and toxicity, and the genetic polymorphism of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P-4502E1(CYPIIE1) were reviewed. In recent studies involving DNA analysis, it was found that a deficiency of the ALDH2 isozyme (ALDH2*2) was responsible for the flushing symptoms as well as other vasomotor symptoms caused by a higher acetaldehyde level after alcohol consumption. Deficiency of ALDH2 activity has been found prevalently only among people of Mongoloid origin, and the deficiency of ALDH2 prevents them from developing alcohol dependence due to the unpleasant physical effects of the flushing symptom. It was reported that Mongoloids such as Japanese and Chinese people carry the enzymatically active (ALDH2*1) subunit and/or the inactive (ALDH2*2) one, and that a low proportion of ALDH2 deficiency (ALDH2*2 allele frequency) was found in alcoholics compared with healthy controls. It was also reported that polymorphism of ALDH2 and/or CYP2E1 may be associated with the susceptibility to alcohol-induced liver injury. Concerning blood ethanol elimination kinetics, it was reported that the c2 gene of CYP2E1 and the ALDH2*1 gene may have greater effects on ethanol and acetaldehyde elimination than the other genotypes, when the blood ethanol level is below 20 m M. [ABSTRACT FROM AUTHOR]

Examines the prevalence of Borna disease virus (BDV) infections among schizophrenic patients in Japan. Relationships of negative syndromes with schizophrenia and BDV; Proportion of patients with anti-BDV antibody; Correlation between BDV infection and dominant contribution by negative syndromes.