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Ru Band Lu

Researcher at National Cheng Kung University

Publications -  312
Citations -  11210

Ru Band Lu is an academic researcher from National Cheng Kung University. The author has contributed to research in topics: Bipolar disorder & Bipolar II disorder. The author has an hindex of 51, co-authored 310 publications receiving 10185 citations. Previous affiliations of Ru Band Lu include National Health Research Institutes & Sun Yat-sen University.

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Journal Article

Alcohol and aldehyde dehydrogenase genotypes and alcoholism in Chinese men.

TL;DR: The genotypes of the ADH2, ADH3, and ALDH2 loci of alcoholic and nonalcoholic Chinese men living in Taiwan are determined using leukocyte DNA amplified by the PCR and allele-specific oligonucleotides, suggesting that genetic variation in both ADH and AL DH, by modulating the rate of metabolism of ethanol and acetaldehyde, influences drinking behavior and the risk of developing alcoholism.
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Interaction between the Functional Polymorphisms of the Alcohol-Metabolism Genes in Protection against Alcoholism

TL;DR: It is suggested that protection afforded by the ADH2*2 allele may be independent of that afforded by ALDH2* 2, and that individuals carrying one or two copies of ADH 2 and a single copy of ALDH 2*2 had the lowest risk for alcoholism, as compared with the ADh2*1/*1 and ALDH1*1 genotype.
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Histone deacetylase inhibitors up-regulate astrocyte GDNF and BDNF gene transcription and protect dopaminergic neurons

TL;DR: It is shown that two additional HDAC inhibitors, sodium butyrate (SB) and trichostatin A (TSA), mimic the survival-promoting and protective effects of VPA on DA neurons in neuron-glia cultures and indicate that HDAC inhibitor up-regulate GDNF and BDNF expression in astrocytes and protect DA neurons, at least in part, through HDAC inhibition.
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A global perspective on genetic variation at the ADH genes reveals unusual patterns of linkage disequilibrium and diversity.

TL;DR: An initial study of the nature of linkage disequilibrium and genetic variation, in population samples from different regions of the world, in a larger segment of the ADH cluster (including the three Class I ADH genes and ADH7), indicates that most ADH-alcoholism association studies have failed to consider many sites in theADH cluster that may harbor etiologically significant alleles and that the relevance of the various ADH sites will be population dependent.