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        Music Enhances Drunkenness: A Phenomenon Related to Increased Dopaminergic Function

        Kayo Akiyama,Den'etsu Sutoo 대한정신약물학회 2010 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.8 No.3

        Objective: Since ancient times, music has been enjoyed in combination with alcohol or to aid the sick. Why do people desire music for pleasure and cure? The effect of music was investigated by examining how music influences the effects of ethanol on brain function. Methods: Male ddY mice were placed in a closed cage equipped with a speaker, and music (Mozart, Adagio from Divertimento,K. 205; average sound level=65 dB) was played repeatedly for 0.5 to 6 h. Immediately after music exposure, ethanol-induced sleep time was analyzed. Results: Ethanol-induced sleep time was prolonged by exposure to music, and the effect was abolished upon inhibition of calcium/calmodulin-dependent dopamine synthesis in the brain. Conclusion: The present study indicates that music leads to an increase in synthesis of the neurotransmitter dopamine in the brain, and the subsequent increase in dopamine enhances the effects of alcohol. Music might regulate and/or affect various brain functions through dopaminergic neurotransmission. Thus, music might attenuate symptoms of various diseases that involve dopamine dysfunction, such as Parkinson's disease, senile dementia, epilepsy, and attention-deficit/hyperactivity disorder.

      • Association between Polymorphisms in UDP-glucuronosyltransferase 1A6 and 1A7 and Colorectal Cancer Risk

        Osawa, Kayo,Nakarai, Chiaki,Akiyama, Minami,Hashimoto, Ryuta,Tsutou, Akimitsu,Takahashi, Juro,Takaoka, Yuko,Kawamura, Shiro,Shimada, Etsuji,Tanaka, Kenichi,Kozuka, Masaya,Yamamoto, Masahiro,Kido, Yosh Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5

        Genetic polymorphisms of uridine diphosphate-glucuronosyltransferases 1A6 (UGT1A6) and 1A7 (UGT1A7) may lead to genetic instability and colorectal cancer carcinogenesis. Our objective was to measure the interaction between polymorphisms of these repair genes and tobacco smoking in colorectal cancer (CRC). A total of 68 individuals with CRC and 112 non-cancer controls were divided into non-smoker and smoker groups according to pack-years of smoking. Genetic polymorphisms of UGT1A6 and UGT1A7 were examined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). We found a weak association of UGT1A6 polymorphisms with CRC risk (crude odds ratio [OR], 1.65;95% confidence interval [95% CI], 0.9-3.1, P=0.107; adjusted OR 1.95%, 95% CI 1.0-3.8, P=0.051). The ORs for the UGT1A7 polymorphisms were statistically significant (crude OR: 26.40, 95% CI: 3.5-198.4, P=0.001; adjusted OR: 21.52, 95% CI: 2.8-164.1, P=0.003). The joint effect of tobacco exposure and UGTIA6 polymorphisms was significantly associated with colorectal cancer risk in non-smokers (crude OR, 2.11; 95% CI, 0.9-5.0, P=0.092; adjusted OR 2.63, 95% CI, 1.0-6.7, P=0.042). In conclusion, our findings suggest that UGT1A6 and UGT1A7 gene polymorphisms are associated with CRC risk in the Japanese population. In particualr, UGT1A6 polymorphisms may strongly increase CRC risk through the formation of carcinogens not associated with smoking.

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