Integrative epigenetic profiling analysis identifies DNA methylation changes associated with chronic alcohol consumption
COMPUTERS IN BIOLOGY AND MEDICINE
Authors: Weng, Julia Tzu-Ya; Wu, Lawrence Shih-Hsin; Lee, Chau-Shoun; Hsu, Paul Wei-Che; Cheng, Andrew T. A.
Abstract
Alcoholism has always been a major public health concern in Taiwan, especially in the aboriginal communities. Emerging evidence supports the association between DNA methylation and alcoholism, though very few studies have examined the effect of chronic alcohol consumption on the epignome. Since 1986, we have been following up on the mental health conditions of four major aboriginal peoples of Taiwan. The 993 aboriginal people who underwent the phase 1 (1986) clinical interviews were followed up through phase 2 (1990-1992), and phase 3 (2003-2009). Selected individuals for the current study included 10 males from the phase 1 normal cohort who remained normal at phase 2 and became dependent on alcohol by phase 3 and 10 control subjects who have not had any drinking problems throughout the study. We profiled the DNA methylation changes in the blood samples collected at phases 2 and 3. Enrichment analyses have identified several biological processes related to immune system responses and aging in the control group. In contrast, differentially methylated genes in the case group were mostly associated with susceptibility to infections, as well as pathways related to muscular contraction and neural degeneration. The methylation levels of six genes were found to correlate with alcohol consumption. These include genes involved in neurogenesis (NPDC1) and inflammation (HERC5), as well as alcoholism-associated genes ADCY9, CKM, and PHOX2A. Given the limited sample size, our approach uncovered genes and disease pathways associated with chronic alcohol consumption at the epigenetic level. The results offer a preliminary methylome map that enhances our understanding of alcohol-induced damages and offers new targets for alcohol injury research. (C) 2014 Elsevier Ltd. All rights reserved.
Quasi-two-body decays B-(s) -> PD0* (2400) -> PD pi in the perturbative QCD approach
PHYSICAL REVIEW D
Authors: Cui, Bo-Yan; Fan, Ying-Ying; Liu, Fu-Hu; Wang, Wen-Fei
Abstract
We study the quasi-two-body decays B -> PD0* (2400) -> PD pi with P = (pi, K, eta, eta') in the perturbative QCD factorization approach. The predicted branching fractions for the considered decays are in the range of 10(-9)-10(-4). The strong Cabibbo-Kobayashi-Maskawa (CKM) suppression factor R-CKM approximate to lambda(4) ((rho) over bar (2) + (eta) over bar (2)) approximate to 3 x 10(-4) results in the great difference of the branching ratios for the decays with D-0* and (D) over bar (0)* as the intermediate states. The ratio R-(D) over bar0*0 between the decays B-0 -> (D) over bar (0)*K-0(0) -> D- pi(+) K-0 and B-0 -> (D) over bar (0)*(0) pi(0) -> D- pi(+) pi(0) is about 0.091(-0.005)(+0.003), consistent with the flavor-SU(3) symmetry result. The ratio for the branching fractions is found to be 1.10(-0.02)(+0.05) between B(B-s(0) -> D-0*(+) K- -> D-0 pi(+) K-) and B(B-0 -> D-0*(+) pi(-) -> D-0 pi(+) pi(-)) and to be 1.03(-0.07)(+0.06) between B(B-s(0) -> (D) over bar (0)*(0) (K) over bar (0) -> D- pi(+) (K) over bar (0)) and 2B(B-0 -> (D) over bar (0)*(0)pi(0) -> D- pi(+) pi(0)). The predictions in this work can be tested by the future experiments.