Peripheral blood gene-expression in heavy vs. moderate drinkers exposed to three types of personalized imagery
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59206 | GEO | 2014/07/09
SECONDARY ACCESSION(S): PRJNA254726
REPOSITORIES: GEO
Similar Datasets
Project description:Alterations in stress-related gene-expression may play a role in stress-related drinking and the risk for alcohol dependence. Microarrays were used to measure changes in gene-expression in peripheral blood in non-smoking, social drinking subjects exposed to three types of personalized imagery: neutral, stressful (but not alcohol- related), and alcohol-related cues. Gene-expression was measured at baseline, immediately after, and 1 hour after stimulus presentation. Subjects were allowed to drink up to 750cc of beer in a “taste-test” following stimulus presentation in each imagery condition, and the amount of beer consumed was recorded. Gene-expression levels were compared in 2 groups of non-smoking subjects (n=11/group): heavy drinkers (HD, defined as regular alcohol use over the past year of at least 8 standard drinks/week for women and at least 15 standard drinks/week for men), and moderate drinkers (MD, defined as up to 7 standard drinks/week for women and 14 standard drinks/week for men). 198 samples total. Total RNA isolated from PAXgene blood RNA tubes from heavy drinkers (n=11) and moderate drinkers (n=11) exposed to 3 different types of personalized imagery (stress, neutral, or alcohol-cue) at three time-points per condition (baseline, immediately after cue presentation,and 1 hour after cue presentation)(9 samples per subject).
2014-07-09 | E-GEOD-59206 | biostudies-arrayexpress
Project description:Background: The most important risk factors for head and neck squamous carcinoma (HNSCC) are tobacco smoking and alcohol consumption, while subgroups are caused by infection with human papillomaviruses (HPV) or Epstein-Barr virus (EBV). Here, we studied alterations of somatic copy-number in whole genome, p16 protein and TP53 mutations by alcohol drinking, smoking and viral infections. Methods: We conducted a prospective cohort study. DNA obtained from tumors and margin samples as well as peripheral blood was assayed by array comparative genomic hybridization using Agilent Whole Human Genome 180K. Mutations of p53 gene by direct sequencing, detection of HPV by polymerase-chain-reaction (PCR), quantification of EBV by reverse transcription-PCR and p16 immunohistochemical (IHC) staining were also performed. prospective cohort study: 225 tumor samples were analyzed by Agilent-022060 SurePrint G3 Human CGH miroarray 4x180K. Log2 Ratio (tumor sample DNA/normal DNA) were compared among none alcohol drinkers, moderate alcohol drinkers, heavy alcohol drinkers, none smokers, moderate smokers, heavy smokers and both. Sample characteristics weres scored as following; Human Papilloma Virus Infection (gene detected by PCR in tumor sample): positive=1; negative=0 p16 protein immunohistochemistry: positive=1; negative=0 tumor grade: matured=0; moderate=1; immature=2 Radiotherapy with or without chemotherapy after operation: performed =1; not performed =0 Recurrence/relapse: rec =1; not rec =0 suvival status:death=1; survive=0 smoking status (Pack year of smoking): none smoker=0; pack-year <20 = 1 (moderate smoker); pack-year <=20 = 2 (heavy smoker) alcohol drinking: Alcohol drinkers were divided into non-drinker or less than one drink per day =0: one and more but less than two drinks per day = moderate drinker 1: two and more drinks per day=heavy drinker 2: during the 20 years preceding their treatment for HNSCC. One drink was defined as containing approximately 10g of alcohol, which is considered equal to 30 ml of hard liquor, 100 ml of wine containing 12% alcohol, or 360 ml of beer.
2013-07-01 | E-GEOD-47443 | biostudies-arrayexpress
Project description:<p>The Australian twin-family study of alcohol use disorder (OZALC study) derives from telephone diagnostic interview studies of two general population volunteer cohorts of Australian twins (cohort 1, mostly born 1940-1964; cohort 2, born 1964-71) and the spouses of the former cohort - a total of over 11,000 families. Three coordinated studies, using a shared assessment protocol and with a shared goal of gene-discovery, were conducted - one funded by the National Institute on Drug Abuse, the others by the National Institute on Alcoholism and Alcohol Abuse - by investigators associated with the Midwest Alcoholism Research Center at Washington University in St. Louis, and investigators at Queensland Institute of Medical Research, Brisbane, Australia (led by Professor Nicholas Martin), using informative families identified from these cohorts. The first of these (NIDA Nicotine Addiction Genetics [NAG] project, PI Pamela Madden) identified index cases from the 3 cohorts with a history of heavy smoking (smoked 20 or more cigarettes daily, or 40 or more cigarettes on 1 or more occasions) and with additional available full siblings who were smokers, and interviewed and obtained blood samples from twins, and cooperative full siblings and parents, in order to identify families that would be informative for linkage analysis of a quantitative heaviness of smoking trait. The second identified additional families with an index case who either reported a history of alcohol dependence (DSM-IV), or scored above the 85th percentile on a quantitative measure of heaviness of alcohol use (alcohol factor score), derived from measures of frequency of heavy drinking, frequency of drinking to intoxication, and typical weekly consumption in standard drinks (all referenced to the respondent's heaviest drinking period) and of lifetime maximum 1-day alcohol consumption and maximum tolerance to alcohol (drinks before getting drunk or before feeling effects of alcohol). Interview and DNA were obtained from index cases and siblings, and DNA only from available parents. The goal of this second study (NIAAA OZ-ALCOHOL EDAC study, PI Andrew Heath) was to identify sibships including pairs who were either extreme concordant for the quantitative consumption measure (both scoring above the 85th percentile) or extreme discordant (one scoring above the 85th percentile and one scoring below the 30th percentile) that would be informative for linkage analysis. The third identified additional sibships solely on the basis of large sibship size, regardless of alcohol or tobacco use phenotypes (NIAAA OZ-BIGSIB study, PIs the late Richard Todd, Andrew Heath). From these coordinated studies a case-control series of alcohol dependent individuals and unaffected controls were constructed for a family-based Genomewide Association Study (OZALC-GWAS) of heaviness of alcohol use and alcohol dependence, funded by the National Institute of Alcoholism and Alcohol Abuse. These data are made available here for all investigators studying outcomes related to alcohol or tobacco use (including major depressive disorder).</p>
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Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.
2020-04-07 | GSE137228 | GEO
Project description:Alcohol exposure is known to impact several components of the one-carbon metabolism pathway, which is vital for providing methyl groups for DNA and peptide synthesis and for methylation modification of nucleotides and proteins. Methylation patterning in DNA is known to be altered across generations in specific situations in humans, including nutrient deprivation and smoking during pregnancy. We were interested in seeing whether heavy alcohol exposure during pregnancy, which is associated with fetal alcohol syndrome, influences genome-wide infant methylation patterning. From Guthrie card spots across over 100 infants of various genders, ethnicities, and maternal smoking and drinking status, we find two loci that are have significantly different methylation patterning associated with maternal drinking; cgXXX and cgYYY, the former near MCOLN3 and the latter in intergenic space. We also use available epidemiological information associated with our data set to replicate maternal smoking with infant methylation changes as well as replicate and expand upon methylation differences between genders and ethnicities.
2016-01-29 | GSE65428 | GEO
Project description:Background: The incidence of alcohol and tobacco co-abuse is as high as 80%. The molecular mechanism underlying this comorbidity is virtually unknown but interactions between these drugs have important implications for the development of, and recovery from drug dependence. Methods: We investigated the effects of chronic tobacco and alcohol abuse and the interaction of the two behaviours on global gene expression in the human nucleus accumbens using cDNA microarrays and 20 alcoholic and control cases, with and without smoking comorbidity. Changes in gene expression were established by two-way ANOVA. Unsupervised hierarchical clustering was utilized to probe the strength of the data sets. Results: Subjecting the data sets derived from microarray gene expression screening to unsupervised hierarchical clustering tied the cases into distinct groups. When considering all alcohol-responsive genes, alcoholics were separated from non alcoholics with the exception of one control case. All smokers were distinguished from non smokers based on similarity in expression of smoking-sensitive genes. In the nucleus accumbens, alcohol-responsive genes were associated with transcription, lipid metabolism and signalling. Smoking-sensitive genes were predominantly assigned to functional groups concerned with RNA processing and the endoplasmic reticulum. Both drugs influenced the expression of genes involved in matrix remodelling, proliferation and cell morphogenesis. Additionally, a gene set encoding proteins involved in the canonical pathway ‘regulation of the actin cytoskeleton’ was induced in response to alcohol and tobacco co-abuse and included. Conclusions: The region-specific modulation of alcohol-sensitive gene expression by smoking may have important consequences for alcohol-induced aberrations within the mesolimbic dopaminergic system. The data set contained individual RNA samples extracted from the nucleus accumbens from 5 non smoking non drinking control case, 5 non smoking alcoholics, 5 non drinking smokers, and 5 smoking alcoholics. An aliquot if each sample was combined to generate a reference pool. Each sample was amplified individually and labelled with Cy3 in the process, the reference samples was amplified and labelled with Cy5. Each sample was hybridised competitively against the reference sample to 1 array.
2010-07-01 | E-GEOD-20568 | biostudies-arrayexpress
Project description:HPV-positive oral squamous cell carcinomas (OSCCs) are specific biological and clinical entities, characterized by a more favorable prognosis compared to HPV-negative OSCCs and occurring generally in non-smoking and non-drinking younger individuals. However, poor information is available on the molecular and the clinical behavior of HPV-positive oral cancers occurring in smoking/drinking subjects. Thus, this study was designed to compare, at molecular level, two OSCC cell lines, both derived from drinking and smoking individuals and differing for presence/absence of HPV infection.
2019-12-01 | E-MTAB-6152 | biostudies-arrayexpress
Project description:Background: The most important risk factors for head and neck squamous carcinoma (HNSCC) are tobacco smoking and alcohol consumption, while subgroups are caused by infection with human papillomaviruses (HPV) or Epstein-Barr virus (EBV). Here, we studied alterations of somatic copy-number in whole genome, p16 protein and TP53 mutations by alcohol drinking, smoking and viral infections. Methods: We conducted a prospective cohort study. DNA obtained from tumors and margin samples as well as peripheral blood was assayed by array comparative genomic hybridization using Agilent Whole Human Genome 180K. Mutations of p53 gene by direct sequencing, detection of HPV by polymerase-chain-reaction (PCR), quantification of EBV by reverse transcription-PCR and p16 immunohistochemical (IHC) staining were also performed.
2013-07-01 | GSE47443 | GEO
Project description:The PRogramming of Intergenerational Stress Mechanisms (PRISM) study is an urban, ethnically diverse pregnancy cohort that was designed to study a range of chemical and non-chemical stressors in relation to maternal health, pregnancy outcomes, and child development. Pregnant women were enrolled from Boston and New York City hospitals and affiliated prenatal clinics beginning in 2011. Eligibility criteria included English or Spanish-speaking, over 18 years of age at enrollment, and singleton pregnancy. Exclusion criteria included HIV+ status or self-reported drinking ≥7 alcoholic drinks per week before pregnancy or any alcohol after pregnancy recognition
2021-06-10 | ST001827 | MetabolomicsWorkbench
Project description:Alcohol use disorders (AUD) are complex, moderately heritable, psychiatric disorders associated with heightened morbidity and mortality. Genome-wide association studies of AUD and drinks per week (DPW) have identified multiple risk loci however few studies have examined the intersection between the loci and genes associated with AUD and DPW, especially with respect to their functional and regulatory significance. In this study we use a muti-omics systems approach to identify causal variants and genes associated with AUD and DPW.
2021-11-20 | GSE189139 | GEO