{"title":"Enhancing the Use of Vehicle Alcohol Interlocks With Emerging Technology.","authors":"Robert B Voas","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Among the earliest applications of health technologies to a safety program was the development of blood alcohol content (BAC) tests for use in impaired-driving enforcement. This led to the development of miniature, highly accurate devices that officers could carry in their pockets. A natural extension of this technology was the vehicle alcohol interlock, which is used to reduce recidivism among drivers convicted of driving under the influence (DUI) by requiring them to install the devices (which will not allow someone with a positive BAC to drive) on their vehicles. While on the vehicle, interlocks have been shown to reduce recidivism by two-thirds. Use of these devices has been growing at the rate of 10 to 15 percent a year, and there currently are more than 300,000 units in use. This expansion in the application of interlocks has benefited from the integration of other emerging technologies into interlock systems. Such technologies include data systems that record both driver actions and vehicle responses, miniature cameras and face recognition to identify the user, Wi-Fi systems to provide rapid reporting on offender performance and any attempt to circumvent the device, GPS tracking of the vehicle, and more rapid means for monitoring the integrity of the interlock system. This article describes how these health technologies are being applied in interlock programs and the outlook for new technologies and new court sanctioning programs that may influence the growth in the use of interlocks in the future. </p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"36 1","pages":"81-9"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic events in liver cancer resulting from alcoholic liver disease.","authors":"Samuel W French","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Epigenetic mechanisms play an extensive role in the development of liver cancer (i.e., hepatocellular carcinoma [HCC]) associated with alcoholic liver disease (ALD) as well as in liver disease associated with other conditions. For example, epigenetic mechanisms, such as changes in the methylation and/or acetylation pattern of certain DNA regions or of the histone proteins around which the DNA is wrapped, contribute to the reversion of normal liver cells into progenitor and stem cells that can develop into HCC. Chronic exposure to beverage alcohol (i.e., ethanol) can induce all of these epigenetic changes. Thus, ethanol metabolism results in the formation of compounds that can cause changes in DNA methylation and interfere with other components of the normal processes regulating DNA methylation. Alcohol exposure also can alter histone acetylation/deacetylation and methylation patterns through a variety of mechanisms and signaling pathways. Alcohol also acts indirectly on another molecule called toll-like receptor 4 (TLR4) that is a key component in a crucial regulatory pathway in the cells and whose dysregulation is involved in the development of HCC. Finally, alcohol use regulates an epigenetic mechanism involving small molecules called miRNAs that control transcriptional events and the expression of genes important to ALD.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"57-67"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prenatal alcohol exposure and cellular differentiation: a role for Polycomb and Trithorax group proteins in FAS phenotypes?","authors":"Kylee J Veazey, Daria Muller, Michael C Golding","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Exposure to alcohol significantly alters the developmental trajectory of progenitor cells and fundamentally compromises tissue formation (i.e., histogenesis). Emerging research suggests that ethanol can impair mammalian development by interfering with the execution of molecular programs governing differentiation. For example, ethanol exposure disrupts cellular migration, changes cell-cell interactions, and alters growth factor signaling pathways. Additionally, ethanol can alter epigenetic mechanisms controlling gene expression. Normally, lineage-specific regulatory factors (i.e., transcription factors) establish the transcriptional networks of each new cell type; the cell's identity then is maintained through epigenetic alterations in the way in which the DNA encoding each gene becomes packaged within the chromatin. Ethanol exposure can induce epigenetic changes that do not induce genetic mutations but nonetheless alter the course of fetal development and result in a large array of patterning defects. Two crucial enzyme complexes--the Polycomb and Trithorax proteins--are central to the epigenetic programs controlling the intricate balance between self-renewal and the execution of cellular differentiation, with diametrically opposed functions. Prenatal ethanol exposure may disrupt the functions of these two enzyme complexes, altering a crucial aspect of mammalian differentiation. Characterizing the involvement of Polycomb and Trithorax group complexes in the etiology of fetal alcohol spectrum disorders will undoubtedly enhance understanding of the role that epigenetic programming plays in this complex disorder.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"77-85"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic targets for reversing immune defects caused by alcohol exposure.","authors":"Brenda J Curtis, Anita Zahs, Elizabeth J Kovacs","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alcohol consumption alters factors that modify gene expression without changing the DNA code (i.e., epigenetic modulators) in many organ systems, including the immune system. Alcohol enhances the risk for developing several serious medical conditions related to immune system dysfunction, including acute respiratory distress syndrome (ARDS), liver cancer, and alcoholic liver disease (ALD). Binge and chronic drinking also render patients more susceptible to many infectious pathogens and advance the progression of HIV infection by weakening both innate and adaptive immunity. Epigenetic mechanisms play a pivotal role in these processes. For example, alcohol-induced epigenetic variations alter the developmental pathways of several types of immune cells (e.g., granulocytes, macrophages, and T-lymphocytes) and through these and other mechanisms promote exaggerated inflammatory responses. In addition, epigenetic mechanisms may underlie alcohol's ability to interfere with the barrier functions of the gut and respiratory systems, which also contribute to the heightened risk of infections. Better understanding of alcohol's effects on these epigenetic processes may help researchers identify new targets for the development of novel medications to prevent or ameliorate alcohol's detrimental effects on the immune system.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"97-113"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31934569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sridevi Balaraman, Joseph D Tingling, Pai-Chi Tsai, Rajesh C Miranda
{"title":"Dysregulation of microRNA expression and function contributes to the etiology of fetal alcohol spectrum disorders.","authors":"Sridevi Balaraman, Joseph D Tingling, Pai-Chi Tsai, Rajesh C Miranda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are members of a large class of non-protein-coding RNA (ncRNA) molecules that represent a significant, but until recently unappreciated, layer of cellular regulation. Assessment of the generation and function of miRNAs suggests that these ncRNAs are vulnerable to interference from genetic, epigenetic, and environmental factors. A small but rapidly expanding body of studies using a variety of animal- and cell culture-based experimental models also has shown that miRNAs are important targets of alcohol during fetal development and that their dysregulation likely plays a significant role in the etiology of fetal alcohol spectrum disorders (FASD). Accordingly, an analysis of the regulation and function of these miRNAs may yield important clues to the management of FASD.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"18-24"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31934151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Community indicators: assessing the impact of alcohol use on communities.","authors":"Andrea Flynn, Samantha Wells","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Community indicators are used to assess the impact of alcohol on communities. This article reviews the main data sources for community indicators, discusses their strengths and limitations, and discusses indicators used in reference to four main topics relating to alcohol use and problems at the community level: alcohol use, patterns, and problems; alcohol availability; alcohol-related health outcomes/trauma; and alcohol-related crime and enforcement. It also reviews the challenges associated with collecting community indicator data, along with important innovations in the field that have contributed to better knowledge of how to collect and analyze community-level data on the impact of alcohol.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"135-49"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41156982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetics--new frontier for alcohol research.","authors":"Shivendra D Shukla, Samir Zakhari","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31934149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Using surveys to calculate disability-adjusted life-years.","authors":"Wolfgang Wiedermann, Ulrich Frick","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 2","pages":"128-33"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marta Varela-Rey, Ashwin Woodhoo, Maria-Luz Martinez-Chantar, José M Mato, Shelly C Lu
{"title":"Alcohol, DNA methylation, and cancer.","authors":"Marta Varela-Rey, Ashwin Woodhoo, Maria-Luz Martinez-Chantar, José M Mato, Shelly C Lu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cancer is one of the most significant diseases associated with chronic alcohol consumption, and chronic drinking is a strong risk factor for cancer, particularly of the upper aerodigestive tract, liver, colorectum, and breast. Several factors contribute to alcohol-induced cancer development (i.e., carcinogenesis), including the actions of acetaldehyde, the first and primary metabolite of ethanol, and oxidative stress. However, increasing evidence suggests that aberrant patterns of DNA methylation, an important epigenetic mechanism of transcriptional control, also could be part of the pathogenetic mechanisms that lead to alcohol-induced cancer development. The effects of alcohol on global and local DNA methylation patterns likely are mediated by its ability to interfere with the availability of the principal biological methyl donor, S-adenosylmethionine (SAMe), as well as pathways related to it. Several mechanisms may mediate the effects of alcohol on DNA methylation, including reduced folate levels and inhibition of key enzymes in one-carbon metabolism that ultimately lead to lower SAMe levels, as well as inhibition of activity and expression of enzymes involved in DNA methylation (i.e., DNA methyltransferases). Finally, variations (i.e., polymorphisms) of several genes involved in one-carbon metabolism also modulate the risk of alcohol-associated carcinogenesis.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"25-35"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic effects of ethanol on the liver and gastrointestinal system.","authors":"Shivendra D Shukla, Robert W Lim","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The widening web of epigenetic regulatory mechanisms also encompasses ethanol-induced changes in the gastrointestinal (GI)-hepatic system. In the past few years, increasing evidence has firmly established that alcohol modifies several epigenetic parameters in the GI tract and liver. The major pathways affected include DNA methylation, different site-specific modifications in histone proteins, and microRNAs. Ethanol metabolism, cell-signaling cascades, and oxidative stress have been implicated in these responses. Furthermore, ethanol-induced fatty liver (i.e., steatohepatitis) and progression of liver cancer (i.e., hepatic carcinoma) may be consequences of the altered epigenetics. Modification of gene and/or protein expression via epigenetic changes also may contribute to the cross-talk among the GI tract and the liver as well as to systemic changes involving other organs. Thus, epigenetic effects of ethanol may have a central role in the various pathophysiological responses induced by ethanol in multiple organs and mediated via the liver-GI axis.</p>","PeriodicalId":56367,"journal":{"name":"Alcohol research : current reviews","volume":"35 1","pages":"47-55"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31933595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}