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[PMID]: 29510883
[Au] Autor:Haass-Koffler CL
[Ad] Address:Center for Alcohol and Addiction Studies, Department of Psychiatry and Human Behavior, Department of Behavioral and Social Sciences, 121 South Main Street, Brown University, Providence, RI 02919, USA; Section on Clinical Psychoneuroendocrinology and Neuropsychopharmacology, NIAAA and NIDA, NIH, 10 Center Drive, Bethesda, MD 20892, USA. Electronic address: carolina_haass-koffler@brown.edu.
[Ti] Title:The corticotropin releasing factor binding protein: A strange case of Dr. Jekyll and Mr. Hyde in the stress system?
[So] Source:Alcohol;, 2017 Oct 13.
[Is] ISSN:1873-6823
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The corticotropin releasing factor (CRF) exerts its effects by acting on its receptors and on the binding protein (CRFBP). Extensive literature suggests a role of CRF in alcohol use disorder (AUD). Less is known about the specific role, if any, of CRFBP in AUD. In this review, we summarize recent interdisciplinary efforts toward identifying the contribution of CRFBP in mediating CRF activation. The role of CRFBP in alcohol-related behaviors has been evaluated with the ultimate goal of designing effective novel therapeutic strategies for AUD. A series of invitro, invivo, exvivo, and genetic studies presented here provides initial evidence that CRFBP may possess both inhibitory and excitatory roles, and supports the original hypothesis that it represents a novel pharmacological target for the treatment of AUD. This report summarizes the proceedings of one of the talks at the Young Investigator Award symposium at the Alcoholism and Stress: A Framework for Future Treatment Strategies Conference, Volterra, Italy.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  2 / 81315 MEDLINE  
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[PMID]: 29496608
[Au] Autor:Zhou Y; Crowley R; Prisinzano T; Kreek MJ
[Ad] Address:Laboratory of the Biology of Addictive Diseases, The Rockefeller University, NY, USA. Electronic address: zhouya@rockefeller.edu.
[Ti] Title:Effects of mesyl salvinorin B alone and in combination with naltrexone on alcohol deprivation effect in male and female mice.
[So] Source:Neurosci Lett;673:19-23, 2018 Feb 26.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Alcohol relapse plays a major role in alcohol dependence and is an important focus for the treatment of alcoholism. The alcohol deprivation effect (ADE) is a widely used paradigm in rodents to model the relapse episodes that occur in human alcoholics. Mesyl Salvinorin B (MSB) is a potent and selective kappa opioid receptor (KOP-r) full agonist, with fewer side effects (e.g., sedation or anhedonia) than classic KOP-r full agonists and a longer duration of action in mice than the structurally similar salvinorin A. We have recently found that MSB prevents cocaine seeking in a rat self-administration model and reduces excessive alcohol drinking in a mouse escalation model via a KOP-r-mediated mechanism. Here, we further investigated whether MSB alone (0.3-3 mg/kg) or in combination with naltrexone (mu-opioid receptor antagonist at 1 mg/kg) altered alcohol "relapse" drinking using a mouse ADE paradigm. Both male and female mice, exposed to 3-week intermittent access alcohol drinking in a two-bottle choice paradigm with 24-h access every other day, developed excessive alcohol intake and then displayed pronounced ADE after 1-week abstinence. Acute administration of MSB prevented the ADE at 3 mg/kg in both male and female mice. Upon investigation of potential synergistic effects between naltrexone and MSB, we found that acute administration of a combination of MSB (0.3 mg/kg) and naltrexone (1 mg/kg) reduced the ADE at doses lower than those individual effective doses, with no sex difference. Our study suggests that the KOP-r full agonist MSB both alone and in combination with naltrexone shows potential in alcohol "relapse" treatment models.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 81315 MEDLINE  
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[PMID]: 29378214
[Au] Autor:Hayes DM; Nickell CG; Chen KY; McClain JA; Heath MM; Deeny MA; Nixon K
[Ad] Address:Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0596, USA. Electronic address: dhayes4@radford.edu.
[Ti] Title:Activation of neural stem cells from quiescence drives reactive hippocampal neurogenesis after alcohol dependence.
[So] Source:Neuropharmacology;133:276-288, 2018 Jan 31.
[Is] ISSN:1873-7064
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neural stem cell-driven adult neurogenesis contributes to the integrity of the hippocampus. Excessive alcohol consumption in alcoholism results in hippocampal degeneration that may recover with abstinence. Reactive, increased adult neurogenesis during abstinence following alcohol dependence may contribute to recovery, but the mechanism driving reactive neurogenesis is not known. Therefore, adult, male rats were exposed to alcohol for four days and various markers were used to examine cell cycle dynamics, the percentage and number of neural progenitor cell subtypes, and the percentage of quiescent versus activated progenitors. Using a screen for cell cycle perturbation, we showed that the cell cycle is not likely altered at 7 days in abstinence. As the vast majority of Bromodeoxyuridine-positive (+) cells were co-labeled with progenitor cell marker, Sox2, we then developed a quadruple fluorescent labeling scheme to examine Type-1, -2a, -2b and-3 progenitor cells simultaneously. Prior alcohol dependence indiscriminately increased all subtypes at 7 days, the peak of the reactive proliferation. An evaluation of the time course of reactive cell proliferation revealed that cells begin proliferating at 5 days post alcohol, where only actively dividing Type 2 progenitors were increased by alcohol. Furthermore, prior alcohol increased the percentage of actively dividing Sox2+ progenitors, which supported that reactive neurogenesis is likely due to the activation of progenitors out of quiescence. These observations were associated with granule cell number returning to normal at 28 days. Therefore, activating stem and progenitor cells out of quiescence may be the mechanism underlying hippocampal recovery in abstinence following alcohol dependence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  4 / 81315 MEDLINE  
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[PMID]: 29281048
[Au] Autor:Hassan L; Shiu E
[Ad] Address:Bangor Business School, College Road, Bangor, Gwynedd LL57 2DG, Wales.
[Ti] Title:Communicating Messages About Drinking.
[So] Source:Alcohol Alcohol;53(1):1-2, 2018 01 01.
[Is] ISSN:1464-3502
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:EDITORIAL; COMMENT
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process
[do] DOI:10.1093/alcalc/agx112

  5 / 81315 MEDLINE  
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[PMID]: 28463821
[Au] Autor:Hoyt LR; Randall MJ; Ather JL; DePuccio DP; Landry CC; Qian X; Janssen-Heininger YM; van der Vliet A; Dixon AE; Amiel E; Poynter ME
[Ad] Address:Vermont Lung Center, University of Vermont, Burlington, VT 05405, USA; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405, USA.
[Ti] Title:Mitochondrial ROS induced by chronic ethanol exposure promote hyper-activation of the NLRP3 inflammasome.
[So] Source:Redox Biol;12:883-896, 2017 Aug.
[Is] ISSN:2213-2317
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Alcohol use disorders are common both in the United States and globally, and are associated with a variety of co-morbid, inflammation-linked diseases. The pathogenesis of many of these ailments are driven by the activation of the NLRP3 inflammasome, a multi-protein intracellular pattern recognition receptor complex that facilitates the cleavage and secretion of the pro-inflammatory cytokines IL-1 and IL-18. We hypothesized that protracted exposure of leukocytes to ethanol would amplify inflammasome activation, which would help to implicate mechanisms involved in diseases associated with both alcoholism and aberrant NLRP3 inflammasome activation. Here we show that long-term ethanol exposure of human peripheral blood mononuclear cells and a mouse macrophage cell line (J774) amplifies IL-1 secretion following stimulation with NLRP3 agonists, but not with AIM2 or NLRP1b agonists. The augmented NRLP3 activation was mediated by increases in iNOS expression and NO production, in conjunction with increases in mitochondrial membrane depolarization, oxygen consumption rate, and ROS generation in J774 cells chronically exposed to ethanol (CE cells), effects that could be inhibited by the iNOS inhibitor SEITU, the NO scavenger carboxy-PTIO, and the mitochondrial ROS scavenger MitoQ. Chronic ethanol exposure did not alter K efflux or Zn homeostasis in CE cells, although it did result in a lower intracellular concentration of NAD . Prolonged administration of acetaldehyde, the product of alcohol dehydrogenase (ADH) mediated metabolism of ethanol, mimicked chronic ethanol exposure, whereas ADH inhibition prevented ethanol-induced IL-1 hypersecretion. Together, these results indicate that increases in iNOS and mitochondrial ROS production are critical for chronic ethanol-induced IL-1 hypersecretion, and that protracted exposure to the products of ethanol metabolism are probable mediators of NLRP3 inflammasome hyperactivation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  6 / 81315 MEDLINE  
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[PMID]: 29524232
[Au] Autor:Ko H; Song YM; Lee SC; Park SW; Sung J; Lee K; Lee E
[Ad] Address:Department of Family Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
[Ti] Title:Association between excessive alcohol consumption and echocardiographic parameters according to the presence of flushing reaction in Korean men: A community based study.
[So] Source:Alcohol Clin Exp Res;, 2018 Mar 10.
[Is] ISSN:1530-0277
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The objective of this study was to investigate the effect of excessive alcohol consumption on heart reflected by various echocardiographic parameters according to the presence or absence of flushing reaction that might reflect acetaldehyde metabolism. METHODS: A total of 854 Korean men without significant cardiovascular diseases who underwent echocardiography and participated in the Korean Healthy Twin Study were used as subjects of this study. These subjects were classified into three categories: non-drinker, moderate drinker (≤ 196 g/week), and heavy drinker (> 196 g/week) within two strata of flushing reaction to alcohol drinking. Association between echocardiographic measurements and categories of the amount of alcohol consumption considering flushing reaction were evaluated using mixed linear regression model. RESULTS: The proportion of flushers among drinkers was 39.5% (278 of 703). In stratified analysis by flushing reaction, non-flushers showed significantly higher left ventricular mass index (: 4.605; 95% CI: 0.966, 8.243) and significantly lower ratio of peak early diastolic velocities (E peak) over peak late diastolic velocities of mitral inflow (: -0.103; 95% CI: -0.198, -0.008) in heavy drinkers compared to non-drinkers. Flushers showed significantly higher left atrial volume index (: 2.712; 95% CI: 0.456, 4.968) in heavy drinkers and significantly lower ratio of E peak over the peak early diastolic mitral annular velocities (: -0.493; 95% CI: -0.902, -0.085) in moderate drinkers compared to non-drinkers. However, the interaction according to flushing reaction was only statistically significant for the association between alcohol consumption and left atrial volume index (p for interaction = 0.004). CONCLUSION: Alcohol consumption is associated with changes in cardiac structure and function. Such association might be influenced by acetaldehyde metabolism. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/acer.13622

  7 / 81315 MEDLINE  
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[PMID]: 29523775
[Au] Autor:Schloss M; Becak D; Tosto ST; Velayati A
[Ad] Address:Medical Student, Alabama College of Osteopathic Medicine, Dothan, AL, USA.
[Ti] Title:A Case of Levofloxacin-Induced Hepatotoxicity.
[So] Source:Am J Case Rep;19:272-276, 2018 Mar 10.
[Is] ISSN:1941-5923
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND Levofloxacin covers a broad spectrum of pathogens and is readily prescribed by clinicians. Hepatotoxicity is a known but unusual complication of levofloxacin use. Here, we present a case of severe transaminitis caused by levofloxacin. CASE REPORT A young man in his thirties with a history of asthma, chronic alcoholism, methamphetamine intravenous drug abuse (IVDA), and non-compliant insulin-dependent diabetes mellitus (IDDM) presented to an emergency department with suicidal ideation. Vital signs were stable and the patient was noted to have cellulitis of the right forearm, for which cultures were drawn, and he received IV clindamycin. He was admitted to behavioral medicine for further care. Blood cultures were positive for gram-negative rods and he was transferred to the medicine ward. Cultures eventually grew Brevundimonas diminuta. Clindamycin was discontinued and he was started on levofloxacin. Transaminase levels measured soon after levofloxacin administration showed aminotransferase levels raised to approximately 50 times baseline within a few days. Levofloxacin was discontinued due to concern about drug-induced hepatotoxicity. After discontinuation, transaminase levels decreased immediately. Work-up for other causes of transaminitis revealed no other etiology. CONCLUSIONS Clinicians should remain mindful that levofloxacin can induce hepatotoxicity in rare cases. In patients presenting with acute liver injury who have recently taken levofloxacin, it would be wise to remain cognizant of the possibility of levofloxacin-induced hepatotoxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  8 / 81315 MEDLINE  
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[PMID]: 28745447
[Au] Autor:Scott MS
[Ad] Address:National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland.
[Ti] Title:Commentary: Perspectives on alcohol-related gene and environment interplay in diverse populations.
[So] Source:Am J Addict;26(5):526-531, 2017 Aug.
[Is] ISSN:1521-0391
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND AND OBJECTIVES: Racial/ethnic groups comprise more than 20% of the U.S. population, but many experience disproportionately high risk for alcohol misuse, often resulting in higher rates of alcohol-associated consequences. Completion of mapping the human genome has launched rapidly evolving research methods aimed at improved understanding of genetic contribution to disease. Despite decades of research on the influence of genetic and environmental risks on alcohol use disorders and outcomes, few studies have included racial/ethnic subpopulations in sufficient numbers to allow for proper statistical analysis. METHODS: The papers in this special issue help to elucidate current knowledge on the etiology of genetic and environmental contributors and potential moderators of alcohol use and associated problems among racial/ethnic populations. The lack of racial/ethnic diversity across many genetic studies contributes to challenges in interpretation of findings and eventually applications to precision medicine. RESULTS: Proposed approaches to overcome disparities in racial/ethnic participant recruitment in genetic studies include methods to address population stratification in allele frequency, improve transparency in subjects' consenting to participate, and engaging interdisciplinary research teams and community involvement to improve recruitment of racial/ethnic minorities. DISCUSSION AND CONCLUSIONS: The reviews presented underscore various gaps in our knowledge of the genetic influences on alcohol use disorders due to the failure to include racially and ethnically diverse populations in genetic and epigenetic study samples. New directions are suggested to overcome the resulting research challenges and ultimately to inform future personalized intervention approaches for racial/ethnic populations. SCIENTIFIC SIGNIFICANCE: Inclusion of heterogeneous populations in genomic research will provide a better comprehension of possible unique genetic factors in the broader general population that may be missed due to exclusion of unique and common variants that may be present in racial/ethnic populations. (Am J Addict 2017;26:526-531).
[Mh] MeSH terms primary: Alcohol Drinking
Alcoholism
Ethnic Groups
Gene-Environment Interaction
Patient Selection
[Mh] MeSH terms secundary: Alcohol Drinking/genetics
Alcohol Drinking/psychology
Alcoholism/genetics
Alcoholism/psychology
Humans
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:170727
[St] Status:MEDLINE
[do] DOI:10.1111/ajad.12584

  9 / 81315 MEDLINE  
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[PMID]: 29519768
[Au] Autor:Qanneta R; Bov Aleu E
[Ad] Address:Hospital Sociosanitario Francol, Tarragona, Espaa. Electronic address: rami_kanita229@hotmail.com.
[Ti] Title:Pie de Charcot asociado con alcoholismo crnico en un paciente no diabtico: una asociacin inusual. Charcot foot associated with chronic alcoholism in a non-diabetic patient: An unusual association.
[So] Source:Reumatol Clin;, 2018 Mar 05.
[Is] ISSN:1885-1398
[Cp] Country of publication:Spain
[La] Language:eng; spa
[Pt] Publication type:LETTER
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 81315 MEDLINE  
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[PMID]: 29495031
[Au] Autor:Buzalaf MAR; Magalhes AC; Rios D
[Ad] Address:Bauru School of Dentistry, University of So Paulo, Alameda Octvio Pinheiro Brisolla, 9-75, Bauru, So Paulo, Brazil 17,012-901.
[Ti] Title:Prevention of erosive tooth wear: targeting nutritional and patient-related risks factors.
[So] Source:Br Dent J;224(5):371-378, 2018 Mar 09.
[Is] ISSN:1476-5373
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:This article provides an overview of the nutritional and patient-related risk factors involved in the aetiology of erosive tooth wear (ETW) and the preventive strategies to counteract them. The first step is to diagnose clinical signs of ETW and to recognise causal factors. Low pH and high buffer capacity of foods/drinks are the major risk factors, while the calcium concentration is the main protective factor. Reduction of frequency of consumption and contact time of erosive foods/drinks with the teeth, use of straws appropriately positioned and consumption of dairy products are advisable. Oral hygiene has a role in the development of ETW, however, postponing toothbrushing is not clinically advisable. In cases of drug abuse, chronic alcoholism, GERD or bulimia, the patient must be referred to a doctor. Immediately after vomiting, patients might be advised to rinse the mouth. Saliva has an important protective role and patients with reduced salivary flow can benefit from the use of chewing gum. Recent studies have focused on improving the protective capacity of the acquired pellicle as well as on the role of protease inhibitors on dentine erosion. However, the degree of evidence for these preventive measures is low. Clinical trials are necessary before these measures can be recommended.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/sj.bdj.2018.173


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