Fernando Oliveira E Silva, António José Cruz, João Nuak
{"title":"Penile Cellulitis Related to Mpox Genital Lesions.","authors":"Fernando Oliveira E Silva, António José Cruz, João Nuak","doi":"10.20344/amp.19832","DOIUrl":"10.20344/amp.19832","url":null,"abstract":"","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"28 1","pages":"51-52"},"PeriodicalIF":1.2,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83362000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-06-17DOI: 10.21203/rs.3.rs-34394/v1
A. Vargas-Martínez, M. Lima-Serrano, M. Trapero-Bertran
BACKGROUND Binge drinking (BD) among adolescents is a public health concern worldwide. This study assessed the cost-effectiveness and cost-utility of a web-based computer-tailored intervention to prevent BD in adolescence. METHODS The sample was drawn from a study evaluating the Alerta Alcohol program. The population consisted of adolescents 15 to 19 years of age. Data were recorded at baseline (January to February 2016) and after 4 months (May to June 2017) and were used to estimate costs and health outcomes, as measured by the number of BD occasions and quality-adjusted life years (QALYs). Incremental cost-effectiveness and cost-utility ratios were calculated from National Health Service (NHS) and societal perspectives and for a time horizon of 4 months. A multivariate deterministic sensitivity analysis of best/worst scenarios by subgroups was used to account for uncertainty. RESULTS The cost of reducing BD occasions by one per month was €16.63 from the NHS perspective, which from the societal perspective resulted in savings of €7986.37. From the societal perspective, the intervention resulted in an incremental cost of €71.05 per QALY gained from the NHS perspective and this was dominant, resulting in savings of €34,126.64 per QALY gained in comparison with the control group. Subgroup analyses showed that the intervention was dominant for girls from both the perspectives and for individuals 17 years or older from the NHS perspective. CONCLUSIONS Computer-tailored feedback is a cost-effective way to reduce BD and increase QALYs among adolescents. However, long-term follow-up is needed to evaluate more fully changes in both BD and health-related quality of life.
{"title":"Cost-effectiveness and cost-utility analyses of a web-based computer-tailored intervention for prevention of binge drinking among Spanish adolescents.","authors":"A. Vargas-Martínez, M. Lima-Serrano, M. Trapero-Bertran","doi":"10.21203/rs.3.rs-34394/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-34394/v1","url":null,"abstract":"BACKGROUND\u0000Binge drinking (BD) among adolescents is a public health concern worldwide. This study assessed the cost-effectiveness and cost-utility of a web-based computer-tailored intervention to prevent BD in adolescence.\u0000\u0000\u0000METHODS\u0000The sample was drawn from a study evaluating the Alerta Alcohol program. The population consisted of adolescents 15 to 19 years of age. Data were recorded at baseline (January to February 2016) and after 4 months (May to June 2017) and were used to estimate costs and health outcomes, as measured by the number of BD occasions and quality-adjusted life years (QALYs). Incremental cost-effectiveness and cost-utility ratios were calculated from National Health Service (NHS) and societal perspectives and for a time horizon of 4 months. A multivariate deterministic sensitivity analysis of best/worst scenarios by subgroups was used to account for uncertainty.\u0000\u0000\u0000RESULTS\u0000The cost of reducing BD occasions by one per month was €16.63 from the NHS perspective, which from the societal perspective resulted in savings of €7986.37. From the societal perspective, the intervention resulted in an incremental cost of €71.05 per QALY gained from the NHS perspective and this was dominant, resulting in savings of €34,126.64 per QALY gained in comparison with the control group. Subgroup analyses showed that the intervention was dominant for girls from both the perspectives and for individuals 17 years or older from the NHS perspective.\u0000\u0000\u0000CONCLUSIONS\u0000Computer-tailored feedback is a cost-effective way to reduce BD and increase QALYs among adolescents. However, long-term follow-up is needed to evaluate more fully changes in both BD and health-related quality of life.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"11 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2020-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87333351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Prenatal alcohol exposure (PAE) is increasingly recognized as being associated with a wide range of physical health problems, in addition to the well-defined neurocognitive difficulties that have been reported (Mattson et al., 2019). In line with other prenatal perturbations, including smoking, inadequate nutrition and exposure to stress, exposure of the fetus to alcohol during critical stages of development may contribute to 'developmental origins of health and disease' (DOHaD), as first proposed by Barker and colleagues (1995). DOHaD suggests that a suboptimal environment in early development may increase susceptibility to conditions such as hypertension, insulin resistance and obesity, which are risk factors for prevalent non-communicable chronic diseases such as cardiovascular disease and type II diabetes (Hanson and Gluckman, 2011). This article is protected by copyright. All rights reserved.
{"title":"Can fetal alcohol exposure increase the risk of hypertension? A new study in children and adolescents diagnosed with fetal alcohol spectrum disorder suggests it can.","authors":"K. Moritz, N. Reid, L. Akison","doi":"10.1111/acer.14175","DOIUrl":"https://doi.org/10.1111/acer.14175","url":null,"abstract":"Prenatal alcohol exposure (PAE) is increasingly recognized as being associated with a wide range of physical health problems, in addition to the well-defined neurocognitive difficulties that have been reported (Mattson et al., 2019). In line with other prenatal perturbations, including smoking, inadequate nutrition and exposure to stress, exposure of the fetus to alcohol during critical stages of development may contribute to 'developmental origins of health and disease' (DOHaD), as first proposed by Barker and colleagues (1995). DOHaD suggests that a suboptimal environment in early development may increase susceptibility to conditions such as hypertension, insulin resistance and obesity, which are risk factors for prevalent non-communicable chronic diseases such as cardiovascular disease and type II diabetes (Hanson and Gluckman, 2011). This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"32 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88186281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Ritz, S. Segobin, C. Lannuzel, A. Laniepce, C. Boudehent, N. Cabé, F. Eustache, F. Vabret, H. Beaunieux, A. Pitel
BACKGROUND Despite severe structural brain abnormalities within the fronto-cerebellar circuit (FCC), cerebellar metabolism studied with FDG-PET is relatively preserved in patients with alcohol use disorder (AUD). The compensatory role of the cerebellum has been explored mainly through fMRI examination of AUD patients with preserved level of performance. The present study aims at examining cerebellar metabolism and its relationship with regional brain metabolism and neuropsychological functioning in AUD patients. METHODS Thirty-two recently detoxified AUD patients and 23 controls underwent an FDG-PET examination at rest. Participants also performed a neuropsychological battery assessing executive functions, verbal memory and ataxia. RESULTS Compared to controls, AUD patients had higher glucose-uptake in the cerebellar lobules VIII, in association with hypometabolism notably in several nodes of the FCC. Cerebellar hypermetabolism correlated negatively with regional hypometabolism in the premotor and frontal cortices. This pattern of regional hypermetabolism and hypometabolism related to ataxia and working memory deficits. CONCLUSIONS These specific brain-behaviour relationships do not fulfil the criteria for brain compensatory processes. Cerebellar hypermetabolism may rather reflect the involvement of different pathological mechanisms, leading to a maladaptive plasticity phenomenon within the FCC in AUD patients who are early in abstinence. Further studies are required to examine the contributions of structural and functional connectivity alterations in the cerebellar hypermetabolism and the changes of these pathological mechanisms with abstinence or relapse. This article is protected by copyright. All rights reserved.
{"title":"Cerebellar hypermetabolism in alcohol use disorder: compensatory mechanism or maladaptive plasticity?","authors":"L. Ritz, S. Segobin, C. Lannuzel, A. Laniepce, C. Boudehent, N. Cabé, F. Eustache, F. Vabret, H. Beaunieux, A. Pitel","doi":"10.1111/acer.14158","DOIUrl":"https://doi.org/10.1111/acer.14158","url":null,"abstract":"BACKGROUND\u0000Despite severe structural brain abnormalities within the fronto-cerebellar circuit (FCC), cerebellar metabolism studied with FDG-PET is relatively preserved in patients with alcohol use disorder (AUD). The compensatory role of the cerebellum has been explored mainly through fMRI examination of AUD patients with preserved level of performance. The present study aims at examining cerebellar metabolism and its relationship with regional brain metabolism and neuropsychological functioning in AUD patients.\u0000\u0000\u0000METHODS\u0000Thirty-two recently detoxified AUD patients and 23 controls underwent an FDG-PET examination at rest. Participants also performed a neuropsychological battery assessing executive functions, verbal memory and ataxia.\u0000\u0000\u0000RESULTS\u0000Compared to controls, AUD patients had higher glucose-uptake in the cerebellar lobules VIII, in association with hypometabolism notably in several nodes of the FCC. Cerebellar hypermetabolism correlated negatively with regional hypometabolism in the premotor and frontal cortices. This pattern of regional hypermetabolism and hypometabolism related to ataxia and working memory deficits.\u0000\u0000\u0000CONCLUSIONS\u0000These specific brain-behaviour relationships do not fulfil the criteria for brain compensatory processes. Cerebellar hypermetabolism may rather reflect the involvement of different pathological mechanisms, leading to a maladaptive plasticity phenomenon within the FCC in AUD patients who are early in abstinence. Further studies are required to examine the contributions of structural and functional connectivity alterations in the cerebellar hypermetabolism and the changes of these pathological mechanisms with abstinence or relapse. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"1 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79832635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ke Xu, J. Montalvo-Ortiz, Xinyu Zhang, S. Southwick, J. Krystal, R. Pietrzak, J. Gelernter
BACKGROUND Hazardous alcohol consumption has significant adverse medical consequences. These effects may be mediated, in part, by alterations in DNA methylation. Thus, DNA methylation signatures in peripheral cells may provide biomarkers of the medical impact of alcohol use and the risk for future alcohol consumption. METHOD Using a high density methylation array, we characterized epigenome-wide DNA methylation in saliva cells with respect to alcohol consumption in a large cohort of male European American veterans. In this study, DNA methylation of over 870,000 CpG DNA sites was profiled in 1,135 European American men. Alcohol consumption was assessed using the Alcohol Use Disorder Identification Test-Consumption (AUDIT-C). Linear regression was applied in an epigenome-wide association study (EWAS), adjusted for confounders. Gene set enrichment analysis was performed in the KEGG database with a correction for gene length. RESULTS We found that a total of 70 CpG sites reached EWAS-corrected significance (p<6E-08) with small effects on alcohol consumption for individual CpG sites, including 64 new CpG sites and six CpG sites that were previously reported as associated with alcohol use disorder, liver function, body mass index, and lipid metabolism. The most significant CpG site was located in SLC7A11(t=-11.34, p=2.66E-28), a gene involved specifically in cysteine and glutamate transportation. The 70 significant CpG sites were located on 44 genes, including genes involved in amino acid transport and metabolism systems. We identified 68 pathways with a false discovery rate <0.05. CONCLUSION We identified novel DNA methylation sites associated with alcohol consumption. Results may shed light on peripheral mechanisms of alcohol consumption on adverse health outcomes among heavy drinkers. This article is protected by copyright. All rights reserved.
{"title":"Epigenome-wide DNA Methylation Association Analysis Identified Novel Loci in Peripheral Cells for Alcohol Consumption among European American Male Veterans.","authors":"Ke Xu, J. Montalvo-Ortiz, Xinyu Zhang, S. Southwick, J. Krystal, R. Pietrzak, J. Gelernter","doi":"10.1111/acer.14168","DOIUrl":"https://doi.org/10.1111/acer.14168","url":null,"abstract":"BACKGROUND\u0000Hazardous alcohol consumption has significant adverse medical consequences. These effects may be mediated, in part, by alterations in DNA methylation. Thus, DNA methylation signatures in peripheral cells may provide biomarkers of the medical impact of alcohol use and the risk for future alcohol consumption.\u0000\u0000\u0000METHOD\u0000Using a high density methylation array, we characterized epigenome-wide DNA methylation in saliva cells with respect to alcohol consumption in a large cohort of male European American veterans. In this study, DNA methylation of over 870,000 CpG DNA sites was profiled in 1,135 European American men. Alcohol consumption was assessed using the Alcohol Use Disorder Identification Test-Consumption (AUDIT-C). Linear regression was applied in an epigenome-wide association study (EWAS), adjusted for confounders. Gene set enrichment analysis was performed in the KEGG database with a correction for gene length.\u0000\u0000\u0000RESULTS\u0000We found that a total of 70 CpG sites reached EWAS-corrected significance (p<6E-08) with small effects on alcohol consumption for individual CpG sites, including 64 new CpG sites and six CpG sites that were previously reported as associated with alcohol use disorder, liver function, body mass index, and lipid metabolism. The most significant CpG site was located in SLC7A11(t=-11.34, p=2.66E-28), a gene involved specifically in cysteine and glutamate transportation. The 70 significant CpG sites were located on 44 genes, including genes involved in amino acid transport and metabolism systems. We identified 68 pathways with a false discovery rate <0.05.\u0000\u0000\u0000CONCLUSION\u0000We identified novel DNA methylation sites associated with alcohol consumption. Results may shed light on peripheral mechanisms of alcohol consumption on adverse health outcomes among heavy drinkers. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"20 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78358917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gloria Brunori, Michelle Weger, Jennifer Schoch, Katarzyna M Targowska-Duda, Megan Barnes, A. M. Borruto, L. Rorick‐Kehn, N. Zaveri, J. Pintar, R. Ciccocioppo, L. Toll, A. Cippitelli
BACKGROUND The nociceptin/orphanin FQ opioid peptide (NOP) receptor and its endogenous ligand N/OFQ have been implicated in the regulation of drug and alcohol use disorders. In particular, evidence demonstrated that NOP receptor activation blocks reinforcing and motivating effects of alcohol across a range of behavioral measures, including alcohol intake, conditioned place preference and vulnerability to relapse. METHODS Here, we show the effects of pharmacological activation and inhibition of NOP receptors on binge-like alcohol consumption, as measured by the "drinking in the dark" (DID) model in C57BL/6J mice. RESULTS We found that two potent and selective NOP agonists AT-202 (0, 0.3, 1, 3 mg/kg) and AT-312 (0, 0.3, 1 mg/kg) did not affect binge alcohol drinking at doses that do not affect locomotor activity. AT-202 also failed to alter DID behavior when administered to mice previously exposed to chronic alcohol treatment with an alcohol-containing liquid diet. Conversely, treatment with either the high affinity NOP receptor antagonist SB-612111 (0, 3, 10, 30 mg/kg) or the selective antagonist LY2817412 (0, 3, 10, 30 mg/kg) decreased binge drinking. SB-612111 was effective at all doses examined, LY2817412 was effective at 30 mg/kg. Consistently, NOP receptor knockout mice consumed less alcohol compared to wild type. SB-612111 reduced DID and increased sucrose consumption at doses that do not appear to affect locomotor activity. However, the high dose of SB-612111 (30 mg/kg) reduced alcohol intake but failed to inhibit preference in a two-bottle choice DID model that can assess moderate alcohol intake. CONCLUSIONS The present results suggest that NOP receptor inhibition rather than activation may represent a valuable approach for treatment of alcohol use disorders characterized by excessive alcohol consumption such as binge drinking. This article is protected by copyright. All rights reserved.
{"title":"NOP receptor antagonists decrease alcohol drinking in the dark in C57BL/6J mice.","authors":"Gloria Brunori, Michelle Weger, Jennifer Schoch, Katarzyna M Targowska-Duda, Megan Barnes, A. M. Borruto, L. Rorick‐Kehn, N. Zaveri, J. Pintar, R. Ciccocioppo, L. Toll, A. Cippitelli","doi":"10.1111/acer.14165","DOIUrl":"https://doi.org/10.1111/acer.14165","url":null,"abstract":"BACKGROUND\u0000The nociceptin/orphanin FQ opioid peptide (NOP) receptor and its endogenous ligand N/OFQ have been implicated in the regulation of drug and alcohol use disorders. In particular, evidence demonstrated that NOP receptor activation blocks reinforcing and motivating effects of alcohol across a range of behavioral measures, including alcohol intake, conditioned place preference and vulnerability to relapse.\u0000\u0000\u0000METHODS\u0000Here, we show the effects of pharmacological activation and inhibition of NOP receptors on binge-like alcohol consumption, as measured by the \"drinking in the dark\" (DID) model in C57BL/6J mice.\u0000\u0000\u0000RESULTS\u0000We found that two potent and selective NOP agonists AT-202 (0, 0.3, 1, 3 mg/kg) and AT-312 (0, 0.3, 1 mg/kg) did not affect binge alcohol drinking at doses that do not affect locomotor activity. AT-202 also failed to alter DID behavior when administered to mice previously exposed to chronic alcohol treatment with an alcohol-containing liquid diet. Conversely, treatment with either the high affinity NOP receptor antagonist SB-612111 (0, 3, 10, 30 mg/kg) or the selective antagonist LY2817412 (0, 3, 10, 30 mg/kg) decreased binge drinking. SB-612111 was effective at all doses examined, LY2817412 was effective at 30 mg/kg. Consistently, NOP receptor knockout mice consumed less alcohol compared to wild type. SB-612111 reduced DID and increased sucrose consumption at doses that do not appear to affect locomotor activity. However, the high dose of SB-612111 (30 mg/kg) reduced alcohol intake but failed to inhibit preference in a two-bottle choice DID model that can assess moderate alcohol intake.\u0000\u0000\u0000CONCLUSIONS\u0000The present results suggest that NOP receptor inhibition rather than activation may represent a valuable approach for treatment of alcohol use disorders characterized by excessive alcohol consumption such as binge drinking. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"103 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74213689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. Petrenko, Elizabeth M. Demeusy, Michelle E. Alto
BACKGROUND When the primary disabilities associated with fetal alcohol spectrum disorders (FASD) are not well supported, individuals are at higher risk for mental health problems and other secondary conditions. The Families on Track intervention was designed to prevent secondary conditions and improve family functioning in children with FASD. Promising results from a pilot study demonstrated positive effects on child and caregiver outcomes immediately following the intervention. The objective of this study was to examine the sustainability of these effects 6-months post-intervention. METHODS Thirty children (ages 4 to 8) with prenatal alcohol exposure and their caregivers were enrolled in the original study. Families were randomized to the Families on Track intervention or an active comparison group that provided comprehensive assessment and individualized feedback. The intervention integrated a positive parenting curriculum and a child skills group. Families were assessed at baseline, post-intervention, and 6-month follow up visits. Follow up data were available for 24 families on child and caregiver outcomes. Data were analyzed using effect size calculations and analysis of variance techniques. RESULTS Relative to the comparison group, intervention families showed continued gains in parenting efficacy and maintained prior improvements in FASD knowledge over the follow-up period. Although intervention families reported a decrease in their needs being met over the follow up period, they continued to report their needs being met to greater extent than those in the comparison group. Consistent with post-intervention outcomes, children in both groups exhibited similar decreases in child disruptive behavior 6 months following the intervention. Unfortunately, positive gains seen at post-intervention for child self-esteem and emotion regulation were attenuated at follow-up. CONCLUSIONS This pilot study yielded promising effects on important areas of caregiver functioning. However, the intervention's impact on child functioning waned over time, suggesting the need for sustained or alternate child intervention.
{"title":"6-month Follow up of the Families on Track Intervention Pilot Trial for Children with Fetal Alcohol Spectrum Disorders and Their Families.","authors":"C. Petrenko, Elizabeth M. Demeusy, Michelle E. Alto","doi":"10.1111/acer.14180","DOIUrl":"https://doi.org/10.1111/acer.14180","url":null,"abstract":"BACKGROUND\u0000When the primary disabilities associated with fetal alcohol spectrum disorders (FASD) are not well supported, individuals are at higher risk for mental health problems and other secondary conditions. The Families on Track intervention was designed to prevent secondary conditions and improve family functioning in children with FASD. Promising results from a pilot study demonstrated positive effects on child and caregiver outcomes immediately following the intervention. The objective of this study was to examine the sustainability of these effects 6-months post-intervention.\u0000\u0000\u0000METHODS\u0000Thirty children (ages 4 to 8) with prenatal alcohol exposure and their caregivers were enrolled in the original study. Families were randomized to the Families on Track intervention or an active comparison group that provided comprehensive assessment and individualized feedback. The intervention integrated a positive parenting curriculum and a child skills group. Families were assessed at baseline, post-intervention, and 6-month follow up visits. Follow up data were available for 24 families on child and caregiver outcomes. Data were analyzed using effect size calculations and analysis of variance techniques.\u0000\u0000\u0000RESULTS\u0000Relative to the comparison group, intervention families showed continued gains in parenting efficacy and maintained prior improvements in FASD knowledge over the follow-up period. Although intervention families reported a decrease in their needs being met over the follow up period, they continued to report their needs being met to greater extent than those in the comparison group. Consistent with post-intervention outcomes, children in both groups exhibited similar decreases in child disruptive behavior 6 months following the intervention. Unfortunately, positive gains seen at post-intervention for child self-esteem and emotion regulation were attenuated at follow-up.\u0000\u0000\u0000CONCLUSIONS\u0000This pilot study yielded promising effects on important areas of caregiver functioning. However, the intervention's impact on child functioning waned over time, suggesting the need for sustained or alternate child intervention.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"1 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82896307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Derrick R. Samuelson, Min Gu, J. Shellito, P. Molina, Christopher M. Taylor, Meng Luo, D. Welsh
BACKGROUND Alcohol use causes significant disruption of intestinal microbial communities, yet exactly how these dysbiotic communities interact with the host is unclear. We sought to understand the role of microbial products associated with alcohol-dysbiosis in mice on intestinal permeability and immune activation in an in-vitro model system. METHODS Microbiota samples from binge-on-chronic alcohol-fed and pair-fed male and female mice were cultured in Gifu Anaerobic Broth for 24 hours under anaerobic conditions. Live/whole organisms were removed, microbial products were collected, and added to human peripheral blood mononuclear cells (PBMC) or polarized C2BBe1 intestinal epithelial monolayers. Following stimulation, transepithelial electrical resistance (TEER) was measured using a volt/ohm meter and immune activation of PBMC was assessed via flow cytometry. RESULTS Microbial products from male and female alcohol-fed mice significantly decreased TEER (mean percentage change from baseline alcohol-fed 0.86 Ω/cm2 v. pair-fed 1.10 Ω/cm2 ) compared to microbial products from control mice. Following ex-vivo stimulation immune activation of PBMC was assessed via flow cytometry. We found that microbial products from alcohol-fed mice significantly increased the percentage of CD38+ CD4+ (mean alcohol-fed 17.32%+0.683% SD v. mean pair-fed 14.2%+1.21% SD, P<0.05) and CD8+ (mean alcohol-fed 20.28%+0.88% SD v. mean pair-fed 12.58%+3.59% SD, P<0.05) T-cells. CONCLUSIONS Collectively, these data suggest that microbial products contribute to immune activation and intestinal permeability associated with alcohol dysbiosis. Further, utilization of these ex-vivo microbial product assays will allow us to rapidly assess the impact of microbial products on intestinal permeability and immune activation and to identify probiotic therapies to ameliorate these defects. This article is protected by copyright. All rights reserved.
{"title":"Intestinal microbial products from alcohol-fed mice contribute to intestinal permeability and peripheral immune activation.","authors":"Derrick R. Samuelson, Min Gu, J. Shellito, P. Molina, Christopher M. Taylor, Meng Luo, D. Welsh","doi":"10.1111/acer.14176","DOIUrl":"https://doi.org/10.1111/acer.14176","url":null,"abstract":"BACKGROUND\u0000Alcohol use causes significant disruption of intestinal microbial communities, yet exactly how these dysbiotic communities interact with the host is unclear. We sought to understand the role of microbial products associated with alcohol-dysbiosis in mice on intestinal permeability and immune activation in an in-vitro model system.\u0000\u0000\u0000METHODS\u0000Microbiota samples from binge-on-chronic alcohol-fed and pair-fed male and female mice were cultured in Gifu Anaerobic Broth for 24 hours under anaerobic conditions. Live/whole organisms were removed, microbial products were collected, and added to human peripheral blood mononuclear cells (PBMC) or polarized C2BBe1 intestinal epithelial monolayers. Following stimulation, transepithelial electrical resistance (TEER) was measured using a volt/ohm meter and immune activation of PBMC was assessed via flow cytometry.\u0000\u0000\u0000RESULTS\u0000Microbial products from male and female alcohol-fed mice significantly decreased TEER (mean percentage change from baseline alcohol-fed 0.86 Ω/cm2 v. pair-fed 1.10 Ω/cm2 ) compared to microbial products from control mice. Following ex-vivo stimulation immune activation of PBMC was assessed via flow cytometry. We found that microbial products from alcohol-fed mice significantly increased the percentage of CD38+ CD4+ (mean alcohol-fed 17.32%+0.683% SD v. mean pair-fed 14.2%+1.21% SD, P<0.05) and CD8+ (mean alcohol-fed 20.28%+0.88% SD v. mean pair-fed 12.58%+3.59% SD, P<0.05) T-cells.\u0000\u0000\u0000CONCLUSIONS\u0000Collectively, these data suggest that microbial products contribute to immune activation and intestinal permeability associated with alcohol dysbiosis. Further, utilization of these ex-vivo microbial product assays will allow us to rapidly assess the impact of microbial products on intestinal permeability and immune activation and to identify probiotic therapies to ameliorate these defects. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"34 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2019-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79446880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-01Epub Date: 2019-07-24DOI: 10.1111/acer.14145
Arturo Hernandez
The liver is a main target of thyroid hormones (TH), which can regulate the expression of multiple genes in this tissue, most notably, those associated with the metabolism and physiology of lipids. Systemic TH status is associated with biochemical parameters dependent on liver function, including cholesterol level. For this reason, the liver is considered a desirable therapeutic target for tissue-specific thyromimetic action. This article is protected by copyright. All rights reserved.
{"title":"Thyroid Hormone and Alcoholic Fatty Liver: The Developmental Input.","authors":"Arturo Hernandez","doi":"10.1111/acer.14145","DOIUrl":"https://doi.org/10.1111/acer.14145","url":null,"abstract":"The liver is a main target of thyroid hormones (TH), which can regulate the expression of multiple genes in this tissue, most notably, those associated with the metabolism and physiology of lipids. Systemic TH status is associated with biochemical parameters dependent on liver function, including cholesterol level. For this reason, the liver is considered a desirable therapeutic target for tissue-specific thyromimetic action. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"43 9","pages":"1834-1837"},"PeriodicalIF":3.2,"publicationDate":"2019-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/acer.14145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37398361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-01Epub Date: 2019-07-16DOI: 10.1111/acer.14140
Damien A Bellos, Dhara Sharma, Megan R McMullen, Jeanette Wat, Paramananda Saikia, Carol A de la Motte, Laura E Nagy
BACKGROUND Specific-sized species of the carbohydrate hyaluronan elicit a variety of cellular responses mediating tissue integrity and repair, as well as regulating inflammatory responses. Orally provided hyaluronan with an average molecular weight of 35kDa (HA35) protects mice from short term ethanol-induced liver injury. This protection was associated with maintenance of the co-localization of zonula occludins-1 (ZO-1) and occludin at tight junctions in the proximal colon. However, it is not known whether HA35 also protects other regions of the intestine or whether protection is due to a direct and/or indirect interaction of HA35 with the intestinal epithelium. METHODS Female C57BL/6J mice were fed an ethanol containing diet or pair-fed control diet (4 days) and treated with or without HA35 via daily gavage during the last 3 days of ethanol feeding. Intestinal morphology and tight junction integrity was assessed. Differentiated Caco-2 cells were transfected or not with scrambled siRNA or siRNA targeting layilin, a hyaluronan receptor. Caco-2 cells were treated with or without HA35 prior to challenge with ethanol. Localization of tight junction proteins, FITC-dextran permeability and transepithelial electrical resistance (TEER) were evaluated. RESULTS While short-term ethanol did not result in any apparent changes in the gross morphology of the intestine, co-localization of ZO-1 and occludin at tight junctions was decreased in proximal and distal colon. HA35 prevented these effects of ethanol. In differentiated Caco-2 cells, ethanol decreased the localization of ZO-1 and occludin at tight junctions and increased permeability of FITC-dextran. At higher concentrations, ethanol also decreased TEER. Pre-treatment with HA35 prevented these changes. When the hyaluronan receptor Layilin was knocked down in Caco-2 cells, HA35 no longer protected cells from ethanol-induced loss of tight junctions. CONCLUSION Taken together, these data indicate that HA35 interacts with Layilin on intestinal epithelial cells and maintains intestinal tight junction integrity during short-term ethanol exposure. This article is protected by copyright. All rights reserved.
{"title":"Specifically Sized Hyaluronan (35 kDa) Prevents Ethanol-Induced Disruption of Epithelial Tight Junctions Through a layilin-Dependent Mechanism in Caco-2 Cells.","authors":"Damien A Bellos, Dhara Sharma, Megan R McMullen, Jeanette Wat, Paramananda Saikia, Carol A de la Motte, Laura E Nagy","doi":"10.1111/acer.14140","DOIUrl":"https://doi.org/10.1111/acer.14140","url":null,"abstract":"BACKGROUND Specific-sized species of the carbohydrate hyaluronan elicit a variety of cellular responses mediating tissue integrity and repair, as well as regulating inflammatory responses. Orally provided hyaluronan with an average molecular weight of 35kDa (HA35) protects mice from short term ethanol-induced liver injury. This protection was associated with maintenance of the co-localization of zonula occludins-1 (ZO-1) and occludin at tight junctions in the proximal colon. However, it is not known whether HA35 also protects other regions of the intestine or whether protection is due to a direct and/or indirect interaction of HA35 with the intestinal epithelium. METHODS Female C57BL/6J mice were fed an ethanol containing diet or pair-fed control diet (4 days) and treated with or without HA35 via daily gavage during the last 3 days of ethanol feeding. Intestinal morphology and tight junction integrity was assessed. Differentiated Caco-2 cells were transfected or not with scrambled siRNA or siRNA targeting layilin, a hyaluronan receptor. Caco-2 cells were treated with or without HA35 prior to challenge with ethanol. Localization of tight junction proteins, FITC-dextran permeability and transepithelial electrical resistance (TEER) were evaluated. RESULTS While short-term ethanol did not result in any apparent changes in the gross morphology of the intestine, co-localization of ZO-1 and occludin at tight junctions was decreased in proximal and distal colon. HA35 prevented these effects of ethanol. In differentiated Caco-2 cells, ethanol decreased the localization of ZO-1 and occludin at tight junctions and increased permeability of FITC-dextran. At higher concentrations, ethanol also decreased TEER. Pre-treatment with HA35 prevented these changes. When the hyaluronan receptor Layilin was knocked down in Caco-2 cells, HA35 no longer protected cells from ethanol-induced loss of tight junctions. CONCLUSION Taken together, these data indicate that HA35 interacts with Layilin on intestinal epithelial cells and maintains intestinal tight junction integrity during short-term ethanol exposure. This article is protected by copyright. All rights reserved.","PeriodicalId":7410,"journal":{"name":"Alcoholism, clinical and experimental research","volume":"43 9","pages":"1848-1858"},"PeriodicalIF":3.2,"publicationDate":"2019-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/acer.14140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37363400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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