Pub Date : 2025-01-04DOI: 10.1016/j.alcohol.2025.01.001
Justin J. Verlinden , Mairead E. Moloney , Olga A. Vsevolozhskaya , Lauren N. Whitehurst , Jessica Weafer
Insomnia is a risk factor for hazardous drinking, yet the mechanisms underlying this risk are not well characterized. Two factors that might contribute to the relationship between insomnia and drinking are stress and depression. Insomnia is strongly associated with increased stress and depression, which are, in turn, strongly linked to hazardous drinking. Here we conducted a preliminary investigation to determine whether perceived stress and depression indirectly explain the relationship between insomnia and hazardous drinking. Heavy drinkers with self-reported insomnia (n = 405: 270 women, 134 men, 1 non-binary) completed self-report measures of hazardous drinking, insomnia, perceived stress, and depression. Results from our primary cross-sectional parallel mediation model with insomnia as the predictor and hazardous drinking as the outcome showed that, when accounting for the influence of both perceived stress and depression, there was a partial indirect effect of insomnia on hazardous drinking through perceived stress, 95% CI [0.014, 0.205], but not depression, 95% CI [-0.080, 0.172]. In our competing cross-sectional parallel mediation model with hazardous drinking as the predictor and insomnia as the outcome, there was a partial indirect effect of hazardous drinking on insomnia through depression 95% CI [0.016, 0.059], but not perceived stress 95% CI: [-0.026, 0.011]. Results suggest that insomnia may be related to hazardous drinking through its effects on stress and that hazardous drinking may be related to insomnia through its effects on depression. These findings lay the groundwork for future longitudinal studies assessing the causal roles of stress and depression in the insomnia-AUD relationship.
{"title":"Indirect effects of perceived stress and depression on the relationship between insomnia symptoms and hazardous drinking","authors":"Justin J. Verlinden , Mairead E. Moloney , Olga A. Vsevolozhskaya , Lauren N. Whitehurst , Jessica Weafer","doi":"10.1016/j.alcohol.2025.01.001","DOIUrl":"10.1016/j.alcohol.2025.01.001","url":null,"abstract":"<div><div>Insomnia is a risk factor for hazardous drinking, yet the mechanisms underlying this risk are not well characterized. Two factors that might contribute to the relationship between insomnia and drinking are stress and depression. Insomnia is strongly associated with increased stress and depression, which are, in turn, strongly linked to hazardous drinking. Here we conducted a preliminary investigation to determine whether perceived stress and depression indirectly explain the relationship between insomnia and hazardous drinking. Heavy drinkers with self-reported insomnia (n = 405: 270 women, 134 men, 1 non-binary) completed self-report measures of hazardous drinking, insomnia, perceived stress, and depression. Results from our primary cross-sectional parallel mediation model with insomnia as the predictor and hazardous drinking as the outcome showed that, when accounting for the influence of both perceived stress and depression, there was a partial indirect effect of insomnia on hazardous drinking through perceived stress, 95% CI [0.014, 0.205], but not depression, 95% CI [-0.080, 0.172]. In our competing cross-sectional parallel mediation model with hazardous drinking as the predictor and insomnia as the outcome, there was a partial indirect effect of hazardous drinking on insomnia through depression 95% CI [0.016, 0.059], but not perceived stress 95% CI: [-0.026, 0.011]. Results suggest that insomnia may be related to hazardous drinking through its effects on stress and that hazardous drinking may be related to insomnia through its effects on depression. These findings lay the groundwork for future longitudinal studies assessing the causal roles of stress and depression in the insomnia-AUD relationship.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"123 ","pages":"Pages 1-9"},"PeriodicalIF":2.5,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-26DOI: 10.1016/j.alcohol.2024.12.007
Tengfei Li , George Luta , Prosper N'Gouemo
Prenatal alcohol exposure (PAE) during pregnancy can increase the prevalence of N-methyl-d-aspartate (NMDA)-induced generalized tonic-clonic seizures (GTCSs) in developing rats. However, it is unclear whether phenobarbital (PB) can suppress these PAE-related seizures. To explore this knowledge gap, we investigated the effects of acute PB treatment on NMDA-induced seizures in postpartum rats, prenatally exposed to alcohol on gestational day 18 (GD18), at two developmental stages: day 7 (P7), the equivalent of pre-term neonates, and day 15 (P15), the equivalent of full-term neonates. Timed-pregnant female Sprague–Dawley rats were given a single dose of alcohol or its vehicle on GD18 during the second-trimester equivalent. Male and female postpartum rats were tested for the effectiveness of single-dose treatment with either PB or its vehicle in suppressing NMDA-induced seizures. These seizures include wild running-like behavior (WRLB), flexion seizures (FSs), clonic seizures (CSs), generalized tonic-clonic seizures (GTCSs), and tonic seizures (TSs) in P7 and P15 rats. Analyses revealed that P7 rats were more likely to develop GTCSs after PB administration than P15 rats; this effect was associated with shorter latencies to develop NMDA-induced seizures. Moreover, PAE-related seizure severity is less responsive to PB treatment in P7 rats than in P15 rats. These findings suggest that the PAE-related GTCS model in P7 rats can be used to investigate the mechanisms underlying PB-resistant seizures in developing rats.
妊娠期产前酒精暴露（PAE）可增加发育大鼠n -甲基- d -天冬氨酸（NMDA）诱导的全身性强直-阵挛性癫痫（GTCSs）的患病率。然而，尚不清楚苯巴比妥（PB）是否能抑制这些与pae相关的癫痫发作。为了探索这一知识差距，我们研究了急性PB治疗对产后大鼠nmda诱导癫痫发作的影响，这些大鼠在妊娠第18天（GD18）暴露于酒精中，在两个发育阶段：第7天（P7），相当于早产儿，第15天（P15），相当于足月新生儿。在妊娠中期等量给予妊娠期雌性Sprague-Dawley大鼠单剂量酒精或其载体GD18。用单剂量PB或其载体对雄性和雌性产后大鼠进行抑制nmda诱导癫痫发作的效果试验。P7和P15大鼠的发作包括狂奔样行为（WRLB）、屈曲性发作（FSs）、阵挛性发作（CSs）、全身性强直-阵挛性发作（GTCSs）和强直性发作（TSs）。分析显示，P7大鼠比P15大鼠更容易在给药后发生gtcs；这种效应与nmda诱发癫痫发作的潜伏期较短有关。此外，P7大鼠与P15大鼠相比，pae相关的gtcs对PB治疗的反应较差。这些发现提示P7大鼠pae相关的GTCS模型可用于研究发育中大鼠pb抵抗性癫痫发作的机制。
{"title":"Age-related impact of phenobarbital in suppressing prenatal alcohol exposure-related seizures in developing rats","authors":"Tengfei Li , George Luta , Prosper N'Gouemo","doi":"10.1016/j.alcohol.2024.12.007","DOIUrl":"10.1016/j.alcohol.2024.12.007","url":null,"abstract":"<div><div>Prenatal alcohol exposure (PAE) during pregnancy can increase the prevalence of <em>N</em>-methyl-<span>d</span>-aspartate (NMDA)-induced generalized tonic-clonic seizures (GTCSs) in developing rats. However, it is unclear whether phenobarbital (PB) can suppress these PAE-related seizures. To explore this knowledge gap, we investigated the effects of acute PB treatment on NMDA-induced seizures in postpartum rats, prenatally exposed to alcohol on gestational day 18 (GD18), at two developmental stages: day 7 (P7), the equivalent of pre-term neonates, and day 15 (P15), the equivalent of full-term neonates. Timed-pregnant female Sprague–Dawley rats were given a single dose of alcohol or its vehicle on GD18 during the second-trimester equivalent. Male and female postpartum rats were tested for the effectiveness of single-dose treatment with either PB or its vehicle in suppressing NMDA-induced seizures. These seizures include wild running-like behavior (WRLB), flexion seizures (FSs), clonic seizures (CSs), generalized tonic-clonic seizures (GTCSs), and tonic seizures (TSs) in P7 and P15 rats. Analyses revealed that P7 rats were more likely to develop GTCSs after PB administration than P15 rats; this effect was associated with shorter latencies to develop NMDA-induced seizures. Moreover, PAE-related seizure severity is less responsive to PB treatment in P7 rats than in P15 rats. These findings suggest that the PAE-related GTCS model in P7 rats can be used to investigate the mechanisms underlying PB-resistant seizures in developing rats.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"123 ","pages":"Pages 39-50"},"PeriodicalIF":2.5,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-24DOI: 10.1016/j.alcohol.2024.12.005
Nathaniel Albright , Ethan Morgan
Introduction
Alcohol use, and its relationship with mental health outcomes, remains a public health priority. Yet, little research has focused on this association among aging sexual and gender minority (SGM) populations with even less dedicated to the unique issues of those aging with HIV, a gap we begin to fill here.
Methods
Data for this analysis originated from the Columbus Healthy Aging Project (CHAP), a cross-sectional survey among adults ≥50 years who reside in the Columbus, Ohio. Multivariable linear regression models were utilized to assess the relationship between alcohol use (via AUDIT score) and several mental health outcomes (e.g., depression, anxiety, perceived stress, and sexual orientation microaggressions), adjusting for demographic characteristics and other risk factors. Models were assessed for moderation by self-reported HIV status.
Results
Among the entire sample (N = 787), mean perceived stress score was 18.2 (SD = 5.5), mean anxiety score was 9.1 (5.9), and mean depression score was 9.9 (SD = 6.7). 32 (7.4%) self-reported as PLWH. Among those reporting any alcohol use, mean AUDIT score use was 10.5 (SD = 10.9). Each of the mental health outcome measures were positively associated with AUDIT score. Meanwhile, there was significant moderation of each of the mental health outcome measures by HIV status, suggesting a stronger association with AUDIT score in each case.
Conclusion
Our results suggest that there are broad stressors impacting alcohol use not only among older SGM broadly but in particular among PLWH. Although a diverse set of results, these data highlight the need for more research on alcohol use among aging SGM populations, particularly PLWH and those identifying as a different gender identity.
{"title":"Assessing the relationship between mental health and AUDIT score among older sexual and gender minorities","authors":"Nathaniel Albright , Ethan Morgan","doi":"10.1016/j.alcohol.2024.12.005","DOIUrl":"10.1016/j.alcohol.2024.12.005","url":null,"abstract":"<div><h3>Introduction</h3><div>Alcohol use, and its relationship with mental health outcomes, remains a public health priority. Yet, little research has focused on this association among aging sexual and gender minority (SGM) populations with even less dedicated to the unique issues of those aging with HIV, a gap we begin to fill here.</div></div><div><h3>Methods</h3><div>Data for this analysis originated from the Columbus Healthy Aging Project (CHAP), a cross-sectional survey among adults ≥50 years who reside in the Columbus, Ohio. Multivariable linear regression models were utilized to assess the relationship between alcohol use (via AUDIT score) and several mental health outcomes (e.g., depression, anxiety, perceived stress, and sexual orientation microaggressions), adjusting for demographic characteristics and other risk factors. Models were assessed for moderation by self-reported HIV status.</div></div><div><h3>Results</h3><div>Among the entire sample (N = 787), mean perceived stress score was 18.2 (SD = 5.5), mean anxiety score was 9.1 (5.9), and mean depression score was 9.9 (SD = 6.7). 32 (7.4%) self-reported as PLWH. Among those reporting any alcohol use, mean AUDIT score use was 10.5 (SD = 10.9). Each of the mental health outcome measures were positively associated with AUDIT score. Meanwhile, there was significant moderation of each of the mental health outcome measures by HIV status, suggesting a stronger association with AUDIT score in each case.</div></div><div><h3>Conclusion</h3><div>Our results suggest that there are broad stressors impacting alcohol use not only among older SGM broadly but in particular among PLWH. Although a diverse set of results, these data highlight the need for more research on alcohol use among aging SGM populations, particularly PLWH and those identifying as a different gender identity.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"123 ","pages":"Pages 51-56"},"PeriodicalIF":2.5,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-21DOI: 10.1016/j.alcohol.2024.12.002
John Marendes (Jr.), Marissa A. Muench, Camille L. Young, Amira A. Ghaly, Brendan J. Tunstall
Introduction
Chronic alcohol exposure in humans and rodents causes tolerance to the analgesic effects of alcohol, and enhances pain sensitivity during alcohol withdrawal (i.e., hyperalgesia). The available literature suggests a bidirectional enhancement between chronic alcohol consumption and chronic pain sensitivity. We previously found that oxytocin administration could reduce alcohol consumption in alcohol-dependent rats, and now hypothesize that oxytocin, through analgesic action in the central nervous system, could ameliorate the hyperalgesia induced by alcohol-dependence. To test this hypothesis, we assessed the ability of central and peripheral oxytocin administration to alter thermal (Hargreaves assay) and mechanical (Von Frey assay) pain sensitivity, in male and female rats, made alcohol dependent through repeated cycles of chronic-intermittent ethanol-vapor exposure (CIEV; compared to air-exposed controls).
Methods
Male and female cohorts of Wistar rats were surgically prepared with an ICV cannula and assigned to two groups matched in terms of initial response in the Hargreaves assay. Rats in the alcohol dependent group were exposed to chronic-intermittent alcohol-vapor, while air-exposed control rats were exposed only to room air and served as the control group. The thermal nociception sensitivity of all rats was monitored via weekly Hargreaves assay to determine alcohol-dependence-induced hyperalgesia in dependent rats. Next, rats were ICV administered oxytocin (0, 0.5, or 5 μg in 2.5 μL saline) prior to Hargreaves testing (Experiment 1) or Von Frey testing (Experiment 2). Finally, rats were IP administered oxytocin (0, 0.1, or 1 mg/kg) prior to Hargreaves testing (Experiment 3) or Von Frey testing (Experiment 4). In a follow-up experiment, female rats were tested to directly compare three methods for applying the Von Frey test.
Results
Male and female alcohol-dependent rats developed hyperalgesia, observed in the Hargreaves assay (Experiment 1 & 3), however, hyperalgesia was not so readily observed when the same rats were tested in the Von Frey assay (Experiments 2 & 4, with the exception of female rats in Experiment 4; follow-up testing indicated that the method of Von Frey test employed is likely important to explain this discrepancy). In both the Hargreaves and Von Frey assays, and in both male and female rats, following central or peripheral administration, oxytocin produced analgesia similarly in both alcohol dependent rats and air-exposed controls.
Conclusion
Together, these data suggest the oxytocin system could be targeted to produce therapeutic action in disease that produce hyperalgesia such as in alcohol dependence. We discuss methodological considerations and future experiments that could further elucidate a role for oxytocin in the overlapping neurobiology of alcohol dependence and chronic pain.
{"title":"Analgesic effect of oxytocin in alcohol-dependent male and female rats","authors":"John Marendes (Jr.), Marissa A. Muench, Camille L. Young, Amira A. Ghaly, Brendan J. Tunstall","doi":"10.1016/j.alcohol.2024.12.002","DOIUrl":"10.1016/j.alcohol.2024.12.002","url":null,"abstract":"<div><h3>Introduction</h3><div>Chronic alcohol exposure in humans and rodents causes tolerance to the analgesic effects of alcohol, and enhances pain sensitivity during alcohol withdrawal (i.e., hyperalgesia). The available literature suggests a bidirectional enhancement between chronic alcohol consumption and chronic pain sensitivity. We previously found that oxytocin administration could reduce alcohol consumption in alcohol-dependent rats, and now hypothesize that oxytocin, through analgesic action in the central nervous system, could ameliorate the hyperalgesia induced by alcohol-dependence. To test this hypothesis, we assessed the ability of central and peripheral oxytocin administration to alter thermal (Hargreaves assay) and mechanical (Von Frey assay) pain sensitivity, in male and female rats, made alcohol dependent through repeated cycles of chronic-intermittent ethanol-vapor exposure (CIEV; compared to air-exposed controls).</div></div><div><h3>Methods</h3><div>Male and female cohorts of Wistar rats were surgically prepared with an ICV cannula and assigned to two groups matched in terms of initial response in the Hargreaves assay. Rats in the alcohol dependent group were exposed to chronic-intermittent alcohol-vapor, while air-exposed control rats were exposed only to room air and served as the control group. The thermal nociception sensitivity of all rats was monitored via weekly Hargreaves assay to determine alcohol-dependence-induced hyperalgesia in dependent rats. Next, rats were ICV administered oxytocin (0, 0.5, or 5 μg in 2.5 μL saline) prior to Hargreaves testing (Experiment 1) or Von Frey testing (Experiment 2). Finally, rats were IP administered oxytocin (0, 0.1, or 1 mg/kg) prior to Hargreaves testing (Experiment 3) or Von Frey testing (Experiment 4). In a follow-up experiment, female rats were tested to directly compare three methods for applying the Von Frey test.</div></div><div><h3>Results</h3><div>Male and female alcohol-dependent rats developed hyperalgesia, observed in the Hargreaves assay (Experiment 1 & 3), however, hyperalgesia was not so readily observed when the same rats were tested in the Von Frey assay (Experiments 2 & 4, with the exception of female rats in Experiment 4; follow-up testing indicated that the method of Von Frey test employed is likely important to explain this discrepancy). In both the Hargreaves and Von Frey assays, and in both male and female rats, following central or peripheral administration, oxytocin produced analgesia similarly in both alcohol dependent rats and air-exposed controls.</div></div><div><h3>Conclusion</h3><div>Together, these data suggest the oxytocin system could be targeted to produce therapeutic action in disease that produce hyperalgesia such as in alcohol dependence. We discuss methodological considerations and future experiments that could further elucidate a role for oxytocin in the overlapping neurobiology of alcohol dependence and chronic pain.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"123 ","pages":"Pages 27-38"},"PeriodicalIF":2.5,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-20DOI: 10.1016/j.alcohol.2024.12.006
J. Daniel Obray , Adam R. Denton , Jayda Carroll-Deaton , Kristin Marquardt , L. Judson Chandler , Michael D. Scofield
Perineuronal nets (PNNs) are specialized components of the extracellular matrix that play a critical role in learning and memory. In a Pavlovian fear conditioning paradigm, degradation of PNNs affects the formation and storage of fear memories. This study examined the impact of adolescent intermittent ethanol (AIE) exposure by vapor inhalation on the expression of PNNs in the adult rat prelimbic (PrL) and infralimbic (IfL) subregions of the medial prefrontal cortex. Results indicated that following AIE, the total number of PNN positive cells in the PrL cortex increased in layer II/III but did not change in layer V. Conversely, in the IfL cortex, the number of PNN positive cells decreased in layer V, with no change in layer II/III. In addition, the intensity of PNN staining was significantly altered by AIE exposure, which narrowed the distribution of signal intensity, reducing the number of high and low intensity PNNs. Given these changes in PNNs, the next experiment assessed the effects of AIE and PNN digestion on extinction of a conditioned fear memory. In Air control rats, digestion of PNNs by bilateral infusion of Chondroitinase ABC (ChABC) into the IfL cortex enhanced fear extinction and reduced contextual fear renewal. In contrast, both fear extinction learning and contextual fear renewal remained unchanged following PNN digestion in AIE exposed rats. These results highlight the sensitivity of prefrontal PNNs to adolescent alcohol exposure and suggest that ChABC-induced plasticity is reduced in the IfL cortex following AIE exposure.
{"title":"Enhanced fear extinction through infralimbic perineuronal net digestion: The modulatory role of adolescent alcohol exposure","authors":"J. Daniel Obray , Adam R. Denton , Jayda Carroll-Deaton , Kristin Marquardt , L. Judson Chandler , Michael D. Scofield","doi":"10.1016/j.alcohol.2024.12.006","DOIUrl":"10.1016/j.alcohol.2024.12.006","url":null,"abstract":"<div><div>Perineuronal nets (PNNs) are specialized components of the extracellular matrix that play a critical role in learning and memory. In a Pavlovian fear conditioning paradigm, degradation of PNNs affects the formation and storage of fear memories. This study examined the impact of adolescent intermittent ethanol (AIE) exposure by vapor inhalation on the expression of PNNs in the adult rat prelimbic (PrL) and infralimbic (IfL) subregions of the medial prefrontal cortex. Results indicated that following AIE, the total number of PNN positive cells in the PrL cortex increased in layer II/III but did not change in layer V. Conversely, in the IfL cortex, the number of PNN positive cells decreased in layer V, with no change in layer II/III. In addition, the intensity of PNN staining was significantly altered by AIE exposure, which narrowed the distribution of signal intensity, reducing the number of high and low intensity PNNs. Given these changes in PNNs, the next experiment assessed the effects of AIE and PNN digestion on extinction of a conditioned fear memory. In Air control rats, digestion of PNNs by bilateral infusion of Chondroitinase ABC (ChABC) into the IfL cortex enhanced fear extinction and reduced contextual fear renewal. In contrast, both fear extinction learning and contextual fear renewal remained unchanged following PNN digestion in AIE exposed rats. These results highlight the sensitivity of prefrontal PNNs to adolescent alcohol exposure and suggest that ChABC-induced plasticity is reduced in the IfL cortex following AIE exposure.</div></div>","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"123 ","pages":"Pages 57-67"},"PeriodicalIF":2.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.alcohol.2024.10.035
N. Shashikanth , L. Basa , R. Rajenthiran, C. Nguyen, P. Raju, S.C. Lee, C. Shekhar, F. Giorgianni, R.K. Rao
{"title":"32. Alcohol-induced tissue injury at the gut-liver-brain axis is more severe in diabetic mice","authors":"N. Shashikanth , L. Basa , R. Rajenthiran, C. Nguyen, P. Raju, S.C. Lee, C. Shekhar, F. Giorgianni, R.K. Rao","doi":"10.1016/j.alcohol.2024.10.035","DOIUrl":"10.1016/j.alcohol.2024.10.035","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"121 ","pages":"Page 217"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143127755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.alcohol.2024.10.015
M.B. Gutierrez, C.M. Coopersmith, M.L. Ford
{"title":"12. Role of Foxp3+ regulatory T cells in chronic ethanol consumption and sepsis pathogenesis","authors":"M.B. Gutierrez, C.M. Coopersmith, M.L. Ford","doi":"10.1016/j.alcohol.2024.10.015","DOIUrl":"10.1016/j.alcohol.2024.10.015","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"121 ","pages":"Page 211"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143127862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1016/j.alcohol.2024.10.023
A. Mandal, A. Ratna, J. Thanikasalam, E. Kurt-Jones, P. Mandrekar
{"title":"20. Myeloid TLR4 deficient mice are not protected from alcohol-mediated liver injury and inflammation: contribution of hepatocytes and neutrophils","authors":"A. Mandal, A. Ratna, J. Thanikasalam, E. Kurt-Jones, P. Mandrekar","doi":"10.1016/j.alcohol.2024.10.023","DOIUrl":"10.1016/j.alcohol.2024.10.023","url":null,"abstract":"","PeriodicalId":7712,"journal":{"name":"Alcohol","volume":"121 ","pages":"Pages 213-214"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143141010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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