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Purpose: Following the beginning of the pandemic brought about by the novel coronavirus which causes COVID-19, the first COVID-19 vaccination received emergency use authorization in the United States of America in December of 2020. Current research has shown the authorized COVID-19 vaccines are safe and effective at preventing severe illness, hospitalizations and death have a good safety profile. Additionally, the side effects associated with these vaccines are typically mild to moderate while the protection against hospitalization and severe disease is substantial. (https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/adverse-events.html). At the time of this study, there appears to be a paucity in the research related to the attitudes toward COVID-19 and COVID-19 vaccines among athletic trainers. The purpose of this study is to describe the attitudes toward COVID-19 and COVID-19 vaccines among athletic trainers. Methods: A total of 186 athletic trainers (age= 43 ± 11, years of certified experience = 20 ± 11) opened and completed the survey. Participants were sent an electronic survey via email that collected demographic information and assessed attitudes toward COVID-19 and COVID-19 vaccines. Data was downloaded and analyzed using a commercially available statistics package. Results: The majority of athletic trainers surveyed had received a COVID-19 vaccination at the time of this study (94.1%, n=175). Most athletic trainers also agreed that the health of their patients was more important than disruption of their competition season due to COVID-19 (82.3%, n=153). In general, the most common reason for vaccine hesitancy was the speed with which currently available COVID-19 vaccines were developed. Conclusions: The findings of this study show the majority of surveyed athletic trainers had received a COVID-19 vaccine. The primary reason for athletic trainers not receiving a COVID-19 vaccination appeared to be the speed at which the currently available COVID-19 vaccines were developed. Given the available information on the new mRNA COVID vaccines, this may indicate a lack of education on the development of the COVID-19 vaccines. As athletic trainers continue to work in day-to-day patient care, it is imperative to determine the best methods for educating athletic trainers on the potential benefits of COVID-19 vaccinations.

Purpose: Burnout is a psychological cognitive-affective syndrome that is defined by emotional exhaustion, depersonalization, and reduced accomplishment. Burnout has been identified as a common issue in several allied healthcare professions, and is often contributed to by stress, workload, and social support. At the time of this study, there appears to be no published research on the relationship between levels of sexual harassment and levels of burnout. The purpose of this was to describe the prevalence of burnout and sexual harassment among allied healthcare professionals and students. A secondary purpose was to examine the potential relationship between sexual harassment and burnout among allied healthcare professionals and students. Methods: A total of 173 allied healthcare professionals and students (age= 43 ± 13, years of certified experience = 17 ± 12) opened and completed the instrument. Participants were sent an electronic survey via email that collected demographic information and assessed levels of burnout and sexual harassment. Data was downloaded and analyzed using a commercially available statistics package. Results: On average, allied healthcare professionals and students were at risk of burnout. There was a significant positive correlation between levels of burnout and sexual harassment. Additionally, females were significantly more likely to report workplace sexual harassment than males. Conclusions: The findings of this study suggest, on average, allied healthcare professionals and students are at risk of burnout. The findings also suggest that female allied healthcare professionals and students are more likely to experience burnout as a result of workplace sexual harassment. There is an evident need for employers to enhance policies and procedures to reduce and eliminate the occurrence of sexual harassment in the workplace. Doing so has the potential to reduce the risk of burnout among female allied healthcare professionals and students.

Purpose: After the widespread transmission of the novel coronavirus that causes COVID-19, the first COVID-19 vaccination received emergency use authorization in the United States in December of 2020. Current research has shown the authorized COVID-19 vaccines to be safe and effective at preventing severe illness. At the time of this study, there appears to be no published research on the attitudes and receipt of COVID-19 vaccinations among occupational therapy professionals and students. The purpose of this study is to describe the attitudes and receipt of COVID-19 vaccinations among occupational therapy professionals and students in early 2021. Methods: A total of 114 occupational therapy professionals and students (age= 41 ± 15, years of certified experience = 13 ± 13) opened the survey link and completed the instrument. Participants were sent an electronic survey via email that collected demographic information and assessed attitudes and receipt of COVID-19 vaccination. Data was downloaded and analyzed using a commercially available statistics package. Results: The majority of occupational therapy professionals in this study agreed on some level that they were comfortable (Strongly Agree = 36.0%, Agree = 16.7%, Somewhat Agree = 10.5%). Most occupational therapy professionals and students stated they had or would receive a COVID-19 vaccination. The majority of participants reported personal, household, and community safety as the primary considerations for receiving a COVID-19 vaccination. In general, these factors were a larger factor for participants than public perception or personal liberties being infringed upon. Conclusions: The findings of this study suggest a majority of occupational therapy professionals and students are comfortable with the current level of approvals for available COVID-19 vaccinations, and at the time of the survey had or intending to be vaccinated. As occupational therapy professionals and students continue to work in day-to-day patient care, it is imperative to consider the best means of educating occupational therapy professionals and students on the potential benefits of COVID-19 vaccinations.

Purpose: Following the widespread transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), multiple business and schools drastically reduced face-to-face services. Additionally, many state and local governments enacted face mask mandates and other legislations aimed at decreasing the spread of the virus. Current research is being conducted to evaluate the epidemiology, recognition, treatment, and prevention of coronavirus disease 2019 (COVID-19), the disease associated with SARS-CoV-2. At the time of this study, there is no published research on the attitudes and usage of face masks or face coverings among certified occupational therapy professionals during the COVID-19 Pandemic. The purpose of this study is to describe the attitudes and usage of face masks or face coverings among occupational therapy professionals in the state of Texas during the COVID-19 pandemic. Methods: A total of 107 occupational therapy professionals (age= 42 ± 12, years of certified experience = 18 ± 11) opened the survey link and completed the instrument. Participants were sent an electronic survey via email that collected demographic information and assessed attitudes and usage of face masks or face coverings. Data was downloaded and analyzed using a commercially available statistics package. Results: The overwhelming majority of occupational therapy professionals in this study agreed on some level that the use of face masks to mitigate the transmission of SARS-CoV2 was strongly supported by the available evidence (Strongly Agree = 65.4%, Agree = 19.6%, Somewhat Agree = 5.6%). Most occupational therapy professionals also reported that their institutions currently had a mandate in place requiring face masks during patient encounters and coworker interactions (Patient Encounters = 94.4%, Coworker Interactions = 86.9%). Most occupational therapy professionals reported wearing face masks the majority of the time when entering public spaces. Occupational therapy professionals cited the influence of their personal use of face masks was for personal health, health of those in their household, and the health of their patients. Conclusions: The findings of this study suggest a majority of occupational therapy professionals in Texas are wearing face masks or face coverings, even when not actively involved in patient care or other aspects of their jobs. Future research should be conducted to assess the use of face masks among other allied health care professions

Background Hepatic stellate cell (HSC) differentiation/activation is central to liver fibrosis and is innately linked to the immune response to liver injury. Exosomes (EXOs) are important means of communication between cell populations. This study sought to characterize EXO release from HSCs and the effect of HSC-EXOs on macrophage cytokine release/function. Methods Liver from a rat fibrosis model was analyzed for EXO expression and localization. Quiescent and culture-activated rat and mouse HSCs and activated human HSCs were analyzed for microRNA expression. Mouse, rat, and human HSCs were culture-activated and EXOs purified from culture medium prior to addition to macrophages, and interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα) mRNA and protein measured. The effect of activated HSC-EXOs on macrophage migration was assayed. Results Activation of rat HSCs led to increased EXO production in vivo, an effect mirrored by in vitro rat HSC culture-activation. Culture activation of mouse and rat HSCs led to altered EXO microRNA profiles, with a similar microRNA profile detected in activated human HSCs. Addition of activated HSC-EXOs to macrophages stimulated IL-6 and TNFα mRNA expression and protein secretion in mouse and human macrophages, but not for rat HSC-EXO-macrophages. Addition of human EXOs to macrophages stimulated migration, effects mirrored by the direct addition of rhIL-6 and rhTNFα. Conclusions HSC-EXOs associate with macrophages and stimulate cytokine synthesis-release and macrophage migration. Constructing a comprehensive understanding of EXO interactions between liver cell populations in the setting of inflammation/fibrosis increases the potential for developing new diagnostic/therapeutic approaches.

Fibrotic liver injury is a significant healthcare burden in the United States. It represents a major cause of morbidity and mortality for which there are no effective Food and Drug Administration-approved treatment strategies. Fibrosis is considered a disruption of the normal wound healing responses mediated by fibroblastic cells, which are triggered and sustained by pro-fibrotic cytokines such as transforming growth factor beta 1 (TGF-β1). TGF-β1-mediated trans-differentiation of hepatic stellate cells (HSCs) from quiescent to activated myofibroblasts is a pivotal event in the development of fibrosis. Activation is accompanied by global changes in microRNA (miR) expression. It has been previously reported that miR19b is decreased in activated HSCs and contributes to increased expression of TGF-β receptor II and connective tissue growth factor, both confirmed targets of miR19b. An adeno-associated virus serotype 2 vector (AAV2) with a miR19b transgene downstream of enhanced green fluorescent protein under the murine collage alpha 1(I) promoter was developed specifically to target HSCs. Male Sprague Dawley rats (250 g) underwent sham or bile-duct ligation (BDL) surgery. Directly after BDL, rats received AAV2-miR19b, AAV2-control, or vehicle normal saline (NS) by portal-vein injection. After 2 weeks, the animals were euthanized, and blood was collected for alanine and aspartate aminotransferase, total and direct bilirubin, and alkaline phosphatase. Tissue was collected for RNA and protein extraction and histology. Fibrosis and measures of hepatic injury were significantly reduced in AAV2-miR19b-treated rats in combination with significant improvements in total and direct bilirubin. Histological analysis of collagen by PicroSirius Red staining revealed a ∼50% reduction compared to AAV2-control or NS-injected animals. Pro-fibrotic markers, smooth-muscle alpha-actin, TGF-β receptor II, and collagen alpha 2(I) mRNA and protein were significantly decreased compared to AAV2-control and NS groups. AAV2-mediated reintroduction of miR-19b, specifically expressed in HSCs, improved liver function, inhibited fibrosis, and improved measures of hepatic injury in a BDL model.

Hepatitis C virus (HCV)-related cirrhosis, one of the most common etiologies of liver cirrhosis in the Western world, is a risk factor for hepatocellular carcinoma. To confirm and improve current effectiveness of screening and prognosis of patients with established cirrhosis, a credible, simple plasma biomarker is needed. Hepatic stellate cell activation, a pivotal event in cirrhosis development, results in increased secretion of extracellular matrix proteins, including tenascin-C (TnC). Herein, we tested TnC as a simple biomarker to identify cirrhotic patients with active HCV infection from those with HCV eradication. A prospective study of subjects with HCV-related cirrhosis, stratified into two groups, HCV or virologic cure, was conducted. Plasma TnC expression was measured by ELISA and Western blots. TnC values were correlated with markers of liver injury and ROC analyses performed between groups. The HCV cirrhotic cohort, consisting mostly of men (56%), Caucasians (76%), and genotype 1a or 1b (84%), was compared to healthy controls (HCs). Plasma TnC was significantly higher in HCV cirrhotic patients with active infection compared to HCs (P

Our data describe autophagic flux in primary rat hepatic stellate cells (rHSCs) treated with pro-fibrotic growth factor, transforming growth factor beta (TGF-β). An autophagy flux experiment determines the rate of synthesis and degradation of the autophagosome marker, LC3-II in the presence and absence of the lysosomal inhibitor bafilomcyin, which blocks LC3-II degradation in lysosomes. The effects of a test agent on LC3-II flux through the autophagic pathway is determined immunochemically by its relative amounts detected in lysates of cells treated with and without bafilomycin. This measurement helps to validate whether exposure to an agent affects the biogenesis or the degradation of autophagosomes during autophagy, a major macromolecular degrading mechanism in eukaryotic cells. (“Rev-erb Agonist and TGF-β Similarly Affect Autophagy but Differentially Regulate Hepatic Stellate Cell Fibrogenic Phenotype” (Thomes et al., in press) [1].

Certain dietary components when combined with alcohol exacerbate alcohol-induced liver injury (ALI). Here, we tested whether fructose, a major ingredient of the western diet, enhances the severity of ALI. We fed mice ethanol for 8 weeks in the following Lieber-DeCarli diets: (a) Regular (contains olive oil); (b) corn oil (contains corn oil); (c) fructose (contains fructose and olive oil) and (d) corn+fructose (contains fructose and corn oil). We compared indices of metabolic function and liver pathology among the different groups. Mice fed fructose-free and fructose-containing ethanol diets exhibited similar levels of blood alcohol, blood glucose and signs of disrupted hepatic insulin signaling. However, only mice given fructose-ethanol diets showed lower insulin levels than their respective controls. Compared with their respective pair-fed controls, all ethanol-fed mice exhibited elevated levels of serum ALT; the inflammatory cytokines TNF-α, MCP-1 and MIP-2; hepatic lipid peroxides and triglycerides. All the latter parameters were significantly higher in mice given fructose-ethanol diets than those fed fructose-free ethanol diets. Mice given fructose-free or fructose-containing ethanol diets each had higher levels of hepatic lipogenic enzymes than controls. However, the level of the lipogenic enzyme fatty acid synthase (FAS) was significantly higher in livers of mice given fructose control and fructose-ethanol diets than in all other groups. Our findings indicate that dietary fructose exacerbates ethanol-induced steatosis, oxidant stress, inflammation and liver injury, irrespective of the dietary fat source, to suggest that inclusion of fructose in or along with alcoholic beverages increases the risk of more severe ALI in heavy drinkers.

Background Exposure to alcohol and its metabolites can initiate hepatic injury and fibrogenesis. Fibrosis is mediated through hepatic stellate cell (HSC) activation, leading to global changes in mRNA and microRNA (miR) expression. miRs are expressed in cells or shuttled to exosomes which can be detected in tissue culture media (TCM) and biological fluids. The mechanisms and function underlying the differential expression and processing of miRs and their downstream effects during hepatic injury remain poorly understood. Methods Expression of primary (pri)-miR17-92. and individual members of this cluster, miR17a, 18a, 19a, 20a, 19b, and 92, were examined in primary HSCs and human LX2 cells exposed to alcohol-conditioned media (CM), liver tissue from a rodent model of alcoholic injury, and in exosomes from TCM and plasma of rodent models and patients with alcoholic liver disease (ALD). miR expression was examined in HSCs transduced with an AAV2 vector carrying GFP-miR19b or GFP-control transgene under the collagen promoter. Results Profibrotic markers were enhanced in primary HSCs and LX2 cells exposed to alcohol-CM, concomitant with decreased miR19b expression and a significant increase in pri-miR17-92. Increased pri-miR17-92 was confirmed in a rodent model of alcohol-induced liver injury. Individual members of the cluster were inversely proportionate in cells and exosomes. AAV2-mediated miR19b overexpression inhibited miR17-92 and altered expression of individual cluster members in cells and exosomes. Expression of individual miR17-92 cluster members in plasma exosomes isolated from patients with ALD was similar to that seen in a rodent model of alcoholic injury and in vitro. Conclusions Reintroduction of miR19b inhibits HSC activation and modulates expression of pri-miR17-92 and the inverse expression of individual cluster members in cells and exosomes. Better understanding of miR17-92 processing may provide mechanistic insights into the role of individual miRs and exosomes during hepatic injury, revealing new therapeutic targets.

Background: Chronic ethanol consumption increases the risk of hepatic cirrhosis and hepatocellular carcinoma (HCC). While sex differences exist in susceptibility to ethanol-induced liver damage/HCC development, little is known about the effects of ethanol on tumor progression. Methods: Neonatal male and female mice were initiated with a single dose of diethylnitrosamine (DEN). Sixteen or 40 weeks later, animals were placed on a 10/20% (v/v) ethanol–drinking water (EtOH-DW; alternate days) regime for 8 weeks. At study end, liver tissue and serum were analyzed for liver pathology/function and cytokine expression. Results: DEN reproducibly induced hepatic foci/tumors in male and female mice. Ethanol diminished hepatic function and increased liver damage, but ethanol alone did not induce hepatic foci/HCC formation. In DEN-initiated EtOH-DW animals, ethanol significantly increased tumor incidence and burden, but only in male mice. Male and female mice (±DEN) demonstrated comparable blood alcohol content at necropsy, yet increased hepatic damage and diminished hepatic function/antioxidant capacity were significantly greater in males. Analysis of liver mRNA for Th1, Th2, or T-regulatory factors demonstrated significantly elevated SMAD3 in male compared to female mice in response to EtOH, DEN initiation, and DEN + EtOH-DW. Conclusions: These data demonstrate male mice are more susceptible to HCC incidence and progression in the setting of chronic ethanol feeding than females. Differences in markers of hepatic immune response in male mice suggest that increased TGFβ-SMAD3 signaling may enhance promotion in this model of HCC progression, effects modulated by chronic ethanol feeding.

Background Alcohol is a significant risk factor for development of hepatocellular carcinoma (HCC). To date, no rodent model has demonstrated formation of hepatic neoplasia in the setting of chronic alcohol consumption alone.

Alcoholic liver disease (ALD) is a major cause of acute and chronic liver disease worldwide. The progressive nature of ALD is well described; however, the complex interactions under which these pathologies evolve remain to be fully elucidated. Clinically there are no clear biomarkers or universally accepted, effective treatment strategies for ALD. Experimental models of ALD are an important component in identifying underlying mechanisms of alcohol-induced injury to develop better diagnostic markers, predictors of disease progression, and therapeutic targets to manage, halt, or reverse disease progression. Rodents remain the most accessible model for studying ALD pathology. Effective rodent models must mimic the natural history of ALD while allowing examination of complex interactions between multiple hepatic, and non-hepatic, cell types in the setting of altered metabolic or oxidative/nitrosative stress, inflammatory responses, and sensitivity to cytotoxic stress. Additionally, mode and duration of alcohol delivery influence hepatic response and present unique challenges in understanding disease pathology. This review provides an overview of rodent models of ALD, their strengths and weaknesses relative to human disease states, and provides insight of the potential to develop novel rodent models to simulate the course of human ALD.

Chronic ethanol consumption is a known risk factor for developing hepatocellular carcinoma (HCC). The use of plant-derived antioxidants is gaining increasing clinical prominence as a potential therapy to ameliorate the effects of ethanol on hepatic disease development and progression. This study demonstrates silibinin, a biologically active flavanoid derived from milk thistle, inhibits cytochrome p4502E1 induction, ethanol metabolism and reactive oxygen species generation in HCC cells in vitro. These silibinin-mediated effects also inhibit ethanol-dependent increases in HCC cell proliferation in culture.

The treatment of alcohol addiction includes a combination of pharmacological and psychotherapeutical treatment. During detoxification, different pharmacological treatment options exist, particularly the use of benzodiazepines (symptome-triggered or fixed-dose regimes) or clomethiazole, which is mainly used in central Europe. Besides these well-established therapies, studies have shown evidence for the application of anticonvulsants like carbamazepine or topiramate, between others. The presentation will give an overview of the current knowledge about pharmacological treatment options for managing alcohol withdrawal. In this context, results from studies on biomarkers will be presented, which can be used for an individualized treatment regime. Several pharmacological options exist for relapse prevention in abstinent alcohol-dependent patients, some well established like disulfiram, acamprosate or naltrexone. Effectiveness and limits of these medications will be discussed, taking into account new studies on already existing compounds like baclofen or topiramate or new developments like nalmefene. Regarding psychotherapeutical treatment of alcohol dependence, several therapeutical approaches have shown effectiveness. This applies for motivational enhancement therapy (MET), cognitive-behavioural therapy (CBT), group therapy, family therapy and psychodynamic therapy/interpersonal therapy (IT). In most centers in Germany, a combination of MET and CBT is used to motivate patients and to prevent relapse. New therapeutical approaches like metacognitive therapy for alcohol addiction will be presented and discussed. # S19.2 THERAPEUTIC APPROACHES TO EXTRAHEPATIC ALCOHOL-ASSOCIATED DISEASES {#article-title-2} The noxious effect of alcohol is not limited to the liver, being systemic. EtOH-related organ damage should be assessed according to: (i) degree of EtOH consumption, (ii) personal and gender risk, (iii) organ susceptibility factors and (iv) clinical suspicion. All active diseases that coexist with liver damage should be treated. (1) Neurological damage is related to direct EtOH effect, thiamine deficiency and malnutrition. Epilepsy improves with EtOH cessation. EtOH abstinence and dellirium requires prevention and early treatment. (2) EtOH cardiovascular damage may induce a diversity of atrial and ventricular arrhythmias. Heart failure and HTA are dose-dependent and should be managed with diuretic and RAA inhibitors. Anti-thrombotic treatment should be established considering risk–benefit balance. Haemorrhagic risk is increased and should be prevented in gastrointestinal, traumatic and neurological damage, with specific suspicion for subdural post-traumatic and hypertensive haematomas. (3) Malnutrition is related to poor diet, malabsorption, metabolic protein and carbohydrate disturbances, interfering with immunity and increasing systemic organ damage. It should be corrected with dietary or parenteral supply. Chronic pancreatitis may cause malabsorption. Vitamin, mineral deficiencies and excess are frequently seen, requiring early correction. (4) Tissue oxidative damage may be corrected with antioxidant therapy. (5) Skeletal myopathy and osteopenia should be treated with protein supply, calcium, D Vitamin and physiotherapy. (6) Particular infections in alcoholism (pneumonia, soft-tissue and sepsis) make to consider the major frequency of Gram-negative bacilli, anaerobes, mycobacteria, fungi and Listeria. (7) Management of alcoholic patient at ICU requires specific considerations concerning to septic shock, drug, anaesthesia and peri-operative management. (8) Pharmacological interaction between EtOH and drugs, with CYP2E1 induction should be considered. (9) EtOH may interfere and increase other pathogenic agents such as HCV, tobacco and cocaine. (10) Consider increased cancer risk in alcoholism. In summary, systemic treatment in alcoholism needs a multidisciplinary approach to consider all causes of tissue damage and the diverse therapeutic response, with specific individual assessment. # S19.5 ALCOHOL AND CARCINOGENESIS {#article-title-3} Following ingestion, ethanol (EtOH) exerts direct and indirect effects on hepatic physiology. Many deleterious consequences of ethanol relate to intrahepatic metabolism and changes in hepatic REDOX status. Previous studies report different hepatic responses to chronic EtOH intake between males and females. The aims of the current studies were to determine effects of EtOH on hepatic tumor progression in male (m) and female (f) mice. Neonatal (m) and (f) B6C3 mice were initiated with single dose diethylnitrosamine (DEN, 1 mg/kg, i.p., 23 days old). Mice were weaned onto, and maintained on, an EtOH–drinking water regime (10/20% ( v/v ); alternate days) beginning at 16 or 40 weeks for 8 weeks. At 24 and 48 weeks, animals were sacrificed and blood-tissue harvested. Significantly more (m) DEN mice developed altered hepatic foci (foci) vs . (f) mice in pair-matched groups at 24 and 48 weeks in the absence of significant differences in BAC (range; 10.43 ± 3.96 to14.13 ± 3.46 mM). Foci area were significantly greater in pair-matched DEN initiated (m) vs . (f) mice, and (m) DEN + EtOH (0.320 ±.033mm2) vs. (m) DEN (0.142 ± 0.042 mm2) at 24 weeks and (0.481 ± 0.029 mm2 (DEN) vs 0.268 ± 0.061 mm2 (DEN + EtOH) at 48 weeks. Measures of hepatic injury were assessed by scoring sections for steatosis, necrosis, inflammation and sirius red staining. Significantly increased liver pathology was identified in (m) vs . (f) DEN + EtOH mice at 24 and 48 weeks. Induction of CYP2E1 was significantly greater in (m) mice maintained on EtOH drinking water compared with (f), as were measurements of malondialdehyde (MDA; indicator of lipid peroxidation). Conversely, glutathione (GSH) was significantly higher in (f) vs . (m) mice in response to EtOH ± DEN initiation. Immunohistochemistry for proliferating cell nuclear antigen (PCNA) identified a 121% increase in staining in (m) DEN + EtOH vs . a 16.9% decrease in (f) DEN + EtOH at 24 weeks and a 79.3% increase in (m) and 14.5% decrease in (f) mice at 48 weeks. Western blot identified corresponding, significant increases in cyclin D1 in (m) vs. (f) DEN + EtOH mice. Finally, inclusion of silibinin, a dietary antioxidant derived from the milk thistle plant, failed to significantly alter hepatic pathology or tumor progression in females. Conversely, dietary silibinin acted to further enhance EtOH-dependent increases in hepatocarcinogenesis in males. These data demonstrate chronic EtOH consumption in the setting of underlying hepatocyte transformation significantly enhances tumorigenesis in (m), but not in (f) mice. Additionally, (f) mice maintain higher GSH levels and appear to more effectively manage EtOH-associated REDOX changes, data further supported by inclusion of a natural, plant-derived dietary antioxidant.