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| 1 | Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells显示文摘AIM:To investigate the role of reactive oxygen species(ROS) in ethanol-mediated cell death of polarized hepatic(WIF-B) cells.METHODS:In this work,WIF-B cultures were treated with pyrazole(inducer of cytochrome P4502E1,CYP2E1) and/or L-buthionine sulfoximine(BSO),a known inhibitor of hepatic glutathione(GSH),followed by evaluation of ROS production,antioxidant levels,and measures of cell injury(apoptosis and necrosis).RESULTS:The results revealed that ethanol treatment alone caused a significant two-fold increase in the activation of caspase-3 as well as a similar doubling in ROS.When the activity of the CYP2E1 was increased by pyrazole pretreatment,an additional two-fold elevation in ROS was detected.However,the CYP2E1-related ROS elevation was not accompanied with a correlative increase in apoptotic cell injury,but rather was found to be associated with an increase in necrotic cell death.Interestingly,when the thiol status of the cells was manipulated using BSO,the ethanol-induced activation of caspase-3 was abrogated.Additionally,ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.CONCLUSION:Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels. | Benita L McVicker Pamela L Tuma Kusum K Kharbanda Serene ML Lee Dean J Tuma | 2009 | World Journal of Gastroenterology2009，15，21： | 5 |
| 2 | Measuring supply chain performance显示文摘 | Benita M. Beamon | 1999 | International Journal of Operations & Production Management1999，，3： | 3 |
| 3 | Characterization of diazepam submicron emulsion interface: Role of oleic acid显示文摘 | M. Y. Levy W. Schutze C. Fuhrer S. Benita | 1994 | Journal of Microencapsulation1994，，1： | 3 |
| 4 | Influence of Emulsion Droplet Surface Charge on Indomethacin Ocular Tissue Distribution显示文摘 | Shmuel Klang Mohammed Abdulrazik Simon Benita* | 2000 | Pharmaceutical Development and Technology2000，，4： | 2 |
| 5 | Self-reported risk of stroke and factors associated with underestimation of stroke risk among older adults with atrial fibrillation: the SAGE-AF study显示文摘Background Though engaging patients with atrial fibrillation(AF) in understanding their stroke risk is encouraged by guidelines, little is known regarding AF patients' perceived stroke risk or its relationship with oral anticoagulation(OAC) use. We aim to identify factors associated with underestimation of stroke risk among older patients with AF and relate this to OAC use. Methods Data are from the ongoing SAGE(Systematic Assessment of Geriatric Elements)-AF study, which included older patients(> 65 years) with non-valvular AF and a CHA2 DS2-VASc score of ≥ 2. Participants reported their perceived risk of having a stroke without OAC. We compared the perceived risk to CHA2 DS2-VASc predicted stroke risk and classified participants as 'over' or 'under' estimators, and identified factors associated with underestimation of risk using multiple logistic regression. Results The average CHA2 DS2-VASc score of 915 participants(average age: 75 years, 47% female, 86% white) was 4.3 ± 1.6, 43% of participants had discordant predicted and self-reported stroke risks. Among the 376 participants at highest risk(CHA2 DS2-VASc score ≥ 5), 46% of participants underestimated their risk. Older participants(≥ 85 years) were more likely and OAC treated patients less likely to underestimate their risk of developing a future stroke than respective comparison groups. Conclusions A significant proportion of study participants misperceived their stroke risk, mostly by overestimating. Almost half of participants at high risk of stroke underestimated their risk, with older patients more likely to do so. Patients on OAC were less likely to underestimate their risk, suggesting that successful efforts to educate patients about their stroke risk may influence treatment choices. | Jordy Mehawej Jane Saczynski Jerry H.Gurwitz Hawa O.Abu Benita A.Bamgbade Wei-Jia WANG Tenes Paul Katherine Trymbulak Connor Saleeba Zi-Yue WANG Catarina I.Kiefe Robert J.Goldberg David D.Mc Manus | 2020 | Journal of Geriatric Cardiology2020，17，8： | 2 |
| 6 | Effect of ethanol on pro-apoptotic mechanisms in polarizedhepatic cells显示文摘Chronic ethanol consumption is associated with serious and potentially fatal alcohol-related liver injuries such as hepatomegaly, alcoholic hepatitis and cirrhosis. Moreover, it has been documented that the clinical progression of alcohol-induced liver damage may be associated with an increase in hepatocellular death that involves apoptotic mechanisms. Although much information has been learned about the clinical manifestations associated with alcohol-related diseases, the search continues for a better understanding of the molecular and/or cellular mechanisms by which ethanol exerts its deleterious effects such as the induction of pro-apoptotic mechanisms and related cell damaging events. As part of the effort to enhance our understanding of those particular cellular pathways and mechanisms associated with ethanol toxicity, researchers over the years have utilized a variety of model systems. Recently, work has come forth demonstrating the utility of a hybrid cell line (WIF-B) as a cell culture model system for the study of alcohol-associated alterations in hepatocellular mechanisms. Success with such emerging model systems could aid in the development of potential therapeutic treatments for the prevention of alcohol- induced apoptotic cell death that may ultimately serve as a significant target in delaying the onset and/or progression of clinical symptoms of alcohol-mediated liver disease. This review article summarizes the current understanding of ethanol-mediated modifications in cell survival and thus the promotion of pro-apoptotic events with emphasis on analyses made in various experimental model systems, particularly the more recently characterized WIF-B cell system. | Benita L McVicker Dean J Tuma Carol A Casey | 2007 | World Journal of Gastroenterology2007，13，37： | 2 |
| 7 | Supply chain design and analysis:显示文摘 | Benita M Beamon | 1998 | International Journal of Production Economics1998，，3： | 2 |
| 8 | Self-dispersing lipid formulations for improving oral absorption of lipophilic drugs显示文摘 | Tatyana Gershanik Simon Benita | 2000 | European Journal of Pharmaceutics and Biopharmaceutics2000，，1： | 2 |
| 9 | The Role of Doctoral Advisors: A Look at Advising from the Advisor’s Perspective显示文摘 | Benita J. Barnes Ann E. Austin | 2009 | Innovative Higher Education2009，，5： | 2 |
| 10 | Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes, and downregulation of carbonic anhydrase-III, in betaine supplemented ethanol-fed rats显示文摘 | Kusum K. Kharbanda Vasanthy Vigneswara Benita L. McVicker Anna U. Newlaczyl Kevin Bailey Dean Tuma David E. Ray Wayne G. Carter | 2009 | Biochemical and Biophysical Research Communications2009，，4： | 2 |
| 11 | Impact of asialoglycoprotein receptor deficiency on the development of liver injury显示文摘The asialoglycoprotein (ASGP) receptor is a wellcharacterized hepatic receptor that is recycled via the common cellular process of receptor-mediated endocytosis (RME). The RME process plays an integral part in the proper traff icking and routing of receptors and ligands in the healthy cell. Thus, the missorting or altered transport of proteins during RME is thought to play a role in several diseases associated with hepatocyte and liver dysfunction. Previously, we examined in detail alterations that occur in hepatocellular RME and associated receptor functions as a result of one particular liver injury, alcoholic liver disease (ALD). The studies revealed profound ethanolmediated impairments to the ASGP receptor and the RME process, indicating the importance of this receptor and the maintenance of proper endocytic events in normal tissue. To further clarify these observations, studies were performed utilizing knockout mice (lacking a functional ASGP receptor) to which were administered several liver toxicants. In addition to alcohol, we examined the effects following administration of antiFas (CD95) antibody, carbon tetrachloride (CCl4) and lipopolysaccharide (LPS)/galactosamine. The results of these studies demonstrated that the knockout mice sustained enhanced liver injury in response to all of the treatments, as shown by increased indices of liver damage, such as enhancement of serum enzyme levels, histopathological scores, as well as hepatocellular death. Overall, the work completed to date suggests a possible link between hepatic receptors and liver injury. In particular, adequate function and content of the ASGP receptor may provide protection against various toxinmediated liver diseases. | Serene ML Lee Carol A Casey Benita L McVicker | 2009 | World Journal of Gastroenterology2009，15，10： | 2 |
| 12 | Interaction of a Self-Emulsifying Lipid Drug Delivery System with the Everted Rat Intestinal Mucosa as a Function of Droplet Size and Surface Charge显示文摘 | Tatyana Gershanik Sharon Benzeno Simon Benita | 1998 | Pharmaceutical Research1998，，6： | 2 |
| 13 | Interaction of a Self-Emulsifying Lipid Drug Delivery System with the Everted Rat Intestinal Mucosa as a Function of Droplet Size and Surface Charge显示文摘 | Tatyana Gershanik Sharon Benzeno Simon Benita | 1998 | Pharmaceutical Research1998，，6： | 2 |
| 14 | Cellular fi bronectin stimulates hepatocytes to produce factors that promote alcohol-induced liver injury显示文摘AIM:To examine the consequences of cellular f ibronectin(cFn)accumulation during alcohol-induced injury,and inv estigate whether increased cFn could have an effect on hepatocytes(HCs)by producing factors that could cont ribute to alcohol-induced liver injury.METHODS:HCs were isolated from rats fed a control or ethanol liquid diet for four to six weeks.Exogenous c Fn(up to 7.5 μg/mL)was added to cells cultured for 20 h,and viability(lactate dehydrogenase),apoptosis(caspase activity)and se cretion of proinflammat-ory cytokines(tumor ne c rosis fac tor alpha,TNF-α and interleukin 6,IL-6),mat rix metalloproteinases(MMPs)and their inhibitors(tissue inhibitors of metall-oproteinases,TIMPs)was det ermined.Degrad ation of iodinated cFn was det ermined over a 3 h time period in the preparations.RESULTS:cFn degradation is impaired in HCs isolated from ethanol-fed animals,leading to its accumulation in the matrix.Addition of exogenous cFn did not affect viability of HCs from control or ethanolfed animals,and apoptosis was affected only at the higher concentration.Sec retion of MMPs,TIMPs,TNF-α and IL-6,however,was increased by exogenously added cFn,with HCs from ethanolfed animals showing increased susceptibility compared to the controls.CONCLUSION:These results suggest that the elevated amounts of cFn observed in alcoholic liver injury can stimulate hepatocytes to produce factors which promote further tissue damage. | Razia S Aziz-Seible Benita L McVicker Kusum K Kharbanda Carol A Casey | 2011 | World Journal of Hepatology2011，3，2： | 2 |
| 15 | Self-dispersing lipid formulations for improving oral absorption of lipophilic drugs显示文摘 | Gershanik T Benita S | 2000 | Eur J Pharm Bio2000，50，2： | 1 |
| 16 | Interaction of a self-emulsifying lipid drug delivery system with the everted rat intestinal mucosa as a function of droplet size and surface charge 显示文摘 | Gershanik G Benzeno S Benita S | 1998 | Pharm Res1998，15，6： | 1 |
| 17 | Self-emulsifying drug delivery systems for improved oral delivery of lipophilic drugs显示文摘 | Gursoy RN Benita S | 2004 | Biomedicine Pharmacotherapy2004，58，： | 1 |
| 18 | Self-emulsifying drug delivery systems(SEDDS)for improved oral delivery of lipophilic drugs显示文摘 | Gursoy R N Benita S | 2004 | Bi-omed Pharmacother2004，58，3： | 1 |
| 19 | System reliability and congestion in a material handling system显示文摘 | Benita M B | 1999 | Computers & Industrial Engineering1999，36，3： | 1 |
| 20 | Influence of oil droplet surface charge on the performance of antibody--emulsion conjugates 显示文摘 | Goldstein D Sader O Benita S | 2007 | BiomedPharmacother2007，61，1： | 1 |
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