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| 1 | No association between cyclooxygenase-2 and uridine diphosphate glucuronosyltransferase 1A6 genetic polymorphisms and colon cancer risk显示文摘AIM:To investigate the association of variations in the cyclooxygenase-2(COX2) and uridine diphosphate glucuronosyltransferase 1A6(UGT1A6) genes and non-steroidal anti-inflammatory drugs(NSAIDs) use with risk of colon cancer.METHODS:NSAIDs,which are known to reduce the risk of colon cancer,act directly on COX2 and reduce its activity.Epidemiological studies have associated variations in the COX2 gene with colon cancer risk,but others were unable to replicate this finding.Similarly,enzymes in the UGT1A6 gene have been demonstrated to modify the therapeutic effect of NSAIDs on colon adenomas.Polymorphisms in the UGT1A6 gene have been statistically shown to interact with NSAID intake to influence risk of developing colon adenomas,but not colon cancer.Here we examined the association of tagging single nucleotide polymorphisms(SNPs) in the COX2 and UGT1A6 genes,and their interaction with NSAID consumption,on risk of colon cancer in a population of 422 colon cancer cases and 481 population controls.RESULTS:No SNP in either gene was individually statistically significantly associated with colon cancer,nor did they statistically significantly change the protective effect of NSAID consumption in our sample.Like others,we were unable to replicate the association of variants in the COX2 gene with colon cancer risk(P > 0.05),and we did not observe that these variants modify the protective effect of NSAIDs(P > 0.05).We were able to confirm the lack of association of variants in UGT1A6 with colon cancer risk,although further studies will have to be conducted to confirm the association of these variants with colon adenomas.CONCLUSION:Our study does not support a role of COX2 and UGT1A6 genetic variations in the development of colon cancer. | Cheryl L Thompson Sarah J Plummer Alona Merkulova Iona Cheng Thomas C Tucker Graham Casey Li Li | 2009 | World Journal of Gastroenterology2009，15，18： | 11 |
| 2 | 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 |
| 3 | 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 |
| 4 | 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 |
| 5 | A new aluminum hydroxide octamer (SO4)5 · 16H2O显示文摘 | Casey W H Olmstead M M Phillips B L | 2005 | Inorg Chem2005，44，： | 1 |
| 6 | Rapid optimization of a peptide inhibitor of malaria parasite invasion by comprehensive N-methyl scanning显示文摘 | HARRIS K S CASEY J L COLEY A M | 2009 | J Biol Chem2009，284，14： | 1 |
| 7 | Purification of bacterially expressed single chain Fv antibodies for clinical applications using metal chelate chromatography显示文摘 | Casey J L Keep P A Chester K A etal | 1995 | J Immun Method1995，179，： | 1 |
| 8 | Mechanism research of cryoanalgesia 显示文摘 | Zhou L Kambin P Casey KF | 1995 | Neurol Res1995，17，4： | 1 |
| 9 | Persistence and fate of 17- estradiol and testosterone in agricultural soils显示文摘 | Z Fan FXM Casey G L Larsen | 2007 | Chemosphere2007，67，： | 1 |
| 10 | Endothelin-1 gene expression and biosynthesis in human endometrial HEC-IA cancer cells 显示文摘 | Economos K Macdonald P C Casey M L | 1992 | Caner Res1992，52，3： | 1 |
| 11 | Mechanism research cryoanalgesia 显示文摘 | ZHOU L KAMBIN P CASEY K F | 1995 | Neurol Res1995，17，4： | 1 |
| 12 | DNA methylation regulatesMicroRNA expression显示文摘 | Han L Witmer PD Casey E | 2007 | Cancer Biol Ther2007，6，8： | 1 |
| 13 | Preferred crystallographic orientation development during the plastic and superplastic flow of calcite rocks显示文摘 | Rutter E H Casey M Burlini L | 1994 | J Struct Geol1994，16，： | 1 |
| 14 | Symptom management in gynecologic malignancies显示文摘 | Casey C Chen L M Rabow M W | 2011 | Expert Rev Anticancer Ther2011，11，7： | 1 |
| 15 | Abnormal Cervical Appearance: What to Do, When to Worry?显示文摘 | Casey Petra M Long Margaret E Marnach Mary L | 2011 | Mayo Clinic Proceedings2011，，2： | 1 |
| 16 | Familial vasopressin-sensitiveACTH-independent macronodular adrenal hyperplasia(VPs-AIMAH):clinical studies of three kindreds显示文摘 | Gagliardi L Hotu C Casey G | 2009 | Clin Endocrinol(Oxf)2009，70，6： | 1 |
| 17 | Music as a therapeutic intervention for anxiety in patients receiving radiation therapy显示文摘 | Smith M Casey L Johnson D | 2001 | Oncol Nurs Forum2001，28，5： | 1 |
| 18 | Fate and transport of 17fl-estradiol in soil-water systems 显示文摘 | Casey F X M Larsen G L Hakk H | 2003 | Environ Sci Technol2003，37，11： | 1 |
| 19 | Comparison of human cerebral activation pattern during cutaneous warmth, heat pain, and deep cold pain显示文摘 | Casey K L Minoshima S Morrow T J | 1996 | J Neurophysiol1996，76，1： | 1 |
| 20 | Sleep-related hypoventilation/hypoxemic syndromes显示文摘 | Casey K R Cantillo K O Brown L K | 2007 | Chest2007，131，6： | 1 |
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