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1Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction显示文摘AIM To comprehensively evaluate mitochondrial(dys) function in preclinical models of nonalcoholic steatohepatitis(NASH).METHODS We utilized two readily available mouse models of nonalcoholic fatty liver disease(NAFLD) with or without progressive fibrosis: Lep^(ob)/Lep^(ob)(ob/ob) and FATZO mice on high trans-fat, high fructose and high cholesterol(AMLN) diet. Presence of NASH was assessed using immunohistochemical and pathological techniques, and gene expression profiling. Morphological features of mitochondria were assessed via transmission electron microscopy and immunofluorescence, and function was assessed by measuring oxidative capacity in primary hepatocytes, and respiratory control and proton leak in isolated mitochondria. Oxidative stress was measured by assessing activity and/or expression levels of Nrf1, Sod1, Sod2, catalase and 8-OHdG. RESULTS When challenged with AMLN diet for 12 wk, ob/ob and FATZO mice developed steatohepatitis in the presence of obesity and hyperinsulinemia. NASH development was associated with hepatic mitochondrial abnormalities, similar to those previously observed in humans, including mitochondrial accumulation and increased proton leak. AMLN diet also resulted in increased numbers of fragmented mitochondria in both strains of mice. Despite similar mitochondrial phenotypes, we found that ob/ob mice developed more advanced hepatic fibrosis. Activity of superoxide dismutase(SOD) was increased in ob/ob AMLN mice, whereas FATZO mice displayed increased catalase activity, irrespective of diet. Furthermore, 8-OHd G, a marker of oxidative DNA damage, was significantly increased in ob/ob AMLN mice compared to FATZO AMLN mice. Therefore, antioxidant capacity reflected as the ratio of catalase:SOD activity was similar between FATZO and C57 BL6 J control mice, but significantly perturbed in ob/ob mice. CONCLUSION Oxidative stress, and/or the capacity to compensate for increased oxidative stress, in the setting of mitochondrial dysfunction, is a key factor for development of hepatic injury and fibrosis in these mouse models.Michelle L Boland Stephanie Oldham Brandon B Boland Sarah Will Jean-Martin Lapointe Silvia Guionaud Christopher J Rhodes James L Trevaskis 2018World Journal of Gastroenterology2018,24,16:7
2Pathogenicity islands and virulence eveluation Listeria显示文摘Vazquez Boland J A Dominguiz Bernal G Gonzalez Zorn B 2001Microbes and Infection2001,69,:1
3Advances in acute and chronic pancreatitis显示文摘Acute pancreatitis(AP)and chronic pancreatitis are the third leading gastrointestinal causes for admissions and readmissions to hospitals in the United States.This review of articles published between 2019-2022(December)from international sources identified four categories of crucial new findings:The report includes(1)New genetic pathogenic mutations(TRPV6);expected genetic outcomes in a Northern European population;(2)a new serum diagnostic marker for AP-fatty acid ethyl esters-distinguishing acute pancreatitis associated with alcohol;explanations of the impact of monocytes/macrophages on the inflammatory process that defines their future in diagnosis,staging,and treatment;(3)innovations in timing of per os low-fat,solid food intake immediately on admission;resolution of concepts of aggressive parenteral fluid intake;dramatic shifts to nonoperative from operative treatment of infected pancreatic necrosis.Each modification reduced interventions,complications,and lengths-of-stay;and(4)authoritarian recommendations for medical treatment of chronic pain.These advances offer opportunities to initiate newly proven treatments to enhance outcomes,alter the natural history,and envision the future of two diseases that have no known cure.Williamson B Strum Clement Richard Boland 2023World Journal of Gastroenterology2023,29,7:1
4Mechanical properties of ultrahigh-strength gold nanowires显示文摘Wu B Heidelberg A Boland J J 2005Nature Materials2005,,4:1
5Drop-on-demand priming of cells and materials for designer tissue con- structs显示文摘BOLAND T TAO X DAMON B J 2007Materials Science and Engineering: C2007,27,3:1
6Distribution of phytate and nutritionally important elements among the morphological components of cereal grains 显示文摘O'Dell B L de Boland A R Koirtyohann 1972J Agric Food Chem1972,20,:1
7Predicting adverse events in children with fever and chemotherapy-indueed neutropenia: the prospective muhieenter SPOG 2003 FN study显示文摘Boland AA Nicole B Andreas H 2010J Clin Oncol2010,28,12:1
8Cations reduce antimi- crobial efficacy of lysozyme-chelator combinations 显示文摘Boland JS Davidson PM Bruce B 2004J Food Prot2004,67,2:1
9Apoptotic changes in the aged brain are triggered by interleukin-1beta-induced activation of p38 and reversed by treatment with eicosapentaenoic acid 显示文摘 Lonergan PE Boland B 2002J Biol Chem2002,277,34:1
10Isocitrate lyase of the facultative intracellular pathogen Rhodococcus equi显示文摘Kelly B G Wall D M Boland C A 2002Microbiology2002,148,3:1
11Abeta-mediated activation of the apoptotic cascade in cultured cortical neurones:a role for Cathepsin-L显示文摘Boland B Campbell V 2004Neurobiol Aging2004,25,1:1
12The RTX haemolysins Apxl and ApxⅡ are major virulence factors of the swine pathogen Actinobacillus pleuropneumoniae:Evidence from nutational analysis显示文摘Tascon R I Vazquez Boland J A Gutierrez Martin c B 1994Molecular Mi crobiology1994,,14:1
13Rapidprototyping of tissue-engineering constructs,usingphotopolymerizable hydrogels and stereolithography显示文摘DHARIWALA B HUNT E BOLAND T 2004Tissue Engineering2004,10,910:1
14Autophagy in- duction and autophagosome clearance in neurons: rela- tionship to autophagic pathology in Alzheimer's disease 显示文摘BOLAND B KUMAR A LEE S 2008J Neurosci2008,28,27:1
15Lysosomal storage disor- ders : the cellular impact of lysosomal dysfunction 显示文摘Platt FM Boland B van der Spoel AC 2012J Cell Biol2012,199,5:1
16Drop-on-demand printing of cells and materials for designer tis-sue constructs显示文摘BOLAND T TAO X DAMON B J 2007Materials Science&Engineering:C Biomimetic and Superamolecular Systems2007,27,:1
17Sacral resection for recurrent rectal cancer:analysis of morbidity and treatment results显示文摘Melton G B Paty P B Boland P J 2006Dis Colon Rectum2006,49,:1
18Esophageal carcinoma: Are modern tar- geted therapies shaking the rock? 显示文摘Boland PM Burtness B 2013Curr Opin Oncol2013,25,:1
19Analysis of centers for Medicaid and Medicare services 'Never events”in elderly patient undergoing bowel operations显示文摘Morse B C Boland B N Blackhurst D W 0,,08:1
20Biology and management of dollar spot (Sclerotinia homoeocarpa):an important disease of turfgrass显示文摘Walsh B Ikeda S D Boland G J 1999HortScience1999,34,:1
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