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| 1 | Alcoholic pancreatitis:New insights into the pathogenesisand treatment显示文摘Acute pancreatitis is a necro-inflammatory disease of the exocrine pancreas that is characterized by inappropriate activation of zymogens, infiltration of the pancreas by inflammatory cells, and destruction of the pancreatic exocrine cells. Acute pancreatitis can progress to a severe life-threatening disease. Currently there is no pharmacotherapy to prevent or treat acute pancreatitis. One of the more common factors associated with acute pancreatitis is alcohol abuse. Although commonly associated with pancreatitis alcohol alone is unable to cause pancreatitis. Instead, it appears that alcohol and its metabolic by-products predispose the pancreas to damage from agents that normally do not cause pancreatitis, or to more severe disease from agents that normally cause mild pancreatic damage. Over the last 10 to 20 years, a tremendous amount of work has defined a number of alcohol-mediated biochemical changes in pancreatic cells. Among these changes are: Sustained levels of intracellular calcium, activation of the mitochondrial permeability transition pore, endoplasmic reticulum stress, impairment in autophagy, alteration in the activity of transcriptional activators, and colocalization of lysosomal and pancreatic digestive enzymes. Elucidation of these changes has led to a deeper understanding of the mechanisms by which ethanol predisposes acinar cells to damage. This greater understanding has revealed a number of promising targets for therapeutic intervention. It is hoped that further investigation of these targets will lead to the development of pharmacotherapy that is effective in treating and preventing the progression of acute pancreatitis. | Dahn L Clemens Katrina J Schneider Christopher K Arkfeld Jaclyn R Grode Mark A Wells Shailender Singh | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，1： | 10 |
| 2 | In vivo radiometric analysis of glucose uptake and distribution in mouse bone显示文摘Bone formation and remodeling occurs throughout life and requires the sustained activity of osteoblasts and osteoclasts,particularly during periods of rapid bone growth.Despite increasing evidence linking bone cell activity to global energy homeostasis,little is known about the relative energy requirements or substrate utilization of bone cells.In these studies,we measured the uptake and distribution of glucose in the skeleton in vivo using positron-emitting^(18)F-fluorodeoxyglucose([^(18)F]-FDG) and non-invasive,high-resolution positron emission tomography/computed tomography(PET/CT) imaging and ex vivo autoradiography.Assessment of [^(18)F]-FDG uptake demonstrated that relative to other tissues bone accumulated a significant fraction of the total dose of the glucose analog.Skeletal accumulation was greatest in young mice undergoing the rapid bone formation that characterizes early development.PET/CT imaging revealed that [^(18)F]-FDG uptake was greatest in the epiphyseal and metaphyseal regions of long bones,which accords with the increased osteoblast numbers and activity at this skeletal site.Insulin administration significantly increased skeletal accumulation of [^(18)F]-FDG,while uptake was reduced in mice lacking the insulin receptor specifically in osteoblasts or fed a high-fat diet.Our results indicated that the skeleton is a site of significant glucose uptake and that its consumption by bone cells is subject to regulation by insulin and disturbances in whole-body metabolism. | Meredith L Zoch Diane S Abou Thomas L Clemens Daniel LJ Thorek Ryan C Riddle | 2016 | Bone Research2016，4，1： | 9 |
| 3 | The hypoxia-inducible factor-1α activates ectopic production of fibroblast growth factor 23 in tumor-induced osteomalacia显示文摘Tumor-induced osteomalacia(TIO) is a rare paraneoplastic syndrome in which ectopic production of fibroblast growth factor 23(FGF23) by non-malignant mesenchymal tumors causes phosphate wasting and bone fractures. Recent studies have implicated the hypoxia-inducible factor-1α(HIF-1α) in other phosphate wasting disorders caused by elevated FGF23, including X-linked hypophosphatemic rickets and autosomal dominant hypophosphatemia. Here we provide evidence that HIF-1α mediates aberrant FGF23 in TIO by transcriptionally activating its promoter. Immunohistochemical studies in phosphaturic mesenchymal tumors resected from patients with documented TIO showed that HIF-1α and FGF23 were co-localized in spindleshaped cells adjacent to blood vessels. Cultured tumor tissue produced high levels of intact FGF23 and demonstrated increased expression of HIF-1α protein. Transfection of MC3T3-E1 and Saos-2 cells with a HIF-1α expression construct induced the activity of a FGF23 reporter construct. Prior treatment of tumor organ cultures with HIF-1α inhibitors decreased HIF-1α and FGF23 protein accumulation and inhibited HIF-1α-induced luciferase reporter activity in transfected cells. Chromatin immunoprecipitation assays confirmed binding to a HIF-1α consensus sequence within the proximal FGF23 promoter, which was eliminated by treatment with a HIF-1α inhibitor. These results show for the first time that HIF-1α is a direct transcriptional activator of FGF23 and suggest that upregulation of HIF-1α activity in TIO contributes to the aberrant FGF23 production in these patients. | Qian Zhang Michele Doucet Ryan E Tomlinson Xiaobin Han L Darryl Quarles Michael T Collins Thomas L Clemens | 2016 | Bone Research2016，4，2： | 6 |
| 4 | Alcoholic pancreatitis:Lessons from the liver显示文摘The association between alcohol consumption and pancreatitis has been recognized for over 100 years. Despite the fact that this association is well recognized, the mechanisms by which alcohol abuse leads to pancreatic tissue damage are not entirely clear. Alcohol abuse is the major factor associated with pancreatitis in the Western world. Interestingly, although most cases of chronic pancreatitis and many cases of acute pancreatitis are associated with alcohol abuse, only a small percentage of individuals who abuse alcohol develop this disease. This situation is reminiscent of the association between alcohol abuse and the incidence of alcoholic liver disease. The liver and the pancreas are developmentally very closely related. Even though these two organs are quite different, they exhibit a number of general structural and functional similarities. Furthermore, the diseases mediated by alcohol abuse in these organs exhibit some striking similarities. The diseases in both organs are characterized by parenchymal cell damage, activation of stellate cells, aberrant wound healing, and fibrosis. Because of the similarities between the liver and the pancreas, and the alcohol-associated diseases of these organs, we may be able to apply much of the knowledge that we have gained regarding the effects of alcohol on the liver to the pancreas. | Dahn L Clemens Katrina J Mahan | 2010 | World Journal of Gastroenterology2010，16，11： | 5 |
| 5 | Phase structure in polypropylene/ PA6/SEBS blends显示文摘 | A N Wilkinson L Laugel M L Clemens | 1999 | Polymer1999，40，： | 1 |
| 6 | Miniemulsion polymerization as a means to encapsulate organic and inorganic materials 显示文摘 | Clemens K W Katharina L | 2010 | Adv Polym Sci2010，233，： | 1 |
| 7 | A Randomized Controlled Trial in Second-Generation Zotarolimus-Eluting Resolute Stents Versus Everolimus-Eluting Xience V Stents in Real-World Patients显示文摘 | Clemens von Birgelen Mounir W.Z. Basalus Kenneth Tandjung K. Gert van Houwelingen Martin G. Stoel J.(Hans) W. Louwerenburg Gerard C.M. Linssen Salah A.M. Sa?d Miep A.W.J. Kleijne Hanim Sen Marije M. L?wik Job van der Palen Patrick M.J. Verhorst Frits H.A. | 2012 | Journal of the American College of Cardiology2012，，15： | 1 |
| 8 | The effect of calcium on the rate and products of steam gasification of char from low rank coal显示文摘 | Clemens A H Damiano L F Matheson T W | 1998 | Fuel1998，77，910： | 1 |
| 9 | Evolution and variability of the asian monsoon system : State of the art and outstanding issues显示文摘 | Wang P X Clemens S Beaufort L | 2005 | Quaternary Science Reviews2005，24，： | 1 |
| 10 | Air and gas pockets in sewerage pressure mains显示文摘 | Lubbers C L Clemens F | 2005 | Water Science and Technology2005，52，3： | 1 |
| 11 | Forum on bone and skel- etal muscle interactions: summary of the proceedings of an ASBMR workshop显示文摘 | Bonewald L F Kiel D P Clemens T L | 2013 | J Bone Miner Res2013，28，9： | 1 |
| 12 | Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile Rhesus monkeys显示文摘 | Christopher L Coe Marian Kramer Boldizsár Czéh Elizabeth Gould Alison J Reeves Clemens Kirschbaum Eberhard Fuchs | 2003 | Biological Psychiatry2003，，10： | 1 |
| 13 | Partition- ing behaviour of some toxic volatile elements during stoker and fluidised bed combustion of alkaline sub- bituminous coal 显示文摘 | Clemens A H Damiano L F Gong D | 1999 | Fuel1999，78，12： | 1 |
| 14 | Assessing Dependence : Some Experimental Results 显示文摘 | Robert T Clemen Gregory W Fischer Robert L Winkler | 2000 | Management Science2000，46，8： | 1 |
| 15 | Treatment of peri-implant defects with guided bone regeneration:A comparative clinical study with various membranes and bone grafts显示文摘 | Martin L Christof P Clemens K | 1998 | Int J OralMaxillofac Implants1998，13，： | 1 |
| 16 | Compound-specific, quantitative characterization of organic fluorochemicals in biological matrices显示文摘 | Hansen K J Clemen L A Ellefson M E | 2001 | Environ Sci Technol2001，35，4： | 1 |
| 17 | Aggregating point estimates:A flexible modeling approach显示文摘 | Clemen R T Winkler R L | 1993 | Management Science1993，39，： | 1 |
| 18 | Analysis of Dscam diversity in regulating axon guidance in Drosophila mushroom bodies 显示文摘 | Zhan X L Clemens J C Neves G | 2004 | Neuron2004，43，5： | 1 |
| 19 | Large-scale hydrological change drove the late Miocene C4 plant expansion in the Himalayan foreland and Arabian Peninsula 显示文摘 | Huang Yongsong Steven C Clemens Liu Weiguo Wang Yi Wmxen L Prell | 2007 | Geology2007，35，6： | 1 |
| 20 | Late Pleistocene variability of Arabian Sea summer monsoon winds and continental aridity: Eolian records from the lithogenic component of deep-sea sediments显示文摘 | Clemens S C Prell W L | 1990 | Paleoceanography1990，5，： | 1 |
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