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| 1 | Hypertriglyceridemia-induced pancreatitis: A case-based review显示文摘Hypertriglyceridemia is an established cause of pancreatitis. In a case-based approach, we present a review of hypertriglyceridemia and how it can cause pancreatitis. We outline how to investigate and manage such patients. A 35 year old man presented to the emergency department with abdominal pain and biochemical evidence of acute pancreatitis. There was no history of alcohol consumption and biliary imaging was normal. The only relevant past medical history was that of mild hyperlipidemia, treated with diet alone. Physical exam revealed epigastric tenderness, right lateral rectus palsy, lipemia retinalis, bitemporal hemianopsia and a delay in the relaxation phase of his ankle reflexes. Subsequent laboratory investigation revealed marked hypertriglyceridemia and panhypopituarism. An enhanced CT scan of the head revealed a large suprasellar mass impinging on the optic chiasm and hypothalamus. The patient was treated supportively; thyroid replacement and lipid lowering agents were started. He underwent a successful resection of a craniopharyngioma. Post- operatively, the patient did well on hormone replacement therapy. He has had no further attacks of pancreatitis. This case highlights many of the factors involved in the regulation of triglyceride metabolism. We review the common causes of hypertriglyceridemia and the proposed mechanisms resulting in pancreatitis. The incidence and management of hypertriglyceridemia- induced pancreatitis are also discussed. | S Ian Gan Alun L Edwards Christopher J Symonds Paul L Beck | 2006 | World Journal of Gastroenterology2006，12，44： | 35 |
| 2 | 1990—2017年中国伤害负担:2017年全球疾病负担研究结果(摘译)显示文摘伤害是全球性的公共卫生挑战,涉及各年龄组和不同性别的人群。过去三十年来,中国经济快速发展,人口老龄化趋势加重,社会呈现出城镇化、机动化和老龄化等特征。随着人们生活环境和生活方式的改变,伤害已跃居人群致死原因第五位,仅排在恶性肿瘤、心脑血管疾病、呼吸系统疾病和心肌梗死之后。据估计,中国每年在伤害方面消耗的直接医疗费用约为650亿元人民币. | 林泽婷(译) 吕来文(译) 黄晓晴(译) 李丽萍(审校) Duan Leilei Ye Pengpeng Juanita A Haagsma Jin Ye Wang Yuan Er Yuliang Deng Xiao Gao Xin Ji Cuirong Wang Linhong Marlena S Bannick W Cli Mountjoy-Venning Caitlin N Hawley Zichen Liu Mari Smith Spencer L James Theo Vos Christopher J L Murray | 2020 | 伤害医学(电子版)2020，9，2： | 15 |
| 3 | Encapsulating peritoneal sclerosis显示文摘Encapsulating peritoneal sclerosis(EPS) is a debilitating condition characterized by a fibrocollagenous membrane encasing the small intestine, resulting in recurrent small bowel obstructions. EPS is most commonly associated with long-term peritoneal dialysis, though medications, peritoneal infection, and systemic inflammatory disorders have been implicated. Many cases remain idiopathic. Diagnosis is often delayed given the rarity of the disorder combined with non-specific symptoms and laboratory findings. Although cross-sectional imaging with computed tomography of the abdomen can be suggestive of the disorder, many patients undergo exploratory laparotomy for diagnosis. Mortality approaches 50% one year after diagnosis. Treatment for EPS involves treating the underlying condition or eliminating possible inciting agents(i.e. peritoneal dialysis, medications, infections) and nutritional support, frequently with total parenteral nutrition. EPSspecific treatment depends on the disease stage. In the inflammatory stage, corticosteroids are the treatment of choice, while in the fibrotic stage, tamoxifen may be beneficial. In practice, distinguishing between stages may be difficult and both may be used. Surgical intervention, consisting of peritonectomy and enterolysis, is timeconsuming and high-risk and is reserved for situations in which conservative medical therapy fails in institutions with surgical expertise in this area. Herein we review the available literature of the etiology, pathogenesis, diagnosis, and treatment of this rare, but potentially devastating disease. | Christopher J Danford Steven C Lin Martin P Smith Jacqueline L Wolf | 2018 | World Journal of Gastroenterology2018，24，28： | 13 |
| 4 | Management of borderline and locally advanced pancreatic cancer:Where do we stand?显示文摘Many patients with pancreas cancer present with locally advanced pancreatic cancer(LAPC).The principle tools used for diagnosis and staging of LAPC include endoscopic ultrasound,axial imaging with computed tomography and magnetic resonance imaging,and diagnostic laparoscopy.The definition of resectability has historically been vague,as there is considerable debate and controversy as to the definition of LAPC.For the patient with LAPC,there is some level of involvement of the surrounding vascular structures,which include the superior mesenteric artery,celiac axis,hepatic artery,superior mesenteric vein,or portal vein.When feasible,most surgeons would recommend possible surgical resection for patients with borderline LAPC,with the goal of an R0 resection.For initially unresectable LAPC,neoadjuvant should be strongly considered.Specifically,these patients should be offered neoadjuvant therapy,and the tumor should be assessed for possible response and eventual resection.The efficacy of neoadjuvant therapy with this approach as a bridge to potential curative resection is broad,ranging from 3%-79%.The different modalities of neoadjuvant therapy include sin-gle or multi-agent chemotherapy combined with radiation,chemotherapy alone,and chemotherapy followed by chemotherapy with radiation.This review focuses on patients with LAPC and addresses recent advances and controversies in the field. | Jin He Andrew J Page Matthew Weiss Christopher L Wolfgang Joseph M Herman Timothy M Pawlik | 2014 | World Journal of Gastroenterology2014，20，9： | 11 |
| 5 | 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 |
| 6 | Nonalcoholic 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 | 2018 | World Journal of Gastroenterology2018，24，16： | 7 |
| 7 | Five-year mortality and coronary heart disease development after normal coronary angiogram显示文摘 | Jason T McMullan Christopher J Lindsell Andra L Blomkalns | 2011 | World Journal of Emergency Medicine2011，2，1： | 6 |
| 8 | Hepatic intra-arterial infusion of yttrium-90 microspheres in the treatment of recurrent hepatocellular carcinoma after liver transplantation: A case report显示文摘Hepatocellular carcinoma (HCC) recurs with a reported frequency of 12%-18% after liver transplantation. Recurrence is associated with a mortality rate exceeding 75%. Approximately one-third of recurrences develop in the transplanted liver and are therefore amenable to local therapy. A variety of treatment modalities have been reported including resection, transarterial chemo- embolization (TACE), radiofrequency ablation (RFA), ethanol ablation, cryoablation, and external beam irradiation. Goals of treatment are tumor control and the minimization of toxic effect to functional parenchyma. Efficacy of treatment is mitigated by the need for ongoing immunosuppression. Yttrium-90 microspheres have been used as a treatment modality both for primary HCC and for pre-transplant management of HCC with promising results. Twenty-two months after liver transplantation for hepatitis C cirrhosis complicated by HCC, a 42-year old man developed recurrence of HCC in his transplant allograft. Treatment of multiple right lobe lesions with anatomic resection and adjuvant chemotherapy was unsuccessful. Multifocal recurrence in the remaining liver allograft was treated with hepatic intra-arterial infusion of yttrium-90 microspheres (SIR-Spheres, Sirtex Medica Inc., Lake Forest, IL, USA). Efficacy was demonstrated by tumor necrosis on imaging and a decrease in alpha-fetoprotein (AFP) level. There were no adverse consequences of initial treatment. | Louis Rivera Huan Giap William Miller Jonathan Fisher Donald J Hillebrand Christopher Marsh Randolph L Schaffer | 2006 | World Journal of Gastroenterology2006，12，35： | 6 |
| 9 | Analysis of a Successful Immune Response against Hepatitis C Virus显示文摘 | Stewart Cooper Ann L Erickson Erin J Adams Joe Kansopon Amy J Weiner David Y Chien Michael Houghton Peter Parham Christopher M Walker | 1999 | Immunity1999，，4： | 3 |
| 10 | SLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueduct显示文摘Pendred syndrome(PS) is characterized by autosomal recessive inheritance of goiter associated with a defect of iodide organification, hearing loss, enlargement of the vestibular aqueduct(EVA), and mutations of the SLC26A4 gene. However, not all EVA patients have PSor SLC26A4 mutations. Two mutant alleles of SLC26A4 are detected in 1/4 of North American or European EVA populations, one mutant allele is detected in another 1/4 of patient populations, and no mutations are detected in the other 1/2. The presence of two mutant alleles of SLC26A4 is associated with abnormal iodide organification, increased thyroid gland volume, increased severity of hearing loss, and bilateral EVA. The presence of a single mutant allele of SLC26A4 is associated with normal iodide organification, normal thyroid gland volume, less severe hearing loss and either bilateral or unilateral EVA. When other underlying correlations are accounted for, the presence of a cochlear malformation or the size of EVA does not have an effect on hearing thresholds. This is consistent with observations of an Slc26a4 mutant mouse model of EVA in which hearing loss is independent of endolymphatic hydrops or inner ear malformations. Segregation analyses of EVA in families suggest that the patients carrying one mutant allele of SLC26A4 have a second, undetected mutant allele of SLC26A4, and the probability of a sibling having EVA is consistent with its segregation as an autosomal recessive trait. Patients without any mutations are an etiologically heterogeneous group in which siblings have a lower probability of having EVA. SLC26A4 mutation testing can provide prognostic information to guide clinical surveillance and management, as well as the probability of EVA affecting a sibling. | Taku Ito Julie Muskett Parna Chattaraj Byung Yoon Choi Kyu Yup Lee Christopher K Zalewski Kelly A King Xiangming Li Philine Wangemann Thomas Shawker Carmen C Brewer Seth L Alper Andrew J Griffith | 2013 | World Journal of Otorhinolaryngology2013，3，2： | 2 |
| 11 | HER-2/neu protein overexpression and gene amplification in human transitional cell carcinoma of the bladder显示文摘 | Christopher L Coogan Carlos R Estrada Shiv Kapur Kenneth J Bloom | 2004 | Urology2004，，4： | 2 |
| 12 | Effect of Ginkgo biloba (EGb 761) and aspirin on platelet aggregation and platelet function analysis among older adults at risk of cardiovascular disease: a randomized clinical trial显示文摘 | Christopher D Gardner James L Zehnder Alison J Rigby Joel R Nicholus John W Farquhar | 2007 | Blood Coagulation & Fibrinolysis2007，，8： | 2 |
| 13 | Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010显示文摘 | Christopher J L Murray Theo Vos Rafael Lozano Mohsen Naghavi Abraham D Flaxman Catherine Michaud Majid Ezzati Kenji Shibuya Joshua A Salomon Safa Abdalla Victor Aboyans Jerry Abraham Ilana Ackerman Rakesh Aggarwal Stephanie Y Ahn Mohammed K Ali Mohammad A | 2012 | The Lancet . 2012 (9859)2012，，9859： | 2 |
| 14 | Liver bioengineering:Current status and future perspectives显示文摘The present review aims to illustrate the strategies that are being implemented to regenerate or bioengineer livers for clinical purposes.There are two general pathways to liver bioengineering and regeneration.The first consists of creating a supporting scaffold,either synthetically or by decellularization of human or animal organs,and seeding cells on the scaffold,where they will mature either in bioreactors or in vivo.This strategy seems to offer the quickest route to clinical translation,as demonstrated by the development of liver organoids from rodent livers which were repopulated with organ specific cells of animal and/or human origin.Liver bioengineering has potential for transplantation and for toxicity testing during preclinical drug development.The second possibility is to induce liver regeneration of dead or resected tissue by manipulating cell pathways.In fact,it is well known that the liver has peculiar regenerative potential which allows hepatocyte hyperplasia after amputation of liver volume.Infusion of autologous bone marrow cells,which aids in liver regeneration,into patients was shown to be safe and to improve their clinical condition,but the specific cells responsible for liver regeneration have not yet been determined and the underlying mechanisms remain largely unknown.A complete understanding of the cell pathways and dynamics and of the functioning of liver stem cell niche is necessary for the clinical translation of regenerative medicine strategies.As well,it will be crucial to elucidate the mechanisms through which cells interact with the extracellular matrix,and how this latter supports and drives cell fate. | Christopher Booth Tom Soker Pedro Baptista Christina L Ross Shay Soker Umar Farooq Robert J Stratta Giuseppe Orlando | 2012 | World Journal of Gastroenterology2012，18，47： | 2 |
| 15 | Production of dimethylfuran for liquid fuels from biomass-derived carbohydrates显示文摘 | Yuriy R L Christopher J B Zhen Y L | 2007 | Nature2007，447，： | 1 |
| 16 | Bacterial RNA chaperones confer abiotic stress tolerance in plants and improved grain yield in maize under water-limited condition 显示文摘 | Paolo C Dave W Robert J B Don C A Jay H Martin S Mark A Ganesh K Sara S Robert D Santiago N Stephanie B Mary F Jayaprakash T Santanu D Christopher B Michael H L Jacqueline E H | 2008 | Plant Physiology2008，147，2： | 1 |
| 17 | Extracting multi-source brain activity from a single electromagnetic channel显示文摘 | Christopher J J David L | 2003 | Artificial Intelligence in Medicine2003，28，1： | 1 |
| 18 | Outcomed and clinicopa thologic variables associated with late recurrence after nephrectomy fkr localiged Renal cell carcinoma显示文摘 | SIMON P K CHRISTOPHER J M BRADLEY C L | 2011 | Urology2011，78，5： | 1 |
| 19 | The role of the natural environment in the emergence of antibiotic resistance in Gram-negative bacteria显示文摘 | Elizabeth MH Wellington Alistair BA Boxall Paul Cross Edward J Feil William H Gaze Peter M Hawkey Ashley S Johnson-Rollings Davey L Jones Nicholas M Lee Wilfred Otten Christopher M Thomas A Prysor Williams | 2013 | The Lancet Infectious Diseases2013，，2： | 1 |
| 20 | 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 |
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