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| 1 | Gastrointestinal complications of diabetes mellitus显示文摘Diabetes mellitus affects virtually every organ system in the body and the degree of organ involvement depends on the duration and severity of the disease,and other co-morbidities.Gastrointestinal(GI) involvement can present with esophageal dysmotility,gastro-esophageal reflux disease(GERD),gastroparesis,enteropathy,non alcoholic fatty liver disease(NAFLD) and glycogenic hepatopathy.Severity of GERD is inversely related to glycemic control and management is with prokinetics and proton pump inhibitors.Diabetic gastroparesis manifests as early satiety,bloating,vomiting,abdominal pain and erratic glycemic control.Gastric emptying scintigraphy is considered the gold standard test for diagnosis.Management includes dietary modifications,maintaining euglycemia,prokinetics,endoscopic and surgical treatments.Diabetic enteropathy is also common and management involves glycemic control and symptomatic measures.NAFLD is considered a hepatic manifestation of metabolic syndrome and treatment ismainly lifestyle measures,with diabetes and dyslipidemia management when coexistent.Glycogenic hepatopathy is a manifestation of poorly controlled type 1 diabetes and is managed by prompt insulin treatment.Though GI complications of diabetes are relatively common,awareness about its manifestations and treatment options are low among physicians.Optimal management of GI complications is important for appropriate metabolic control of diabetes and improvement in quality of life of the patient.This review is an update on the GI complications of diabetes,their pathophysiology,diagnostic evaluation and management. | Babu Krishnan Shithu Babu Jessica Walker Adrian B Walker Joseph M Pappachan | 2013 | World Journal of Diabetes2013，4，3： | 10 |
| 2 | Rising incidence of intrahepatic cholangiocarcinoma in the United States: a true increase?显示文摘 | Yasser H Shaib Jessica A Davila Kathryn McGlynn Hashem B El-Serag | 2003 | Journal of Hepatology2003，，3： | 3 |
| 3 | Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in Parkinson’s disease Philip显示文摘This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson’s disease(PD).Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation,but as an integral part of this process,superoxides and other reactive oxygen species are also produced.Excessive free radical production contributes to oxidative stress.Cells have evolved to handle such stress via various endogenous anti-oxidant proteins.One such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner membrane.There are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural cells.In a series of previous publications,we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium(MPP+;toxic metabolite of MPTP)and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential,and reducing oxidative stress.We also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in UCP4.Furthermore,we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin(hormone produced by adipocytes)acting via UCP2 against MPP+-induced toxicity.There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD.Their expression,which can be induced,may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease. | WL Ho Jessica WM Ho Hui-Fang Liu Danny HF So Zero HM Tse Koon-Ho Chan David B Ramsden Shu-Leong Ho | 2012 | Translational Neurodegeneration2012，1，1： | 3 |
| 4 | Requirement for cyclin D3 in germinal center formation and function显示文摘第二等的淋巴的纸巾的幼芽的中心(GC ) 对装高亲密关系的体液的有免疫力的回答批评。当多样化他们的抗体基因时,在 GC 以内的 B 房间经历快速的同种细胞的扩大和选择。尽管 GC B 房间采用一个唯一的 proliferative 程序提供这些进程,这通常被相信,很少联系 GC 的房间周期怎么被安排被知道。D 类型 cyclins 组成使房间能对生理的变化作出回应的房间周期引擎的一个重要部件。房间类型 -- 并且 D 类型 cyclins 的发展阶段特定的角色被描述了,但是 cyclin D 要求没在 GC 反应期间被探讨。在这研究,我们报导 cyclin D3 为切换的增长和 Ig 班大部分是非必需的在 vitro 激活的 B 房间。相反,在 Ccnd3 的 GC 开发 ?/ ?老鼠显著地被损害,作为是 T 房间依赖者抗体反应。在 GC 以内,尽管切换, unswitched B 房间被 cyclin D3 inactivation 影响, IgM?水池更严重地被减少。有趣地尽管有 cyclin D2 表示的补偿增加, Ccnd3 的一个重要数字 ?/ ?GC B 房间处于静止 G0 状态积累。最后,尽管 cyclin D3 inactivation 没在 GC B 房间破坏 BCL6 表示,支持 BCL6 overexpression 的效果完全堵住了 GC,建议 cyclin D3 调整 GC 形成的 BCL6 下游地行动。这是 cyclin D3 玩的第一示范在 B 房间开发的 GC 阶段的一个重要、唯一的角色。 | Jonathan U Peled J Jessica Yu Jeganathan Venkatesh Enguang Bi B Belinda Ding Melissa Krupski-Downs Rita Shaknovich Piotr Sicinski Betty Diamond Matthew D Scharff B Hilda Ye | 2010 | Cell Research2010，20，6： | 3 |
| 5 | Colorectal cancer in the young显示文摘 | Jessica B O’Connell Melinda A Maggard Edward H Livingston Cifford K Yo | 2004 | The American Journal of Surgery2004，，： | 2 |
| 6 | Preschooler's physical activity levels and associations with lesson context,teacher's behavior,and environment during preschool physical education显示文摘 | Van Cauwenberghe E Valery L Jessica G Ilse D B Greet C | 2012 | Early Childhood Research Quarterly2012，27，2： | 1 |
| 7 | Early control of H5NI influenza virus replication by the type I interferon response in Mice显示文摘 | KristyJ S Shivaprakash G Jessica A B | 2009 | J Virol2009，83，11： | 1 |
| 8 | Evaluation of a rapid diagnostic test (CareStartTM Malaria HRP-2/pLDH (Pf/pan) Combo test) for the diagnosis of malaria in reference setting显示文摘 | Jessica M Philippe G Emmanuel B | 2010 | Malar J2010，，9： | 1 |
| 9 | Recovery of valuable elements from spent Li-batteries 显示文摘 | JESSICA F P NATALIA G B JLrLIO C A | 2008 | Journal of Hazardous Materi- als2008，150，： | 1 |
| 10 | Use of a real time PCR assay for detection of the ctxA gene of Vibrio cholerae in an environmental survey of Mobile Bay显示文摘 | GEORGE M B JESSICA L N MICHAEL D B | 2007 | J Microbiol Methods2007，68，： | 1 |
| 11 | Genome sequence of the palaeopolyploid soybean 显示文摘 | Jeremy S Steven B C Jessica S | 2010 | Nature2010，463，： | 1 |
| 12 | Vascular smooth muscle tumors:13 cases and a review of the literature显示文摘 | Jagdish B Gursharan S Jessica H | 2006 | Int J Angiol2006，15，1： | 1 |
| 13 | Metformin therapy in a transgenic mouse model of Huntington's disease 显示文摘 | THONG C M JESSICA L B BENJAMIN O | 2007 | Neurosci Lett2007，411，2： | 1 |
| 14 | Normative Social Influence is Underdetected显示文摘 | Jessica M Nolan Wesley Schuhz P Robert B Cialdini | 2008 | So- ciety for Personality and Social Psychology2008，34，7： | 1 |
| 15 | Position of the American Dietetic Association:Fat Replacers显示文摘 | Satya S J Julie M J Jessica D B | | 0，，： | 1 |
| 16 | Adhesion to extracellular matrix proteins modulates bovine neutrophil responses to inflammatory mediators显示文摘 | Jessica D B Mark T Q Steve D S | 2002 | J Leukoc Biol2002，71，： | 1 |
| 17 | GC-MS analysis of the lipophilic principles of Echinacea purpurea and evaluation of cucumber mosaic cucumovims (CMV) infection 显示文摘 | Mohammad H Jessica F Maria G B | 2002 | J Pharm Biomed Anal2002，29，： | 1 |
| 18 | Synthesis of unsymmetrical 3, 4-diaryl-3-pyrrolin-2-ones utilizing pyrrole weinreb amides 显示文摘 | JESSICA G G SARCH P Y NATH R B | 2011 | J Org Chem2011，76，20： | 1 |
| 19 | Beliefs about papanicolaou smears and compliance with papanicolaou smear follow-up in adolescents 显示文摘 | Jessica A Kahn V Chiou B A | 1999 | Arch Pediatr Adolesc Med1999，153，10： | 1 |
| 20 | Seasonal abundance of total and pathogenic Vibrio parahaemolyticus in alabama oysters显示文摘 | Angelo D Jessica LN Johnc B | 2003 | Appl Environ Microbiol2003，69，3： | 1 |
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