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| 1 | Gastroenteropancreatic neuroendocrine tumours显示文摘 | Irvin M Modlin Kjell Oberg Daniel C Chung Robert T Jensen Wouter W de Herder Rajesh V Thakker Martyn Caplin Gianfranco Delle Fave Greg A Kaltsas Eric P Krenning Steven F Moss Ola Nilsson Guido Rindi Ramon Salazar Philippe Ruszniewski Anders Sundin | 2008 | Lancet Oncology2008，，1： | 8 |
| 2 | Juvenile polyposis syndrome显示文摘Juvenile polyposis syndrome is a rare autosomal dominant syndrome characterized by multiple distinct juvenile polyps in the gastrointestinal tract and an increased risk of colorectal cancer.The cumulative life-time risk of colorectal cancer is 39% and the relative risk is 34.Juvenile polyps have a distinctive histology characterized by an abundance of edematous lamina propria with inflammatory cells and cystically dilated glands lined by cuboidal to columnar epithelium with reactive changes.Clinically,juvenile polyposis syndrome is defined by the presence of 5 or more juvenile polyps in the colorectum,juvenile polyps throughout the gastrointestinal tract or any number of juvenile polyps and a positive family history of juvenile polyposis.In about 50%-60% of patients diagnosed with juvenile polyposis syndrome a germline mutation in the SMAD4 or BMPR1A gene is found.Both genes play a role in the BMP/TGF-beta signalling pathway.It has been suggested that cancer in juvenile polyposis may develop through the socalled 'landscaper mechanism' where an abnormal stromal environment leads to neoplastic transformation of the adjacent epithelium and in the end invasive carcinoma.Recognition of this rare disorder is important for patients and their families with regard to treatment,follow-up and screening of at risk individuals.Each clinician confronted with the diagnosis of a juvenile polyp should therefore consider the possibility of juvenile polyposis syndrome.In addition,juvenile polyposis syndrome provides a unique model to study colorectal cancer pathogenesis in general and gives insight in the molecular genetic basis of cancer.This review discusses clinical manifestations,genetics,pathogenesis and management of juvenile polyposis syndrome. | Lodewijk AA Brosens Danielle Langeveld W Arnout van Hattem Francis M Giardiello G Johan A Offerhaus | 2011 | World Journal of Gastroenterology2011，17，44： | 7 |
| 3 | 儿童期肥胖、成年期肥胖和心血管风险因子显示文摘过去30年,儿童超重或肥胖的发生率明显增加[1]。儿童期肥胖是死亡率增加的预测因子,这主要是由于儿童期肥胖可导致心血管疾病发生率增加。相关的预测研究提示"肥胖流行症"可能改变目前心血管疾病死亡率下降的趋势,使现今儿童的寿命缩短。 | Juonala M Magnussen CG Berenson GS Venn A Burns TL Sabin MA Srinivasan SR Daniels SR Davis PH Chen W Sun C Cheung M Viikari JS Dwyer T Raitakari OT 叶鹏 | 2012 | 中华高血压杂志2012，20，1： | 6 |
| 4 | On tolerability and safety of a maintenance treatment with 6-thioguanine in azathioprineor 6-mercaptopurine intolerant IBD patients显示文摘AIM: To determine the tolerability and safety profile of a low-dose maintenance therapy with 6-TG in azathioprine (AZA) or 6-mercaptopurine (6-MP) intolerant inflammatory bowel disease (IBD) patients over a treatment period of at least 1 year.METHODS: Database analysis.RESULTS: Twenty out of ninety-five (21%) patients discontinued 6-TG (mean dose 24.6 mg; mean 6-TGN level 540 pmol/8×108 RBC) within 1 year. Reasons for discontinuation were GI complaints (31%), malaise (15%)and hepatotoxicity (15%). Hematological events occurred in three patients, one discontinued treatment. In the 6-TG-tolerant group, 9% (7/75) could be classified as hepatotoxicity. An abdominal ultrasound was performed in 54% of patients, one patient had splenomegaly.CONCLUSION: The majority of AZA or 6-MP-intolerant IBD patients (79%) is able to tolerate maintenance treatment with 6-TG (dosages between 0.3 and 0.4 mg/kg per d). 6-TG may still be considered as an escape maintenance immunosuppressant in this difficult to treat group of patients, taking into account potential toxicity and efficacy of other alternatives. The recently reported hepatotoxicity is worrisome and 6-TG should therefore be administered only in prospective trials. | Nanne KH de Boer Luc JJ Derijks Lennard PL Gilissen Daniel W Hommes Leopold GJB Engels Sybrand Y de Boer Gijsbertus den Hartog Piet M Hooymans Anja BU M(?)kelburg Barend D Westerveld Anton HJ Naber Chris JJ Mulder Dirk J de Jong | 2005 | World Journal of Gastroenterology2005，11，35： | 4 |
| 5 | Langerhans cell histiocytosis masquerading as acute appendicitis: Case report and review显示文摘Langerhans cell histiocytosis(LCH) is a rare syndrome characterized by unifocal,multifocal unisystem,or disseminated/multi-system disease that commonly involves the bone,skin,lymph nodes,pituitary,or sometimes lung(almost exclusively in smokers) causing a variety of symptoms from rashes and bone lesions to diabetes insipidus or pulmonary infiltrates.We present a previously unreported case of gastrointestinal LCH as well as a novel characteristic lesion affecting the colon of a young woman who presented with signs and symptoms mimicking acute on chronic appendicitis.Immunohistochemical analysis of appendectomy specimen and nodular specimens on colonoscopy demonstrated S-100,CD1a,and langerin reactivity.The patient underwent systemic chemotherapy with cytarabine and demonstrated excellent response to therapy. | Mohammad M Karimzada Michele N Matthews Samuel W French Daniel De Ugarte Dennis Y Kim | 2017 | World Journal of Gastrointestinal Endoscopy2017，9，3： | 3 |
| 6 | Ron receptor-dependent gene regulation in a mouse model of endotoxin-induced acute liver failure显示文摘BACKGROUND:Prior experimentation has shown that loss of the tyrosine kinase(TK) signaling domain of the Ron receptor leads to marked hepatocyte protection in a model of lipopolysaccharideinduced acute liver failure(ALF) in D-galactosamine(GalN)sensitized mice.The aim of this study was to identify the role of Ron in the regulation of hepatic gene expression.METHODS:Microarray analyses were performed on liver RNA isolated sequentially from wild-type(WT) and TK-/mice during the progression of ALF.Gene array data were validated using Western and immunohistochemistry analyses as well as with ex vivo culture systems.RESULTS:At baseline,101 genes were differentially expressed between WT and TK-/-livers,which regulate processes involved in hypoxia,proliferation,apoptosis and metabolism.One hour after ALF induction,WT livers exhibited increased cytokine expression compared to TK-/-livers,and after 4 hours,an induction of suppressor of cytokine signaling(SOCS) genes as well as JAK-STAT pathway activation were prominent in TK-/livers compared to controls.CONCLUSION:Our studies suggest a novel hepato-protective mechanism in Ron TK-/-mice wherein increased and sustained SOCS production and JAK-STAT activation in the hepatocyte may inhibit the destructive proinflammatory milieu and promote survival factors which blunt hepatic death and the ensuing development of ALF. | Rishikesh M Kulkarni Louis W Kutcher William D Stuart Daniel J Carson Mike A Leonis Susan E Waltz | 2012 | Hepatobiliary & Pancreatic Diseases International2012，11，4： | 3 |
| 7 | 一种房颤风险评分系统的建立(Framingham心脏研究):基于社区的队列研究显示文摘背景房颤导致了发病率和病死率的显著上升。本研究旨在建立一种预测个体罹患房颤绝对风险的风险评分系统,并提供研究人员评价新危险因素的流程。方法作者评估了Framingham心脏研究中于1968年6月至1987年9月间进行了8044次检测的4764例参与者(55%为女性,年龄45~95岁)。此后,参与者被随访至房颤首发,随访期最长达10年。多变量Coxi回归确认出1(1年内罹患房颤的临床危险因素。次级分析纳入了常规超声心动图检测指标(5152例4参与者,7156次检测)对房颤风险进行再分层评估,并评价超声检测指标能否提高风险预测能力。结果4764例参与者中的457例4(10%)罹患房颤。年龄、性别、体重指数、收缩压、降压治疗、PR间期、有临床意义的心脏杂音及心力衰竭与房颤相关,并被纳入了风险评分模型(除体重指数P=0.08外,其余均为P〈0.05),模型的C统计量为0.78(95%CI0.76~0.80)。10年房颤风险随年龄变化:年龄〈65岁的人群中53例(1%)风险高于15%,而〉65岁的人群中为783例(27%)。为提高预测能力而纳入超声检测指标仅使模型C统计量略微增高,由0.78(95%C10.75~0.80)增至0.79(95%CI0.77~0.82:P=0.005)。超声心动图检测指标并不能改善风险再分层评估(P=0.18)。结论基于社区医疗中易得的临床因素建立的风险评分系统,有助于确认社区个体罹患房颤的风险,评估技术或标志物能否改善风险预测,以及针对高危个体采取预防措施。 | Renate B Schnabel Lisa M Sullivan Daniel Levy Michael J Pencina Joseph M Massaro Ralph B D'Agostino Sr Christopher Newton-Cheh Jennifer F Yamamoto Jared W Magnani Thomas M Tadros William B Kannel Thomas J Wang Patrick T Ellinor Philip A Wolf Ramachanclran S Vasan Emelia J Benjamin 黄刚(译) | 2009 | 世界临床医学2009，，9： | 2 |
| 8 | Central line-associated bloodstream infection among children with biliary atresia listed for liver transplantation显示文摘BACKGROUND Pre-transplant nutrition is a key driver of outcomes following liver transplantation in children.Patients with biliary atresia(BA) may have difficulty achieving satisfactory weight gain with enteral nutrition alone,and parenteral nutrition(PN) may be indicated.While PN has been shown to improve anthropometric parameters of children with BA listed for liver transplantation,less is known about the risks,particularly infectious,associated with this therapy among this specific group of patients.AIM To describe the incidence,microbiology,and risk factors of central line-associated bloodstream infection(CLABSI) among children with BA listed for liver transplantation.METHODS Retrospective review of children aged ≤ 2-years of age with BA who were listed for primary liver transplantation at Texas Children's Hospital from 2008 through2015(n = 96).Patients with a central line for administration of PN(n = 63) were identified and details of each CLABSI event were abstracted.We compared the group of patients who experienced CLABSI to the group who did not,to determine whether demographic,clinical,or laboratory factors correlated with development of CLABSI.RESULTS Nineteen of 63 patients(30%,95%CI:19,43) experienced 29 episodes of CLABSI during 4800 line days(6.04 CLABSI per 1000 line days).CLABSI was predominantly associated with Gram-negative organisms(14/29 episodes,48%)including Klebsiella spp.,Enterobacter spp.,and Escherichia coli.The sole polymicrobial infection grew Enterobacter cloacae and Klebsiella pneumoniae.Grampositive organisms(all Staphylococcus spp.) and fungus(all Candida spp.)comprised 9/29(31%) and 6/29(21%) episodes,respectively.No demographic,clinical,or laboratory factors were significantly associated with an increased risk for the first CLABSI event in Cox proportional hazards regression analysis CONCLUSION There is substantial risk for CLABSI among children with BA listed for liver transplantation.No clinical,demographic,or laboratory factor we tested emerged as an independent predictor of CLABSI.While our data did not show an impact of CLABSI on the short-term clinical outcome,it would seem prudent to implement CLABSI reduction strategies in this population to the extent that each CLABSI event represents potentially preventable hospitalization,unnecessary healthcare dollar expenditures,and may exact an opportunity cost,in terms of missed allograft offers. | Nicole D Triggs Stacey Beer Sonam Mokha Kat Hosek Danielle Guffey Charles G Minard Flor M Munoz Ryan W Himes | 2019 | World Journal of Hepatology2019，11，2： | 2 |
| 9 | Label-retaining liver cancer cells are relatively resistant to sorafenib显示文摘 | Hong-Wu Xin Chenwi M Ambe Danielle M Hari Gordon W Wiegand Tyler C Miller Jin-Qiu Chen Andrew J Anderson Satyajit Ray John E Mullinax Tomotake Koizumi Russell C Langan Douglas Burka Michelle A Herrmann Paul K Goldsmith Alexander Stojadinovic Udo Rudloff S | 2013 | Gut2013，，12： | 2 |
| 10 | Activitybased costing accounting for a market orientation 显示文摘 | Daniel J G Greg W M William B C | 1998 | Industrial Marketing Management1998，，127： | 1 |
| 11 | Catalytic combustion of methane on Co/MgO:characterisation of active cobalt sites显示文摘 | Ulla M A Spretz R Lombardo E Daniell W Knozinger H | | 0，，： | 1 |
| 12 | Vocal response to pain in piglets显示文摘 | Daniel M W Leah A B David F | 1998 | Applied Animal Behaviour Science1998，56，2： | 1 |
| 13 | Global update on the susceptibility of human influenza viruses to neuraminidase inhibitors, 2012-2013显示文摘 | Meijer A Rebelo-de-Andrade H Correia V Besselaar T Drager-Dayal R Fry A Gregory V Gubareva L Kageyama T Laekenby A Lo J Odagiri T Pere- yaslov D Siqueira M M Takashita E Tashiro M Wang D Wong S Zhang W Daniels R S Hurt A C | 2014 | An- tiviral Research2014，110，： | 1 |
| 14 | Preferred risk allocation in target cost contracts in con- struction显示文摘 | Joseph H L Chan Daniel W M Chan Patrick T I Lam | 2011 | Facilities2011，29，1314： | 1 |
| 15 | A mechanism for zinc toxicity in neuroblastoma cells显示文摘 | Daniels W M U Hendricks J Salie R | 2004 | Metabolic Brain Disease2004，19，12： | 1 |
| 16 | Twenty years of inten- sive fertilization and competing vegetation suppression in loblolly pine plantations: Impacts on soil C,N, and microbial biomass显示文摘 | Sami W R Daniel M Bruce B | 2010 | Soil Biology & Biochemistry2010，42，5： | 1 |
| 17 | Regulation of the human catalytic subunit of telomerase (hTERT) 显示文摘 | Daniel M Peek G W Tollefsbol T O | 2012 | Gene2012，498，2： | 1 |
| 18 | Suppression of allergic immune responses to house dust mite (HDM) in rats exposed to 2,3,7,8-TCDD显示文摘 | Luebke R W Copeland C B Daniels M | 2001 | Toxicol Sci2001，62，1： | 1 |
| 19 | Solid-state modification of poly (butylene terephthalate)with a bio-based fatty acid dimer diol furnishing copolyesters with unique morphologies显示文摘 | Erik G Lidia J W Daniel H M | 2013 | Macromolecules2013，46，： | 1 |
| 20 | Incorporating observational data into the formulary decision-making process- summary of aroundtable discussion显示文摘 | ANKE-PEGGY H JOHN B W DANIEL M | 2008 | J Managed Care Pharma- cy2008，14，3： | 1 |
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