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| 1 | Gastrointestinal radiation injury:Symptoms,risk factors and mechanisms显示文摘Ionising radiation therapy is a common treatment modality for different types of cancer and its use is expected to increase with advances in screening and early detection of cancer.Radiation injury to the gastrointestinal tract is important factor working against better utility of this important therapeutic modality.Cancer survivors can suffer a wide variety of acute and chronic symptoms following radiotherapy,which significantly reduces their quality of life as well as adding an extra burden to the cost of health care.The accurate diagnosis and treatment of intestinal radiation injury often represents a clinical challenge to practicing physicians in both gastroenterology and oncology.Despite the growing recognition of the problem and some advances in understanding the cellular and molecular mechanisms of radiation injury,relatively little is known about the pathophysiology of gastrointestinal radiation injury or any possible susceptibility factors that could aggravate its severity.The aims of this review are to examine the various clinical manifestations of post-radiation gastrointestinal symptoms,to discuss possible patient and treatment factors implicated in normal gastrointestinal tissue radiosensitivity and to outline different mechanisms of intestinal tissue injury. | Abobakr K Shadad Frank J Sullivan Joseph D Martin Laurence J Egan | 2013 | World Journal of Gastroenterology2013，19，2： | 35 |
| 2 | Gastrointestinal radiation injury:Prevention and treatment显示文摘With the recent advances in detection and treatment of cancer,there is an increasing emphasis on the efficacy and safety aspects of cancer therapy.Radiation therapy is a common treatment for a wide variety of cancers,either alone or in combination with other treatments.Ionising radiation injury to the gastrointestinal tract is a frequent side effect of radiation therapy and a considerable proportion of patients suffer acute or chronic gastrointestinal symptoms as a result.These side effects often cause morbidity and may in some cases lower the efficacy of radiotherapy treatment.Radiation injury to the gastrointestinal tract can be minimised by either of two strategies:technical strategies which aim to physically shift radiation dose away from the normal intestinal tissues,and biological strategies which aim to modulate the normal tissue response to ionising radiation or to increase its resistance to it.Although considerable improvement in the safety of radiotherapy treatment has been achieved through the use of modern optimised planning and delivery techniques,biological techniques may offer additional further promise.Different agents have been used to prevent or minimize the severity of gastrointestinal injury induced by ionising radiation exposure,including biological,chemical and pharmacological agents.In this review we aim to discuss various technical strategies to prevent gastrointestinal injury during cancer radiotherapy,examine the different therapeutic options for acute and chronic gastrointestinal radiation injury and outline some examples of research directions and considerations for prevention at a pre-clinical level. | Abobakr K Shadad Frank J Sullivan Joseph D Martin Laurence J Egan | 2013 | World Journal of Gastroenterology2013，19，2： | 32 |
| 3 | Imaging of bone metastasis: An update显示文摘Early detection of skeletal metastasis is critical for accurate staging and optimal treatment. This paper briefly reviews our current understanding of the biological mechanisms through which tumours metastasise to bone and describes the available imaging methods to diagnose bone metastasis and monitor response to treatment. Among the various imaging modalities currently available for imaging skeletal metastasis, hybrid techniques whichfuse morphological and functional data are the most sensitive and specific, and positron emission tomography(PET)/computed tomography and PET/magnetic resonance imaging will almost certainly continue to evolve and become increasingly important in this regard. | Gerard J O'Sullivan Fiona L Carty Carmel G Cronin | 2015 | World Journal of Radiology2015，7，8： | 10 |
| 4 | D-二聚体预测稳定型冠状动脉性心脏病患者的长期病因特异性死亡率、心血管事件和癌症显示文摘交联纤维蛋白的降解产物D-二聚体是高凝状态和血栓形成事件的标志。D-二聚体水平中度升高与血管疾病患者静脉和动脉事件的风险相关。在缺血性疾病长期普伐他汀干预(long-term intervention with pravastatin in ischemic disease,LIPID)试验中,研究者在存在其他危险因素的背景下,评估了D-二聚体水平在预测长期血管转归、病因特异性死亡率和新发癌症中的作用。 | 刘青 叶鹏 Simes J Robledo KP White HD Espinoza D Stewart RA Sullivan DR Zeller T Hague W Nestel PJ Glasziou PP Keech AC Elliott J Blankenberg S Tonkin AM LIPID study investigators | 2018 | 中华高血压杂志2018，26，3： | 6 |
| 5 | Osteoprotegerin: A Novel Secreted Protein Involved in the Regulation of Bone Density显示文摘 | W.S Simonet D.L Lacey C.R Dunstan M Kelley M.-S Chang R Lüthy H.Q Nguyen S Wooden L Bennett T Boone G Shimamoto M DeRose R Elliott A Colombero H.-L Tan G Trail J Sullivan E Davy N Bucay L Renshaw-Gegg T.M Hughes D Hill W Pattison P Campbell S Sander G Van | 1997 | Cell1997，，2： | 6 |
| 6 | Osteoprotegerin Ligand Is a Cytokine that Regulates Osteoclast Differentiation and Activation显示文摘 | D.L Lacey E Timms H.-L Tan M.J Kelley C.R Dunstan T Burgess R Elliott A Colombero G Elliott S Scully H Hsu J Sullivan N Hawkins E Davy C Capparelli A Eli Y.-X Qian S Kaufman I Sarosi V Shalhoub G Senaldi J Guo J Delaney W.J Boyle | 1998 | Cell1998，，2： | 4 |
| 7 | 脂质组学改善传统危险因素预测的2型糖尿病患者的心血管事件显示文摘临床脂质测定并未显示出糖尿病或心血管病相关的脂质代谢改变的复杂性。脂质组学则能够评估可作为疾病风险潜在标志物的数百种脂质种类。方法:纳入来自糖尿病治疗和血管保护行动。 | 刘莉 叶鹏 Alshehry ZH Mundra PA Barlow CK Mellett NA Wong G McConville MJ Simes J Tonkin AM Sullivan DR Barnes EH Nestel PJ Kingwell BA Marre M Neal B Poulter NR Rodgers A Williams B Zoungas S Hillis GS Chalmers J Woodward M Meikle PJ | 2016 | 中华高血压杂志2016，24，10： | 3 |
| 8 | 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 |
| 9 | Regulation of Wnt/β-catenin signaling by herpesviruses显示文摘The Wnt/β-catenin signaling pathway is instrumental in successful differentiation and proliferation of mammalian cells. It is therefore not surprising that the herpesvirus family has developed mechanisms to interact with and manipulate this pathway. Successful coexistence with the host requires that herpesviruses establish a lifelong infection that includes periods of latency and reactivation or persistence. Many herpesviruses establish latency in progenitor cells and viral reactivation is linked to host-cell proliferation and differentiation status. Importantly, Wnt/β-catenin is tightly connected to stem/progenitor cell maintenance and differentiation. Numerous studies have linked Wnt/β-catenin signaling to a variety of cancers, emphasizing the importance of Wnt/β-catenin pathways in development, tissue homeostasis and disease. This review details how the alpha-, beta-, and gammaherpesviruses interact and manipulate the Wnt/β-catenin pathway to promote a virus-centric agenda. | Kevin J Zwezdaryk Joseph A Combs Cindy A Morris Deborah E Sullivan | 2016 | World Journal of Virology2016，5，4： | 2 |
| 10 | Effects of UV- B on seedling growth in the Pinaceae显示文摘 | Sullivan J H Teremura A H | 1988 | Amer J Bot1988，75，4： | 2 |
| 11 | Measurement of piezoelectrically induced charge in GaN/A1GaN heterostructure field - effect transistors 显示文摘 | Yu E T Sullivan G J Asbeck P M | 1997 | Appl Phys Lett1997，71，19： | 1 |
| 12 | Identification and characterization of an off virus homo logue of the vaccinia virusgene encoding the major envelop antigen p37k显示文摘 | Mercer A A Flening S B | 1994 | Virology1994，202，： | 1 |
| 13 | Sleep disturbance as the hallmark of posttraumatic stress disorder 显示文摘 | Ross R J Ball W A Sullivan K A | 1989 | Am J Psychiatry1989，146，： | 1 |
| 14 | Characterization of plant p23-like proteins for their co-chaperone activities 显示文摘 | Zhang Z M Sullivan W Felts S J | 2010 | Cell Stress Chaperones2010，15，5： | 1 |
| 15 | Schottky-barrier inhomogeneity at epitaxial NiSi2 interfaces on Si(100) 显示文摘 | TUNG R T LEVI A F J SULLIVAN J P | 1991 | Phys Rev Lett1991，66，1： | 1 |
| 16 | The Fas counterattack : a molecular mechenism of tumor immune privilege 显示文摘 | O'Connell J Bennett M W O'Sullivan G C et aL | 1997 | Mol Med1997，3，： | 1 |
| 17 | PWM-Switch modeling of DC-DC converters 显示文摘 | Van Dijk E Spruijt J N O'Sullivan D M | 1995 | IEEE Trans on Power Electronics1995，10，6： | 1 |
| 18 | Factors affecting choice of community residential care setting 显示文摘 | Sales AE Hedrick SC Sullivan J | 2005 | J Aging Health2005，17，2： | 1 |
| 19 | Do BITs Really Work?An Evaluation of Bilateral Investment Treaties and Their Grand Bargain显示文摘 | SALACUSE J W SULLIVAN N P | 2005 | Harvard International Law Journal2005，46，1： | 1 |
| 20 | Exacerbation of damage and altered NF-kappa B activation in mice lacking tumor necrosis factor receptors after traumatic brain injury显示文摘 | Sullivan P G Bruce-Keller A J Rabchevsky A G | 1999 | J Neurosci1999，19，15： | 1 |
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