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| 1 | Pancreatic cancer: A review of clinical diagnosis, epidemiology, treatment and outcomes显示文摘This review aims to outline the most up-to-date knowledge of pancreatic adenocarcinoma risk, diagnostics, treatment and outcomes, while identifying gaps that aim to stimulate further research in this understudied malignancy. Pancreatic adenocarcinoma is a lethal condition with a rising incidence, predicted to become the second leading cause of cancer death in some regions. It often presents at an advanced stage, which contributes to poor five-year survival rates of 2%-9%, ranking firmly last amongst all cancer sites in terms of prognostic outcomes for patients. Better understanding of the risk factors and symptoms associated with this disease is essential to inform both health professionals and the general population of potential preventive and/or early detection measures. The identification of high-risk patients who could benefit from screening to detect pre-malignant conditions such as pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasms and mucinous cystic neoplasms is urgently required, however an acceptable screening test has yet to be identified. The management of pancreatic adenocarcinoma is evolving, with the introduction of new surgical techniques and medical therapies such as laparoscopic techniques and neo-adjuvant chemoradiotherapy, however this has only led to modest improvements in outcomes. The identification of novel biomarkers is desirable to move towards a precision medicine era, where pancreatic cancer therapy can be tailored to the individual patient, while unnecessary treatments that have negative consequences on quality of life could be prevented for others. Research efforts must also focus on the development of new agents and delivery systems. Overall, considerable progress is required to reduce the burden associated with pancreatic cancer. Recent, renewed efforts to fund large consortia and research into pancreatic adenocarcinoma are welcomed, but further streams will be necessary to facilitate the momentum needed to bring breakthroughs seen for other cancer sites. | Andrew McGuigan Paul Kelly Richard C Turkington Claire Jones Helen G Coleman R Stephen McCain | 2018 | World Journal of Gastroenterology2018，24，43： | 140 |
| 2 | Platelet thromboxane(11-dehydro-Thromboxane B_2) and aspirin response in patients with diabetes and coronary artery disease显示文摘Aspirin(ASA) irreversibly inhibits platelet cyclooxygenase-1(COX-1) leading to decreased thromboxane-mediated platelet activation. The effect of ASA ingestion on thromboxane generation was evaluated in patients with diabetes(DM) and cardiovascular disease. Thromboxane inhibition was assessed by measuring the urinary excretion of 11-dehydro-thromboxane B2(11dhTxB2), a stable metabolite of thromboxane A2. The mean baseline urinary 11dhTxB2 of DM was 69.6% higher than healthy controls(P = 0.024): female subjects(DM and controls) had 50.9% higher baseline 11dhTxB2 than males(P = 0.0004), while age or disease duration had no influence. Daily ASA ingestion inhibited urinary 11dhTxB2 in both DM(71.7%) and controls(75.1%, P < 0.0001). Using a pre-established cut-off of 1500 pg/mg of urinary 11dhTxB2, there were twice as many ASA poor responders(ASA 'resistant') in DM than in controls(14.8% and 8.4%, respectively). The rate of ASA poor responders in two populations of acute coronary syndrome(ACS) patients was 28.6 and 28.7%, in spite of a significant(81.6%) inhibition of urinary 11dhTxB2(P < 0.0001). Both baseline 11dhTxB2 levels and rate of poor ASA responders were significantly higher in DM and ACS compared to controls. Underlying systemic oxidative inflammation may maintain platelet function in atherosclerotic cardiovascular disease irrespective of COX-1 pathway inhibition and/or increase systemic generation of thromboxane from non-platelet sources. | Luis R Lopez Kirk E Guyer Ignacio Garcia De La Torre Kelly R Pitts Eiji Matsuura Paul RJ Ames | 2014 | World Journal of Diabetes2014，5，2： | 13 |
| 3 | Nat Genet:单基因突变导致过敏性皮炎的发生显示文摘最近,研究者们鉴定出了一类导致神经性皮炎发生的关键基因突变:CARDll。来自美国NIH过敏与传染病研究所的研究者们通过对四个没有血缘关系的患病家庭进行分析,发现了这一导致疾病产生的基因、 | Chi A Ma, Yuan Zhang, Michael A Weinreich, Jonathan J Lyons, Celeste G Nelson, Thomas DiMaggio, Kelly D Stone, Joshua D Milner Jeffrey R Stinson, Elisa Ruffo, Batsukh Dorjbal, Swadhinya Arjunaraja, Kelsey Voss, Andrew L Snow Jordan K Abbott, Pia J Hauk, Paul R Reynolds, Erwin W Gelfand Elisa Ruffo Salomé Glauzy, Natsuko Yamakawa, Eric Meffre Jennifer Stoddard, Julie Niemela, Sergio D Rosenzweig Yu Zhang, Helen F Matthews Joshua J McElwee Nina Jones Alejandro Palma, Matías Oleastro, Emma Prieto, Andrea R Bernasconi, Geronimo Dubra, Silvia Danielian, Jonathan Zaiat, Marcelo A Marti Brian Kim Megan A Cooper Neil Romberg | 2017 | 现代生物医学进展2017，17，27： | 3 |
| 4 | Gastrointestinal pathology in the University Teaching Hospital, Lusaka, Zambia: review of endoscopic and pathology records显示文摘 | Paul Kelly Mwamba Katema Beatrice Amadi Lameck Zimba Sylvia Aparicio Victor Mudenda K. Sridutt Baboo Isaac Zulu | 2007 | Transactions of the Royal Society of Tropical Medicine and Hygiene2007，，2： | 3 |
| 5 | Does low volume high-intensity interval training elicit superior benefits to continuous low to moderate-intensity training in cancer survivors?显示文摘AIM To determine the impact ofm low volume high-intensity interval training(LVHIIT) and continuous low to moderate-intensity exercise training(CLMIT) on cardiovascular disease(CVD) risk and health outcomes in cancer survivors.METHODS Sedentary cancer survivors(n=75,aged 51±12year)within 24 months of diagnosis,were randomised into three groups for 12 wk of LVHIIT(n=25),CLMIT(n=25)or control group(n=25).The exercise intervention involved 36 sessions(three sessions per week).The LVHIIT group performed 7 x 30 s intervals(≥85%predicted maximal heart rate)with a 60 s rest between intervals,and the CLMIT group performed continuous aerobic training for 20 min(≤55%predicted maximal heart rate)on a stationary bike.Outcome variables were measured at baseline and at12 weeks and analysed using a 3 x 2(group x time)repeated measures ANCOVA to evaluate main and interaction effects.RESULTS Significant improvements(time)were observed for seven of the 22 variables(ES 0.35-0.97,P≤0.05).There was an interaction effect(P<0.01)after 12 in the LVHIIT group for six-minute walk test(P<0.01;d=0.97;95%CI:0.36,1.56;large),sit to stand test(P<0.01;d=-0.83;95%CI:-1.40,-0.22;large)and waist circumference reduction(P=0.01;d=-0.48;95%CI:-1.10,0.10;medium).An interaction effect(P<0.01)was also observed for quality of life in both the LVHIIT(d=1.11;95CI:0.50,1.72;large)and CLMIT(d=0.57;95%CI:-0.00,1.20;moderate)compared with the control group(d=-0.15;95%CI:-0.95,0.65;trivial).CONCLUSION Low-volume high-intensity training shows promise as an effective exercise prescription within the cancer population,showing greater improvements in cardiorespiratory fitness,lower body strength and waist circumference compared with traditional CLMIT and control groups.Both LVHIIT and CLMIT improved quality of life.A proposed benefit of LVHIIT is the short duration(3 min)of exercise required,which may entice more cancer survivors to participate in exercise,improving health outcomes and lowing the risk of CVD. | Kellie Toohey Kate Pumpa Andrew McKune Julie Cooke Katrina D DuBose Desmond Yip Paul Craft Stuart Semple | 2018 | World Journal of Clinical Oncology2018，9，1： | 3 |
| 6 | Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse显示文摘Hyaluronan(HA)production by dendritic cells(DCs)is known to promote antigen presentation and to augment T-cell activation and proliferation.We hypothesized that pericellular HA can function as intercellular‘glue’directly mediating T cell–DC binding.Using primary human cells,we observed HA-dependent binding between T cells and DCs,which was abrogated upon pre-treatment of the DCs with 4-methylumbelliferone(4-MU),an agent which blocks HA synthesis.Furthermore,T cells regulate HA production by DCs via T cell-derived cytokines in a T helper(Th)subset-specific manner,as demonstrated by the observation that cell-culture supernatants from Th1 but not Th2 clones promote HA production.Similar effects were seen upon the addition of exogenous Th1 cytokines,IL-2,interferon c(IFN-c)and tumor necrosis factor a(TNF-a).The critical factors which determined the extent of DC–T cell binding in this system were the nature of the pre-treatment the DCs received and their capacity to synthesize HA,as T-cell clones which were pre-treated with monensin,added to block cytokine secretion,bound equivalently irrespective of their Th subset.These data support the existence of a feedforward loop wherein T-cell cytokines influence DC production of HA,which in turn affects the extent of DC–T cell binding.We also document the presence of focal deposits of HA at the immune synapse between T-cells and APC and on dendritic processes thought to be important in antigen presentation.These data point to a pivotal role for HA in DC–T cell interactions at the IS. | Paul L Bollyky Stephen P Evanko Rebecca P Wu Susan Potter-Perigo S Alice Long Brian Kinsella Helena Reijonen Kelly Guebtner Brandon Teng Christina K Chan Kathy R Braun John A Gebe Gerald T Nepom Thomas N Wight | 2010 | Cellular & Molecular Immunology2010，7，3： | 3 |
| 7 | Esophageal squamous cell cancer in a highly endemic region显示文摘AIM: To identify risk factors associated with esophageal cancer in Zambia and association between dietary intake and urinary 8-iso prostaglandin F2α(8-iso PGF2α).METHODS: We conducted a prospective, case control study at the University Teaching Hospital. Subjects included both individuals admitted to the hospital and those presenting for an outpatient upper endoscopy. Esophageal cancer cases were compared to age and sex-matched controls. Cases were defined as patients with biopsy proven esophageal cancer; controls were defined as subjects without endoscopic evidence ofesophageal cancer. Clinical and dietary data were collected using a standard questionnaire, developed a priori. Blood was collected for human immunodeficiency virus(HIV) serology. Urine was collected, and 8-iso PGF2α was measured primarily by enzyme-linked immunosorbent assay and expressed as a ratio to creatinine.RESULTS: Forty five controls(mean age 54.2 ± 15.3, 31 male) and 27 cases(mean age 54.6 ± 16.4, 17 males) were studied. Body mass index was lower in cases(median 16.8) than controls(median 23.2), P = 0.01. Histopathologically, 25/27(93%) were squamous cell carcinoma and 2/27(7%) adenocarcinoma. More cases smoked cigarettes(OR = 11.24, 95%CI: 1.37-92.4, P = 0.02) but alcohol consumption and HIV seropositivity did not differ significantly(P = 0.14 for both). Fruit, vegetables and fish consumption did not differ significantly between groups(P = 0.11, 0.12, and 0.10, respectively). Mean isoprostane level was significantly higher in cases(0.03 ng/mg creatinine) than controls(0.01 ng/mg creatinine)(OR = 2.35, 95%CI: 1.19-4.65, P = 0.014).CONCLUSION: Smoking and isoprostane levels were significantly associated with esophageal cancer in Zambians, but diet, HIV status, and alcohol consumption were not. | Akwi W Asombang Violet Kayamba Mpala M Lisulo Kathryn Trinkaus Victor Mudenda Edford Sinkala Stayner Mwanamakondo Themba Banda Rose Soko Paul Kelly | 2016 | World Journal of Gastroenterology2016，22，9： | 2 |
| 8 | Gastric cancer in Africa: what do we know about incidence and risk factors?显示文摘 | Akwi W. Asombang Paul Kelly | 2011 | Transactions of the Royal Society of Tropical Medicine and Hygiene2011，，2： | 2 |
| 9 | Late paleocene to eocene paleocenography of the equatorial pacific ocean: stable isotopes recorded at ocean drilling program site 865, allison guyot显示文摘 | Zachos J C Thomas E Parrow M Paul C K Kelly D C Silva I P Sliter W V Lohmann K C | 1995 | Paleoceanography1995，10，： | 1 |
| 10 | Modeling a vuggy carbonate reservoir,McElroy Field,West Texas显示文摘 | Kaveh Dehghani Paul Mitch Harris Kelly A Edwards | 1999 | AAPG Bulletin1999，83，： | 1 |
| 11 | SU11248 inhibits tumor growth and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model显示文摘 | Lesley J. Murray Tinya J. Abrams Kelly R. Long Theresa J. Ngai Lisa M. Olson Weiru Hong Paul K. Keast Jacqueline A. Brassard Anne Marie O’Farrell Julie M. Cherrington Nancy K. Pryer | 2003 | Clinical and Experimental Metastasis2003，，8： | 1 |
| 12 | Role of L-glutamine in critical illness: new insights显示文摘 | David Kelly Paul E. Wischmeyer | 2003 | Current Opinion in Clinical Nutrition and Metabolic Care2003，，2： | 1 |
| 13 | Role of L-glutamine in critical illness: new insights显示文摘 | Kelly D Paul E Wischmeyer | 2003 | Curr Opin Clin Nutr Metab Care2003，6，2： | 1 |
| 14 | Global Analysis of Host-Pathogen Interactions that Regulate Early-Stage HIV-1 Replication显示文摘 | Renate K?nig Yingyao Zhou Daniel Elleder Tracy L. Diamond Ghislain M.C. Bonamy Jeffrey T. Irelan Chih-yuan Chiang Buu P. Tu Paul D. De Jesus Caroline E. Lilley Shannon Seidel Amanda M. Opaluch Jeremy S. Caldwell Matthew D. Weitzman Kelli L. Kuhen Sourav B | 2008 | Cell2008，，1： | 1 |
| 15 | 原发性免疫缺陷病患者肿瘤发生情况:美国免疫缺陷网络注册患者肿瘤发病率分析显示文摘研究背景评估了在美国免疫缺陷网络(USIDNET)注册的原发性免疫缺陷病(PIDDs)患者的总体和器官特异性肿瘤发病率,并与监测、流行病学和最终结果项目(SEER)数据库中经年龄校正的人群的肿瘤发病率进行比较。目的假设PIDD患者由于免疫功能受损,肿瘤发病率会增加。方法将2003年至2015年在USIDNET注册中心注册的PIDD (n=3658)患者的总体和器官特异性肿瘤发病率进行评估,并与SEER数据库中经年龄校正的人群发病率进行比较。结果与年龄相匹配的SEER人群相比,观察到PIDD患者罹患肿瘤的相对危险率为1. 42倍(P<0. 001)。PIDD的男性患癌症的风险是年龄校正的男性人群的1. 91倍(P<0. 001),而PIDD女性患者的总体肿瘤发病率与经年龄校正的女性人群相比并无差异。对SEER数据库中最常见的4个恶性肿瘤——肺癌、结肠癌、乳腺癌和前列腺癌的发病率进行分析,PIDD患者中这些肿瘤的发病没有显著增加。男性和女性PIDD患者的淋巴瘤发病率均显著增加(男性10倍,P<0. 001;女性8. 34倍,P<0. 001)。结论 PIDD患者的肿瘤发病率较高。在特定的PIDD人群中淋巴瘤发病率的增高是导致总体肿瘤发病率提高的主要原因,而常见的实体肿瘤的风险没有增加。这些数据表明免疫系统在预防特定肿瘤方面有一定的作用。 | Paul C.Mayor Kevin H.Eng Kelly L.Singel Scott I.Abrams Kunle Odunsi Kirsten B.Moysich Ramsay Fuleihan Elizabeth Garabedian Patricia Lugar Hans D.Ochs Francisco A.Bonilla Rebecca H.Buckley Kathleen E.Sullivan Zuhair K.Ballas Charlotte Cunningham-Rundles Brahm H.Segal 白炜 曾小峰 | 2018 | 中华临床免疫和变态反应杂志2018，12，2： | 1 |
| 16 | New chemotherapeutic a gents prolong survival and improve quality of life in non small cell lung cancer: a review of the literature and fu ture directions显示文摘 | Paul A Bunn PAJr Kelly K | 1998 | Clin Cancer Res1998，4，5： | 1 |
| 17 | The Intracellular Sensor NLRP3 Mediates Key Innate and Healing Responses to Influenza A Virus via the Regulation of Caspase-1显示文摘 | Paul G. Thomas Pradyot Dash Jerry R. Aldridge Ali H. Ellebedy Cory Reynolds Amy J. Funk William J. Martin Mohamed Lamkanfi Richard J. Webby Kelli L. Boyd Peter C. Doherty Thirumala-Devi Kanneganti | 2009 | Immunity2009，，4： | 1 |
| 18 | Peer support for pa tients with type 2 diabetes~ cluster randomised controlled trial显示文摘 | Smith S M Paul G Kelly A | 2011 | BMJ2011，3，2： | 1 |
| 19 | Health Literacy and Adherence to Glaucoma Therapy显示文摘 | Kelly W. Muir Cecile Santiago-Turla Sandra S. Stinnett Leon W. Herndon R. Rand Allingham Pratap Challa Paul P. Lee | 2006 | American Journal of Ophthalmology2006，，2： | 1 |
| 20 | Randomized phase III trial of paclitaxel plus carboplatin versus vinorelbine plus cisplatin in the treatment of patients with advanced Non-small Cell Lung Cancer:A Southwest Oncology Group Trial显示文摘 | Kelly K Crowley J Paul AB | 2001 | J Clin Oncol2001，19，： | 1 |
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