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| 1 | Hematological disorders and pulmonary hypertension显示文摘Pulmonary hypertension(PH),a serious disorder with a high morbidity and mortality rate,is known to occur in a number of unrelated systemic diseases.Several hematological disorders such as sickle cell disease,thalassemia and myeloproliferative diseases develop PH which worsens the prognosis.Associated oxidant injury and vascular inflammation cause endothelial damage and dysfunction.Pulmonary vascular endothelial damage/dysfunction is an early event in PH resulting in the loss of vascular reactivity,activation of proliferative and antiapoptotic pathways leading to vascular remodeling,elevated pulmonary artery pressure,right ventricular hypertrophy and premature death.Hemolysis observed in hematological disorders leads to free hemoglobin which rapidly scavenges nitric oxide(NO),limiting its bioavailability,and leading to endothelial dysfunction.In addition,hemolysis releases arginase into the circulation which converts L-arginine to ornithine,thus bypassing NO production.Furthermore,treatments for hematological disorders such as immunosuppressive therapy,splenectomy,bone marrow transplantation,and radiation have been shown to contribute to the development of PH.Recent studies have shown deregulated iron homeostasis in patients with cardiopulmonary diseases including pulmonary arterial hypertension(PAH).Several studies have reported low iron levels in patients with idiopathic PAH,and iron deficiency is an important risk factor.This article reviews PH associated with hematological disorders and its mechanism:and iron homeostasis and its relevance to PH. | Rajamma Mathew Jing Huang Joseph M Wu John T Fallon Michael H Gewitz | 2016 | World Journal of Cardiology2016，8，12： | 6 |
| 2 | Cardiac papillary fibroelastoma:The need for a timely diagnosis显示文摘Cardiac papillary fibroelastomas(CPFs) are the second most common primary cardiac tumors and the most common cardiac valvular tumors. Although they are histologically benign and usually asymptomatic, CPFs can lead to serious and life-threatening complications like myocardial infarction, stroke, pulmonary embolus, cardiac arrest etc. CPFs represent a rare entity in clinical medicine and literature regarding their management is limited. We report two cases which illustrate such complications arising from undiagnosed CPFs on the aortic valve. We further stress on the importance of identifying CPFs early so that they can be managed appropriately based on recommendations from the available literature. | Srikanth Yandrapalli Bella Mehta Pratik Mondal Tanush Gupta Pallavi Khattar John Fallon Randy Goldberg Sachin Sule Wilbert S Aronow | 2017 | World Journal of Clinical Cases2017，5，1： | 2 |
| 3 | Retroperitoneal lipoblastoma: A discussion of current management显示文摘 | Daniela Burchhardt Sara C. Fallon Monica E. Lopez Eugene S. Kim John Hicks Mary L. Brandt | 2012 | Journal of Pediatric Surgery2012，，10： | 1 |
| 4 | Human Monocyte-Derived Macrophages Induce Collagen Breakdown in Fibrous Caps of Atherosclerotic Plaques: Potential Role of Matrix- Degrading Metalloproteinases and Implications for Plaque Rupture显示文摘 | Prediman K. Shah Erling Falk Juan J. Badimon Antonio Fernandez-Ortiz Alessandra Mailhac Gerardo Villareal-Levy John T. Fallon Jan Regnstrom Valentin Fuster | 1995 | Circulation1995，，6： | 1 |
| 5 | A protocol for determining lake acidification pathways显示文摘 | David R. Marmorek David P. Bernard Christopher H. R. Wedeles Glenn Sutherland John A. Malanchuk William E. Fallon | 1989 | Water Air and Soil Pollution (-)1989，，3： | 1 |
| 6 | Role of serial multiparametric magnetic resonance imaging in prostate cancer active surveillance显示文摘AIM:To examine whether addition of 3T multiparametric magnetic resonance imaging(mp MRI)to an active surveillance protocol could detect aggressive or progressive prostate cancer.METHODS:Twenty-three patients with low risk disease were enrolled on this active surveillance study,all of which had Gleason score 6 or less disease.All patients had clinical assessments,including digital rectal examination and prostate specific antigen(PSA)testing,every 6 mo with annual 3T mp MRI scans with gadolinium contrast and minimum sextant prostate biopsies.The MRI images were anonymized of patient identifiers and clinical information and each scan underwentradiological review without the other results known.Descriptive statistics for demographics and follow-up as well as the sensitivity and specificity of mp MRI to identify prostate cancer and progressive disease were calculated.RESULTS:During follow-up(median 24.8 mo)11 of 23 patients with low-risk prostate cancer had disease progression and were taken off study to receive definitive treatment.Disease progression was identified through upstaging of Gleason score on subsequent biopsies for all 11 patients with only 2 patients also having a PSA doubling time of less than 2 years.All 23 patients had biopsy confirmed prostate cancer but only 10 had a positive index of suspicion on mp MRI scans at baseline(43.5% sensitivity).Aggressive disease prediction from baseline mpM RI scans had satisfactory specificity(81.8%)but low sensitivity(58.3%).Twentytwo patients had serial mp MRI scans and evidence of disease progression was seen for 3 patients all of whom had upstaging of Gleason score on biopsy(30% specificity and 100% sensitivity).CONCLUSION:Addition of mp MRI imaging in active surveillance decision making may help in identifying aggressive disease amongst men with indolent prostate cancer earlier than traditional methods. | Larissa J Vos Michele Janoski Keith Wachowicz Atiyah Yahya Oleksandr Boychak John Amanie Nadeem Pervez Matthew B Parliament Edith Pituskin B Gino Fallone Nawaid Usmani | 2016 | World Journal of Radiology2016，8，4： | 1 |
| 7 | A mechanistic analysis of the role of microcalcifications in atherosclerotic plaque stability: potential implications for plaque rupture显示文摘 | Natalia Maldonado Adreanne Kelly-Arnold Yuliya Vengrenyuk Damien Laudier John T. Fallon Renu Virmani Luis Cardoso Sheldon Weinbaum | 2012 | AJP: Heart and Circulatory Physiology2012，，5： | 1 |
| 8 | Noninvasive In Vivo Human Coronary Artery Lumen and Wall Imaging Using Black-Blood Magnetic Resonance Imaging显示文摘 | Zahi A. Fayad Valentin Fuster John T. Fallon Timothy Jayasundera Stephen G. Worthley Gerard Helft J. Gilberto Aguinaldo Juan J. Badimon Samin K. Sharma | 2000 | Circulation: Journal of the American Heart Association2000，，5： | 1 |
| 9 | Comparison of response evaluation criteria in solid tumors with volumetric measurements for estimation of tumor burden in pancreatic adenocarcinoma and hepatocellular carcinoma显示文摘 | Jessemae L. Welsh Kellie Bodeker Elizabeth Fallon Sundershan K. Bhatia John M. Buatti Joseph J. Cullen | 2012 | The American Journal of Surgery2012，，5： | 1 |
| 10 | Hedgehog-Regulated Processing of Gli3 Produces an Anterior/Posterior Repressor Gradient in the Developing Vertebrate Limb显示文摘 | Baolin Wang John F Fallon Philip A Beachy | 2000 | Cell2000，，4： | 1 |
| 11 | Macrophage Infiltration in Acute Coronary Syndromes: Implications for Plaque Rupture显示文摘 | Pedro R. Moreno Erling Falk Igor F. Palacios John B. Newell Valentín fuster John T. Fallon | 1994 | Circulation1994，，2： | 1 |
| 12 | Suppressors of Cytokine Signaling 2 and 3 Diametrically Control Macrophage Polarization显示文摘 | Shaun Spence Amy Fitzsimons Caroline R. Boyd Julia Kessler Denise Fitzgerald Joanne Elliott Joan Ní Gabhann Siobhan Smith Antonio Sica Emily Hams Sean P. Saunders Caroline A. Jefferies Padraic G. Fallon Danny F. McAuley Adrien Kissenpfennig James A. Johns | 2013 | Immunity2013，，1： | 1 |
| 13 | Fibroblast Growth Factors as Multifunctional Signaling Factors显示文摘 | Gy?rgyi Szebenyi John F. Fallon | 1999 | International Review of Cytology1999，，： | 1 |
| 14 | Accelerated Flap Prefabrication with Vascular Endothelial Growth Factor显示文摘 | Qing Li Ernane Reis Wen Zhang Lester Silver John Fallon Hubert Weinberg | 2000 | J reconstr Microsurg2000，，01： | 1 |
| 15 | Fat embolization and fatal cardiac arrest during hip arthroplasty with methylmethacrylate显示文摘 | Fallon Katherine M Fuller John G | 2001 | Can J Anesth2001，48，7： | 1 |
| 16 | Inhibition of Intimal Thickening After Balloon Angioplasty in Porcine Coronary Arteries by Targeting Regulators of the Cell Cycle显示文摘 | Richard Gallo Adrian Padurean Thottala Jayaraman Steven Marx Merce Roque Steven Adelman James Chesebro John Fallon Valentin Fuster Andrew Marks Juan Jose Badimon | 1999 | Circulation1999，，16： | 1 |
| 17 | Coronary Composition and Macrophage Infiltration in Atherectomy Specimens From Patients With Diabetes Mellitus显示文摘 | Pedro R. Moreno Alvaro M. Murcia Igor F. Palacios Miltiadis N. Leon Victor H. Bernardi Valentín Fuster John T. Fallon | 2000 | Circulation: Journal of the American Heart Association2000，，： | 1 |
| 18 | Phase I/II trial of formoterol fumarate combined with megestrol acetate in cachectic patients with advanced malignancy显示文摘 | C. A. Greig N. Johns C. Gray A. MacDonald N. A. Stephens R. J. E. Skipworth M. Fallon L. Wall G. M. Fox K. C. H. Fearon | 2014 | Supportive Care in Cancer2014，，5： | 1 |
| 19 | Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice显示文摘 | Reigh-Yi Lin Robin P. Choudhury Weijing Cai Min Lu John T. Fallon Edward A. Fisher Helen Vlassara | 2003 | Atherosclerosis2003，，2： | 1 |
| 20 | 胆固醇酯转运蛋白抑制剂anacetrapib对血脂异常患者脂蛋白及健康个体24h动态血压的影响:2项双盲、随机、安慰剂对照Ⅰ期研究显示文摘背景抑制胆固醇酯转运蛋白(CETP)被认为有望成为治疗血脂异常的一种新策略。Anacetrapib(MK-0859)是目前正在研发的一种CETP抑制剂。本研究旨在评估anacetrapib作为单一治疗对低密度脂蛋白胆固醇(LDL—C)和高密度脂蛋白胆固醇(HDL-C)以及24h动态血压的影响。
方法作者进行了两项双盲、随机、安慰剂对照Ⅰ期研究。第一项研究中,50例年龄18~75岁的血脂异常患者(LDL—C1000~1900mg/L;治疗组40例,安慰剂组10例)接受anacetrapib治疗,剂量分别为每日餐后口服0mg、10mg、40mg、150mg或300mg,连续28d。采用标准的脂质和脂蛋白监测以及安全性监测,同时测定anacetrapib浓度进行药代动力学分析。第二项研究中,22例年龄为45~75岁的健康受试者接受每日餐后口服anacetrapib150mg或等量安慰剂治疗,连续10d,然后随机交换接受另一种治疗方法,各治疗期之间至少有14d洗脱期。研究过程中,每个治疗期的前1天和第10天进行24h动态血压监测。通过监测临床不良反应、体格检查、生命体征、12导联心电图和实验室安全性来评估两项研究安全性和耐受性的主要终点或次要终点。统计分析方法的选择符合方案分析。这两项试验均在ClinicalTrials.gov进行了注册,注册号分别为NCT00565292和NCT00565006。
结果血脂异常研究中,1例患者撤回知情同意书,1例因没有完整的服药前测定结果而在分析HDL—C和LDL—C数据时被剔除。Anacetrapib具有剂量依赖性调脂作用,对血脂异常患者其最大调脂作用为HDL—C增加129%[x=511(s=38)~x=1149(s=79)mg/L],而LDL-C降低38%[x=1382(s=114)~x=776(s=79)mg/L]。健康个体24h动态血压研究中,第10天时anacetrapib组和安慰剂组之间的最小方差为收缩压0.60mmHg(1mmHg≈0.133kPa)(90%CI-1.54~2.74;P=0.634),舒张压0.47mmHg(90%CI-0.90~1.84;P=0.561)。
结论Anacetrapib升高HDL-C的作用似乎远大于其他同类试验药物,而降低LDL-C的作用似乎与他汀类药物相似。尽管调脂作用强于其他同类药物,但anacetrapib似乎并不升高血压,这提示有效抑制CETP本身并不会使血压升高。 | Rajesh Krishna Matt S Anderson Arthur J Bergman Bo Jin Marissa Fallon Josee Cote Kim Rosko Cynthia Chavez-Eng Ryan Lutz Daniel MBloomfi eld Maria Gutierrez James Doherty Fredrick Bieberdorf Jeffrey Chodakewitz Keith M Gottesdiener John A Wagner 王亭忠(译) | 2008 | 世界临床医学2008，2，3： | 0 |
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