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| 1 | Pancreatic ductal adenocarcinoma: Risk factors, screening, and early detection显示文摘Pancreatic cancer is the fourth most common cause of cancer-related deaths in the United States, with over 38000 deaths in 2013. The opportunity to detect pancreatic cancer while it is still curable is dependent on our ability to identify and screen high-risk populations before their symptoms arise. Risk factors for developing pancreatic cancer include multiple genetic syndromes as well as modifiable risk factors. Genetic conditions include hereditary breast and ovarian cancer syndrome, Lynch Syndrome, familial adenomatous polyposis, Peutz-Jeghers Syndrome, familial atypical multiple mole melanoma syndrome, hereditary pancreatitis, cystic fibrosis, and ataxia-telangiectasia; having a genetic predisposition can raise the risk of developing pancreatic cancer up to 132-fold over the general population. Modifiable risk factors, which include tobacco exposure, alcohol use, chronic pancreatitis, diet, obesity, diabetes mellitus, as well as certain abdominal surgeries and infections, have also been shown to increase the risk of pancreatic cancer development. Several largevolume centers have initiated such screening protocols, and consensus-based guidelines for screening high-riskgroups have recently been published. The focus of this review will be both the genetic and modifiable risk factors implicated in pancreatic cancer, as well as a review of screening strategies and their diagnostic yields. | Andrew E Becker Yasmin G Hernandez Harold Frucht Aimee L Lucas | 2014 | World Journal of Gastroenterology2014，20，32： | 24 |
| 2 | Autoantibody to MOG suggests two distinct clinical subtypes of NMOSD显示文摘We characterized a unique group of patients with neuromyelitis optica spectrum disorder(NMOSD) who carried autoantibodies of aquaporin-4(AQP4) and myelin-oligodendrocyte glycoprotein(MOG). Among the 125 NMOSD patients, 10(8.0%) were AQP4- and MOG-ab double positive, and 14(11.2%) were MOG-ab single positive. The double-positive patients had a multiphase disease course with a high annual relapse rate(P=0.0431), and severe residual disability(P<0.0001). Of the double-positive patients, 70% had MS-like brain lesions, more severe edematous, multifocal regions on spinal magnetic resonance imaging(MRI), pronounced decreases of retinal nerve fiber layer thickness and atrophy of optic nerves. In contrast, patients with only MOG-ab had a higher ratio of monophasic disease course and mild residual disability. Spinal cord MRI illustrated multifocal cord lesions with mild edema, and brain MRIs showed more lesions around lateral ventricles. NMOSD patients carrying both autoantibodies to AQP4 and MOG existed and exhibited combined features of prototypic NMO and relapsing-remitting form of MS, whereas NMOSD with antibodies to MOG only exhibited an 'intermediate' phenotype between NMOSD and MS. Our study suggests that antibodies against MOG might be pathogenic in NMOSD patients and that determination of anti-MOG antibodies maybe instructive for management of NMOSD patients. | Yaping Yan Yujing Li Ying Fu Li Yang Lei Su Kaibin Shi Minshu Li Qiang Liu Aimee Borazanci Yaou Liu Yong He Jeffrey L Bennett Timothy L Vollmer Fu-Dong Shi | 2016 | Science China(Life Sciences)2016，59，12： | 20 |
| 3 | Novel interactions of mitochondria and reactive oxygen/nitrogen species in alcohol mediated liver disease显示文摘Mitochondrial dysfunction is known to be a contributing factor to a number of diseases including chronic alcohol induced liver injury. While there is a detailed understanding of the metabolic pathways and proteins of the liver mitochondrion, little is known regarding how changes in the mitochondrial proteome may contribute to the development of hepatic pathologies. Emerging evidence indicates that reactive oxygen and nitrogen species disrupt mitochondrial function through post-translational modifications to the mitochondrial proteome. Indeed, various new affinity labeling reagents are available to test the hypothesis that post-translational modification of proteins by reactive species contributes to mitochondrial dysfunction and alcoholic fatty liver disease. Specialized proteomic techniques are also now available, which allow for identification of defects in the assembly of multi-protein complexes in mitochondria and the resolution of the highly hydrophobic proteins of the inner membrane. In this review knowledge gained from the study of changes to the mitochondrial proteome in alcoholic hepatotoxicity will be described and placed into a mechanistic framework to increase understanding of the role of mitochondrial dysfunction in liver disease. | Sudheer K Mantena Adrienne L King Kelly K Andringa Aimee Landar Victor Darley-Usmar Shannon M Bailey | 2007 | World Journal of Gastroenterology2007，13，37： | 7 |
| 4 | MicroRNA in pancreatic ductal adenocarcinoma and its precursor lesions显示文摘Pancreatic ductal adenocarcinoma(PDAC) is the 4^(th) deadliest cancer in the United States, due to its aggressive nature, late detection, and resistance to chemotherapy. The majority of PDAC develops from 3 precursor lesions, pancreatic intraepithelial lesions(PanIN), intraductual papillary mucinous neoplasm(IPMN), and mucinous cystic neoplasm. Early detection and surgical resection can increase PDAC 5-year survival rate from 6% for Stage Ⅳ to 50% for Stage Ⅰ. To date, there are no reliable biomarkers that can detect PDAC. MicroRNAs(miRNA) are small noncoding RNAs(18-25 nucleotides) that regulate gene expression by affecting translation of messenger RNA(mRNA). A large body of evidence suggests that miRNAs are dysregulated in various types of cancers. MiRNA has been profiled as a potential biomarker in pancreatic tumor tissue, blood, cyst fluid, stool, and saliva. Four mi RNA biomarkers(miR-21, miR-155, miR-196, and miR-210) have been consistently dysregulated in PDAC. MiR-21, miR-155, and miR-196 have also been dysregulated in IPMN and PanIN lesions suggesting their use as early biomarkers of this disease. In this review, we explore current knowledge of miRNA sampling, miR NA dysregulation in PDAC and its precursor lesions, and advances that have been made in using miRNA as a biomarker for PDAC and its precursor lesions. | yasmin g hernandez aimee l lucas | 2016 | World Journal of Gastrointestinal Oncology2016，8，1： | 6 |
| 5 | Requirement for IGF-I in Epidermal Growth Factor-Mediated Cell Cycle Progression of Mammary Epithelial Cells显示文摘 | MALINDA A S MONICA M R AIMEE V L | 2002 | Endocrinology2002，143，5： | 1 |
| 6 | A comparison of myeorrhizal and saprotrophic fungus tolerance to creosote in vitro 显示文摘 | Dana L Jennifer I Aimee L | 2003 | Int Biode- ter Biodegr2003，51，3： | 1 |
| 7 | Low temperature H2S dry-desulfurization with zinc oxide 显示文摘 | Hector F G Hugo M G Luis J G Jennifer H Aimee M Steven L S | 2010 | Microporous and Mesoporous Materials2010，127，： | 1 |
| 8 | Association between endometriosis and risk of histological subtypes of ovarian cancer: a pooled analysis of case–control studies显示文摘 | Celeste Leigh Pearce Claire Templeman Mary Anne Rossing Alice Lee Aimee M Near Penelope M Webb Christina M Nagle Jennifer A Doherty Kara L Cushing-Haugen Kristine G Wicklund Jenny Chang-Claude Rebecca Hein Galina Lurie Lynne R Wilkens Michael E Carney Mar | 2012 | Lancet Oncology2012，，： | 1 |
| 9 | Persis- tent Colonization by HaeraopHilus influenzae in chronic obstructive pul- monary disease 显示文摘 | Timothy FMurphy Aimee L Brauer Andrew T Schiffmacher | 2004 | Am J Repir Crit Care Med2004，170，3： | 1 |
| 10 | Effect of Stay-in-Place Metal Forms on Per- formanee of Concrete Bridge Decks显示文摘 | Guthrie W Spencer Stephen L Forst Birdsall Aimee W | 2006 | Transportation Research Record2006，，1958： | 1 |
| 11 | Frequency dependence of antidepressant response to left prefrontal repetitive transcranial magnetic stimulation (rTMS) as a function of baseline cerebral glucose metabolism显示文摘 | Timothy A Kimbrell John T Little Robert T Dunn Mark A Frye Benjamin D Greenberg Eric M Wassermann Jennifer D Repella Aimee L Danielson Mark W Willis Brenda E Benson Andrew M Speer Elizabeth Osuch Mark S George Robert M Post | 1999 | Biological Psychiatry1999，，12： | 1 |
| 12 | High molecular-weight hyaluronan inhibits macrophage proliferation and cytokine release in the early wound of a preclinical postlaminectomy rat model显示文摘 | Aimee L Schimizzi Jennifer B Massie Mark Murphy | 2006 | The Spine Journal2006，6，5： | 1 |
| 13 | Assessment of the pediatric index of mortality 2 with the PaO2/FIO2 ratio derived from the SpO2/FIO2 ratio:a prospective pilot study in a French pediatric intensive care unit显示文摘 | Stephane L Marie D Aimee D | 2011 | Pediatr Crit Care Med2011，12，4： | 1 |
| 14 | Expression of tumor markers hyaluronic acid and hyaluronidase (HYAL1) in head and neck tumors显示文摘 | Aimee L Franzmann Grethchen L Schroeder William Jarrard Goodwin | 2003 | International Journal of Cancer2003，106，3： | 1 |
| 15 | Knowledge transfer between groups via personnel rotation: effects of social identity and knowledge quality 显示文摘 | AIMeE A K L ARGOTEB J M LEVlNEC | 2005 | Organizational behavior and human Decision processes2005，，96： | 1 |
| 16 | Assessment of the pediatric in- dex of mortality 2 with the PaO2/FIO2 ratio derived from the SpO2/ FIO2 ratio: a prospective pilot study in a French pediatric intensive care unit显示文摘 | Stephane L Marie D Aimee D | 2011 | Pediatr Crit Care Med2011，12，4： | 1 |
| 17 | lligh molecular-weight hyaluronan inhibits macrophage proliferation and cytokine release in the early wound of a preclinical post- laminectomy rat model显示文摘 | Aimee L Schimizzi Jennifer B Massie Mark Murphy | 2006 | Spine J2006，6，5： | 1 |
| 18 | Population-based drug-related anaphylaxis in children and adolescents captured by South Carolina Emergency Room Hospital Discharge Database(SCERHDD)(2000-2002)显示文摘 | SUZANNE L W AIMEE A D A TAMAR R K | 2007 | Pharm Drug Safety2007，16，2： | 1 |
| 19 | Or- ganizational Identity Formation and Change显示文摘 | Dennis A Gioia Shubha D Patvardhan Aimee L | 2013 | The Acade- my of Management Annals2013，7，1： | 1 |
| 20 | Ghrelin ceils replace insulin producing cells in two mouse models of pancreas development 显示文摘 | Catherine L Aimee E Prado | 2004 | PNAS2004，101，9： | 1 |
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