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| 1 | Sonographic markers for early diagnosis of fetal malformations显示文摘Fetal malformations are very frequent in industrialized countries.Although advanced maternal age may affect pregnancy outcome adversely,80%-90%of fetal malformations occur in the absence of a specific risk factor for parents.The only effective approach for prenatal screening is currently represented by an ultrasound scan.However,ultrasound methods present two important limitations:the substantial absence of quantitative parameters and the dependence on the sonographer experience.In recent years,together with the improvement in transducer technology,quantitative and objective sonographic markers highly predictive of fetal malformations have been developed.These markers can be detected at early gestation(11-14 wk)and generally are not pathological in themselves but have an increased incidence in abnormal fetuses.Thus,prenatal ultrasonography during the second trimester of gestation provides a'genetic sonogram',including,for instance,nuchal translucency,short humeral length,echogenic bowel,echogenic intracardiac focus and choroid plexus cyst,that is used to identify morphological features of fetal Down’s syndrome with a potential sensitivity of more than 90%.Other specific and sensitive markers can be seen in the case of cardiac defects and skeletal anomalies.In the future,sonographic markers could limit even more the use of invasive and dangerous techniques of prenatal diagnosis(amniocentesis,etc.). | Maria Daniela Renna Paola Pisani Francesco Conversano Emanuele Perrone Ernesto Casciaro Gian Carlo Di Renzo Marco Di Paola Antonio Perrone Sergio Casciaro | 2013 | World Journal of Radiology2013，5，10： | 12 |
| 2 | Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics显示文摘Classically, the non-alcoholic fatty liver disease(NAFLD) physiopathology and progression has been summarized in the two hits hypothesis. The first hit is represented by the action of hyperinsulinemia and insulin resistance, accompanying obesity, that leads to liver steatosis increasing the absolute non esterified fatty acids uptake in the liver and the esterification to form triacylglycerol. The oxidative stress is involved in the second hit leading to the progression to nonalcoholic steatohepatitis(NASH) because of its harmful action on steatosic hepatocytes. However, at the present time, the two hits hypothesis needs to be updated because of the discover of genetic polymorphisms involved both in the liver fat accumulation and progression to NASH that make more intriguing understanding the NAFLD pathophysiological mechanisms. In this editorial, we want to underline the role of PNPLA3 I148 M, GPR120 R270 H and TM6SF2 E167 K in the pediatric NAFLD development because they add new pieces to the comprehension of the NAFLD pathophysiological puzzle. The PNPLA3 I148 M polymorphism encodes for an abnormal protein which predisposes to intrahepatic triglycerides accumulation both for a loss-of-function of its triglyceride hydrolase activity and for a gain-of-function of its lipogenic activity.Therefore, it is involved in the first hit, such as TM6SF2 E167 K polymorphisms that lead to intrahepatic fat accumulation through a reduced very low density lipoprotein secretion. On the other hand, the GPR120 R270 H variant, reducing the anti-inflammatory action of the GPR120 receptor expressed by Kuppfer cells, is involved in the second hit leading to the liver injury. | Pierluigi Marzuillo Anna Grandone Laura Perrone Emanuele Miraglia del Giudice | 2015 | World Journal of Hepatology2015，7，11： | 9 |
| 3 | A Molecular Framework for the Control of Adventitious Rooting by TIR1/AFB2-Aux/IAADependent Auxin Signaling in Arabidopsis显示文摘In Arabidopsis thaliana,canonical auxin-dependent gene regulation is mediated by 23 transcription factors from the AUXIN RESPONSE FACTOR(ARF)family that interact with auxin/indole acetic acid repressors(Aux/IAAs),which themselves form co-receptor complexes with one of six TRANSPORT INHIBITOR*!/AUXIN-SIGNALLING F-BOX(TIR1/AFB)proteins.Different combinations of co-receptors drive specific sensing outputs,allowing auxin to control a myriad of processes.ARF6 and ARF8 are positive regulators of adventitious root initiation upstream of jasmonate,but the exact auxin co-receptor complexes controlling the transcriptional activity of these proteins has remained unknown.Here,using loss-of-function mutants we show that three Aux/IAA genes,IAA6,IAA9,and IAA17,act additively in the control of adventitious root(AR)initiation.These three IAA proteins interact with ARF6 and/or ARF8 and likely repress their activity in AR development.We show that TIR1 and AFB2 are positive regulators of AR formation and TIR1 plays a dual role in the control of jasmonic acid(JA)biosynthesis and conjugation,as several JA biosynthesis genes are up-regulated in the tir1-1 mutant.These results lead us to propose that in the presence of auxin,TIR1 and AFB2 form specific sensing complexes with IAA6,IAA9,and/or IAA17 to modulate JA homeostasis and control AR initiation. | Abdellah Lakehal Salma Chaabouni Emilie Cavel Rozenn Le Hir Alok Ranjan Zahra Raneshan Ondrej Novak Daniel IPacurar Irene Perrone Frangois Jobert Laurent Gutierrez Laszlo Bako Catherine Bellini | 2019 | Molecular Plant2019，12，11： | 5 |
| 4 | Fetal programming and early identification of newborns at high risk of free radical-mediated diseases显示文摘Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, preeclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity. | Serafina Perrone Antonino Santacroce Anna Picardi Giuseppe Buonocore | 2016 | World Journal of Clinical Pediatrics2016，5，2： | 4 |
| 5 | DNA end binding activity and Ku70/80 heterodimer expression in human colorectal tumor显示文摘AIM: To determine the DNA binding activity and protein levels of the Ku70/80 heterodimer, the functional mediator of the NHEJ activity, in human colorectal carcinogenesis.METHODS: The Ku70/80 DNA-binding activity was determined by electrophoretic mobility shift assays in 20 colon adenoma and 15 colorectal cancer samples as well as matched normal colonic tissues. Nuclear and cytoplasmic protein expression was determined by immunohistochemistry and Western blot analysis.RESULTS: A statistically significant difference was found in both adenomas and carcinomas as compared to matched normal colonic mucosa (P<0.00). However,changes in binding activity were not homogenous with approximately 50% of the tumors showing a clear increase in the binding activity, 30% displaying a modest increase and 15% showing a decrease of the activity.Tumors, with increased DNA-binding activity, also showed a statistically significant increase in Ku70 and Ku86nuclear expression, as determined by Western blot and immunohistochemical analyses (P<0.001). Cytoplasmic protein expression was found in pathological samples,but not in normal tissues either from tumor patients or from healthy subjects.CONCLUSION: Overall, our DNA-binding activity and protein level are consistent with a substantial activation of the NHEJ pathway in colorectal tumors. Since the NHEJ is an error prone mechanism, its abnormal activation can result in chromosomal instability and ultimately lead to tumorigenesis. | Paola Mazzarelli Paola Parrella Davide Seripa Emanuela Signori Giuseppe Perrone Carla Rabitti Domenico Borzomati Armando Gabbrielli Maria Giovanna Matera Carolina Gravina Marco Caricato Maria Luana Poeta Monica Rinaldi Sergio Valeri Roberto Coppola Vito Michele Fazio | 2005 | World Journal of Gastroenterology2005，11，42： | 4 |
| 6 | Abdominal fat interacts with PNPLA 3 I148M, but not with the APOC 3 variant in the pathogenesis of liver steatosis in chronic hepatitis C显示文摘 | R. Zampino N. Coppola G. Cirillo A. Boemio M. Pisaturo A. Marrone M. Macera E. Sagnelli L. Perrone L. E. Adinolfi E. Miraglia del Giudice | 2013 | J Viral Hepat2013，，8： | 3 |
| 7 | ESC/EAS Guidelines for the management of dyslipidaemias显示文摘 | Alberico L. Catapano ?eljko Reiner Guy De Backer Ian Graham Marja-Riitta Taskinen Olov Wiklund Stefan Agewall Eduardo Alegria M. John Chapman Paul Durrington Serap Erdine Julian Halcox Richard Hobbs John Kjekshus Pasquale Perrone Filardi Gabriele Riccardi | 2011 | Atherosclerosis2011，，： | 3 |
| 8 | Feasibility of robotic pancreaticoduodenectomy显示文摘 | U. Boggi S. Signori N. De Lio V. G. Perrone F. Vistoli M. Belluomini C. Cappelli G. Amorese F. Mosca | 2013 | Br J Surg2013，，7： | 3 |
| 9 | 青少年甘油磷酸胆碱代谢和心血管病的危险因素:一项队列研究显示文摘甘油磷酸胆碱(glycerophosphocholine,GPC)代谢物可调节动脉粥样硬化,从而导致心血管病风险。临床前期心血管病可能从青春期就开始。研究人员应用靶向血清脂质组学鉴定一组新的GPC,并测试在青春期时这些GPC中的任何一种是否与心血管病传统危险因子,如过量内脏脂肪、升高的血压、胰岛素抵抗和致动脉粥样硬化血脂异常相关。 | Syme C Czajkowski S Shin J Abrahamowicz M Leonard G Perron M Richer L Veillette S Gaudet D Strug L Wang Y Xu H Taylor G Paus T Bennett S Pausova Z 刘莉 叶鹏 | 2016 | 中华高血压杂志2016，24，10： | 3 |
| 10 | Radiofrequency Ablation of Small Hepatocellular Carcinoma in Cirrhotic Patients Awaiting Liver Transplantation: A Prospective Study显示文摘 | Vincenzo Mazzaferro Carlo Battiston Stefano Perrone Andrea Pulvirenti Enrico Regalia Raffaele Romito Dario Sarli Marcello Schiavo Francesco Garbagnati Alfonso Marchianò Carlo Spreafico Tiziana Camerini Luigi Mariani Rosalba Miceli Salvatore Andreola | 2004 | Annals of Surgery2004，，5： | 3 |
| 11 | Clear cell adenocarcinoma of the colon is a unique morphological variant of intestinal carcinoma:Case report with molecular analysis显示文摘Here we report a new case of clear cell adenocarcinoma (CCA) of the colon in a 54-year-old Caucasian man. Despite of the previous reported cases, the lesion was located in the right colon and was not associated with the conventional adenoma. We performed immunohistochemical and molecular analyses in order to explore whether the CCA had the molecular features generally associated with conventional colorectal carcinoma. The immunohistochemical and molecular analyses showed that the different morphology of CCA does not reflect a distinct biological entity but only an unusual morphological variant of intestinal carcinoma. | Marta Barisella Andrea Lampis Federica Perrone Antonino Carbone | 2008 | World Journal of Gastroenterology2008，14，42： | 3 |
| 12 | Abdominal fat interacts with PNPLA 3 I148M, but not with the APOC 3 variant in the pathogenesis of liver steatosis in chronic hepatitis C显示文摘 | R. Zampino N. Coppola G. Cirillo A. Boemio M. Pisaturo A. Marrone M. Macera E. Sagnelli L. Perrone L. E. Adinolfi E. Miraglia del Giudice | 2013 | J Viral Hepat2013，，8： | 3 |
| 13 | 常染色体显性遗传性多囊肾病早期的血压控制显示文摘常染色体显性遗传性多囊肾病(autosomal dominant polycystic kidney disease,ADPKD)的早期常出现高血压且与ADPKD患者进展至终末期肾病(endstage renal disease,ESRD)及死于心血管疾病相关。临床研究表明肾素血管紧张素醛固酮系统(rennin angiotensin aldsterone system,RAAS)在ADPKD患者高血压发生过程中发挥关键作用。但采用更积极的降压治疗或增加RAAS阻断剂的使用是否能延迟ADPKD患者ESRD的发生,目前还不清楚。 | Schrier RW Abebe KZ Perrone RD 张刘锋 叶鹏 | 2015 | 中华高血压杂志2015，23，3： | 3 |
| 14 | Experience with peritoneal mesothelioma at the Milan National Cancer Institute显示文摘Diffuse malignant peritoneal mesothelioma (DMPM) is an uncommon and rapidly fatal tumor.Therapeutic options have traditionally been limited and ineffective.The biologic and molecular events correlated with poor responsiveness to therapy are still poorly understood.In recent years,an innovative treatment approach involving aggressive cytoreductive surgery (CRS) and perioperative intraperitoneal chemotherapy has reportedly resulted in improved outcome,as compared to historical controls.Since 1995,at the National Cancer Institute (NCI) of Milan (Italy),patients with DMPM have been treated with CRS and hyperthermic intraperitoneal chemotherapy (HIPEC).In the present paper,clinical experiences and basic science investigations on DMPM at Milan NCI are reviewed.Perioperative and long-term outcome results with CRS and HIPEC are presented.Clinico-pathological prognostic factors were investigated by multivariate analysis.The pathologic features and immunohistochemical markers related to DMPM biologic behavior were assessed in a large case-series uniformly treated at our institution.The prevalence and prognostic role of telomere maintenance mechanisms,which account for the limitless cell replicative potential of many malignancies,were studied.The dysregulation of the apoptotic pathways may play a role in the relative chemo-resistance of DMPM and a better understanding of apoptosis-related mechanisms could result in novel targeted therapeutic strategies.On this basis,the expression of survivin and other IAP family members (IAP-1,IAP-2,and X-IAP),the pro-apoptotic protein Smac/DIABLO,and antigens associated with cell proliferation (Ki-67) and apoptosis (caspase-cleaved cytokeratin-18) were analyzed.Finally,analyses of EGFR,PDGFRA and PDGFRB were performed to ascertain if deregulation of RTK could offer useful alternative therapeutic targets. | Marcello Deraco Dario Baratti Antonello Domenico Cabras Nadia Zaffaroni Federica Perrone Raffaella Villa Jenny Jocollè Maria Rosaria Balestra Shigeki Kusamura Barbara Laterza Silvana Pilotti | 2010 | World Journal of Gastrointestinal Oncology2010，2，2： | 3 |
| 15 | Nuclear imaging in detection and monitoring of cardiotoxicity显示文摘Cardiotoxicity as a result of cancer treatment is a novel and serious public health issue that has a significant impact on a cancer patient’s management and outcome.The coexistence of cancer and cardiac disease in the same patient is more common because of aging population and improvements in the efficacy of antitumor agents.Left ventricular dysfunction is the most typical manifestation and can lead to heart failure.Left ventricular ejection fraction measurement by echocardiography and multigated radionuclide angiography is the most common diagnostic approach to detect cardiac damage,but it identifies a late manifestation of myocardial injury.Early non-invasive imaging techniques are needed for the diagnosis and monitoringof cardiotoxic effects.Although echocardiography and cardiac magnetic resonance are the most commonly used imaging techniques for cardiotoxicity assessment,greater attention is focused on new nuclear cardiologic techniques,which can identify high-risk patients in the early stage and visualize the pathophysiologic process at the tissue level before clinical manifestation.The aim of this review is to summarize the role of nuclear imaging techniques in the non-invasive detection of myocardial damage related to antineoplastic therapy at the reversible stage,focusing on the current role and future perspectives of nuclear imaging techniques and molecular radiotracers in detection and monitoring of cardiotoxicity. | Carmen D’Amore Paola Gargiulo Stefania Paolillo Angela Maria Pellegrino Tiziana Formisano Antonio Mariniello Giuseppe DellaRatta Elisabetta Iardino Marianna D’Amato Lucia La Mura Irma Fabiani Flavia Fusco Pasquale Perrone Filardi | 2014 | World Journal of Radiology2014，6，7： | 2 |
| 16 | Non-cirrhotic portal hypertension with large regenerative nodules: A diagnostic challenge显示文摘Non-cirrhotic portal hypertension is a poorly understood condition characterized by portal hypertension in the absence of conventional hepatic cirrhosis and described in association with blood coagulation disorders, myeloproliferative and immunological diseases and with exposure to toxic drugs. Very recently, precise classification criteria have been proposed in order to define four distinct subcategories. The present case highlights how the clinical presentation, the confounding results from imaging studies, and the difficulties in the histological evaluation often render cases of non-cirrhotic portal hypertension a real diagnostic challenge. It also underscores the classification problems which can be faced once this diagnosis is performed. Indeed, the different subcategories proposed result from the prevalent subtypes in a spectrum of hepatic regenerative responses to a variety of injuries determining microcirculatory dis-turbances. More flexibility in classification should derive from this etiopathogenic background. | Umberto Vespasiani Gentilucci Paolo Gallo Giuseppe Perrone Riccardo Del Vescovo Giovanni Galati Sandro Spataro Chiara Mazzarelli Adriano Pellicelli Antonella Afeltra Antonio Picardi | 2011 | World Journal of Gastroenterology2011，17，20： | 2 |
| 17 | Is human hepatocellular carcinoma a hormone-responsive tumor?显示文摘Before the positive results recently obtained with multitarget tyrosine kinase inhibitor sorafenib,there was no standard systemic treatment for patients with advanced hepatocellular carcinoma(HCC).Sex hormones receptors are expressed in a significant proportion of HCC samples.Following preclinical and epidemiological studies supporting a relationship between sex hormones and HCC tumorigenesis,several randomized controlled trials (RCTs)tested the efficacy of the anti-estrogen tamoxifen as systemic treatment.Largest among these trials showed no survival advantage from the administration of tamoxifen,and the recent Cochrane systematic review produced a completely negative result.This questions the relevance of estrogen receptor-mediated pathways in HCC.However,a possible explanation for these disappointing results is the lack of proper patients selection according to sex hormones receptors expression,but unfortunately the interaction between this expression and efficacy of tamoxifen has not been studied adequately.It has been also proposed that negative results might be explained if tamoxifen acts in HCC via an estrogen receptor-independent pathway,that requires higher doses than those usually administered, but an Asian RCT conducted to assess dose-response effect was completely negative.Interesting,preliminaryresults have been obtained when hormonal treatment (tamoxifen or megestrol)has been selected according to the presence of wild-type or variant estrogen receptors respectively,but no large RCTs are available to support this strategy.Negative results have been obtained also with anti-androgen therapy.In conclusion,there is no robust evidence to consider HCC a hormone-responsive tumor.Hormonal treatments should not be part of the current management of HCC. | Massimo Di Maio Bruno Daniele Sandro Pignata Ciro Gallo Ermelinda De Maio Alessandro Morabito Maria Carmela Piccirillo Francesco Perrone | 2008 | World Journal of Gastroenterology2008，14，11： | 2 |
| 18 | Does Trust Matter? Exploring the Effects of Interorganizational and Interpersonal Trust on Performance显示文摘 | Akbar Zaheer Bill McEvily Vincenzo Perrone | 1998 | Organization Science1998，，2： | 2 |
| 19 | Association Between a Polymorphism in Cannabinoid Receptor 2 and Severe Necroinflammation in Patients With Chronic Hepatitis C显示文摘 | Nicola Coppola Rosa Zampino Giulia Bellini Margherita Macera Aldo Marrone Mariantonietta Pisaturo Adriana Boemio Bruno Nobili Giuseppe Pasquale Sabatino Maione Luigi Elio Adinolfi Laura Perrone Evangelista Sagnelli Emanuele Miraglia Del Giudice Francesca | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 2 |
| 20 | 从胚胎的干细胞塑造眼睛: 生物、医药的含意显示文摘 Organogenesis is regulated by a complex network of intrinsic cues, diffusible signals and cell/cell or cell/matrix interactions that drive the cells of a prospective organ to differentiate and collectively organize in three dimensions. Generating organs in vitro from embryonic stem (ES) cells may provide a simplified system to decipher how these processes are orchestrated in time and space within particular and between neighboring tissues. Recently, this field of stem cell research has also gained considerable interest for its potential applications in regenerative medicine. Among human pathologies for which stem cell-based therapy is foreseen as a promising therapeutic strategy are many retinal degenerative diseases, like retinitis pigmentosa and age-related macular degeneration. Over the last decade, progress has been made in producing ES-derived retinal cells in vitro, but engineering entire synthetic retinas was considered beyond reach. Recently however, major breakthroughs have been achieved with pioneer works describing the extraordinary self-organization of murine and human ES cells into a three dimensional structure highly resembling a retina. ES-derived retinal cells indeed assemble to form a cohesive neuroepithelial sheet that is endowed with the intrinsic capacity to recapitulate, outside an embryonic environment, the main steps of retinal morphogenesis as observed in vivo. This represents a tremendous advance that should help resolving fundamental questions related to retinogenesis. Here, we will discuss these studies, and the potential applications of such stem cell-based systems for regenerative medicine. | Gabriele Colozza Morgane Locker Muriel Perron | 2012 | World Journal of Stem Cells2012，4，8： | 2 |
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