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| 1 | Primary hepatic carcinoid:A case report and literature review显示文摘Carcinoids are tumors derived from neuroendocrine cells and often produce functional peptide hormones.Approximately 54.5% arise in the gastrointestinal tract and frequently metastasize to the liver.Primary hepatic carcinoid tumors(PHCT) are extremely rare;only 95 cases have been reported.A 65-year-old man came to our attention due to occasional ultrasound findings in absence of clinical manifestations.His previous medical history,since 2003,included an echotomography of the dishomogeneous parenchymal area but no focal lesions.A computed tomography scan performed in 2005 showed an enhanced pseudonodular-like lesion of about 2 cm.Cholangio-magnetic resonance imaging identified the lesion as a possible cholangiocarcinoma.No positive findings were obtained with positron emission tomography.Histology suggested a secondary localization in the liver caused by a low-grade malignant neuroendocrine tumor.Immunohistochemistry was positive for anti chromogranin antibodies,Ki67 antibodies and synaptophysin.Octreoscan scintigraphy indicated intense activity in the lesion.Endoscopic investigations were performed to exclude the presence of extrahepatic neoplasms.Diagnosis of PHCT was established.The patient underwent left hepatectomy,followed by hormone therapy with sandostatine LAR.Two months after surgery he had a lymph nodal relapse along the celiac trunk and caudate lobe,which was histologically confirmed.The postoperative clinical course was uneventful,with a negative follow-up for hematochemical,clinical and radiological investigations at 18 mo post-surgery.Diagnosis of PHCT is based principally on the histopathological confi rmation of a carcinoid tumor and the exclusion of a non-hepatic primary tumor.Surgical resection is the recommended primary treatment for PHCT.Recurrence rate and survival rate in patients treated with resection were 18% and 74%,respectively. | Luigi Maria Fenoglio Sara Severini Domenico Ferrigno Giovanni Gollè Cristina Serraino Christian Bracco Elisabetta Castagna Chiara Brignone Fulvio Pomero Elena Migliore Ezio David Mauro Salizzoni | 2009 | World Journal of Gastroenterology2009，15，19： | 14 |
| 2 | Bioactive polymeric materials and electrical stimulation strategies for musculoskeletal tissue repair and regeneration显示文摘Electrical stimulation(ES)is predominantly used as a physical therapy modality to promote tissue healing and functional recovery.Research efforts in both laboratory and clinical settings have shown the beneficial effects of this technique for the repair and regeneration of damaged tissues,which include muscle,bone,skin,nerve,tendons,and ligaments.The collective findings of these studies suggest ES enhances cell proliferation,extracellular matrix(ECM)production,secretion of several cytokines,and vasculature development leading to better tissue regeneration in multiple tissues.However,there is still a gap in the clinical relevance for ES to better repair tissue interfaces,as ES applied clinically is ineffective on deeper tissue.The use of a conducting material can transmit the stimulation applied from skin electrodes to the desired tissue and lead to an increased function on the repair of that tissue.Ionically conductive(IC)polymeric scaffolds in conjunction with ES may provide solutions to utilize this approach effectively.Injectable IC formulations and their scaffolds may provide solutions for applying ES into difficult to reach tissue types to enable tissue repair and regeneration.A better understanding of ES-mediated cell differentiation and associated molecular mechanisms including the immune response will allow standardization of procedures applicable for the next generation of regenerative medicine.ES,along with the use of IC scaffolds is more than sufficient for use as a treatment option for single tissue healing and may fulfill a role in interfacing multiple tissue types during the repair process. | Bryan Ferrigno Rosalie Bordett Nithyadevi Duraisamy Joshua Moskow Michael R.Arul Swetha Rudraiah Syam P.Nukavarapu Anthony T.Vella Sangamesh G.Kumbar | 2020 | Bioactive Materials2020，5，3： | 8 |
| 3 | Review: Bioengineering approach for the repair and regeneration of peripheral nerve显示文摘Complex craniofacial surgeries of damaged tissues have several limitations,which present complications and challenges when trying to replicate facial function and structure.Traditional treatment techniques have shown suitable nerve function regeneration with various drawbacks.As technology continues to advance,new methods have been explored in order to regenerate damaged nerves in an effort to more efficiently and effectively regain original function and structure.This article will summarize recent bioengineering strategies involving biodegradable composite scaffolds,bioactive factors,and external stimuli alone or in combination to support peripheral nerve regeneration.Particular emphasis is made on the contributions of growth factors and electrical stimulation on the regenerative process. | Joshua Moskow Bryan Ferrigno Nikhil Mistry Devina Jaiswal Ketan Bulsara Swetha Rudraiah Sangamesh G.Kumbar | 2019 | Bioactive Materials2019，4，1： | 6 |
| 4 | Role of matrix metalloproteinases in cholestasis and hepatic ischemia/reperfusion injury:A review显示文摘Matrix metalloproteinases(MMPs) are a family ofproteases using zinc-dependent catalysis to break down extracellular matrix(ECM) components, allowing cell movement and tissue reorganization. Like many other proteases, MMPs are produced as zymogens, an inactive form, which are activated after their release from cells. Hepatic ischemia/reperfusion(I/R) is associated with MMP activation and release, with profound effects on tissue integrity: their inappropriate, prolonged or excessive expression has harmful consequences for the liver. Kupffer cells and hepatic stellate cells can secrete MMPs though sinusoidal endothelial cells are a further source of MMPs. After liver transplantation, biliary complications are mainly attributable to cholangiocytes, which, compared with hepatocytes, are particularly susceptible to injury and ultimately a major cause of increased graft dysfunction and patient morbidity. This paper focuses on liver I/R injury and cholestasis and reviews factors and mechanisms involved in MMP activation together with synthetic compounds used in their regulation. In this respect, recent data have demonstrated that the role of MMPs during I/R may go beyond the mere destruction of the ECM and may be much more complex than previously thought. We thus discuss the role of MMPs as an important factor in cholestasis associated with I/R injury. | Giuseppina Palladini Andrea Ferrigno Plinio Richelmi Stefano Perlini Mariapia Vairetti | 2015 | World Journal of Gastroenterology2015，21，42： | 6 |
| 5 | Metabolic shift in liver: Correlation between perfusion temperature and hypoxia inducible factor-1α显示文摘AIM: To study at what temperature the oxygen carried by the perfusate meets liver requirements in a model of organ perfusion. METHODS: in this study, we correlated hypoxia induciblefactor(Hi F)-1α expression to the perfusion temperature and the hepatic oxygen uptake in a model of isolated perfused rat liver. Livers from Wistar rats were perfused for 6 h with an oxygenated medium at 10, 20, 30 and 37 ℃. Oxygen uptake was measured by an oxygen probe; lactate dehydrogenase activity, lactate release and glycogen were measured spectrophotometrically; bile flow was gravitationally determined; p H of the perfusate was also evaluated; Hi F-1α m RNA and protein expression were analyzed by real time-polymerase chain reaction and ELi SA, respectively. RESULTS: Livers perfused at 10 and 20 ℃ showed no difference in lactate dehydrogenase release after 6 h of perfusion(0.96 ± 0.23 vs 0.93 ± 0.09 m U/min per g) and had lower hepatic damage as compared to 30 and 37 ℃(5.63 ± 0.76 vs 527.69 ± 45.27 m U/min per g, respectively, P s < 0.01). After 6 h, tissue ATP was significantly higher in livers perfused at 10 and 20 ℃than in livers perfused at 30 and 37 ℃(0.89 ± 0.06 and 1.16 ± 0.05 vs 0.57 ± 0.09 and 0.33 ± 0.08 nmol/mg, respectively, P s < 0.01). No sign of hypoxia was observed at 10 and 20 ℃, as highlighted by low lactate release respect to livers perfused at 30 and 37 ℃(121.4 ± 12.6 and 146.3 ± 7.3 vs 281.8 ± 45.3 and 1094.5 ± 71.7 nmol/m L, respectively, P s < 0.02), and low relative Hi F-1α m RNA(0.40 ± 0.08 and 0.20 ± 0.03 vs 0.60 ± 0.20 and 1.47 ± 0.30, respectively, P s < 0.05) and protein(3.72 ± 0.16 and 3.65 ± 0.06 vs 4.43 ± 0.41 and 6.44 ± 0.82, respectively, P s < 0.05) expression.CONCLUSION: Livers perfused at 10 and 20 ℃ show no sign of liver injury or anaerobiosis, in contrast to livers perfused at 30 and 37 ℃. | Andrea Ferrigno Laura Giuseppina Di Pasqua Alberto Bianchi Plinio Richelmi Mariapia VairettiAndrea Ferrigno | 2015 | World Journal of Gastroenterology2015，21，4： | 5 |
| 6 | Localization and role of metabotropic glutamate receptors subtype 5 in the gastrointestinal tract显示文摘Metabotropic glutamate receptor subtype 5(mGluR5) is a Group I mGlu subfamily of receptors coupled to the inositol trisphosphate/diacylglycerol pathway. Like other m Glu R subtypes, mGluR5 s contain a phylogenetically conserved, extracellular orthosteric binding site and a more variable allosteric binding site, located on the heptahelical transmembrane domain. The mGluR5 receptor has proved to be a key pharmacological target in conditions affecting the central nervous system(CNS) but its presence outside the CNS underscores its potential role in pathologies affecting peripheral organs such as the gastrointestinal(GI) tract and accessory digestive organs such as the tongue, liver and pancreas. Following identification of mGluR5s in the mouth, various studies have subsequently demonstrated its involvement in mechanical allodynia, inflammation, pain and oral cancer. mGluR5 expression has also been identified in gastroesophageal vagal pathways. Indeed, experimental and human studies have demonstrated that mGluR5 blockade reduces transient lower sphincter relaxation and reflux episodes. In the intestine, mGluR5s have been shown to be involved in the control of intestinal inflammation, visceral pain and the epithelial barrier function. In the liver, mGluR5s have a permissive role in the onset of ischemic injury in rat and mice hepatocytes. Conversely, livers from mice treated with selective negative allosteric modulators and mGluR5 knockout mice are protected against ischemic injury. Similar results have been observed in experimental models of free-radical injury and in vivo mouse models of acetaminophen intoxication. Finally, mGluR5s in the pancreas are associated with insulin secretion control. The picture is, however, far from complete as the review attempts to establish in particular as regards identifying specific targets and innovative therapeutic approaches for the treatment of GI disorders. | Andrea Ferrigno Clarissa Berardo Laura G Di Pasqua Veronica Siciliano Plinio Richelmi Mariapia Vairetti | 2017 | World Journal of Gastroenterology2017，23，25： | 3 |
| 7 | Lobe-Specific Heterogeneity and Matrix Metalloproteinase Activation after Ischemia/Reperfusion Injury in Rat Livers显示文摘 | Giuseppina Palladini Andrea Ferrigno Vittoria Rizzo Eleonora Boncompagni Plinio Richelmi Isabel Freitas Stefano Perlini Mariapia Vairetti | 2012 | Toxicologic Pathology2012，，5： | 2 |
| 8 | Liver plays a central role in asymmetric dimethylargininemediated organ injury显示文摘Asymmetric-dimethylarginine(ADMA) competes with L-arginine for each of the three isoforms of nitric oxide synthase:endothelial;neuronal;inducible.ADMA is synthesized by protein methyltransferases followed by proteolytic degradation.ADMA is metabolized to citrulline and dimethylamine,by dimethylarginine dimethylaminohydrolase(DDAH) and enters cells through cationic amino-acid transporters extensively expressed in the liver.The liver plays a crucial role in ADMA metabolism by DDAH-1 and,as has been recently demonstrated,it is also responsible for ADMA biliary excretion.A correlation has been demonstrated between plasma ADMA levels and the degree of hepatic dysfunction in patients suffering from liver diseases with varying aetiologies:plasma ADMA levels are increased in patients with liver cirrhosis,alcoholic hepatitis and acute liver failure.The mechanism by which liver dysfunction results in raised ADMA concentrations is probably due to impaired activity of DDAH due to severe inflammation,oxidative stress,and direct damage to DDAH.High plasma ADMA levels are also relevant as they are associated with the onset of multiorgan failure(MOF).Increased plasma concentration of ADMA was identified as an independent risk factor for MOF in critically-ill patients causing enhanced Intensive Care Unit mortality:a significant reduction in nitric oxide synthesis,leading to malperfusion in various organs,eventually culminating in multi organs dysfunction. | Andrea Ferrigno Laura G Di Pasqua Clarissa Berardo Plinio Richelmi Mariapia Vairetti | 2015 | World Journal of Gastroenterology2015，21，17： | 2 |
| 9 | Animal modeling in bone research—Should we follow the White Rabbit?显示文摘Animal models are live subjects applied to translational research.They provide insights into human diseases and enhance biomedical knowledge.Livestock development has favored the pace of human social development over millennia.Today's society is more aware of animal welfare than past generations.The general public has marked objections to animal research and many species are falling into disuse.The search for an ideal methodology to replace animal use is on,but animal modeling still holds great importance to human health.Bone research,in particular,has unmet requirements that in vitro technologies cannot fully address.Standardizing novel models remains necessary and rabbits are gaining in popularity as potential bone models.Our aim here is to provide a broad overview of animal modeling and its ethical implications,followed by a narrower focus on bone research and the role rabbits are playing in the current scenario. | Aline Schafrum Macedo Caroline Cezaretti Feitosa Fernando Yoiti Kitamura Kawamoto Paulo Vinicius Tertuliano Marinho Isis dos Santos Dal‐Bo Bianca Fiuza Monteiro Leonardo Prado Thales Bregadioli Gabriel Antonio Covino Diamante Cassio Ricardo Auada Ferrigno | 2019 | Animal Models and Experimental Medicine2019，2，3： | 2 |
| 10 | Haemostatic abnormalities in lung cancer: prognostic implications显示文摘 | Buccheri G Ferrigno D Ginardi C | 1997 | Eur J Cancer1997，33，1： | 1 |
| 11 | Lung tumor markers in onlogy practice:a study of TPA and CA125显示文摘 | Buccheri G Ferrigno D | 2002 | Br J Cancer2002，87，10： | 1 |
| 12 | Vinorelbine in elderly patients with inoperable non-small cell lung carcinoma :a phase Ⅱ study 显示文摘 | Buechcfi G Ferrigno D | 2000 | Cancer2000，88，12： | 1 |
| 13 | Clinical equivalence of two cytokeratin markers in non-small cell lung cancer:A study of tissue polypeptide antigen and cytokeratin 19 fragments显示文摘 | Buccheri G Torchio P Ferrigno D | 2003 | Chest2003，124，2： | 1 |
| 14 | Lung tumor markers in oncology practice: a study of TPA and CA125 显示文摘 | Buccheri G Ferrigno D | 2002 | Br J Cancer2002，87，10： | 1 |
| 15 | Whole brain radiation therapy in management of brain metastasis: results and prognostic factors显示文摘 | Saito EY Viani GA Ferrigno R | 2006 | Radiat Oncol2006，1，6： | 1 |
| 16 | Dental implants placement in conjunction with osteotome sinus floor elevation: a 12-year lifetable analysis from a prospective study on 588 ITI implants 显示文摘 | Ferrigno N Laureti M Fanali S | 2006 | Clin Oral implants Res2006，17，2： | 1 |
| 17 | Regulated nucleo/ cytoplasmic exchange of HOG1 MAPK requires the importin beta homologs NMD5 and XPOI显示文摘 | Ferrigno P Posas F Koepp D | 1998 | EMBO J1998，17，19： | 1 |
| 18 | Plasma levels of D-dimer in lung carcinoma: clinical and prognostic significance 显示文摘 | Buccheri G Torchio P Ferrigno D | 2003 | Cancer2003，97，12： | 1 |
| 19 | Baseline cataract type and 10year mortality in the Italian - American case - control study of age - related cataract显示文摘 | Williams S L Ferrigno L Mora P | | American journal of epidemiology0，156，2： | 1 |
| 20 | Prognositic significance of blood coagulation tests in lung cancer显示文摘 | FERRIGNO D BUCCHERI G RICCA I | 2001 | Eur Respir J2001，17，： | 1 |
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