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13. Augmented reality (AR) in minimally invasive surgery (MIS) training: where are we now in Italy? The Italian Society of Endoscopic Surgery (SICE) ARMIS survey

Author

Balla, Andrea, Sartori, Alberto, Botteri, Emanuele, Podda, Mauro, Ortenzi, Monica, Silecchia, Gianfranco, Guerrieri, Mario, Agresta, Ferdinando, Antonino, Agrusa, Daniele, Aguzzi, Mariantonietta, Alagia, Laura, Alberici, Marco Ettore Allaix, Luisa, Ambrosio, Alfonso, Amendola, Michele, Ammendola, Pietro Maria Amodio, Gabriele, Anania, Jacopo, Andreuccetti, Alfredo, Annichiarico, Pietro, Anoldo, Alessandro, Anselmo, Giovanni, Aprea, Giacomo, Arcuri, Alberto, Arezzo, Giulia, Armatura, Giulia, Bagaglini, Francesco, Bagolini, Beatrice, Bailetti, Gianluca, Baiocchi, Edoardo, Baldini, Elisa, Bannone, Mirko, Barone, Gianluca, Baronio, Raffaele, Basile, Bellucci, Marco, Andrea Benedetti Cacciaguerra, Ilaria, Benzoni, Francesco, Bianco, Giuseppe, Boccia, Cristina, Bombardini, Luigi, Boni, Dario, Bono, Luca Domenico Bonomo, Giulia, Bonventre, Andrea, Bottari, Claudio, Botti, Giacomo, Brentegani, Mattia, Buonomo, Umberto, Bracale, Cosimo, Callari, Luca, Calligaris, Pietro Giorgio Calò, Angelo, Cangiano, Lorenzo, Capezzuoli, Gabriella Teresa Capolupo, Marianna, Capuano, Filippo, Carannante, Eugenia, Cardamone, Teresa, Carfora, Chiara, Caricato, Pietro, Carnevali, Francesco Maria Carrano, Lorenzo, Casali, Gianmaria Casoni Pataccini, Gianluca, Cassese, Simone, Castiglioni, Flavia, Cavicchi, Ceccarelli, Graziano, Giovanni, Cestaro, Pasquale, Cianci, Claudio, Cimmino, Marco, Clementi, Coletta, Diego, Riccardo, Conventi, Corallino, Diletta, Maurizio, Costantini, Lorenzo, Crepaz, Diego, Cuccurullo, Curci, FABIO PIO, Giuseppe, Currò, Giorgio, Dalmonte, Giovanni, D'Alterio, Michele, D'Ambra, D'Ambrosio, Giancarlo, Anna, D'Amore, Michele De Capua, Simona, Deidda, Daniele, Delogu, Maurizio De Luca, Nicolò De Manzini, DE STEFANI, Elena, Giuseppe Di Buono, Marcello Di Martino, DI TOMASO, Anna, Ugo, Elmore, CORDOVA HERENCIA, INGRID ELVA, Giovanni, Emiliani, Sofia, Esposito, Fazio, Federico, Federico, Festa, Marcello, Filotico, Fiocca, Fausto, Irene, Fiume, Francesco, Fleres, Giulia, Fontana, Tommaso, Fontana, Edoardo, Forcignanò, Giampaolo, Formisano, Laura, Fortuna, Uberto Fumagalli Romario, Andrea, Galderisi, Raffaele, Galleano, Carlo, Gazia, Alessio, Giordano, Giorgio, Giraudo, Maria Carmela Giuffrida, Simona, Giura, Anna, Guida, Antonio Maria Iannello, Marco, Inama, Sara, Ingallinella, Iossa, Angelo, Livio, Iudici, Laracca, GIOVANNI GUGLIELMO, LARGHI LAUREIRO, Zoe, Saverio, Latteri, Luca, Leonardi, Pasquale, Lepiane, Edelweiss, Licitra, Paolo, Locurto, Sarah Lo Faso, Nicola, Luciani, Luzza, Luigi, Magaletti, Sara, Michele, Manigrasso, Alessandra, Marano, Francesco, Marchetti, Alessandra, Marello, Nicolò, Mariani, Jacopo Nicolò Marin, Gennaro, Martines, Laura, Mastrangelo, Antonio, Matarangolo, Marco, Materazzo, Mazzarella, Gennaro, Giorgio, Mazzarolo, Maria Paola Menna, Meoli, Francesca, Marco, Milone, Elisabetta, Moggia, Davide, Moioli, Sarah, Molfino, Vitantonio, Mongelli, Roberto, Montalti, Giulia, Montori, Luca, Morelli, Gianluigi, Moretto, Muttillo, EDOARDO MARIA, Irnerio, Muttillo, Francesca, Notte, Alessandro, M Paganini, Gianluca, Pagano, Palmieri, Livia, Giuseppe, Palomba, Valentina, Palumbo, Panetta, Cristina, Giulia, Paradiso, Beniamino, Pascotto, Passannanti, Daniele, Renato, Patrone, Francesca, Pecchini, Francesca, Pego, Fabio, Pelle, Perrotta, Nicola, Wanda, Petz, Biagio, Picardi, Picchetto, Andrea, Chiara, Piceni, Pietricola, Giulia, Enrico, Pinotti, Felice, Pirozzi, Paolo, Pizzini, Poillucci, Gaetano, Ilaria, Puccica, Lorenzo, Ramaci, Rapanotti, Eleonora, Daniela, Rega, Angelica, Reggiani, Giorgio, Romano, Gregorio, Romeo, Luigi, Romeo, Gianluca, Rompianesi, Stefano, Rossi, Edoardo, Saladino, Roberto, Santambrogio, Federica, Saraceno, Giuliano, Sarro, Diego, Sasia, Grazia, Savino, Rosa, Scaramuzzo, Antonio, Sciuto, Michela, Scollica, Giovanni, Scudo, Ardit, Seitaj, Carlo, Serra, Francesco, Serra, Pierpaolo, Sileri, Leandro, Siragusa, Carmen, Sorrentino, Giuseppe, Surfaro, Ernesto, Tartaglia, Beatrice, Torre, Andrea, Tufo, Matteo, Uccelli, Alessandro, Ussia, Vaccari, Samuele, Marina, Valente, Sara, Vertaldi, Alessandro, Vitali, Luca, Zaccherini, Luigi, Zorcolo, Noemi, Zorzetti, Balla, A., Sartori, A., Botteri, E., Podda, M., Ortenzi, M., Silecchia, G., Guerrieri, M., Agresta, F., Agrusa, A., Aguzzi, D., Alagia, M., Alberici, L., Allaix, M. E., Ambrosio, L., Amendola, A., Ammendola, M., Amodio, P. M., Anania, G., Andreuccetti, J., Annichiarico, A., Anoldo, P., Anselmo, A., Aprea, G., Arcuri, G., Arezzo, A., Armatura, G., Bagaglini, G., Bagolini, F., Bailetti, B., Baiocchi, G., Baldini, E., Bannone, E., Barone, M., Baronio, G., Basile, R., Bellucci, M., Cacciaguerra, A. B., Benzoni, I., Bianco, F., Boccia, G., Bombardini, C., Boni, L., Bono, D., Bonomo, L. D., Bonventre, G., Bottari, A., Botti, C., Brentegani, G., Buonomo, M., Bracale, U., Callari, C., Calligaris, L., Calo, P. G., Cangiano, A., Capezzuoli, L., Capolupo, G. T., Capuano, M., Carannante, F., Cardamone, E., Carfora, T., Caricato, C., Carnevali, P., Carrano, F. M., Casali, L., Pataccini, G. C., Cassese, G., Castiglioni, S., Cavicchi, F., Ceccarelli, G., Cestaro, G., Cianci, P., Cimmino, C., Clementi, M., Coletta, D., Conventi, R., Corallino, D., Costantini, M., Crepaz, L., Cuccurullo, D., Curci, F. P., Curro, G., Dalmonte, G., D'Alterio, G., D'Ambra, M., D'Ambrosio, G., D'Amore, A., De Capua, M., Deidda, S., Delogu, D., De Luca, M., De Manzini, N., De Stefani, E., Di Buono, G., Di Martino, M., Di Tomaso, A., Elmore, U., Herencia, I. E. C., Emiliani, G., Esposito, S., Fazio, F., Festa, F., Filotico, M., Fiocca, F., Fiume, I., Fleres, F., Fontana, G., Fontana, T., Forcignano, E., Formisano, G., Fortuna, L., Romario, U. F., Galderisi, A., Galleano, R., Gazia, C., Giordano, A., Giraudo, G., Giuffrida, M. C., Giura, S., Guida, A., Iannello, A. M., Inama, M., Ingallinella, S., Iossa, A., Iudici, L., Laracca, G. G., Laureiro, Z. L., Latteri, S., Leonardi, L., Lepiane, P., Licitra, E., Locurto, P., Faso, S. L., Luciani, N., Luzza, L., Magaletti, S., Manigrasso, M., Marano, A., Marchetti, F., Marello, A., Mariani, N., Marin, J. N., Martines, G., Mastrangelo, L., Matarangolo, A., Materazzo, M., Mazzarella, G., Mazzarolo, G., Menna, M. P., Meoli, F., Milone, M., Moggia, E., Moioli, D., Molfino, S., Mongelli, V., Montalti, R., Montori, G., Morelli, L., Moretto, G., Muttillo, E. M., Muttillo, I., Notte, F., Paganini, A. M., Pagano, G., Palmieri, L., Palomba, G., Palumbo, V., Panetta, C., Paradiso, G., Pascotto, B., Passannanti, D., Patrone, R., Pecchini, F., Pego, F., Pelle, F., Perrotta, N., Petz, W., Picardi, B., Picchetto, A., Piceni, C., Pietricola, G., Pinotti, E., Pirozzi, F., Pizzini, P., Poillucci, G., Puccica, I., Ramaci, L., Rapanotti, E., Rega, D., Reggiani, A., Romano, G., Romeo, G., Romeo, L., Rompianesi, G., Rossi, S., Saladino, E., Santambrogio, R., Saraceno, F., Sarro, G., Sasia, D., Savino, G., Scaramuzzo, R., Sciuto, A., Scollica, M., Scudo, G., Seitaj, A., Serra, C., Serra, F., Sileri, P., Siragusa, L., Sorrentino, C., Surfaro, G., Tartaglia, E., Torre, B., Tufo, A., Uccelli, M., Ussia, A., Vaccari, S., Valente, M., Vertaldi, S., Vitali, A., Zaccherini, L., Zorcolo, L., Zorzetti, N., Balla, Andrea, Sartori, Alberto, Botteri, Emanuele, Podda, Mauro, Ortenzi, Monica, Silecchia, Gianfranco, Guerrieri, Mario, Agresta, Ferdinando, de Manzini, Nicolo, and ARMIS (Augmented Reality in Minimally Invasive Surgery) Collaborative, Group

Subjects
Virtual reality (VR), minimally invasive surgery (MIS), Augmented reality (AR), Minimally invasive surgery (MIS), Mixed reality (MR), Survey, Training, training, augmented reality (AR), mixed reality (MR), survey, virtual reality (VR), Settore MED/18 - Chirurgia Generale, Surgery
Abstract

Minimally invasive surgery (MIS) is a widespread approach in general surgery. Computer guiding software, such as the augmented reality (AR), the virtual reality (VR) and mixed reality (MR), has been proposed to help surgeons during MIS. This study aims to report these technologies' current knowledge and diffusion during surgical training in Italy. A web-based survey was developed under the aegis of the Italian Society of Endoscopic Surgery (SICE). Two hundred and seventeen medical doctors' answers were analyzed. Participants were surgeons (138, 63.6%) and residents in surgery (79, 36.4%). The mean knowledge of the role of the VR, AR and MR in surgery was 4.9 ± 2.4 (range 1-10). Most of the participants (122, 56.2%) did not have experience with any proposed technologies. However, although the lack of experience in this field, the answers about the functioning of the technologies were correct in most cases. Most of the participants answered that VR, AR and MR should be used more frequently for the teaching and training and during the clinical activity (170, 80.3%) and that such technologies would make a significant contribution, especially in training (183, 84.3%) and didactic (156, 71.9%). Finally, the main limitations to the diffusion of these technologies were the insufficient knowledge (182, 83.9%) and costs (175, 80.6%). Based on the present study, in Italy, the knowledge and dissemination of these technologies are still limited. Further studies are required to establish the usefulness of AR, VR and MR in surgical training.

Published
2023

14. Laparoscopic sleeve gastrectomy with Rossetti fundoplication: long-term (5-year) follow-up.

Author

Uccelli M, Cesana GC, Ciccarese F, Oldani A, Giorgi R, De Carli SM, Villa R, Zanoni AAG, Ismail A, Di Capua F, Bonaldi M, Rubicondo C, Moioli D, and Olmi S

Subjects
Adult, Follow-Up Studies, Fundoplication methods, Gastrectomy methods, Humans, Middle Aged, Prospective Studies, Weight Loss, Barrett Esophagus diagnosis, Barrett Esophagus surgery, Esophagitis etiology, Esophagitis surgery, Gastroesophageal Reflux complications, Gastroesophageal Reflux surgery, Laparoscopy methods, Obesity, Morbid complications
Abstract

Background: Gastroesophageal reflux disease (GERD), including erosive esophagitis, is highly prevalent in the obese population. Barrett's esophagus is the consequence of untreated GERD. Laparoscopic sleeve gastrectomy is one of the most frequently performed bariatric procedures. This study presents results after 5 years of follow-up of combined LSG and Rossetti fundoplication for the treatment of GERD, esophagitis, and Barrett's esophagus in patients with morbid obesity., Objective: To evaluate long-term results after sleeve gastrectomy with Rossetti fundoplication., Setting: Public university hospital in Italy., Methods: Since January 2015, more than 450 patients with obesity underwent sleeve gastrectomy with a Rossetti fundoplication procedure as part of prospective studies underway at our center performed by 4 different expert bariatric surgeons. Currently, 127 patients have a follow-up of 5 years or more., Results: Mean patient age was 42.9 ± 10.3 years, and mean body mass index was 42.4 ± 6.1 kg/m 2 . In total, 74.8% of patients were experiencing GERD before surgery. In 29 of 127 patients (22.8%), preoperative gastroscopy showed signs of esophagitis and/or Barrett's esophagus. In particular, 23 of 127 patients (18.1%) had grade A esophagitis, 2 of 127 (1.6%) had grade B, 2 of 127 (1.6%) had grade C, and 2 of 127 (1.6%) had Barrett's esophagus. Mean operative time was 51 ± 21 minutes. No intraoperative complications or conversions were reported. A regular postoperative course was seen in 91.3% of patients. Sixty months after surgery, more than 95% of patients did not experience any reflux symptoms. Percent total weight loss at follow-up was comparable with that with sleeve gastrectomy. Endoscopic follow-up demonstrated improvement of esophagitis lesions (including Barrett's esophagus) present in the preoperative setting., Conclusion: Laparoscopic sleeve gastrectomy with Rossetti fundoplication is well tolerated, feasible, and safe in patients with obesity, providing adequate weight loss results and complete resolution of clinical signs of GERD. We have recorded an improvement in esophagitis lesions present at preoperative gastroscopy and complete resolution of Barrett's esophagus within 5 years of follow-up., (Copyright © 2022 American Society for Metabolic and Bariatric Surgery. Published by Elsevier Inc. All rights reserved.)

Published
2022
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15. Protein load impairs factor H binding promoting complement-dependent dysfunction of proximal tubular cells.

Author

Buelli S, Abbate M, Morigi M, Moioli D, Zanchi C, Noris M, Zoja C, Pusey CD, Zipfel PF, and Remuzzi G

Subjects
Cell Line, Complement Activation, Disease Progression, Humans, Kidney Diseases etiology, Kidney Diseases pathology, Protein Binding, Serum Albumin pharmacology, Transferrin pharmacology, Complement Factor H metabolism, Complement System Proteins metabolism, Kidney Tubules, Proximal pathology, Proteins pharmacology
Abstract

Intrarenal complement activation plays an important role in the progression of chronic kidney disease. A key target of the activated complement cascade is the proximal tubule, a site where abnormally filtered plasma proteins and complement factors combine to promote injury. This study determined whether protein overloading of human proximal tubular cells (HK-2) in culture enhances complement activation by impairing complement regulation. Addition of albumin or transferrin to the cells incubated with diluted human serum as a source of complement caused increased apical C3 deposition. Soluble complement receptor-1 (an inhibitor of all 3 activation pathways) blocked complement deposition while the classical and lectin pathway inhibitor, magnesium chloride-EGTA, was, ineffective. Media containing albumin as well as complement had additive proinflammatory effects as shown by increased fractalkine and transforming growth factor-beta mRNA expression. This paralleled active C3 and C5b-9 generations, effects not shared by transferrin. Factor H, one of the main natural inhibitors of the alternative pathway, binds to heparan sulfate proteoglycans. Both the density of heparan sulfate and factor H binding were reduced with protein loading, thereby enhancing the albumin- and serum-dependent complement activation potential. Thus, protein overload reduces the ability of the tubule cell to bind factor H and counteract complement activation, effects instrumental to renal disease progression.

Published
2009
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16. Involvement of renal tubular Toll-like receptor 9 in the development of tubulointerstitial injury in systemic lupus.

Author

Benigni A, Caroli C, Longaretti L, Gagliardini E, Zoja C, Galbusera M, Moioli D, Romagnani P, Tincani A, Andreoli L, and Remuzzi G

Subjects
Animals, Biopsy, Cells, Cultured, Female, Gene Expression Regulation drug effects, Humans, Kidney Tubules, Proximal pathology, Lupus Erythematosus, Systemic genetics, Lupus Erythematosus, Systemic metabolism, Mice, Mice, Inbred NZB, Mice, Inbred Strains, Nephritis, Interstitial genetics, Nephritis, Interstitial metabolism, Protein Kinase Inhibitors pharmacology, Purines pharmacology, RNA, Messenger genetics, RNA, Messenger metabolism, Roscovitine, Toll-Like Receptor 9 genetics, Kidney Tubules, Proximal metabolism, Lupus Erythematosus, Systemic complications, Nephritis, Interstitial etiology, Toll-Like Receptor 9 metabolism
Abstract

Objective: Toll-like receptor 9 (TLR-9), a receptor for CpG DNA, has been implicated in the activation of immune cells in lupus. We undertook this study to determine whether the expression of TLR-9 in resident renal cells in lupus nephritis is related to the development of tubulointerstitial injury., Methods: TLR-9 was analyzed in selectively retrieved renal tissue from (NZB x NZW)F1 mice at different stages of disease by laser capture microdissection combined with real-time quantitative reverse transcriptase-polymerase chain reaction, and in renal biopsy specimens from lupus nephritis patients by immunohistochemistry. We investigated for the molecular component responsible for TLR-9 activation by cultured proximal tubular cells in serum from patients with lupus., Results: Renal tissue from NZB x NZW mice displayed robust TLR-9 expression localized to proximal tubular cells. TLR-9 levels correlated with proteinuria and tubulointerstitial injury to the extent that a cyclin-dependent kinase inhibitor, while reducing proteinuria and renal structural damage, prevented tubular TLR-9 generation in lupus mice. Consistently, exaggerated TLR-9 staining was found in proximal tubular cells of lupus patients, which correlated with tubulointerstitial damage. DNA-containing immune complexes purified from sera of patients with lupus induced TLR-9 in cultured proximal tubular cells. This was prevented by CCGG-rich short oligonucleotides, specific antagonists of CpG DNA, indicating that the DNA component of immune complexes was required for TLR-9 stimulation., Conclusion: These findings suggest that tubular TLR-9 activation has a pathogenetic role in tubulointerstitial inflammation and damage in experimental and human lupus nephritis, and they indicate a novel target for future therapies.

Published
2007
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17. Shigatoxin-induced endothelin-1 expression in cultured podocytes autocrinally mediates actin remodeling.

Author

Morigi M, Buelli S, Zanchi C, Longaretti L, Macconi D, Benigni A, Moioli D, Remuzzi G, and Zoja C

Subjects
Animals, Antigens, Tumor-Associated, Carbohydrate metabolism, Cell Differentiation, Cell Membrane Permeability, Cells, Cultured, Cytoskeleton metabolism, Endothelin-1 biosynthesis, Mice, Mitogen-Activated Protein Kinases metabolism, NF-kappa B physiology, Signal Transduction, Transcription Factor AP-1 physiology, Transcription, Genetic, Up-Regulation, Actins metabolism, Endothelin-1 metabolism, Podocytes drug effects, RNA, Messenger metabolism, Shiga Toxin 2 pharmacology
Abstract

Shigatoxin (Stx) is the offending agent of post-diarrheal hemolytic uremic syndrome, characterized by glomerular ischemic changes preceding microvascular thrombosis. Because podocytes are highly sensitive to Stx cytotoxicity and represent a source of vasoactive molecules, we studied whether Stx-2 modulated the production of endothelin-1 (ET-1), taken as candidate mediator of podocyte dysfunction. Stx-2 enhanced ET-1 mRNA and protein expression via activation of nuclear factor kappaB (NF-kappaB) and activator protein-1 (Ap-1) to the extent that transfection with the dominant-negative mutant of IkappaB-kinase 2 or with Ap-1 decoy oligodeoxynucleotides reduced ET-1 mRNA levels. We propose a role for p38 and p42/44 mitogen-activated protein kinases (MAPKs) in mediating NF-kappaB-dependent gene transcription induced by Stx-2, based on data that Stx-2 phosphorylated p38 and p42/44 MAPKs and that MAPK inhibitors reduced transcription of NF-kappaB promoter/luciferase reporter gene construct induced by Stx-2. Stx-2 caused F-actin redistribution and intercellular gaps via production of ET-1 acting on ETA receptor, because cytoskeleton changes were prevented by ETA receptor blockade. Exogenous ET-1 induced cytoskeleton rearrangement and intercellular gaps via phosphatidylinositol-3 kinase and Rho-kinase pathway and increased protein permeability across the podocyte monolayer. These data suggest that the podocyte is a target of Stx, a novel stimulus for the synthesis of ET-1, which may control cytoskeleton remodeling and glomerular permeability in an autocrine fashion.

Published
2006
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