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Pancreatic Neoplasms: HELP
Articles by Marco E. Bianchi
Based on 2 articles published since 2008
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Between 2008 and 2019, Marco Bianchi wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Interobserver agreement in contrast harmonic endoscopic ultrasound. 2012

Fusaroli, Pietro / Kypraios, Dimitrios / Mancino, Maria Grazia / Spada, Alessia / Benini, Maria Chiara / Bianchi, Marco / Bocus, Paolo / De Angelis, Claudio / De Luca, Leonardo / Fabbri, Carlo / Grillo, Antonino / Marzioni, Marco / Reggio, Dario / Togliani, Thomas / Zanarini, Stefano / Caletti, Giancarlo. ·Department of Clinical Medicine, GI Unit, University of Bologna/Imola Hospital, Italy Gastroenterology Unit, Bellaria Hospital, Bologna, Italy. pietro.fusaroli@unibo.it ·J Gastroenterol Hepatol · Pubmed #22414180.

ABSTRACT: BACKGROUND AND AIM: Contrast harmonic endoscopic ultrasound (CH-EUS) was recently introduced to clinical practice; its reproducibility among endosonographers is unknown. Our aim was to assess the interobserver agreement (IA) in CH-EUS. METHODS: Fifteen endosonographers (eight experienced and seven non-experienced) from 11 Italian EUS centers evaluated 80 video-cases (40 solid pancreatic lesions, 20 pancreatic cystic lesions and 20 submucosal lesions) of CH-EUS, according to the degree of enhancement, the pattern of distribution and the washout of the contrast agent. IA within each group and between the two groups of observers was assessed with the Fleiss kappa statistic. RESULTS: Overall IA was moderate for the uptake and fair for the pattern of distribution and the washout. In solid pancreatic lesions, IA was moderate for the uptake and fair for the pattern and the washout. In cystic pancreatic lesions, IA was uniformly moderate for the assessment of uptake, slight for the pattern and fair for the washout. In submucosal tumors, IA was substantial for the uptake, slight for the pattern and fair for the washout. Non-experienced endosonographers demonstrated, in most cases, comparable IA with the experienced ones. CONCLUSIONS: Interobserver agreement among endosonographers for CH EUS was satisfactory. In particular, overall IA varied from slight to substantial, being fair in the majority of cases. Inherent structural features of the lesions, as well as technical differences between the variables assessed, could have accounted for the fluctuation of the results. Outcomes of IA were reproducible between experienced and non-experienced endosonographers.

2 Article Endogenous HMGB1 regulates autophagy. 2010

Tang, Daolin / Kang, Rui / Livesey, Kristen M / Cheh, Chun-Wei / Farkas, Adam / Loughran, Patricia / Hoppe, George / Bianchi, Marco E / Tracey, Kevin J / Zeh, Herbert J / Lotze, Michael T. ·Damage Associated Molecular Pattern Molecule Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA. tangd2@upmc.edu ·J Cell Biol · Pubmed #20819940.

ABSTRACT: Autophagy clears long-lived proteins and dysfunctional organelles and generates substrates for adenosine triphosphate production during periods of starvation and other types of cellular stress. Here we show that high mobility group box 1 (HMGB1), a chromatin-associated nuclear protein and extracellular damage-associated molecular pattern molecule, is a critical regulator of autophagy. Stimuli that enhance reactive oxygen species promote cytosolic translocation of HMGB1 and thereby enhance autophagic flux. HMGB1 directly interacts with the autophagy protein Beclin1 displacing Bcl-2. Mutation of cysteine 106 (C106), but not the vicinal C23 and C45, of HMGB1 promotes cytosolic localization and sustained autophagy. Pharmacological inhibition of HMGB1 cytoplasmic translocation by agents such as ethyl pyruvate limits starvation-induced autophagy. Moreover, the intramolecular disulfide bridge (C23/45) of HMGB1 is required for binding to Beclin1 and sustaining autophagy. Thus, endogenous HMGB1 is a critical pro-autophagic protein that enhances cell survival and limits programmed apoptotic cell death.