Bruno

Institut de Recherche sur la Fusion par Confinement Magnétique

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Radioembolisation and portal vein embolization before resection of large hepatocellular carcinoma

世界胃肠病学杂志：英文版 (2015)

Fikri Bouazza Arthur Arthur Poncelet Camilo

Resectability of hepatocellular carcinoma in patients with chronic liver disease is dramatically limited by the need to preserve sufficient remnant liver in order to avoid postoperative liver insufficiency. Preoperative treatments aimed at downsizing the tumor and promoting hypertrophy of the future remnant liver may improve resectability and reduce operative morbidity. Here we report the case of a patient with a large hepatocellular carcinoma arising from chronic liver disease. Preoperative treatment, including tumor downsizing with transarterial radioembolization and induction of future remnant liver hypertrophy with right portal vein embolization, resulted in a 53% reduction in tumor volume and compensatory hypertrophy in the contralateral liver. The patient subsequently underwent extended right hepatectomy with no postoperativesigns of liver decompensation. Pathological examination demonstrated a margin-free resection and major tumor response. This new therapeutic sequence, combining efficient tumor targeting and subsequent portal vein embolization, could improve the feasibility and safety of major liver resection for hepatocellular carcinoma in patients with liver injury.

Portal vein embolization

Portography

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Management of recto-vaginal fistulas after prosthetic reinforcement treatment for pelvic organ prolapse

世界胃肠病学杂志：英文版（电子版） (2010)

Mehdi Ouassi Silvia silvia Cresti Giger

AIM: To communicate our findings on successful treat-ment of recto-vaginal fistulas (RVFs) after prosthetic reinforcement surgery of pelvic organ prolapse (POP). METHODS: A retrospective single center study between 1998 and 2008 was performed. A total of 80 patients with RVF were identified, of which five patients (6%), with a mean age of 65 years (range: 52-73), had undergone previous surgery for POP with pros-thetic reinforcement. RESULTS: All patients complained about ongoing vaginal infections and febri...

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Gene transfer and therapy with adenoviral vector in rats with diethylnitrosamine-induced hepatocellular carcinoma

中国实验血液学杂志 (1997)

M.D. Miguel Idoate Roberto Cachán Cruz Bilbao Bruno

Viral-mediated gene transfer of thymidine kinase ofherpes simplex virus (HSV-tk) has been used to confercytotoxic sensitivity to ganciclovir (GCV) in a variety oftnmor cells. HSV-tk converts GCV into a phosphorylatedcompound which is toxic for dividing cells by blockingDNA synthesis. Our previous study has shown that

Thymidine kinase

Gene transfer

Transduction (biophysics)

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CCDC 2182918: Experimental Crystal Structure Determination

The Cambridge Structural Database (2023)

Noschang Cabral Bruno Fonseca Rodrigues Jessica Roca Jungfer

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.

10.5517/ccdc.csd.cc2c8hqw

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CCDC 2182919: Experimental Crystal Structure Determination

The Cambridge Structural Database (2023)

Noschang Cabral Bruno Fonseca Rodrigues Jessica Roca Jungfer

10.5517/ccdc.csd.cc2c8hrx

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Arrhythmogenic right ventricular cardiomyopathy: From genetics to diagnostic and therapeutic challenges

世界心脏病学杂志：英文版（电子版） (2014)

Bruno Pinamonti Francesca Francesca Brun Luísa

Arrhythmogenic right ventricular cardiomyopathy(ARVC) is a genetic disease characterized by myocyte loss and fibro-fatty tissue replacement. Diagnosis of ARVC remains a clinical challenge mainly at its early stages and in patients with minimal echocardiographic right ventricular(RV) abnormalities. ARVC shares some common features with other cardiac diseases, such as RV outflow ventricular tachycardia, Brugada syndrome, and myocarditis, due to arrhythmic expressivity and biventricular involvement. The identification of ARVC can be often challenging, because of the heterogeneous clinical presentation, highly variable intra- and inter-family expressivity and incomplete penetrance. This genotypephenotype “plasticity” is largely unexplained. A familial history of ARVC is present in 30% to 50% of cases, and the disease is considered a genetic cardiomyopathy, usually inherited in an autosomal dominant pattern with variable penetrance and expressivity; in addition, autosomal recessive forms have been reported(Naxos disease and Carvajal syndrome). Diagnosis of ARVC relays on a scoring system, with major or minorcriteria on the Revised Task Force Criteria. Implantable cardioverter defibrillators(ICDs) are increasingly utilized in patients with ARVC who have survived sudden death(SD)(secondary prevention). However, there are few data available to help identifying ARVC patients in whom the prophylactic implantation of an ICD is truly warranted. Prevention of SD is the primary goal of management. Pharmacologic treatment of arrhythmias, catheter ablation of ventricular tachycardia, and ICD are the mainstay of treatment of ARVC.

Penetrance

Expressivity

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Systemic therapy of hepatocellular carcinoma:Current status and future perspectives

世界胃肠病学杂志：英文版（电子版） (2014)

Domênico Germano Bruno Danièle

The management of hepatocellular carcinoma(HCC)has substantially changed in the past few decades,the introduction of novel therapies(such as sorafenib)have improved patient survival.Nevertheless,HCC remains the third most common cause of cancer-related deaths worldwide.Decision-making largely relies on evidencebased criteria,as showed in the US and European clinical practice guidelines,which endorse five therapeutic recommendations:resection;transplantation;radiofrequency ablation;chemoembolization;and sorafenib.Many molecularly targeted agents that inhibit angiogenesis,epidermal growth factor receptor,and mammalian target of rapamycin are at different stages of clinical development in advanced HCC.Future research should continue to unravel the mechanism of hepatocarcinogenesis and to identify key relevant molecular targets for therapeutic intervention.Identification and validation of potential surrogate and predictive biomarkers hold promise to individualize patient’s treatment to maximize clinical benefit and minimize the toxicity and cost of targeted agents.

Targeted Therapy

Systemic therapy

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Helicobacter pylori and functional dyspepsia: An unsolved issue?

世界胃肠病学杂志：英文版（电子版） (2014)

Angelo Angelo Zullo Cesare Hassan Vincenzo

Patients with Helicobacter pylori(H. pylori) infection may complain of dyspeptic symptoms without presence of macroscopic lesions on gastroduodenal mucosa. Such a condition is usually recognized as functional dyspepsia, and different pathogenetic mechanisms are involved. The role of H. pylori in these patients is controversial. Several trials assessed the potential role of H. pylori eradication in improving dyspeptic symptoms, and data of some meta-analyses demonstrated that cure of infection is associated with a small(10%), but significant therapeutic gain as compared to placebo. The reason for which dyspeptic symptoms regress in some patients following bacterial eradication, but persist in others remains unclear. Regrettably, trials included in the meta-analyses are somewhat different for study design, definition of symptoms, assessment of symptoms changes, and some may be flawed by potential pitfalls. Consequently, the information could be not consistent. We critically reviewed the main available trials, attempting to address future research in this field

Helicobacter Infections

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CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes

世界胃肠病学杂志：英文版（电子版） (2014)

Toni Urbanik Bruno Christian Koehler

AIM:To analyze the role of CYLD for receptor-mediated cell death of murine hepatocytes in acute liver injury models.METHODS:Hepatocyte cell death in CYLD knockout mice(CYLD-/-)was analyzed by application of liver injury models for CD95-(Jo2)and tumor necrosis factor(TNF)-α-[D-Gal N/lipopolysaccharide(LPS)]induced apoptosis.Liver injury was assessed by measurement of serum transaminases and histological analysis.Apoptosis induction was quantified by cleaved PARP staining and Western blotting of activated caspases.Nuclear factor(NF)-κB,ERK,Akt and jun amino-terminal kinases signaling were assessed.Primary Hepatocytes were isolated by two step-collagenase perfusion and treated with recombinant TNF-αand with the CD95-ligand Jo2.Cell viability was analyzed by MTT-assay.RESULTS:Livers of CYLD-/-mice showed increased anti-apoptotic NF-κB signaling.In both applied liver injury models CYLD-/-mice showed a significantly reduced apoptosis sensitivity.After D-Gal N/LPS treatment CYLD-/-mice exhibited significantly lower levels of alanine aminotransferase(ALT)(295 U/L vs 859 U/L,P<0.05)and aspartate aminotransferase(AST)(560 U/L vs 1025 U/L,P<0.01).After Jo injection CYLD-/-mice showed 2-fold lower ALT(50 U/L vs 110 U/L,P<0.01)and lower AST(250 U/L vs 435 U/L,P<0.01)serumlevels compared to WT mice.In addition,isolated CYLD-/-primary murine hepatocytes(PMH)were less sensitive towards death receptor-mediated apoptosis and showed increased levels of Bcl-2,XIAP,c IAP1/2,survivin and c-FLIP expression upon TNF-and CD95-receptor triggering,respectively.Inhibition of NF-κB activation by the inhibitor of NF-κB phosphorylation inhibitor BAY 11-7085 inhibited the expression of antiapoptotic proteins and re-sensitized CYLD-/-PMH towards TNF-and CD95-receptor mediated cell death.CONCLUSION:CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-κB dependent anti-apoptotic signaling.

XIAP

Caspase 8

Viability assay

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Two-dimensional nonlinear finite element analysis of well damage due to reservoir compaction, well-to-well interactions, and localization on weak layers

L.B. Hilbert J. T. Fredrich Bruno G.L. Deitrick E.P. de Rouffignac

In this paper the authors present the results of a coupled nonlinear finite element geomechanics model for reservoir compaction and well-to-well interactions for the high-porosity, low strength diatomite reservoirs of the Belridge field near Bakersfield, California. They show that well damage and failures can occur under the action of two distinct mechanisms: shear deformations induced by pore compaction, and subsidence, and shear deformations due to well-to-well interactions during production or water injection. They show such casting damage or failure can be localized to weak layers that slide or slip under shear due to subsidence. The magnitude of shear displacements and surface subsidence agree with field observations.

Geomechanics

Slip line field

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