209 research outputs found

    Expert Opinion on Hostile Neck Definition in Endovascular Treatment of Abdominal Aortic Aneurysms (a Delphi Consensus)

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    Endovascular aneurysm repair (EVAR) is currently accepted as an alternative to open repair for the treatment of abdominal aortic aneurysm (AAA). Approximately 40-60% of AAA patients are not considered eligible for EVAR due to unfavorable anatomy. There is currently no consensus on the definition of "hostile" aortic neck for EVAR procedure

    Effects of Venous Angioplasty on Cerebral Lesions in Multiple Sclerosis: Expanded Analysis of the Brave Dreams Double-Blind, Sham-Controlled Randomized Trial

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    Purpose: To evaluate if jugular vein flow restoration in various venographic defects indicative of chronic cerebrospinal venous insufficiency (CCSVI) in multiple sclerosis (MS) patients can have positive effects on cerebral lesions identified using magnetic resonance imaging (MRI). Materials and Methods: The Brave Dreams trial ( identifier NCT01371760) was a multicenter, randomized, parallel group, double-blind, sham-controlled trial to assess the efficacy of jugular venoplasty in MS patients with CCSVI. Between August 2012 and March 2016, 130 patients (mean age 39.9 +/- 10.6 years; 81 women) with relapsing/remitting (n=115) or secondary/progressive (n=15) MS were randomized 2:1 to venography plus angioplasty (n=86) or venography (sham; n=44). Patients and study personnel (except the interventionist) were masked to treatment assignment. MRI data acquired at 6 and 12 months after randomization were compared to the preoperative scan for new and/or >30% enlargement of T2 lesions plus new gadolinium enhancement of pre-existing lesions. The relative risks (RR) with 95% confidence interval (CI) were estimated and compared. In a secondary assessment, venograms of patients who underwent venous angioplasty were graded as "favorable" (n=38) or "unfavorable" (n=30) for dilation according to the Giaquinta grading system by 4 investigators blinded to outcomes. These subgroups were also compared. Results: Of the 130 patients enrolled, 125 (96%) completed the 12-month MRI follow-up. Analysis showed that the likelihood of being free of new cerebral lesions at 1 year was significantly higher after venoplasty compared to the sham group (RR 1.42, 95% CI 1.00 to 2.01, p=0.032). Patients with favorable venograms had a significantly higher probability of being free of new cerebral lesions than patients with unfavorable venograms (RR 1.82, 95% CI 1.17 to 2.83, p=0.005) or patients in the sham arm (RR 1.66, 95% CI 1.16 to 2.37, p=0.005). Conclusion: Expanded analysis of the Brave Dreams data that included secondary/progressive MS patients in addition to the relapsing/remitting patients analyzed previously showed that venoplasty decreases new cerebral lesions at 1 year. Secondary analysis confirmed the efficacy of the Giaquinta grading system in selecting patients appropriate for venoplasty who were more likely to be free from accumulation of new cerebral lesions at MRI

    Erratum: Unibody endograft using AFX 2 for less invasive and faster endovascular aortic repair: Protocol for a multicenter nonrandomized study (JMIR Research Protocols (2020) 9:4 (e16959) DOI: 10.2196/16959)

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    In “Unibody Endograft Using AFX 2 for Less Invasive and Faster Endovascular Aortic Repair: Protocol for a Multicenter Nonrandomized Study” (JMIR Res Protoc 2020;9(4):e16959) there were two errors in the Collaborators List. The collaborator Sonia Ronchey was inadvertently not included in the collaborator list. Additionally, the collaborator name Pietro Volpet should have been listed as Pietro Volpe. The Collaborator List was initially published as follows: The LIVE Study Collaborators are as follows: Giancarlo Accarino; Dimitri Apostolou; Guido Bajardi; Stefano Bartoli; Filippo Benedetto; Franco Briolini; Stefano Camparini; Emidio Costantini; Giovanni Credi; Ruggiero Curci; Raffaello Dallatana; Gianmarco de Donato; Carlo Dionisi; Vittorio Dorrucci; Leonardo Ercolini; Gianfranco Fadda; Mauro Ferrari; Loris Flora; Andrea Gaggiano; Roberto Gattuso; Franco Grego; Sabrina Grimaldi; Giovanni Impedovo; Arnaldo Ippoliti; Antonio Jannello; Sergio Losa; Nicola Mangialardi; Isaac Martinez; Javier Martinez; Stefano Michelagnoli; Giancarlo Palasciano; Vincenzo Palazzo; Domenico Palombo; Raffaele Pulli; Giovanni Rossi; Antonino Scolaro; Gianantonio Simoni; Francesco Spinelli; Francesco Talarico; Maurizio Taurino; Marco Trogolo; Nicola Tusini; Gianfranco Veraldi; Pier Francesco Veroux; Gennaro Vigliotti; and Pietro Volpet. The Collaborator List has now been updated to the following: The LIVE Study Collaborators are as follows: Giancarlo Accarino; Dimitri Apostolou; Guido Bajardi; Stefano Bartoli; Filippo Benedetto; Franco Briolini; Stefano Camparini; Emidio Costantini; Giovanni Credi; Ruggiero Curci; Raffaello Dallatana; Gianmarco de Donato; Carlo Dionisi; Vittorio Dorrucci; Leonardo Ercolini; Gianfranco Fadda; Mauro Ferrari; Loris Flora; Andrea Gaggiano; Roberto Gattuso; Franco Grego; Sabrina Grimaldi; Giovanni Impedovo; Arnaldo Ippoliti; Antonio Jannello; Sergio Losa; Nicola Mangialardi; Isaac Martinez; Javier Martinez; Stefano Michelagnoli; Giancarlo Palasciano; Vincenzo Palazzo; Domenico Palombo; Raffaele Pulli; Sonia Ronchey; Giovanni Rossi; Antonino Scolaro; Gianantonio Simoni; Francesco Spinelli; Francesco Talarico; Maurizio Taurino; Marco Trogolo; Nicola Tusini; Gianfranco Veraldi; Pier Francesco Veroux; Gennaro Vigliotti; and Pietro Volpe. The correction will appear in the online version of the paper on the JMIR website on June 24, 2020, together with the publication of this correction notice. Because this was made after submission to PubMed, PubMed Central, and other full-text repositories, the corrected article has also been resubmitted to those repositories

    Risk of de novo cancers after transplantation : Results from a cohort of 7217 kidney transplant recipients, Italy 1997-2009

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    To assess incidence and risk factors for de novo cancers (DNCs) after kidney transplant (KT), we carried out a cohort investigation in 15 Italian KT centres. Seven thousand two-hundred seventeen KT recipients (64.2% men), transplanted between 1997 and 2007 and followed-up until 2009, represented the study group. Person years (PY) were computed from 30 days after transplant to cancer diagnosis, death, return to dialysis or to study closure. The number of observed DNCs was compared to that expected in the general population of Italy through standardised incidence ratios (SIR) and 95% confidence intervals (CI). To identify risk factors, incidence rate ratios (IRR) were computed. Three-hundred ninety five DNCs were diagnosed during 39.598 PYs, with Kaposi's sarcoma (KS), post-transplant lymphoproliferative disorders (PTLD), particularly non-Hodgkin' lymphoma (NHL), lung, kidney and prostate as the most common types. The overall IR was 9.98/1.000 PY, with a 1.7-fold augmented SIR (95% CI: 1.6-1.9). SIRs were particularly elevated for KS (135), lip (9.4), kidney carcinoma (4.9), NHL (4.5) and mesothelioma (4.2). KT recipients born in Southern Italy were at reduced risk of kidney cancer and solid tumors, though at a higher KS risk, than those born in Northern Italy. Use of mTOR inhibitors (mTORi) exerted, for all cancers combined, a 46% significantly reduced risk (95% CI: 0.4-0.7). Our study findings confirmed, in Italy, the increased risks for cancer following KT, and they also suggested a possible protective effect of mTORi in reducing the frequency of post transplant cancers. © 2012 Elsevier Ltd. All rights reserved

    Pharmacological induction of heme-oxygenase-1 inhibits iNOS and oxidative stress in renal ischemia-reperfusion injury

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    Nitric oxide (NO), produced by nitric oxide synthase, is implicated in the pathophysiology of renal ischemia/reperfusion (I/R) injury. This study sought to elucidate the impact of pharmacological induction of heme oxygenase-1 (HO-1) on renal I/R injury. Rats were subjected to 45 minutes of renal ischemia followed by various times of reperfusion (30 minutes, 1 hour, or 3 hours). Plasma from sacrificed rats was obtained, and the kidneys processed for the expression of iNOS, cleaved caspase-3, p38MAPK and for immunohistochemical analysis. Furthermore, we determined renal and plasma levels of lipid hydroperoxides, total thiol groups, and plasmatic NO2 /NO3 formation. Our results showed a time-dependent increase in iNOS expression, which was also confirmed by increased plasma formation of NO2 /NO3 . Interestingly, this effect was reversed by pretreatment (12 hours) with SnCl2, a potent and specific inducer of renal HO-1 expression and activity, or by intraperitoneal injection of biliverdin (10 mg/kg). Furthermore,we observed a concomitant reduction in plasma and renal LOOH formation, a normalization of renal total thiol content, a reduction of caspase-3-mediated apoptosis, and a significant increase in p38MAPK phosphoration. Taken together, these results suggested that HO-1 and its byproduct biliverdin play major roles in the pathophysiological cascade leading to renal I/R injury
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