108 research outputs found
Correction to: Ostomy closure rate during COVID-19 pandemic: an Italian multicentre observational study (Updates in Surgery, (2022), 74, 3, (1017-1025), 10.1007/s13304-022-01274-w)
No full textWhile typesetting the article the Collaborators were not included in the proofs. The collaborators names are provided below: DOC Collaborative Group: Laura Agostinelli, Ferdinando Agresta, Gabriele Anania, Laura Antolino, Pietro Anoldo, Emanuele Botteri, Umberto Bracale, Fabio Carbone, Massimo Carlini, Francesco Maria Carrano, Giorgia Casadei, Diego Coletta, Francesco Crafa, Nicola de’Angelis, Paolo Delrio, Giovanni Domenico De Palma, Marcello Di Martino, Ugo Elmore, Lorenzo Gozzini, Michele Grieco, Giovanni Battista Levi Sandri, Edelweiss Licitra, Andrea Lucchi, Marco Massani, Riccardo Memeo, Marco Milone, Dario Oppici, Monica Ortenzi, Alberto Patriti, Francesca Pecchini, Roberto Peltrini, Micaela Piccoli, Adolfo Pisanu, Mauro Podda, Gilberto Poggioli, Maria Chiara Ranucci, Daniela Rega, Riccardo Rosati, Francesco Roscio, Matteo Rottoli, Roberto Santoro, Alberto Sartori, Antonino Spinelli, Serafino Vanella, Giovanni Vennarecci, Nereo Vettoretto. The original article has been corrected
DISTINCT CARDIAC AND RENAL EFFECTS OF ETA RECEPTOR ANTAGONIST AND ACE INHIBITOR IN EXPERIMENTAL TYPE 2 DIABETES
No full textDiabetic nephropathy is associated with cardiovascular morbidity. ACE inhibitors provide imperfect renoprotection in advanced type 2 diabetes and cardiovascular risk remains elevated. Endothelin (ET)-1 has a role in renal and cardiac dysfunction in diabetes. Here we assessed whether combination therapy with ACE inhibitor and ETA receptor antagonist provided reno- and cardioprotection in rats with overt type 2 diabetes. Four groups of Zucker diabetic fatty (ZDF) rats were treated orally from 4 (when proteinuric) to 8 months with: vehicle; ramipril (1mg/kg); sitaxsentan (60mg/kg); ramipril plus sitaxsentan. Lean rats served as controls. Combined therapy ameliorated proteinuria and glomerulosclerosis mostly as a result of the action of ramipril. Simultaneous blockade of Ang II and ET-1 pathways normalized renal MCP-1 and interstitial inflammation. Cardiomyocyte loss, volume enlargement and capillary rarefaction were prominent abnormalities of ZDF myocardium.
Myocyte volume was reduced by ramipril and sitaxsentan, which also ameliorated heart capillary density. Drug combination restored myocardial structure, and re-established an adequate capillary network in the presence of increased cardiac expression of VEGF/VEGFR-1, and significant reduction of oxidative stress.
In conclusion, in type 2 diabetes concomitant blockade of Ang II synthesis and ET-1 biological activity through ETA receptor antagonist led to substantial albeit not complete renoprotection, almost due to the ACE inhibitor. The drug combination also showed cardioprotective properties which however were mainly dependent on the contribution of ETA receptor antagonist through the action of VEGF
Author response to: Comment on: Effect of centre volume on pathological outcomes and postoperative complications after surgery for colorectal cancer: results of a multicentre national study
No full textTra la foresta e il lago. Il sito all'aperto dell’Epigravettiano recente di Arco via Serafini (Trento, Italia settentrionale)
No full textThe open-air multi-layered site of Arco Via Serafini (Trento, Northern Italy), is situated in the flood plain of the River Sarca (80 m a.s.l.).The stratigraphic sequence allowed documentation of two phases of Late Epigravettian occupation with 14 structured areas in the context of the Younger Dryas
Erratum: Chitotriosidase: a biomarker of activity and severity in patients with sarcoidosis (Respiratory Research (2020) 21 (6) DOI: 10.1186/s12931-019-1263-z)
No full textAfter publication of our article [1] the authors have notified us that one of the names has been incorrectly tagged. Original name tagging: Given name: d Alessandro Family name: Miriana Correct name tagging: Given name: Miriana Family name: d Alessandro The original article has been corrected. Author details
Effects of MCP-1 inhibition by bindarit therapy in a rat model of polycystic kidney disease
No full textBackground/Aims: Experimental and clinical evidence suggested that monocyte chemoattractant protein-1 (MCP-1/CCL2) has a role in the development of interstitial inflammation and renal failure in polycystic kidney disease (PKD). We investigated whether bindarit, an inhibitor of MCP-1/CCL2 synthesis, could influence the evolution of PKD in PCK rats. Methods: PCK rats were treated from 5 to 15 weeks of age with vehicle or bindarit. Sprague-Dawley rats served as control. For in vitro studies, murine podocytes were exposed to albumin with or without bindarit. Results: MCP-1 mRNA was upregulated in the kidney of PCK rats and reduced by bindarit. Treatment limited overexpression of MCP-1 protein by epithelial cells of dilated tubules and cysts, and interstitial inflammatory cells. Excessive renal accumulation of mono-cytes/macrophages was lowered by bindarit by 41%. Serum creatinine slightly increased in PCK rats on vehicle and was similar to controls after bindarit. Kidney and liver cysts were not affected by treatment. Bindarit significantly reduced progressive proteinuria of PCK rats. The antiproteinuric effect was associated with the restoration of the defective nephrin expression in podocytes of PCK rats. Bindarit limited podocyte foot process effacement and ameliorated slit diaphragm frequency. In cultured podocytes, bindarit reduced MCP-1 production in response to albumin and inhibited albumin-induced cytoskeletal remodeling and cell migration. Conclusion: This study showed that although bindarit did not prevent renal cyst growth, it limited interstitial inflammation and renal dysfunction and reduced proteinuria in PKD. Thus, bindarit could be considered a therapeutic intervention complementary to therapies specifically acting to block renal cyst growth
Add-On Cyclic Angiotensin-(1-7) with Cyclophosphamide Arrests Progressive Kidney Disease in Rats with ANCA Associated Glomerulonephritis
No full textRapidly progressive crescentic glomerulonephritis associated with anti-neutrophil cytoplasmic antibodies (ANCA-GN) is a major cause of renal failure. Current immunosuppressive therapies are associated with severe side effects, intensifying the need for new therapeutic strategies. The activation of Mas receptor/Angiotensin-(1-7) axis exerted renoprotection in chronic kidney disease. Here, we investigated the effect of adding the lanthionine-stabilized cyclic form of angiotensin-1-7 [cAng-(1-7)] to cyclophosphamide in a rat model of ANCA-GN. At the onset of proteinuria, Wistar Kyoto rats with ANCA-GN received vehicle or a single bolus of cyclophosphamide, with or without daily cAng-(1-7). Treatment with cAng-(1-7) plus cyclophosphamide reduced proteinuria by 85% vs. vehicle, and by 60% vs. cyclophosphamide, and dramatically limited glomerular crescents to less than 10%. The addition of cAng-(1-7) to cyclophosphamide protected against glomerular inflammation and endothelial rarefaction and restored the normal distribution of parietal epithelial cells. Ultrastructural analysis revealed a preserved GBM, glomerular endothelium and podocyte structure, demonstrating that combination therapy provided an additional layer of renoprotection. This study demonstrates that adding cAng-(1-7) to a partially effective dose of cyclophosphamide arrests the progression of renal disease in rats with ANCA-GN, suggesting that cAng-(1-7) could be a novel clinical approach for sparing immunosuppressants
Author response to: Comment on: Effect of centre volume on pathological outcomes and postoperative complications after surgery for colorectal cancer: results of a multicentre national study
No full textPostoperative complications; Surgery for colorectal cancerComplicaciones posoperatorias; Cirugía para el cáncer colorrectalComplicacions postoperatòries; Cirurgia per al càncer colorecta
Dataset related to: Sirtuin 3 Deficiency Aggravates Kidney Disease in Response to High-Fat Diet through Lipotoxicity-Induced Mitochondrial Damage
No full textThe files contain all the dataset included in the manuscript divided by figures.
Abstract: Sirtuin 3 (SIRT3) is the primary mitochondrial deacetylase that controls the antioxidant
pathway and energy metabolism. We previously found that renal Sirt3 expression and activity were
reduced in mice with type 2 diabetic nephropathy associated with oxidative stress and mitochondrial
abnormalities and that a specific SIRT3 activator improved renal damage. SIRT3 is modulated by
diet, and to assess whether Sirt3 deficiency aggravates mitochondrial damage and accelerates kidney
disease in response to nutrient overloads, wild-type (WT) and Sirt3-/- mice were fed a high-fat-diet
(HFD) or standard diet for 8 months. Sirt3-/- mice on HFD exhibited earlier and more severe
albuminuria compared to WT mice, accompanied by podocyte dysfunction and glomerular capillary
rarefaction. Mesangial matrix expansion, tubular vacuolization and inflammation, associated with
enhanced lipid accumulation, were more evident in Sirt3-/- mice. After HFD, kidneys from Sirt3-/-
mice showed more oxidative stress than WT mice, mitochondria ultrastructural damage in tubular
cells, and a reduction in mitochondrial mass and energy production. Our data demonstrate that Sirt3
deficiency renders mice more prone to developing oxidative stress and mitochondrial abnormalities
in response to HFD, resulting in more severe kidney diseases, and this suggests that mitochondria
protection may be a method to prevent HFD-induced renal injury.The study was partially supported by Fondazione Cariplo
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