81 research outputs found
Trento Longaretti collezionista. Piccola curiosa raccolta di un pittore
No full textQuesta pubblicazione documenta la collezione artistica di Trento Longaretti, già direttore dell’Accademia Carrara di Bergamo. Pittore a sua volta, Longaretti ha riunito, nel corso della vita, una serie di dipinti, disegni, incisioni e sculture di altri artisti, che costituiscono un’interessante testimonianza del gusto di un artista.
Il catalogo delle opere - databili tra la fine del XV secolo e il XX secolo - è suddiviso in pittura, grafica e scultura ed è preceduto da un saggio di Giovanni Valagussa.
Tra gli artisti presenti nella collezione, spiccano i nomi di Pellizza da Volpedo, Tullio Garbari, Piero Marussig, Ennio Morlotti, Mario Sironi e Gianfranco Ferroni
Il magmatismo dell'avampaese Ibleo (Sicilia orientale) tra il Trias e il Quaternario: dati di sottosuolo dal Pleistocene al Miocene medio
No full textEvoluzione del magmatismo nel sottosuolo della Sicilia sud-orientale: dati sul chimismo dei clinopirosseni
No full textSirtuin3 Dysfunction Is the Key Determinant of Skeletal Muscle Insulin Resistance by Angiotensin II.
No full textAngiotensin II promotes insulin resistance. The mechanism underlying this abnormality, however, is still poorly defined. In a different setting, skeletal muscle metabolism and insulin signaling are regulated by Sirtuin3.Here, we investigate whether angiotensin II-induced insulin resistance in skeletal muscle is associated with Sirtuin3 dysregulation and whether pharmacological manipulation of Sirtuin3 confers protection.Parental and GLUT4-myc L6 rat skeletal muscle cells exposed to angiotensin II are used as in vitro models of insulin resistance. GLUT4 translocation, glucose uptake, intracellular molecular signals such as mitochondrial reactive oxygen species, Sirtuin3 protein expression and activity, along with its downstream targets and upstream regulators, are analyzed both in the absence and presence of acetyl-L-carnitine. The role of Sirtuin3 in GLUT4 translocation and intracellular molecular signaling is also studied in Sirtuin3-silenced as well as over-expressing cells.Angiotensin II promotes insulin resistance in skeletal muscle cells via mitochondrial oxidative stress, resulting in a two-fold increase in superoxide generation. In this context, reactive oxygen species open the mitochondrial permeability transition pore and significantly lower Sirtuin3 levels and activity impairing the cell antioxidant defense. Angiotensin II-induced Sirtuin3 dysfunction leads to the impairment of AMP-activated protein kinase/nicotinamide phosphoribosyltransferase signaling. Acetyl-L-carnitine, by lowering angiotensin II-induced mitochondrial superoxide formation, prevents Sirtuin3 dysfunction. This phenomenon implies the restoration of manganese superoxide dismutase antioxidant activity and AMP-activated protein kinase activation. Acetyl-L-carnitine protection is abrogated by specific Sirtuin3 siRNA.Our data demonstrate that angiotensin II-induced insulin resistance fosters mitochondrial superoxide generation, in turn leading to Sirtuin3 dysfunction. The present results also highlight Sirtuin3 as a therapeutic target for the insulin-sensitizing effects of acetyl-L-carnitine
Sirtuin 3-dependent mitochondrial dynamic improvements protect against acute kidney injury
No full textAcute kidney injury (AKI) is a public health concern with an annual mortality rate that exceeds those of breast and prostate cancer, heart failure, and diabetes combined. Oxidative stress and mitochondrial damage are drivers of AKI-associated pathology; however, the pathways that mediate these events are poorly defined. Here, using a murine cisplatin-induced AKI model, we determined that both oxidative stress and mitochondrial damage are associated with reduced levels of renal sirtuin 3 (SIRT3). Treatment with the AMPK agonist AICAR or the antioxidant agent acetyl-l-carnitine (ALCAR) restored SIRT3 expression and activity, improved renal function, and decreased tubular injury in WT animals, but had no effect in Sirt3-/- mice. Moreover, Sirt3-deficient mice given cisplatin experienced more severe AKI than WT animals and died, and neither AICAR nor ALCAR treatment prevented death in Sirt3-/- AKI mice. In cultured human tubular cells, cisplatin reduced SIRT3, resulting in mitochondrial fragmentation, while restoration of SIRT3 with AICAR and ALCAR improved cisplatin-induced mitochondrial dysfunction. Together, our results indicate that SIRT3 is protective against AKI and suggest that enhancing SIRT3 to improve mitochondrial dynamics has potential as a strategy for improving outcomes of renal injury
Ketogenic diet in Lafora disease: a long term follow-up pilot study
No full textPURPOSE: Lafora body disease (LBD) is severe and rapidly worsening progressive myoclonus epilepsy (PME), not treatable with specific therapy. In LBD patients, typical polyglucosan accumulations result from alterations of proteins involved in the regulation of glycogen metabolism. Thus, a ketogenic regimen might reasonably be expected to counteract the disease progression. We set out to assess the feasibility and tolerability of a long-term ketogenic diet (KD) in LBD patients and to make a preliminary evaluation of its effect on the disease course. METHODS: We treated five LBD patients with KD and evaluated the changes in the clinical, neuropsychological and neurophysiological findings over 10-30 months. RESULTS: The KD was well tolerated in all the patients for the first 16 months. Nutritional measures and laboratory findings remained substantially stable. The disease progressed in all the patients, reaching an advanced stage in one. Electrophysiological findings indicated the presence of increased cortical excitability in four patients, paralleling the worsening of the myoclonus.
CONCLUSION: KD was unable to stop the disease progression. However, given the considerable heterogeneity of the natural history of LBD, we cannot exclude the possibility that KD has the potential to slow down the disease progression. The application of this nutritional approach should be further evaluated in larger case series
Liver metastases: sulphur hexafluoride-enhanced ultrasonography for lesion detection: a systematic review.
No full textThis is a systematic review to evaluate the accuracy of contrast-enhanced ultrasonography (CEUS) performed with "SonoVue" (sulphur hexafluoride) in the detection of hepatic metastases. The MEDLINE, EMBASE and COCHRANE Databases were searched, regardless of language, for relevant articles published before December 2009. Two reviewers independently assessed study eligibility using a standardized form and methodological quality using the quality assessment of diagnostic accuracy studies (QUADAS) Checklist. Sensitivity estimates were calculated on a per-patient and/or per-lesion basis. The search for published articles yielded 718 potentially relevant abstracts. Of these, 14 papers were eligible but only three articles fulfilled the inclusion criteria, which comprised a total of 450 patients (patient sample number: range 12 to 365; cancer prevalence: 14.8 to 71.2%). Estimated per-patient sensitivity ranged from 79-100%. Although the quality assessment of diagnostic accuracy studies checklist showed the papers were of good quality, a meta-analysis was not applicable because of the lack of eligible studies. In conclusion, CEUS seems to be promising in the detection of liver metastases; however, there have not been enough studies to conduct meta-analysis. Further studies are required before this promising method can be widely used
Transfer of growth factor receptor mRNA via exosomes unravels the regenerative effect of mesenchymal stem cells
No full textBone marrow-mesenchymal stem cells (BM-MSC) ameliorate renal dysfunction and repair tubular damage of acute kidney injury by locally releasing growth factors, including the insulin-like growth factor-1 (IGF-1). The restricted homing of BM-MSC at the site of injury led us to investigate a possible gene-based communication mechanism between BM-MSC and tubular cells. Human BM-MSC (hBM-MSC) released microparticles and exosomes (Exo) enriched in mRNAs. A selected pattern of transcripts was detected in Exo versus parental cells. Exo expressed the IGF-1 receptor (IGF-1R), but not IGF-1 mRNA, while hBM-MSC contained both mRNAs. R- cells lacking IGF-1R exposed to hBM-MSC-derived Exo acquired the human IGF-1R transcript that was translated in the corresponding protein. Transfer of IGF-1R mRNA from Exo to cisplatin-damaged proximal tubular cells (proximal tubular epithelial cell [PTEC]) increased PTEC proliferation. Coincubation of damaged PTEC with Exo and soluble IGF-1 further enhanced cell proliferation. These findings suggest that horizontal transfer of the mRNA for IGF-1R to tubular cells through Exo potentiates tubular cell sensitivity to locally produced IGF-1 providing a new mechanism underlying the powerful renoprotection of few BM-MSC observed in vivo. © 2013, Mary Ann Liebert, Inc
Impaired oxygen extraction in metabolic myopathies: detection and quantification by near-infrared spectroscopy
No full textAdeno-associated virus-mediated CTLA4Ig gene transfer protects MHC-mismatched renal allografts from chronic rejection
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