La proposta progettuale di Andrea Palladio per il completamento della Basilica di San Petronio: ricostruzione della facciata esistente attraverso il rilievo fotogrammetrico e sua ultimazione tramite metodi digitali

Obiettivo di questo elaborato di tesi è l’analisi e la ricostruzione con metodi digitali di uno dei progetti che Andrea Palladio realizza attorno al 1572 per il completamento della facciata della Basilica di San Petronio a partire da un rilievo fotogrammetrico e da una restituzione dell’intero corpus dei disegni conservati al museo di San Petronio. Il lavoro si iscrive nella ormai lunga serie dei tentativi fatti per trasformare i piatti schemi del disegno in una forma tridimensionale costruibile, al pari di molti altri tra cui quelli di James Ackermann e Scott Schiamberg per il disegno conservato alla Worcester College Library ad Oxford. Il metodo con cui è stato portato avanti lo studio segue due strade principali.In una prima fase, la realizzazione del rilievo fotogrammetrico ha permesso di prendere conoscenza e consapevolezza della facciata odierna, permettendo di contestualizzare il progetto di Palladio. La fase successiva è stata invece riservata alla restituzione bidimensionale dei disegni ottenuta ricalcando l’originale, regolarizzando le parti più approssimate e completando quelle mancanti. Attraverso questo metodo tradizionale, affiancato dall’analisi e confronto con la produzione scritta palladiana, è stato possibile risolvere una prima serie di ambiguità acquisendo un risultato conforme alla semantica dell’architetto veneto. Ottenuti i disegni definitivi, è stato selezionato un progetto su cui approfondire l’analisi attraverso l’applicazione di tecniche di modellazione 3D. Il disegno, inventariato con il numero 64 (sezione D-D), è caratterizzato dal mantenimento quasi integrale della fascia inferiore della facciata, già realizzata al tempo del progetto. Il processo di digitalizzazione ha permesso di dare interpretazione in tre dimensioni al pensiero palladiano, risolvendo le criticità scaturite con l’aggiunta della terza grandezza. Nella fase finale sono state sfruttate le potenzialità del rendering per calarlo più concretamente nella realtà odierna

Sulfonates-PMMA nanoparticles conjugates: A versatile system for multimodal application

a b s t r a c t We report herein the viability of a novel nanoparticles (NPs) conjugated system, namely the attachment, based on ionic and hydrophobic interactions, of different sulfonated organic salts to positively charged poly(methylmethacrylate) (PMMA)-based core-shell nanoparticles (EA0) having an high density of ammonium groups on their shells. In this context three different applications of the sulfonates@EA0 systems have been described. In detail, their ability as cytotoxic drugs and pro-drugs carriers was evaluated in vitro on NCI-H460 cell line and in vivo against human ovarian carcinoma IGROV-1 cells. Besides, 8-hydroxypyrene-1,3,6-trisulfonic acid, trisodium salt (HPTS) was chosen for NPs loading, and its internalization as bioimaging probe was evaluated on Hep G2 cells. Overall, the available data support the interest for these PMMA NPs@sulfonates systems as a promising formulation for theranostic applications. In vivo biological data strongly support the potential value of these core-shell NPs as delivery system for negatively charged drugs or biologically active molecules. Additionally, we have demonstrated the ability of these PMMA core-shell nanoparticles to act as efficient carriers of fluorophores. In principle, thanks to the high PMMA NPs external charge density, sequential and very easy post-loading of different sulfonates is achievable, thus allowing the preparation of nanocarriers either with bi-modal drug delivery behaviour or as theranostic systems

Inflammatory hepatocellular adenomatosis, metabolic syndrome, polycystic ovary syndrome and non-alcoholic steatohepatitis: Chance tetrad or association by necessity?

case repor

Clinical features and natural history of cryptogenic cirrhosis compared to hepatitis C virus-related cirrhosis

AIM To characterize natural history of cryptogenic cirrhosis (CC) and compare its clinical features and outcomes to those of hepatitis C virus (HCV)-related cirrhosis. METHODS A prospective cohort of 102 consecutive patients at their first diagnosis of CC were enrolled in this study. The clinical data and outcomes were compared to an age-and Child-Pugh class-matched cohort of 110 patients with HCV-related cirrhosis. Diagnosis of cirrhosis was based on compatible clinical and laboratory parameters, ultrasound/endoscopic parameters and, whenever possible, on histological grounds and transient elastography. All cases of cirrhosis without a definite etiology were enrolled in the CC group. The parameters assessed were: (1) severity of liver disease at the time of first diagnosis; (2) liver decompensation during follow-up; (3) hepatocellular carcinoma (HCC); (4) orthotopic liver transplantation; and (5) death. The independent associated factors were evaluated by multiple logistic regression analysis, and survival and its determinants by the Kaplan-Meier model, log-rank test and Cox regression. RESULTS At the first observation, median age was 66 and 65 years and male gender was 36% and 58% for CC and HCV cirrhosis, respectively. CC showed Child-Pugh class A/B/C of 47%/31%/22%, respectively. Compared to HCV cirrhosis, CC exhibited a significantly higher prevalence of metabolic syndrome (12% vs 54%, respectively), overweight/obesity, high BMI, impaired glucose tolerance, high blood pressure, dyslipidemia, hyperuricemia, cardiovascular diseases, extrahepatic cancer, and gallstones. Over a median period of 42 mo of follow-up, liver decompensation, HCC development and death for CC and HCV-related cirrhosis were 60.8%, and 54.4%, 16.7% and 17.2%, 39.2% and 30%, respectively. The median survival was 60 mo for CC. Independent predictors of death were age and Child-Pugh class at diagnosis. CC showed an approximately twofold higher incidence of HCC in Child-Pugh class A. CONCLUSION Undiagnosed nonalcoholic fatty liver disease has an etiologic role in CC that is associated with a poor prognosis, early HCC development, high risk of cardiovascular disease and extrahepatic cancer

Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPAR. activation in high fructose diet-induced metabolic syndrome

Background: The AGE-RAGE-oxidative stress (AROS) axis is involved in the onset and progression of metabolic syndrome induced by a high-fructose diet (HFD). PPAR\u3b3 activation is known to modulate metabolic syndrome; however a systems-level investigation looking at the protective effects of PPAR\u3b3 activation as related to the AROS axis has not been performed. The aim of this work is to simultaneously characterize multiple molecular parameters within the AROS axis, using samples taken from different body fluids and tissues of a rat model of HFD-induced metabolic syndrome, in the presence or absence of a PPAR\u3b3 agonist, Rosiglitazone (RGZ). Methods: Rats were fed with 60% HFD for the first half of the treatment duration (21 days) then continued with either HFD alone or HFD plus RGZ for the second half. Results: Rats receiving HFD alone showed metabolic syndrome manifestations including hypertension, dyslipidemia, increased glucose levels and insulin resistance, as well as abnormal kidney and inflammatory parameters. Systolic blood pressure, plasma triglyceride and glucose levels, plasma creatinine, and albuminuria were significantly improved in the presence of RGZ. The following molecular parameters of the AROS axis were significantly upregulated in our rat model: carboxymethyl lysine (CML) in urine and liver; carboxyethyl lysine (CEL) in urine; advanced glycation end products (AGEs) in plasma; receptor for advanced glycation end products (RAGE) in liver and kidney; advanced oxidation protein products (AOPP) in plasma; and 4-hydroxynonenal (HNE) in plasma, liver, and kidney. Conversely, with RGZ administration, the upregulation of AOPP and AGEs in plasma, CML and CEL in urine, RAGE in liver as well as HNE in plasma and liver was significantly counteracted/prevented. Conclusions: Our data demonstrate (i) the systems-level regulatory landscape of HFD-induced metabolic syndrome involving multiple molecular parameters, including HNE, AGEs and their receptor RAGE, and (ii) attenuation of metabolic syndrome by PPAR\u3b3 modulation