Gli studi medievistici di Cornelio Desimoni, un 'pioniere' della storia del territorio

ITALIANO: L’articolo consiste in una rassegna critica dell’opera di Cornelio Desimoni, storico molto versatile, dedicata fra il 1859 e il 1896 al periodo medievale. Accanto a commenti puntuali e all’esegesi di singoli documenti, a recensioni di testi di vario argomento, alla compilazione dei ponderosi annali della propria cittadina natale (Gavi), Desimoni ha affrontato ripetutamente un tema importante di storia politico-territoriale, in cui hanno pesato le sue competenze nel campo del diritto, con risultati molto maturi per l’epoca: le marche e i loro sviluppi nell’Italia a partire dal secolo IX. / ENGLISH: This article is a critical survey of the work that Cornelio Desimoni, a very versatile historian, dedicated to the middle ages during the period between 1859 and 1896. Apart from proffering precise comments, analyses of single documents, reviews of texts on various subjects and compiling the ponderous annals of his birth town (Gavi), Desimoni repeatedly tackled an important theme in political-territorial history: the marches and their development in Italy as from the 9th century. This latter accomplishment, which produced mature results for the time, was favoured by his competence in jurisprudence

Inhibition of in-stent stenosis by oral administration of bindarit in porcine coronary arteries

<p><b>Objective:</b> We have previously demonstrated that bindarit, a selective inhibitor of monocyte chemotactic proteins (MCPs), is effective in reducing neointimal formation in rodent models of vascular injury by reducing smooth muscle cell proliferation and migration and neointimal macrophage content, effects associated with the inhibition of MCP-1/CCL2 production. The aim of the current study was to evaluate the efficacy of bindarit on in-stent stenosis in the preclinical porcine coronary stent model.</p> <p><b>Methods and Results:</b> One or 2 bare metal stents (Multi-Link Vision, 3.5 mm) were deployed (1:1.2 oversize ratio) in the coronary arteries of 42 pigs (20 bindarit versus 22 controls). Bindarit (50 mg/kg per day) was administered orally from 2 days before stenting until the time of euthanasia at 7 and 28 days. Bindarit caused a significant reduction in neointimal area (39.4%, P<0.001, n=9 group), neointimal thickness (51%, P<0.001), stenosis area (37%, P<0.001), and inflammatory score (40%, P<0.001) compared with control animals, whereas there was no significant difference in the injury score between the 2 groups. Moreover, treatment with bindarit significantly reduced the number of proliferating cells (by 45%, P<0.05; n=6 group) and monocyte/macrophage content (by 55%, P<0.01; n=5–6 group) in stented arteries at day 7 and 28, respectively. These effects were associated with a significant (P<0.05) reduction of MCP-1 plasma levels at day 28. In vitro data showed that bindarit (10–300 micromol/L) reduced tumor necrosis factor-alpha (50 ng/mL)–induced pig coronary artery smooth muscle cell proliferation and inhibited MCP-1 production.</p> <p><b>Conclusion:</b> Our results show the efficacy of bindarit in the prevention of porcine in-stent stenosis and support further investigation for clinical application of this compound.</p&gt

Estrategias de recuperación : comida chatarra : un patrón alimentario que atenta contra la salud

Fil: Macri, Elisa Vanesa. Universidad de Buenos Aires. Facultad de Medicina; Argentina.Fil: Guglielmotti, María Beatriz. Universidad de Buenos Aires. Facultad de Odoontología; Argentina.Fil: Friedman, Silvia María. Universidad de Buenos Aires. Facultad de Odontología; Argentina.La "comida basura" define un patrón alimentario que,\nunido a un estilo de vida sedentaria y a la exposición a\nsustancias nocivas, impacta en los procesos bioquímicos que,\ncontrolados genéticamente, predisponen a enfermedades\ncrónicas y al aumento de la morbimortalidad. Incluye aquellos\nalimentos industriales, no saludables, nutricionalmente\ndesequilibrados, con un alto contenido de azúcares,\ngrasas y/o sal y baja en cantidad de fibra, minerales y\nvitaminas

Influencia de componentes dietarios en el téjido óseo : sonrisas sanas

Fil: Gorustovich, Alejandro A. Universidad de Buenos Aires. Facultad de Odonotología; ArgentinaFil: Steimetz, Tammy. Universidad de Buenos Aires. Facultad de Odontología; ArgentinaFil: Nielsen, Forrest H. Universidad de Buenos Aires. Facultad de Odontología; ArgentinaFil: Guglielmotti, María Beatriz. Universidad de Buenos Aires.Facultad de Odontología; ArgentinaDada la importancia nutricional de ciertos elementos minerales, como por ejemplo\nfósforo, sodio, potasio, magnesio, cobre, zinc, silicio y boro, sobre la formación y\nmantenimiento de los tejidos cartilaginoso y óseo, investigadores de la UBA, juntamente\ncon el Departamento de Agricultura de los Estados Unidos de Norteamérica (USDA), han\nestudiado el efecto de la deficiencia nutricional de boro sobre la reparación, modelado y\nremodelado del tejido óseo

The Chemokine CCL2 Mediates the Seizure-enhancing Effects of Systemic Inflammation

Epilepsy is a chronic disorder characterized by spontaneous recurrent seizures. Brain inflammation is increasingly recognized as a critical factor for seizure precipitation, but the molecular mediators of such proconvulsant effects are only partly understood. The chemokine CCL2 is one of the most elevated inflammatory mediators in patients with pharmacoresistent epilepsy, but its contribution to seizure generation remains unexplored. Here, we show, for the first time, a crucial role for CCL2 and its receptor CCR2 in seizure control. We imposed a systemic inflammatory challenge via lipopolysaccharide (LPS) administration in mice with mesial temporal lobe epilepsy. We found that LPS dramatically increased seizure frequency and upregulated the expression of many inflammatory proteins, including CCL2. To test the proconvulsant role of CCL2, we administered systemically either a CCL2 transcription inhibitor (bindarit) or a selective antagonist of the CCR2 receptor (RS102895). We found that interference with CCL2 signaling potently suppressed LPS-induced seizures. Intracerebral administration of anti-CCL2 antibodies also abrogated LPS-mediated seizure enhancement in chronically epileptic animals. Our results reveal that CCL2 is a key mediator in the molecular pathways that link peripheral inflammation with neuronal hyperexcitability

Bindarit inhibits human coronary artery smooth muscle cell proliferation, migration and phenotypic switching

Bindarit, a selective inhibitor of monocyte chemotactic proteins (MCPs) synthesis, reduces neointimal formation in animal models of vascular injury and recently has been shown to inhibit in-stent late loss in a placebo-controlled phase II clinical trial. However, the mechanisms underlying the efficacy of bindarit in controlling neointimal formation/restenosis have not been fully elucidated. Therefore, we investigated the effect of bindarit on human coronary smooth muscle cells activation, drawing attention to the phenotypic modulation process, focusing on contractile proteins expression as well as proliferation and migration. The expression of contractile proteins was evaluated by western blot analysis on cultured human coronary smooth muscle cells stimulated with TNF-α (30 ng/mL) or fetal bovine serum (5%). Bindarit (100-300 µM) reduced the embryonic form of smooth muscle myosin heavy chain while increased smooth muscle α-actin and calponin in both TNF-α- and fetal bovine serum-stimulated cells. These effects were associated with the inhibition of human coronary smooth muscle cell proliferation/migration and both MCP-1 and MCP-3 production. The effect of bindarit on smooth muscle cells phenotypic switching was confirmed in vivo in the rat balloon angioplasty model. Bindarit (200 mg/Kg/day) significantly reduced the expression of the embryonic form of smooth muscle myosin heavy chain, and increased smooth muscle α-actin and calponin in the rat carodid arteries subjected to endothelial denudation. Our results demonstrate that bindarit induces the differentiated state of human coronary smooth muscle cells, suggesting a novel underlying mechanisms by which this drug inhibits neointimal formation