La disuguaglianza «negata»: strategie di promozione e di difesa sociale nel Salento settecentesco

ItL'accentuarsi delle disuguaglianze socioeconomiche negli ultimi anni ha suggerito una verifica delle risposte che nel passato sono state adottate per scongiurare le asimmetrie allora molto più marcate. L'area salentina costituisce un laboratorio particolarmente interessante in questa direzione per le sperequazioni presenti al suo interno, per la radicata mentalità signorile che caratterizzava i ceti borghesi e per la rassegnazione che informava le strategie di difesa sociale dei ceti contadini. Anziché dar luogo ad atteggiamenti autonomi di riscatto e di comportamento relazionale sono emersi metodi e pratiche di integrazione piuttosto che di vera e conflittuale dialettica sociale.EnThe increase of socioeconomic inequalities in recent years has led us to investigate the solutions that had been taken in the past to prevent deeper asymmetries. In this context the Salento area is a particularly interesting case study because of the strong inequalities within this area, the rooted aristocratic mentality that characterized the middle classes, and the sense of resignation that informed the peasantry's strategies of social defense. Instead of autonomous attitudes of redemption and relational behavior, there emerged methods and practices inspired by forms of integration rather than by a genuine and conflictual social dialectic

Oxysterols in the pathogenesis of major chronic diseases.

Pathological accumulation of 27-carbon intermediates or end-products of cholesterol metabolism, named oxysterols, may contribute to the onset and especially to the development of major chronic diseases in which inflammation, but also oxidative damage and to a certain extent cell death, are hallmarks and primary mechanisms of progression. Indeed, certain oxysterols exercise strong pro-oxidant and pro-inflammatory effects at concentrations detectable in the lesions typical of atherosclerosis, neurodegenerative diseases, inflammatory bowel diseases, age-related macular degeneration, and other pathological conditions characterized by altered cholesterol uptake and/or metabolism

Lipid oxidation products in the pathogenesis of inflammation-related gut diseases

Background: A defective mucosal barrier function is the principal cause of the uncontrolled onset and progression of a number of human inflammatory gut diseases, most of which are characterized by chronic intermittent immune and inflammatory responses leading to structural intestinal damage, which can represent a potential risk for colorectal cancer development. During the active disease phase the production of pro-inflammatory cytokines and chemokines, and the induction of oxidative reactions by activated leukocytes and epithelial cells represent the main event in the intestinal inflammation. Objective: Oxidative stress plays a key role in the development of intestinal damage. Indeed reactive oxygen species and their oxidized by-products regulate redox-sensitive signaling pathways and transcription factors, which sustain inflammation within the intestinal layer. Methods: Polyunsaturated fatty acids and cholesterol are the principal targets of oxidative modifications. These lipids, which are cell membrane constituents or are present in food, readily undergo non-enzymatic oxidation to form chemically-reactive species that can induce a wide range of biological effects including inflammation, programmed cell death, and proliferation. Results and Conclusions: In this review we summarize the current knowledge on the role of lipid oxidation products in regulating redox pathways involved in the pathogenesis of inflammation- related gut diseases. In particular, lipid peroxidation end products, such as isoprostanes and aldehydes, and cholesterol oxidation-derived oxysterols are taken into consideration. Results and Conclusions: The control of oxidative damage and consequently tissue local over-production of lipid oxidation products by using specific antioxidant and anti-inflammatory molecules in the diet may have clinical and therapeutic benefits. </jats:sec

Sull'attuazione delle ordinanze possessorie non seguite dal giudizio di merito

Il contributo, muovendo da una pronuncia giurisprudenziale in forza della quale il procedimento possessorio non ha natura cautelare, in quanto esso è, si, regolato dalle disposizioni sul procedimento cautelare uniforme (669 bis e ss. c.p.c.), ma solo nei limiti della loro compatibilità con il procedimento possessorio, si snoda attraverso l'analisi della giurisprudenza formatasi in questa materia e si conclude con riflessioni personali al riguardo

Inflammatory bowel disease: mechanisms, redox considerations, and therapeutic targets.

Oxidative stress is thought to play a key role in the development of intestinal damage in inflammatory bowel disease (IBD), because of its primary involvement in intestinal cells' aberrant immune and inflammatory responses to dietary antigens and to the commensal bacteria. During the active disease phase, activated leukocytes generate not only a wide spectrum of pro-inflammatory cytokines, but also excess oxidative reactions, which markedly alter the redox equilibrium within the gut mucosa, and maintain inflammation by inducing redox-sensitive signaling pathways and transcription factors. Moreover, several inflammatory molecules generate further oxidation products, leading to a self-sustaining and auto-amplifying vicious circle, which eventually impairs the gut barrier. The current treatment of IBD consists of long-term conventional anti-inflammatory therapy and often leads to drug refractoriness or intolerance, limiting patients' quality of life. Immune modulators or anti-tumor necrosis factor α antibodies have recently been used, but all carry the risk of significant side effects and a poor treatment response. Recent developments in molecular medicine point to the possibility of treating the oxidative stress associated with IBD, by designing a proper supplementation of specific lipids to induce local production of anti-inflammatory derivatives, as well as by developing biological therapies that target selective molecules (i.e., nuclear factor-κB, NADPH oxidase, prohibitins, or inflammasomes) involved in redox signaling. The clinical significance of oxidative stress in IBD is now becoming clear, and may soon lead to important new therapeutic options to lessen intestinal damage in this disease. Antioxid. Redox Signal. 19, 1711–1747