La valutazione dei finanziamenti pubblici per le politiche strutturali

Il regolamento 1083/2006 del consiglio della UE, che definisce le regole fondamentali per i fondi strutturali europei per il periodo di programmazione 2007-2013, ha stabilito l’obbligo dei paesi beneficiari di determinare il contributo richiesto all’UE come cofinanziamento non rimborsabile per la costruzione di infrastrutture, tenendo conto delle entrate attese dai pagamenti da parte degli utenti dei servizi erogati dalle infrastrutture stesse. Il principio, di semplice applicazione per gli aspetti di pianificazione finanziaria che ne sono alla base, comporta non poche difficoltà nella pratica della programmazione e della progettazione, e potrebbe generare significative conseguenze sulla attuazione dei programmi operativi dei fondi strutturali, specie nelle regioni dell’obiettivo convergenza. In questo contributo ci si propone di analizzare gli aspetti metodologici rilevanti nelle diverse fasi del ciclo di progetto, di analizzare lo stato di attuazione di questa regola soprattutto nelle regioni italiane dell’obiettivo convergenza , ed infine di discutere alcuni aspetti critici. La programmazione 2007-2013 dei fondi strutturali sta entrando nella fase centrale dell’attuazione, ed al livello nazionale ed europeo si osserva un dibattito vivace sulla efficienza ed efficacia della politica di coesione e sulle opzioni per continuare questo intervento oltre il 2013 (EC DG regional development. Fifth report on Europe’s future 2011), specie nei paesi vecchi membri della Unione, dove i risultati di oltre un ventennio di intervento sono sottoposti a numerose critiche in termini di efficacia e di efficienza della gestione. La modulazione del cofinanziamento Europeo in funzione della sostenibilità finanziaria degli investimenti per lo sviluppo, che attua i principi fondamentali della politica di coesione, trova nelle infrastrutture generatrici di entrate un caso particolarmente interessante. In Italia, un’efficace e piena attuazione di questo principio potrebbe dare un utile contributo al successo della politica di coesione europea

Endogenous annexin A1 counter-regulates bleomycin-induced lung fibrosis

PMCID: PMC3212807This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Resolution of inflammation: an integrated view

O.S. is supported by the NWO (VIDI project 91712303), theDFG (SO876/3-1, SO876/6-1, FOR809, SFB914 TPB08), theGerman-Israeli Foundation, and the Else Kro¨ner FreseniusStiftung. M.P. is supported by the Wellcome Trust (program086867/Z/08), the Arthritis Research UK, the British HeartFoundation (PG/09/060 and PG/11/48/28981) and the MedicalResearch Council

Chemerin15 inhibits neutrophil-mediated vascular inflammation and myocardial ischemia-reperfusion injury through ChemR23

Neutrophil activation and adhesion must be tightly controlled to prevent complications associated with excessive inflammatory responses. The role of the anti-inflammatory peptide chemerin15 (C15) and the receptor ChemR23 in neutrophil physiology is unknown. Here, we report that ChemR23 is expressed in neutrophil granules and rapidly upregulated upon neutrophil activation. C15 inhibits integrin activation and clustering, reducing neutrophil adhesion and chemotaxis in vitro. In the inflamed microvasculature, C15 rapidly modulates neutrophil physiology inducing adherent cell detachment from the inflamed endothelium, while reducing neutrophil recruitment and heart damage in a murine myocardial infarction model. These effects are mediated through ChemR23. We identify the C15/ChemR23 pathway as a new regulator and thus therapeutic target in neutrophil-driven pathologies

A novel mutation in SACS gene in a family from southern Italy

A form of autosomal recessive spastic ataxia (ARSACS) has been described in the Charlevoix and Saguenay regions of Quebec. So far a frameshift and a nonsense mutation have been identified in the SACS gene. The authors report a new mutation (1859insC), leading to a frameshift with a premature termination of the gene product sacsin, in two sisters from consanguineous parents. The phenotype is similar to previously described patients with ARSACS

Biphasic Modulation of NOS Expression, Protein and Nitrite Products by Hydroxocobalamin Underlies Its Protective Effect in Endotoxemic Shock: Downstream Regulation of COX-2, IL-1 beta, TNF-alpha, IL-6, and HMGB1 Expression

Background. NOS/•NO inhibitors are potential therapeutics for sepsis, yet they increase clinical mortality. However, there has been no in vivo investigation of the (in vitro) •NO scavenger, cobalamin’s (Cbl) endogenous effects on NOS/•NO/inflammatory mediators during the immune response to sepsis. Methods. We used quantitative polymerase chain reaction (qPCR), ELISA, Western blot, and NOS Griess assays, in a C57BL/6 mouse, acute endotoxaemia model. Results. During the immune response, pro-inflammatory phase, parenteral hydroxocobalamin (HOCbl) treatment partially inhibits hepatic, but not lung, iNOS mRNA and promotes lung eNOS mRNA, but attenuates the LPS hepatic rise in eNOS mRNA, whilst paradoxically promoting high iNOS/eNOS protein translation, but relatively moderate •NO production. HOCbl/NOS/•NO regulation is reciprocally associated with lower 4 h expression of TNF-α, IL-1β, COX-2, and lower circulating TNF-α, but not IL-6. In resolution, 24 h after LPS, HOCbl completely abrogates a major late mediator of sepsis mortality, high mobility group box 1 (HMGB1) mRNA, inhibits iNOS mRNA, and attenuates LPS-induced hepatic inhibition of eNOS mRNA, whilst showing increased, but still moderate, NOS activity, relative to LPS only. experiments (LPS+D-Galactosamine) HOCbl afforded significant, dose-dependent protection in mice Conclusions. HOCbl produces a complex, time- and organ-dependent, selective regulation of NOS/•NO during endotoxaemia, corollary regulation of downstream inflammatory mediators, and increased survival. This merits clinical evaluation

Una mirada de lo educativo a partir de los discursos y prácticas pedagógicas sobre la condición humana en su unidad y diversidad : (o de esperanzas a partir de pedagogías que privilegian la narratividad)

Las incertidumbres y turbaciones vivenciadas a lo largo del siglo XX en torno a la condición humana, aparecen hoy en un renacer que nos deja nuevamente perplejos, preocupados: fundamentalismos raciales y religiosos, ideologías con una base ético-política que se levantan prohibiendo, persiguiendo; las ideas de Nietzsche sobre el "eterno retorno" se instalan en discursos y prácticas sociales; urge pensar modos de abordaje que nos provoquen un pensar crítico que opere sobre las realidades; que vaya más allá de meros análisis: al respecto dice Ricoeur pasar de una hermenéutica del texto a una de la acción. Las perspectivas sobre la educación que emergen a finales del siglo XX responden a demandas epistémicas que cuestionan algunos lugares del saber pedagógico dando espacio a la incertidumbre, y a la posibilidad de repensar cuestiones pasadas a la vera de reflexiones vigentes. La crítica de la modernidad, la consagración y el anuncio del fin de la posmodernidad, el surgimiento de renovadas propuestas humanistas, han conmovido el campo pedagógico con planteos provenientes de las ciencias sociales y humanas que irrumpen en un pensamiento crítico que se interroga acerca de la condición humana, la unidad y la diversidad, la esperanza de una educación encaminada hacia la utopía de un futuro mejor.Fil: Catalini, Sandra Cecilia. Universidad Nacional de San Luis.Fil: Perretti Matera, Carina. Universidad Nacional de San Luis.Fil: Gómez, Sergio Raúl. Universidad Nacional de San Luis

Resource partitioning revisited: evidence from Italian television broadcasting

The theory of resource partitioning proposes that competition among generalists in the center of a market can trigger a process of resource release that engenders a proliferation of specialist producers outside the center. Previous research has generally examined the relationship between this proliferation and market concentration—a correlate of competitive intensity in the center of the market. In this paper, we extend the theory by arguing that resource release also occurs as the degree of competitive overlap among producers in the center intensifies, even when concentration or other structural features do not vary; we expand its implications by demonstrating that increased competitive overlap in the market center can enhance the viability of producers positioned near the center more than those in the periphery; and we enrich and complete it by specifying the additional assumptions needed to extend the theory of resource partitioning to entry processes. Consistent with our expectations, an empirical examination of the Italian broadcast television industry, from 1992 to 2003, finds that the failure rates of both near-center and peripheral stations decline with greater competitive overlap in the programming of the national broadcasters, with the failure rates of the near-center stations falling more than those of peripheral stations. Greater competitive overlap similarly stimulates the entry of near-center stations more than peripheral one

Definition of a Novel Pathway Centered on Lysophosphatidic Acid To Recruit Monocytes during the Resolution Phase of Tissue Inflammation.

Blood-derived monocytes remove apoptotic cells and terminate inflammation in settings as diverse as atherosclerosis and Alzheimer's disease. They express high levels of the proresolving receptor ALX/FPR2, which is activated by the protein annexin A1 (ANXA1), found in high abundance in inflammatory exudates. Using primary human blood monocytes from healthy donors, we identified ANXA1 as a potent CD14+CD16- monocyte chemoattractant, acting via ALX/FPR2. Downstream signaling pathway analysis revealed the p38 MAPK-mediated activation of a calcium independent phospholipase A2 with resultant synthesis of lysophosphatidic acid (LPA) driving chemotaxis through LPA receptor 2 and actin cytoskeletal mobilization. In vivo experiments confirmed ANXA1 as an independent phospholipase A2-dependent monocyte recruiter; congruently, monocyte recruitment was significantly impaired during ongoing zymosan-induced inflammation in AnxA1-/- or alx/fpr2/3-/- mice. Using a dorsal air-pouch model, passive transfer of apoptotic neutrophils between AnxA1-/- and wild-type mice identified effete neutrophils as the primary source of soluble ANXA1 in inflammatory resolution. Together, these data elucidate a novel proresolving network centered on ANXA1 and LPA generation and identify previously unappreciated determinants of ANXA1 and ALX/FPR2 signaling in monocytes