La gestione delle risorse umane in Italia : bilancio di un decennio

Le ricerche internazionali pi\uf9 recenti sottolineano che, nella gestione delle risorse umane, le imprese si stanno spostando da modelli in cui le persone sono considerate un costo da minimizzare verso modelli caratterizzati da una gestione integrata nel business, all\u2019interno della quale le persone sono ritenute strategiche per il conseguimento di un vantaggio competitivo durevole per l\u2019impresa. Il presente contributo si basa su una survey condotta nel 2009 sulla Direzione delle Risorse Umane di 102 imprese operanti in Italia, utilizzando lo stesso strumento di raccolta dati utilizzato in una survey simile condotta nel 1999. Sulla base dei dati emergenti l\u2019articolo raggiunge due risultati: presenta un\u2019analisi longitudinale sulla gestione delle risorse umane in Italia, confrontando le evidenze del 1999 con quelle del 2009; ed analizza in che misura le politiche di gestione delle risorse umane dichiarate sono coerenti con le pratiche effettivamente implementate, anche qui offendo un raffronto a distanza di dieci anni

Human Resource Management: evoluzione o involuzione?

QUESTO ARTICOLO INDAGA IN CHE MISURA LE DIREZIONI DELLE RISORSE UMANE OPERANTI IN ITALIA ABBIANO FATTO PROPRI, NELLA PROSPETTIVA DELLO HUMAN RESOURCE MAN - AGEMENT, I MODELLI ORIENTATI ALLA VALORIZZAZIONE DELLE RISORSE UMANE O QUELLI CHE ENFATIZZANO LA COERENZA TRA GESTIONE DELLE RISORSE UMANE E STRATEGIE DELL\u2019ORGANIZZAZIONE. NELLA PRIMA SEZIONE SI ESPONGONO I PRESUPPOSTI TEORICI DELLA RICERCA; LA SECONDA SEZIONE PRESENTA GLI OBIETTIVI SPECIFICI DELLA RICERCA E LA METODOLOGIA USATA PER LA RACCOLTA E L\u2019ANALISI DEI DATI; I RISULTATI SONO ILLUSTRATI ALL\u2019INTERNO DELLA TERZA SEZIONE DEL DOCUMENTO. L\u2019ARTICOLO SI CHIUDE CON LA DISCUSSIONE DEI RISULTATI, IN CUI SI EVIDENZIANO ALCUNI ELEMENTI CRITICI CHE IL CONTESTO ITALIANO REGISTRA IN MERITO AL PASSAGGIO A UNA PROSPETTIVA DI HUMAN RESOURCE MANAGEMENT

Universit\ue0 e terza missione: il partenariato didattico per una knowledge city

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Gliadin as a stimulator of innate responses in celiac disease

In celiac disease (CD) we have the prototype of an immune mediated response dominated by the activation of the adaptive immune system and in particular of CD4+ HLA class II restricted T cells. Various seminal studies have established the precise mechanism of how antigen (prolamine) specific activation of CD4+ mucosal T cells occurs. Thus, CD is a condition in which T cells and their activation is the essential hinge in the pathogenic process. These functional studies have provided the explanation for the genetic association between CD and certain HLA alleles (HLA DQ2 and DQ8). These genetic, molecular and functional studies have permitted the clarification of a powerful Th1 dominated pro-inflammatory response that characterises the small intestine of active CD patients. Despite this unassailable set of information and reports there are some intriguing points that have been raised by a series of studies which have indicated that CD is not only defined by an aberrant prolamine-induced activation of the adaptive immune system. New evidence and re-assessments of old studies, point to a more complex pathogenic cascade, which may help to unravel some of the residual obscure points of CD pathogenesis. Here, we outline the current concepts that indicate a direct involvement of the adaptive immune system and we discuss all the evidence supporting a direct activation of the innate immune system by fragments of prolamines, which are not recognized T cell epitopes and how they could influence CD. The gliadin-induced activation of the ‘innate’ immune system might also have a significant role in the induction and persistence of many CD complications and most definitively for the most aggressive one, namely mucosal T cell lymphomas. We further suggest a novel way to harness the unwanted immune response to toxic prolamine, and thus indicate new potential therapeutic strategies to treat or at least control CD

INTERLEUKIN 15 MEDIATES EPITHELIAL CHANGES IN CELIAC DISEASE

Villous atrophy and crypt proliferation are key epithelial features of untreated celiac disease. We tried to define whether cytokines such as interleukin (IL)-15, IL-2, IL-4, and IL-7, which share chains of their receptors, could influence the epithelial modifications. Methods: Duodenal biopsy specimens (14 treated and 13 untreated celiac patients, 7 controls) were cultured in vitro for 24 hours with or without gliadin (1 mg/mL), IL-15, IL-7, IL-4, or IL-2 (10 ng/mL). Tumor necrosis factor (TNF)-α and interferon (IFN)-γ were also used in some specimens of untreated celiacs. Epithelial expression of Ki67, FAS, and transferrin receptor (TFR) was detected by immunohistochemistry, and apoptosis by TUNEL technique (percentage of positive enterocytes). IL-15–positive cells were detected by immunohistochemistry in celiac disease and control biopsy specimens; presence of IL-15 was also determined by semiquantitative polymerase chain reaction. Results: Only IL-15 induced enterocyte expression of Ki67, TFR, and FAS in treated celiac (P < 0.01 vs. medium) and enterocyte apoptosis in untreated celiac disease specimens. Anti–IL-15 monoclonal antibodies neutralized gliadin-induced enterocyte TFR and FAS expression in treated celiac and enterocyte apoptosis in untreated celiac disease specimens (P < 0.05 vs. gliadin). IL-15–positive cells were increased in untreated celiacs (P < 0.001 vs. treated celiacs and controls). Conclusions: IL-15 is involved in the modulation of epithelial changes in celiac disease, indicating that this cytokine has an unforeseen role in the pathologic manifestations of celiac diseas