PUBBLICAZIONI E REPORT DI RILIEVO
REPORTS IN EVIDENZA
La valutazione del grado di fragilità e del fabbisogno di assistenza continuativa degli ultrasessantaquattrenni nel Lazio
Dipartimento di Biomedicina e Prevenzione Università di Roma Tor Vergata - Collegio IPASVI
L’invecchiamento della popolazione porta con se il cambiamento della domanda di servizi, sottolineando la necessità di nuovi modelli di intervento sul territorio e di nuovi percorsi di accesso alle prestazioni assistenziali. L’attuale frammentazione delle prestazioni assistenziali in tanti servizi diretti a poche persone e spesso ad intensità limitata risente della mancanza di criteri chiari per l’accesso alle prestazioni e di modalità operative standardizzate ed omogenee. L’interesse crescente negli ultimi decenni intorno alla definizione della fragilità individuale fa di questo parametro una potenziale chiave di lettura della domanda di assistenza da coniugare ad un approccio proattivo al dimensionamento della domanda ed alla individuazione dei soggetti a rischio di esiti negativi quali il decesso, o l’istituzionalizzazione. Una precoce individuazione della fragilità attraverso strumenti di valutazione multidimensionale di rapido impiego utilizzati nel quadro di un’attività routinaria di screening,può permettere di reimpostare le politiche sociali regionali centrandole su un approccio preventivo... download testo completo
PUBBLICAZIONI IN EVIDENZA
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The research to fight myelodysplastic syndromesRome - 16 November 2020
Dear colleagues, It is a pleasure announce that Prof. Voso Maria Teresa et al. has published an innovative paper on the prestigious journal "Nature Medicine": "Implications of TP53 allelic state for genome stability, clinical presentation and outcomes in myelodysplastic syndromes" LINK. 
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P. Fenaux, U. Platzbecker, G.J. Mufti, G. Garcia‑Manero, R. Buckstein, V. Santini, M. Díez‑Campelo, C. Finelli, M. Cazzola, O. Ilhan, M.A. Sekeres, J.F. Falantes, B. Arrizabalaga, F. Salvi, V. Giai, P. Vyas, D. Bowen, D. Selleslag, A.E. DeZern, J.G. Jurcic, U. Germing, K.S. Götze, B. Quesnel, O. Beyne‑Rauzy, T. Cluzeau, M.-T. Voso, D. Mazure, E. Vellenga, P.L. Greenberg, E. Hellström‑Lindberg, A.M. Zeidan, L. Adès, A. Verma, M.R. Savona, A. Laadem, A. Benzohra, J. Zhang, A. Rampersad, D.R. Dunshee, P.G. Linde, M.L. Sherman, R.S. Komrokji, and A.F. List. "Luspatercept in Patients with Lower-Risk Myelodysplastic Syndromes". The New England Journal of Medicine. n engl j med 382;2
Orecchini E, Doria M, Antonioni A, Galardi S, Ciafrè SA, Frassinelli L, Mancone C, Montaldo C, Tripodi M, Michienzi A. ADAR1 restricts LINE-1 retrotransposition. Nucleic Acids Res. 2016 Sep 21. pii: gkw834
Abstract
Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosines to inosines in double-stranded RNAs. ADAR1 was demonstrated to be functional on different viruses exerting either antiviral or proviral effects. Concerning HIV-1, several studies showed that ADAR1 favors viral replication. The aim of this study was to investigate the composition of the ADAR1 ribonucleoprotein complex during HIV-1 expression. By using a dual-tag affinity purification procedure in cells expressing HIV-1 followed by mass spectrometry analysis, we identified 14 non-ribosomal ADAR1-interacting proteins, most of which are novel. A significant fraction of these proteins were previously demonstrated to be associated to the Long INterspersed Element 1 (LINE1 or L1) ribonucleoparticles and to regulate the life cycle of L1 retrotransposons that continuously re-enter host-genome.Hence, we investigated the function of ADAR1 in the regulation of L1 activity.By using different cell-culture based retrotransposition assays in HeLa cells, we demonstrated a novel function of ADAR1 as suppressor of L1 retrotransposition. Apparently, this inhibitory mechanism does not occur through ADAR1 editing activity. Furthermore, we showed that ADAR1 binds the basal L1 RNP complex. Overall, these data support the role of ADAR1 as regulator of L1 life cycle.
Fairchild, G et al. Mapping the structural organization of the brain in conduct disorder: replication of findings in two independent samples.Journal of Child Psychology and Psychiatry; 14/06/2016; doi:10.1111/jcpp.12581
Abstract
BACKGROUND:Neuroimaging methods that allow researchers to investigate structural covariance between brain regions are increasingly being used to study psychiatric disorders. Structural covariance analyses are particularly well suited for studying disorders with putative neurodevelopmental origins as they appear sensitive to changes in the synchronized maturation of different brain regions. We assessed interregional correlations in cortical thickness as a measure of structural covariance, and applied this method to investigate the coordinated development of different brain regions in conduct disorder (CD). We also assessed whether structural covariance measures could differentiate between the childhood-onset (CO-CD) and adolescence-onset (AO-CD) subtypes of CD, which may differ in terms of etiology and adult outcomes.
METHODS:We examined interregional correlations in cortical thickness in male youths with CO-CD or AO-CD relative to healthy controls (HCs) in two independent datasets. The age range in the Cambridge sample was 16-21 years (mean: 18.0), whereas the age range of the Southampton sample was 13-18 years (mean: 16.7). We used FreeSurfer to perform segmentations and applied structural covariance methods to the resulting parcellations.
RESULTS:In both samples, CO-CD participants displayed a strikingly higher number of significant cross-cortical correlations compared to HC or AO-CD participants, whereas AO-CD participants presented fewer significant correlations than HCs. Group differences in the strength of the interregional correlations were observed in both samples, and each set of results remained significant when controlling for IQ and comorbid attention-deficit/hyperactivity disorder symptoms.
CONCLUSIONS:This study provides new evidence for quantitative differences in structural brain organization between the CO-CD and AO-CD subtypes, and supports the hypothesis that both subtypes of CD have neurodevelopmental origins.
Abstract
BACKGROUND:Neuroimaging methods that allow researchers to investigate structural covariance between brain regions are increasingly being used to study psychiatric disorders. Structural covariance analyses are particularly well suited for studying disorders with putative neurodevelopmental origins as they appear sensitive to changes in the synchronized maturation of different brain regions. We assessed interregional correlations in cortical thickness as a measure of structural covariance, and applied this method to investigate the coordinated development of different brain regions in conduct disorder (CD). We also assessed whether structural covariance measures could differentiate between the childhood-onset (CO-CD) and adolescence-onset (AO-CD) subtypes of CD, which may differ in terms of etiology and adult outcomes.
METHODS:We examined interregional correlations in cortical thickness in male youths with CO-CD or AO-CD relative to healthy controls (HCs) in two independent datasets. The age range in the Cambridge sample was 16-21 years (mean: 18.0), whereas the age range of the Southampton sample was 13-18 years (mean: 16.7). We used FreeSurfer to perform segmentations and applied structural covariance methods to the resulting parcellations.
RESULTS:In both samples, CO-CD participants displayed a strikingly higher number of significant cross-cortical correlations compared to HC or AO-CD participants, whereas AO-CD participants presented fewer significant correlations than HCs. Group differences in the strength of the interregional correlations were observed in both samples, and each set of results remained significant when controlling for IQ and comorbid attention-deficit/hyperactivity disorder symptoms.
CONCLUSIONS:This study provides new evidence for quantitative differences in structural brain organization between the CO-CD and AO-CD subtypes, and supports the hypothesis that both subtypes of CD have neurodevelopmental origins.