207 research outputs found
S. Calabrese – F. Fioroni, Leggere la mente. La lettura come stile di vita, Bologna, Archetipolibri, 2012, pp. 129 (ISBN 978-88-6633-023-3
No full textLe riflessioni relative agli effetti della letteratura sui lettori o spettatori risalgono all’antichità classica, traendo origine dal concetto aristotelico di catarsi, ma è solo a partire dagli anni Settanta che sono emersi approcci reader-oriented, interessati a investigare sul contributo fondamentale del lettore nella costruzione del significato del testo. Ogni processo di decodificazione, in particolare di un testo narrativo, rappresenta dunque un fenomeno cognitivo e affettivo di transfert del lettore nel mondo finzionale del testo.Tra gli anni Settanta e Ottanta, ossia a partire dalla schema theory e dalle ricerche sulle strutture della memoria, si colloca l'apporto cruciale del cognitivismo, poi proseguito dalle neuroscienze: in particolare, esperimenti condotti con l'ausilio delle tecniche di neuroimaging – le quali consentono di osservare e analizzare il funzionamento cerebrale nel momento stesso in cui decodifica e comprende un testo – hanno permesso di illustrare le basi neuronali dell'atto del leggere, evidenziandone ulteriormente la complessità. Questo libro inquadra le più recenti riflessioni neuroscientifiche nell'ambito di una teoria unificata della lettura, focalizzandosi poi su aspetti specifici quali gli effetti patemici della suspense, l'identificazione empatica nello storyworld e le strategie di lettura messe in atto dai bambini soprattutto nel momento in cui sono alle prese con testi controfattuali quali le fiabe
Maltrattamenti in famiglia e verso i minori: indagine svolta alla Procura della Repubblica presso il Tribunale di Perugia (1995-2002).
No full textLeggere la mente. La lettura come stile di vita
No full textLe riflessioni relative agli effetti della letteratura sui lettori risalgono all'antichità classica, ma solo negli ultimi anni sono emerse analisi interessate a valutare il contributo del lettore nella costruzione del significato testuale: a partire dalla schema theory, cognitivismo e neuroscienze hanno cominciato ad affrontare problemi di interesse letterario, consentendoci addirittura di identificare le basi neuronali dell'atto del leggere. Questo libro inquadra le più recenti riflessioni nell'ambito di una teoria unificata della lettura, focalizzandosi su problemi specifici quali gli effetti patemici della suspense e le strategie di "mindreading" messe in atto dai bambini soprattutto quando interagiscono con testi a elevato indice di irrealtà quali le fiabe
Triphenylphosphite neuropathy in hens.
No full textSingle doses of triphenyl phosphite (TPP), a triester of trivalent phosphorus, cause ataxia and paralysis in hens. Characteristics of neurotoxicity were described as somewhat different from organophosphate induced delayed polyneuropathy (OPIDP), which is caused by triesters of pentavalent phosphorus. The onset of TPP neuropathy was reported to occur earlier than that of OPIDP (5-10 versus 7-14 days after dosing, respectively), and chromatolysis, neuronal necrosis and lesions in certain areas of the brain were found in TPP neuropathy only. Pretreatment with phenylmethanesulfonyl fluoride (PMSF) protects from OPIDP, but it either partially protected from effects of low doses or exacerbated those of higher doses of TPP. In order to account for these differences with OPIDP, it was suggested that TPP neuropathy results from the combination of two independent mechanisms of toxicity: typical OPIDP due to inhibition of neuropathy target esterase (NTE) plus a second neurotoxicity related with other target(s). We explored TPP neuropathy in the hen with attention to the phenomena of promotion and protection which are both caused by PMSF when given in combination with typical neuropathic OPs. When PMSF is given before neuropathic OPs it protects from OPIDP; when given afterwards it exaggerates OPIDP. The former effect is due to interactions with NTE, the latter to interactions with an unknown site. The time course of NTE reappearance after TPP (60 or 90 mg/kg i.v.) inhibition showed a longer half-life when compared to that after PMSF (30 mg/kg s.c.) (10-15 versus 4-6 days, respectively). The clinical signs of TPP neuropathy (60 or 90 mg/kg i.v.) were similar to those observed in OPIDP, appeared 7-12 days after treatment, correlated with more than 70% NTE inhibition/aging and were preceded by a reduction of retrograde axonal transport in sciatic nerve of hens. TPP (60 mg/kg i.v.) neuropathy was promoted by PMSF (120 mg/kg s.c.) given up to 12 days afterwards and was partially protected by PMSF (10-120 mg/kg s.c.) when given 24 h before TPP (60 or 90 mg/kg i.v.). The previously reported early onset of TPP neuropathy might be related to the higher dose used in those experiments and to the resulting more severe neuropathy. The lack of full protection might be explained by the slow kinetics of TPP, which would cause substantial NTE inhibition when PMSF effects on NTE had subsided. Since PMSF also affects the promotion site when given before initiation of neuropathy, the resulting neuropathy would then be due to both protection from and promotion of TPP effects by PMSF. No promotion by PMSF (120 mg/kg s.c.) was observed in TPP neuropathy (90 mg/kg i.v.) partially protected by PMSF (10-30 mg/kg s.c.). This might also be explained by the concurrent effects on NTE and on the promotion site obtained with PMSF pretreatment. We conclude that TPP neuropathy in the hen is likely to be the same as typical OPIDP. The unusual effects of combined treatment to hens with TPP and PMSF are explained by the prolonged pharmacokinetics of TPP and by the dual effect of PMSF i.e. protection from and promotion of OPIDP
Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine.
No full textTo assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma beta-endorphin (beta-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 micrograms iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both beta-EP (F = 5.86, p less than 0.002) and cortisol (F = 4.43, p less than 0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for beta-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased beta-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal beta-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p less than 0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity
Giosetta Fioroni lettrice di Paul Celan: percorsi tra il dolore e il silenzio del XX secolo
No full textUn saggio su come Giosetta Fioroni ha riletto all'inizio del XX secolo l'opera di Paul Celan
Paleogene calcareous nannofossil biostratigraphic updates from equatorial Indian Ocean
No full textBiostratigrafia e paleoceanografia di sedimenti provenienti dall'Oceano indiano equatorial
La criminalità minorile: indagine svolta presso il Tribunale per i minorenni di Perugia
No full text- …
