28 research outputs found
Caratterizzazione della penetrazione di proiettili ad alta velocità in acqua e progettazione di un apparato di verifica a fuoco delle armi di piccolo calibro = Characterization of high velocity projectiles penetration into water and design of a light weapons test device
No full textDal momento in cui ho iniziato ad interessarmi di balistica terminale mi ha sempre affascinato la caratterizzazione della penetrazione di corpi solidi ad alta velocità in acqua. Occorre preliminarmente sottolineare come lo studio degli armamenti non debba essere inteso come un interessamento alle modalità di recare offesa alla libertà dei popoli, bensì come puro interesse scientifico in un campo in cui la letteratura spesso offre pochi contributi. Questo ambito risulta di particolare attenzione poiché, sebbene la letteratura offra una pletora di teorie relative all’impatto di corpi ad alta velocità contro bersagli solidi,l’impatto di corpi solidi dotati di elevata velocità contro fluidi è ancora oggi un problema aperto. Il primo approccio alla problematica risale al 1877 e si deve all’austriaco F. Uchatius; lo stesso allestì un apparato sperimentale semplice che dimostrava come fosse possibile sparare in acqua con un fucile e come la penetrazione del proietto nella stessa fosse molto limitata rispetto al moto dell’ogiva in aria. La prima formalizzazione analitica del fenomeno si deve a B. J. Noonan e H. K. Steves , che nel 1970 individuarono l’equazione generale che governa il fenomeno. Per addivenire alla formalizzazione di B. J. Noonan e H. K. Steves tuttavia era stato trascurato il ruolo giocato nel fenomeno dalla cavitazione. A tal proposito, il lavoro di Chen-Xing Jiang e di Feng-Chen Li, nel 2014 ha reso disponibile una trattazione analitica del fenomeno che tiene nella dovuta considerazione anche l’effetto prodotto dalle bolle di cavitazione generate dal moto del proietto nel fluido. L’approccio seguito in questo lavoro è stato quello di confrontare i risultati analitici dell’impatto ad alta velocità di munizioni di varia tipologia contro l’acqua con i risultati sperimentali ottenuti attraverso l’allestimento di un apposito apparato strumentale e l’impiego di una camera ad elevato frame-rate. A valle dell’attività analitica e sperimentale, è stato elaborato un metodo di simulazione numerica che consentisse, una volta validato, di ottenere celermente i dati di penetrazione in acqua di corpi di varia forma. In questo lavoro si è fatto uso di un particolare metodo di simulazione numerica del tipo meshless, la Smoothed Particle Hydrodynamics. La stessa, originariamente impiegata per simulare problemi di astrofisica ha successivamente trovato applicazione nella meccanica dei corpi solidi e fluidi attraverso l’utilizzo di tecniche di tipo statistico volte ad individuare le espressioni analitiche delle variabili fisiche di una distribuzione nota di elementi. A valle della raccolta e del confronto tra i risultati sperimentali, le simulazioni numeriche e le determinazioni analitiche, si è proceduto all’attività di tipo progettuale. In particolare, è stato progettato un apparato atto a consentire le verifiche di funzionamento a fuoco con l’impiego di vari tipi di munizioni. L’approccio ingegneristico seguito ha quindi consentito, soddisfatta la curiosità scientifica e validato un modello di caratterizzazione del fenomeno, di porre le basi per la progettazione di uno strumento di lavoro per il collaudo di apparati di difesa
ADAM10 in Synaptic Physiology and Pathology
No full textGeneration of amyloid-β peptide is at the beginning of a cascade that leads to Alzheimer's disease. Amyloid precursor protein (APP) as well as β- and γ-secretases are the principal players involved in amyloid-β (Aβ) production, while α-secretase cleavage on APP prevents Aβ deposition. A disintegrin and metalloproteinase 10 (ADAM10) has been demonstrated to act as α-secretase in neurons. Objective: Although localization of ADAM10 in the synaptic membrane is the key for its shedding activity, currently, very little is known about the mechanisms that control the synaptic abundance of ADAM10. Results: Two established forms of long-term activity-dependent plasticity, i.e. long-term potentiation and long-term depression (LTD), differentially regulate the synaptic availability and activity of ADAM10. Long-term potentiation decreases ADAM10 surface levels and activity by promoting its endocytosis. This process is mediated by activity-regulated association of ADAM10 with the clathrin adaptor protein 2 (AP2) complex. Conversely, LTD fosters ADAM10 insertion in the membrane and stimulates its activity. Furthermore, ADAM10 interaction with synapse-associated protein 97 (SAP97) is necessary for LTD-induced ADAM10 trafficking and required for LTD maintenance and LTD-induced spine morphology changes. Conclusions: Regulated interaction of ADAM10 with SAP97 and AP2 discloses a novel physiological mechanism of ADAM10 activity regulation at the synapses. This phenomenon produces a situation whereby synaptically regulated ADAM10 activity is positioned to modulate synaptic functionin
Peptidi attivatori dell'enzima ADAM10 e relativi usi nel trattamento delle patologie caratterizzate da un aumento del peptide β-amiloide
No full textThe present intervention relates to new peptides that increase the activity of the enzyme ADAM10 by acting at various levels in the cascade of events that leads to the accumulation of the beta-amyloid peptide. Pharmaceutical compositions are also contemplated comprising activator peptides of the enzyme ADAM10 and the related uses in the medical field for the treatment and/or prevention of the pathologies wherein the increase or accumulation of the beta-amyloid peptide occurs, such as Alzheimer's Disease, head injury and post-traumatic stress disorder
Valutazione della variabilità intra- ed inter-specifica nella componente polisaccaridica del genere Ophrys L.
No full text
Amyloid-β oligomers regulate ADAM10 synaptic localization through aberrant plasticity phenomena
No full textA disintegrin and metalloproteinase 10 (ADAM10) is a synaptic enzyme that has been previously shown to limit amyloid-β1-42 (Aβ1-42) peptide formation in Alzheimer's disease (AD). Furthermore, ADAM10 participates to spine shaping through the cleavage of adhesion molecules and its activity is under the control of synaptic plasticity events. In particular, long-term depression (LTD) promotes ADAM10 synaptic localization triggering its forward trafficking to the synapse, while long-term potentiation elicits ADAM10 internalization. Here, we show that a short-term in vitro exposure to Aβ1-42 oligomers, at a concentration capable of inducing synaptic depression and spine loss, triggers an increase in ADAM10 synaptic localization in hippocampal neuronal cultures. However, the Aβ1-42 oligomers-induced synaptic depression does not foster ADAM10 delivery to the synapse, as the physiological LTD, but impairs ADAM10 endocytosis. Moreover, Aβ1-42 oligomers-induced inhibition of ADAM10 internalization requires neuronal activity and the activation of the NMDA receptors. These data suggest that, at the synaptic level, Aβ1-42 oligomers trigger an aberrant plasticity mechanism according to which Aβ1-42 oligomers can downregulate Aβ generation through the modulation of ADAM10 synaptic availability. Moreover, the increased activity of ADAM10 towards its synaptic substrates could also affect the structural plasticity phenomena. Overall, these data shed new lights on the strict and complex relationship existing between synaptic activity and the primary mechanisms of AD pathogenesis
Occult colon cancer in a patient with an unexplained episode of pulmonary embolism
No full textThe association between venous thromboembolism and cancer has been widely documented and the main factor responsible for cancer-induced venous thromboembolism is considered mostly linked to a hypercoagulation state induced by the cancer itself. There is no consensus on investigative strategies for occult cancer in a patient with a thrombophilic condition. We report a patient who manifested an isolated episode of pulmonary embolism without specific evident sources of venous thromboembolism. The routine clinical and laboratory work-up to detect an occult cancer did not reveal any malignancy. A history of duodenal ulcer in association with a recent slight alteration in bowel habits led us to perform an esophagogastroduodenoscopy which was negative for malignancy, and a barium enema followed by colonoscopy, which revealed the presence of a tumor limited to the large intestine. An unexplained clinically evident hypercoagulation state, even in the presence of mild clinical symptoms, needs more thorough diagnostic strategies when simple methods of screening for occult cancer are negative
Cocaine-evoked negative symptoms require AMPA receptor trafficking in the lateral habenula
No full textSerum Total Tryptase Level Confirms Itself as a More Reliable Marker of Mast Cells Burden in Mast Cell Leukaemia (Aleukaemic Variant)
No full textMast cell leukemia (MCL) is a very rare form of systemic mastocytosis (SM) with a short median survival of 6 months. We describe a case of a 65-year-old woman with aleukaemic variant of MCL with a very high serum total tryptase level of 2255 μg/L at diagnosis, which occurred following an episode of hypotensive shock. She fulfilled the diagnostic criteria of SM, with a bone marrow smear infiltration of 50–60% of atypical mast cells (MCs). She tested negative for the KIT D816V mutation, without any sign of organ damage (no B- or C-findings) and only few mediator-related symptoms. She was treated with antihistamine alone and then with imatinib for the appearance of anemia. She maintained stable tryptase level and a very indolent clinical course for twenty-two months; then, she suddenly progressed to acute MCL with a serum tryptase level up to 12960 μg/L. The patient died due to haemorrhagic diathesis twenty-four months after diagnosis. This clinical case maybe represents an example of the chronic form of mast cell leukemia, described as unpredictable disease, in which the serum total tryptase level has confirmed itself as a reliable marker of mast cells burden regardless of the presence of other signs or symptoms
