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Dysfunction of the glutamate system is increasingly considered a core feature of stress-dependent neuropsychiatric disorders. Clinical neuroimaging studies have shown consistent volumetric changes in limbic and cortical areas, while preclinical studies with stress protocols in rodents found dendritic remodeling and reduction of synapses in the same areas, suggesting that destabilization of glutamate release/transmission, in turn induced by stress and glucocorticoids, is crucial for cognitive function and neural architecture. We found that acute stress rapidly enhances depolarization-evoked glutamate release/transmission in prefrontal and frontal cortex (PFC/FC), an effect mediated by stimulation of synaptic corticosterone receptors. Corticosterone rapidly increases the readily releasable pool of glutamate vesicles, through activation of synaptic receptor-mediated nongenomic mechanisms in PFC/FC. Moreover, we have shown that chronic antidepressants are able to prevent the enhancement of glutamate release induced by acute stressors in these areas.

Recently, ultra-intense laser-driven ion acceleration has turned out to be an extremely interesting phenomenon, capable to produce ion beams which could potentially be suitable for applications as hadron therapy or dense matter diagnostics. The present PhD thesis is addressed to the study of Target Normal Sheath Acceleration (TNSA), namely the laser-based ion acceleration mechanism which dominates the presently accessible experimental conditions. The work is focused in particular on the theoretical modeling of TNSA, motivated by the need for an effective description which, by adopting proper approximations that can limit the required computational efforts, is capable to provide reliable predictions on the resulting ion beam features, given an initial laser-target configuration. Indeed, the development of a robust TNSA theoretical model would mean a deeper comprehension of the key physical factors governing the process, allowing at the same time to draw guidelines for potential experiments in the next future. In this dissertation, in order to achieve a significant advancement in the TNSA modeling field, the results of two original works are reported, the first is focused on a critical, quantitative analysis of existing descriptions, and the second, starting from the conclusions of such an analysis, is dedicated to the extension of a specific model, aiming at the inclusion of further, crucial, TNSA aspects. The quantitative analysis consists in the comparison of six well-known published descriptions, relying on their capability in estimating the maximum ion energy, which is tested over an extensive database of published TNSA experimental results, covering a wide range of laser-target conditions. Such a comparative study, despite the technical issues to be faced in order to reduce the arbitrariness of the results, allows to draw some interesting conclusions about the effectiveness of the six models considered and about TNSA effective modeling in general. According to t

A theoretical model of the Target Normal Sheath Acceleration (TNSA) process, able to go beyond the limits of available descriptions, is developed. It allows to achieve a more satisfactory interpretation of TNSA. The theory, also supported by two dimensional particle-in-cell simulations, elucidates the role played by the main laser and target parameters. Comparison between model predictions and experimental data related to the target thickness dependence of the maximum ion energy is discussed, showing satisfactory agreement. The model can be used as a simple but effective tool to guide the design of future experiments. © 2013 AIP Publishing LLC.

Ultra-intense laser interaction with solid targets appears to be an extremely promising technique to accelerate ions up to several MeV, producing beams that exhibit interesting properties for many foreseen applications. Nowadays, most of all the published experimental results can be theoretically explained in the framework of the target normal sheath acceleration (TNSA) mechanism proposed by Wilks [Phys. Plasmas 8(2), 542 (2001)10.1063/1.1333697]. As an alternative to numerical simulation various analytical or semi-analytical TNSA models have been published in the latest years, each of them trying to provide predictions for some of the ion beam features, given the initial laser and target parameters. However, the problem of developing a reliable model for the TNSA process is still open, which is why the purpose of this work is to enlighten the present situation of TNSA modeling and experimental results, by means of a quantitative comparison between measurements and theoretical predictions of the maximum ion energy. Moreover, in the light of such an analysis, some indications for the future development of the model proposed by Passoni and Lontano [Phys. Plasmas 13(4), 042102 (2006)10.1063/1.2184067] are then presented. © 2012 American Institute of Physics.

During the last 10 years of research it has been experimentally demonstrated that ions can be accelerated up to energies of tens of MeV as a consequence of the ultra-intense laser pulse interaction with a solid target. This process has been shown to take place via the so-called Target Normal Sheath Acceleration (TNSA) mechanism. A fundamental challenge in the investigation of this phenomenon is to understand the dependencies of the ion beam features on the laser and target properties. In order to achieve this goal, several TNSA theoretical models have been proposed. In the present work a collection of maximum ion energies experimentally measured has been compared to the values predicted by six different theoretical descriptions. The models we chose to compare are based either on a fluid approach, on a quasi-static approach, or on a combination of the before-mentioned. On the basis of such a quantitative comparison we aim to provide a reliable test of these theoretical descriptions, in which their strengths, weaknesses, open problems and capability in predicting the ion energy are underlined. © 2011 Elsevier B.V.

A growing body of evidence suggests that oxidative stress plays a key role in the pathogenesis of micro- and macrovascular diabetic complications. The increased oxidative stress in subjects with type 2 diabetes is a consequence of several abnormalities, including hyperglycemia, insulin resistance, hyperinsulinemia, and dyslipidemia, each of which contributes to mitochondrial superoxide overproduction in endothelial cells of large and small vessels as well as the myocardium. The unifying pathophysiological mechanism that underlies diabetic complications could be explained by increased production of reactive oxygen species (ROS) via: (1) the polyol pathway flux, (2) increased formation of advanced glycation end products (AGEs), (3) increased expression of the receptor for AGEs, (4) activation of protein kinase C isoforms, and (5) overactivity of the hexosamine pathway. Furthermore, the effects of oxidative stress in individuals with type 2 diabetes are compounded by the inactivation of two critical anti-atherosclerotic enzymes: endothelial nitric oxide synthase and prostacyclin synthase. Of interest, the results of clinical trials in patients with type 2 diabetes in whom intensive management of all the components of the metabolic syndrome (hyperglycemia, hypercholesterolemia, and essential hypertension) was attempted (with agents that exert a beneficial effect on serum glucose, serum lipid concentrations, and blood pressure, respectively) showed a decrease in adverse cardiovascular end points. The purpose of this review is (1) to examine the mechanisms that link oxidative stress to micro- and macrovascular complications in subjects with type 2 diabetes and (2) to consider the therapeutic opportunities that are presented by currently used therapeutic agents which possess antioxidant properties as well as new potential antioxidant substances.

Femtosecond laser pulse propagation in monomode optical fibers is demonstrated and investigated numerically (by simulations) and experimentally in this paper. A passively mode locked Nd:glass laser giving a pulse duration of about 200 fsec at 1053 nm wavelength and 120 mW average optical power with 100 MHz repetition rate is used in the experimental work. Numerical simulations are done by solving the nonlinear Schrödinger equation with the aid of Matlab program. The results show that self phase modulation (SPM) leads to compression of the spectral width from 5 nm to 2.1 nm after propagation of different optical powers (34, 43, 86 and 120 mW) in fibers of different length (5, 15, 35 m). The varying optical powers produced a varying phase shift. The output spectral width also changed with the fiber length at a given peak power. © 2009 World Scientific Publishing Company.

nPKCdelta is a phospholipid-dependent and calcium-independent PKC isoform, whose over expression in BL6T murine melanoma cells, modifies their proliferative and metastatic potential in vivo, We focus here on the possible relationship between the subcellular localisation of nPKCdelta and distinct phase of the cell cycle. Our findings show a dynamic localisation of nPKCdelta in dependence of the phase of the cell cycle. Actually, this isoform is preferentially localised to the cytoplasm in serum-starved cells, shifting to the nucleus during the S-phase and becoming peri-nuclear, associated to the Golgi apparatus, in G2-M phase. Therefore, taken together our findings demonstrate that the subcellular localisation of nPKCdelta changes dynamically during the cell cycle in dependence of the requirement of the enzyme at a particular place of the cell. (C) 2002 Elsevier Science (USA). All rights reserved.