Effect of laser irradiation on failure mechanism of TiCp reinforcedtitanium composite coating produced by laser cladding

Laser cladding is an effective technique to coat a metallic substrate with a layer of a different nature.It has been widely reported that the most important combined parameters controlling the quality ofthe coating are the specific energy (E) and the powder density ( ). In the present work, clad depositsof Ti6Al4V + 60 wt.% TiC were prepared on a Ti6Al4V substrate using an optimum combination of Ec= 24 J/mm2 and c= 3 mg/mm2. These experiments were performed using a laser power of 400 and600 W, in order to study the effect of laser power on the properties of the clad. The microstructure, phasecomposition and nanohardness of the coatings were investigated by optical microscopy, scanning elec-tron microscopy and X-ray diffraction. During laser processing, TiC can be partially converted to TiCX(X = 0.5) due mainly to the TiC dissolution into the laser-generated melting pool and subsequent precipi-tation during cooling. It was observed that the lower laser power limit reduces primary TiC dissolution butit also promotes secondary carbide alignment at the interface. On the other hand, the damage mechanisminduced by high laser power is dominated by primary TiC particle cracking by the high stress concentra-tion at the particle matrix interface followed by ductile failure of the matrix. It is also remarkable thatirradiance affects the TiC/TiCxratio despite Ecand care fixed and it determines hardness distributioninside the coating.Authors thank MINECO funding in special the Training of Research Staff programme with the help BES-2009-013589 and the support of the Comision Interministerial de Ciencia y Tecnologia (CICYT), Spain, under Grant MAT2012-39124. This work was developed at the Materials Technology Unit of the Polytechnic University of Valencia associated to CSIC through the National Centre for Metallurgical Research (CENIM). Finally, thank the EU for the funding received through the FEDER help in the project UPOV08-3E-005 for the purchase of equipment and the Generalitat Valenciana for the help ACOMP/2012/094.Candel Bou, JJ.; Jiménez, J.; Franconetti Rodríguez, P.; Amigó Borrás, V. (2014). Effect of laser irradiation on failure mechanism of TiCp reinforcedtitanium composite coating produced by laser cladding. Journal of Materials Processing Technology. 214(11):2325-2332. https://doi.org/10.1016/j.jmatprotec.2014.04.035S232523322141

Alcohol use and abuse in training conscripts of the Hellenic navy

OBJECTIVES: Alcohol abuse and addiction are big current problems of the developed world having multivariate causality and multiple effects. Alcohol abuse in young people is a matter of central importance due to its wide range long lasting effects, especially so in Greece where the problem has only recently started growing. The Hellenic Navy is interested in the complications of alcohol abuse in training conscripts. Because young conscripts will be placed in demanding positions, but also because in Greece the military service is obligatory and represents an important period for the socialization of young men. METHODS: In the present study, levels of alcohol use and abuse were measured in a sample of 650 male training conscripts of the Hellenic Navy. The tools used are: (a) two questionnaires measuring frequency and quantity of alcohol consumption and psychosocial variables, (b) the CAGE test, which is a questionnaire measuring hidden alcoholism. RESULTS: 38,1% conscripts were characterized problematic drinkers according the adolescents criteria. Additional psychological complications were related to alcohol use. Using the stricter criterion for adults (plus psychological complications) 8.9% were found to be problematic drinkers. The use of CAGE questionnaire which is measuring hidden alcoholism, identified 16% of the total sample as hidden alcoholics. DISCUSSION: The findings regarding unregular levels of alcohol use and abuse are presented as well as their relation to psychosocial complications and to demographic characteristics. The results are discussed in the light of Creek and international bibliography

Levodopa-Induced Dyskinesia Is Associated with Increased Thyrotropin Releasing Hormone in the Dorsal Striatum of Hemi-Parkinsonian Rats

Background Dyskinesias associated with involuntary movements and painful muscle contractions are a common and severe complication of standard levodopa (L-DOPA, L-3,4-dihydroxyphenylalanine) therapy for Parkinson's disease. Pathologic neuroplasticity leading to hyper-responsive dopamine receptor signaling in the sensorimotor striatum is thought to underlie this currently untreatable condition. Methodology/Principal Findings Quantitative real-time polymerase chain reaction (PCR) was employed to evaluate the molecular changes associated with L-DOPA-induced dyskinesias in Parkinson's disease. With this technique, we determined that thyrotropin releasing hormone (TRH) was greatly increased in the dopamine-depleted striatum of hemi-parkinsonian rats that developed abnormal movements in response to L-DOPA therapy, relative to the levels measured in the contralateral non-dopamine-depleted striatum, and in the striatum of non-dyskinetic control rats. ProTRH immunostaining suggested that TRH peptide levels were almost absent in the dopamine-depleted striatum of control rats that did not develop dyskinesias, but in the dyskinetic rats, proTRH immunostaining was dramatically up-regulated in the striatum, particularly in the sensorimotor striatum. This up-regulation of TRH peptide affected striatal medium spiny neurons of both the direct and indirect pathways, as well as neurons in striosomes. Conclusions/Significance TRH is not known to be a key striatal neuromodulator, but intrastriatal injection of TRH in experimental animals can induce abnormal movements, apparently through increasing dopamine release. Our finding of a dramatic and selective up-regulation of TRH expression in the sensorimotor striatum of dyskinetic rat models suggests a TRH-mediated regulatory mechanism that may underlie the pathologic neuroplasticity driving dopamine hyper-responsivity in Parkinson's disease.Morris K. Udall Center for Excellence in Parkinson’s Research at MGH/MITNational Institutes of Health (U.S.) (NIH NS38372)American Parkinson Disease Association, Inc.University of Alabama at BirminghamMassachusetts General HospitalNational Institute of Diabetes and Digestive and Kidney Diseases (U.S.) (NIDDK/NIH grant R01 DK58148)National Institute of Neurological Disorders and Stroke (U.S.) (R01 NINDS/NIH grant NS045231)Stanley H. and Sheila G. Sydney FundMichael J. Fox Foundation for Parkinson's Researc

A new framework for cortico-striatal plasticity: behavioural theory meets In vitro data at the reinforcement-action interface

Operant learning requires that reinforcement signals interact with action representations at a suitable neural interface. Much evidence suggests that this occurs when phasic dopamine, acting as a reinforcement prediction error, gates plasticity at cortico-striatal synapses, and thereby changes the future likelihood of selecting the action(s) coded by striatal neurons. But this hypothesis faces serious challenges. First, cortico-striatal plasticity is inexplicably complex, depending on spike timing, dopamine level, and dopamine receptor type. Second, there is a credit assignment problem—action selection signals occur long before the consequent dopamine reinforcement signal. Third, the two types of striatal output neuron have apparently opposite effects on action selection. Whether these factors rule out the interface hypothesis and how they interact to produce reinforcement learning is unknown. We present a computational framework that addresses these challenges. We first predict the expected activity changes over an operant task for both types of action-coding striatal neuron, and show they co-operate to promote action selection in learning and compete to promote action suppression in extinction. Separately, we derive a complete model of dopamine and spike-timing dependent cortico-striatal plasticity from in vitro data. We then show this model produces the predicted activity changes necessary for learning and extinction in an operant task, a remarkable convergence of a bottom-up data-driven plasticity model with the top-down behavioural requirements of learning theory. Moreover, we show the complex dependencies of cortico-striatal plasticity are not only sufficient but necessary for learning and extinction. Validating the model, we show it can account for behavioural data describing extinction, renewal, and reacquisition, and replicate in vitro experimental data on cortico-striatal plasticity. By bridging the levels between the single synapse and behaviour, our model shows how striatum acts as the action-reinforcement interface

Asymmetric spike-timing dependent plasticity of striatal nitric oxide-synthase interneurons

International audienc

l-DOPA dosage is critically involved in dyskinesia via loss of synaptic depotentiation

The emergence of levodopa (l-DOPA)-induced dyskinesia and motor fluctuations represents a major clinical problem in Parkinson's disease (PD). While it has been suggested that the daily dose of l-DOPA can play a critical role, the mechanisms linking l-DOPA dosage to the occurrence of motor complications have not yet been explored. Using an experimental model of PD we have recently demonstrated that long-term l-DOPA treatment leading to the induction of abnormal involuntary movements (AIMs) alters corticostriatal bidirectional synaptic plasticity. Dyskinetic animals, in fact, lack the ability to reverse previously induced long-term potentiation (LTP). This lack of depotentiation has been associated to a defect in erasing unessential motor information. Here chronic l-DOPA treatment was administered at two different doses to hemiparkinsonian rats, and electrophysiological recordings were subsequently performed from striatal spiny neurons. Both low and high doses of l-DOPA restored normal LTP, which was disrupted following dopamine (DA) denervation. By the end of the chronic treatment, however, while the low l-DOPA dose induced AIMs only in half of the rats, the high dose caused motor complications in all the treated animals. Interestingly, the dose-related expression of motor complications was associated with a lack of synaptic depotentiation. Our study provides further experimental evidence to support a direct correlation between the daily dosage of l-DOPA and the induction of motor complications and establishes a critical pathophysiological link between the lack of synaptic depotentiation and the expression of AIMs

GABAergic Circuits Control Spike-Timing-Dependent Plasticity

International audienc

Inhibition of phosphodiesterases rescues striatal long-term depression and reduces levodopa-induced dyskinesia

The aim of the present study was to evaluate the role of the nitric oxide/cyclic guanosine monophosphate pathway in corticostriatal long-term depression induction in a model of levodopa-induced dyskinesia in experimental parkinsonism. Moreover, we have also analysed the possibility of targeting striatal phosphodiesterases to reduce levodopa-induced dyskinesia. To study synaptic plasticity in sham-operated rats and in 6-hydroxydopamine lesioned animals chronically treated with therapeutic doses of levodopa, recordings from striatal spiny neurons were taken using either intracellular recordings with sharp electrodes or whole-cell patch clamp techniques. Behavioural analysis of levodopa-induced abnormal involuntary movements was performed before and after the treatment with two different inhibitors of phosphodiesterases, zaprinast and UK-343664. Levodopa-induced dyskinesia was associated with the loss of long-term depression expression at glutamatergic striatal synapses onto spiny neurons. Both zaprinast and UK-343664 were able to rescue the induction of this form of synaptic plasticity via a mechanism requiring the modulation of intracellular cyclic guanosine monophosphate levels. This effect on synaptic plasticity was paralleled by a significant reduction of abnormal movements following intrastriatal injection of phosphodiesterase inhibitors. Our findings suggest that drugs selectively targeting phosphodiesterases can ameliorate levodopa-induced dyskinesia, possibly by restoring physiological synaptic plasticity in the striatum. Future studies exploring the possible therapeutic effects of phosphodiesterase inhibitors in non-human primate models of Parkinson's disease and the involvement of striatal synaptic plasticity in these effects remain necessary to validate this hypothesis

Raman spectroscopy of (n,m)-identified individual single-walled carbon nanotubes

0370-1972International audienceThe goal of our "complete experimental" approach was to relate the Raman response of an individual single-walled carbon nanotubes (SWNT) to its (n,m) structure determined from an independent way. In this aim, a procedure including transmission electronic microscopy (TEM), Raman spectroscopy, and electron diffraction experiments on the same SAINT has been developed. The independent determinations of both structure and Raman features of semiconducting and metallic nanotubes allows to discuss several questions concerning: (i) the relation between diameter of the tubes and the radial breathing mode (RBM) frequency, (ii) the values and the nature of the E-33(S) and E-44(S) optical transition energies. (c) 2007 WELEY-VCH Veriag GmbH & Co. KGaA, Weinheim

Greenhouse module for space systems: A lunar greenhouse design

This presentation describes the results of the Greenhouse Module for Space Systems project carried out by DLR and its partners within the framework of the Micro-Ecological Life Support System Alternative (MELiSSA) program. The presentation gives an overview of the final design, which was further detailed in a concurrent engineering design study. Based on the study, the consortium also identified technology and knowledge gaps, which have to be addressed in future projects