Quadratic deformation of Minkowski space

We present a deformation of the Minkowski space as embedded into the conformal space (in the formalism of twistors) based in the quantum versions of the corresponding kinematic groups. We compute explicitly the star product, whose Poisson bracket is quadratic. We show that the star product although defined on the polynomials can be extended differentiably. Finally we compute the Eucliden and Minkowskian real forms of the deformation.Comment: Presented at XVII European Workshop on String Theory 2011. Padova (Italy) September 05-09; Fortschr. Phys. 1-7 (2012

Thermodynamics modeling of deep learning systems for a temperature based filter pruning technique

We analyse the dynamics of convolutional filters' parameters of a convolutional neural networks during and after training, via a thermodynamic analogy which allows for a sound definition of temperature. We show that removing high temperature filters has a minor effect on the performance of the model, while removing low temperature filters influences majorly both accuracy and loss decay. This result could be exploited to implement a temperature-based pruning technique for the filters and to determine efficiently the crucial filters for an effective learning

Quantization of Projective Homogeneous Spaces and Duality Principle

We introduce a general recipe to construct quantum projective homogeneous spaces, with a particular interest for the examples of the quantum Grassmannians and the quantum generalized flag varieties. Using this construction, we extend the quantum duality principle to quantum projective homogeneous spaces.Comment: Final version (after correcting the journal's proofs), to appear in "Journal of Noncommutative Geometry

On the deformation quantization of affine algebraic varieties

We compute an explicit algebraic deformation quantization for an affine Poisson variety described by an ideal in a polynomial ring, and inheriting its Poisson structure from the ambient space

Supersymmetry in noncommutative superspaces

Non commutative superspaces can be introduced as the Moyal-Weyl quantization of a Poisson bracket for classical superfields. Different deformations are studied corresponding to constant background fields in string theory. Supersymmetric and non supersymmetric deformations can be defined, depending on the differential operators used to define the Poisson bracket. Some examples of deformed, 4 dimensional lagrangians are given. For extended superspace (N>1), some new deformations can be defined, with no analogue in the N=1 case.Comment: 23 pages, AMS-LaTeX. Misprints corrected, references adde

Acute exposure to lead increases myocardial contractility independent of hypertension development

Abstract We studied the effects of the acute administration of small doses of lead over time on hemodynamic parameters in anesthetized rats to determine if myocardial contractility changes are dependent or not on the development of hypertension. Male Wistar rats received 320 mg/kg lead acetate iv once, and their hemodynamic parameters were measured for 2 h. Cardiac contractility was evaluated in vitro using left ventricular papillary muscles as were Na + ,K + -ATPase and myosin Ca 2+ -ATPase activities. Lead increased left-(control: 112 ± 3.7 vs lead: 129 ± 3.2 mmHg) and right-ventricular systolic pressures (control: 28 ± 1.2 vs lead: 34 ± 1.2 mmHg) significantly without modifying heart rate. Papillary muscles were exposed to 8 mM lead acetate and evaluated 60 min later. Isometric contractions increased (control: 0.546 ± 0.07 vs lead: 0.608 ± 0.06 g/mg) and time to peak tension decreased (control: 268 ± 13 vs lead: 227 ± 5.58 ms), but relaxation time was unchanged. Post-pause potentiation was similar between groups (n = 6 per group), suggesting no change in sarcoplasmic reticulum activity, evaluated indirectly by this protocol. After 1-h exposure to lead acetate, the papillary muscles became hyperactive in response to a b-adrenergic agonist (10 mM isoproterenol). In addition, post-rest contractions decreased, suggesting a reduction in sarcolemmal calcium influx. The heart samples treated with 8 mM lead acetate presented increased Na + ,K + -ATPase (approximately 140%, P , 0.05 for control vs lead) and myosin ATPase (approximately 30%, P , 0.05 for control vs lead) activity. Our results indicated that acute exposure to low lead concentrations produces direct positive inotropic and lusitropic effects on myocardial contractility and increases the right and left ventricular systolic pressure, thus potentially contributing to the early development of hypertension

Acute Lead Exposure Increases Arterial Pressure: Role of the Renin-Angiotensin System

Background: Chronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension. Methodology/Principal Findings: Wistar rats were treated with lead acetate (i.v. bolus dose of 320 μg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na+,K+-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 μg/dL, which is below the reference blood concentration (60 μg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na+,K+-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na+,K+-ATPase, AT1 and AT2. Pre-treatment with an AT1 receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect. Conclusion: Acute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular diseaseThis study was supported by grants from CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior) and CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico)/FAPES (Fundação de Amparo à Pesquisa do Espírito Santo)/FUNCITEC (Fundação de Ciência e Tecnologia)(39767531/07), Brazil and from MCINN (Ministerio de Ciencia e Innovación) (SAF 2009- 07201) and ISCIII (Instituto de Salud Carlos III) (Red RECAVA- Red Temática de Investigación en Enfermedades Cardiovasculares del Instituto de Salud Carlos III, RD06/0014/0011), Spai