Rigorous derivation of coherent resonant tunneling time and velocity in finite periodic systems

The velocity $v_{res}$ of resonant tunneling electrons in finite periodic structures is analytically calculated in two ways. The first method is based on the fact that a transmission of unity leads to a coincidence of all still competing tunneling time definitions. Thus, having an indisputable resonant tunneling time $\tau_{res},$ we apply the natural definition $v_{res}=L/\tau_{res}$ to calculate the velocity. For the second method we combine Bloch's theorem with the transfer matrix approach to decompose the wave function into two Bloch waves. Then the expectation value of the velocity is calculated. Both different approaches lead to the same result, showing their physical equivalence. The obtained resonant tunneling velocity $v_{res}$ is smaller or equal to the group velocity times the magnitude of the complex transmission amplitude of the unit cell. Only at energies where the unit cell of the periodic structure has a transmission of unity $v_{res}$ equals the group velocity. Numerical calculations for a GaAs/AlGaAs superlattice are performed. For typical parameters the resonant velocity is below one third of the group velocity.Comment: 12 pages, 3 figures, LaTe

Use of reciproc instruments with different motions: cyclic fatigue testing with simulation of the body temperature

Aim: To assess the influence of different motions on the cyclic fatigue resistance of Reciproc instruments simulating the temperature of the clinical conditions. Methods: The sample size was determined using statistical software set with the following parameters: \u3b1=0.05, \u3b2=0.20, \u3b4=30.0, \u3c3=28.0. The experiment required 54 Reciproc files. Brand new R25 files were randomly allocated to three groups defined by the tested motion: continuous rotation at 300 rpm (n=18), \u201cRECIPROC\u201d mode (n=18), and \u201cWAVEONE\u201d mode (n=18). The same endodontic motor was used for all groups (X-Smart IQ). All files were rotated/reciprocated until fracture inside a custom-designed artificial canal with 60\ub0 angle and 5-mm radius of curvature milled in a stainless-steel block. The testing device was electrically heated to keep its internal temperature at 35\ub11\ub0C, which was constantly monitored with a thermometer. After file separation, the time to failure was registered with a digital chronometer and the length of the fractured fragment measured with a digital calliper. The fracture surface of each file was observed at the scanning electron microscope to perform a qualitative fractographic analysis. The collected data (time to fracture and fracture length) were tested for the normality of the distribution and the equality of variances with a Shapiro-Wilk and a Levene test, respectively. The dependent variables were compared amongst groups by means of a multivariate analysis of variance and Tuckey post-hoc test (p=0.05). Results: The continuous rotation group exhibited the shortest lifespan among the considered groups (85.4\ub19.5 s to failure). Both reciprocating motions were associated with a significant improvement of fatigue resistance (p<0.001). The \u201cRECIPROC\u201d mode allowed for longer time to failure than the \u201cWAVEONE\u201d mode, with 141.6\ub119.4 s and 117.2\ub111.2 s to failure, respectively. The absence of differences among the considered groups in terms of fracture length confirmed the correct positioning of the files inside the artificial canal. The scanning electron microscopic analysis showed signs of file separation ascribable to cyclic fatigue. Conclusion: The present study preliminary demonstrated that the native \u201cRECIPROC\u201d motion use of R25 Reciproc files should be preferred over other types of motions to prevent file separation in the clinical setting

Bianchi type I universe with viscous fluid: A qualitative analysis

The nature of cosmological solutions for a homogeneous, anisotropic Universe given by a Bianchi type-I (BI) model in the presence of a Cosmological constant $\Lambda$ is investigated by taking into account dissipative process due to viscosity. The system in question is thoroughly studied both analytically and numerically. It is shown the viscosity, as well as the $\Lambda$ term exhibit essential influence on the character of the solutions. In particular a negative $\Lambda$ gives rise to an ever-expanding Universe, whereas, a suitable choice of initial conditions plus a positive $\Lambda$ can result in a singularity-free oscillatory mode of expansion. For some special cases it is possible to obtain oscillations in the exponential mode of expansion of the BI model even with a negative $\Lambda$, where oscillations arise by virtue of viscosity.Comment: RevTex, 16 pages, 32 figure

CB1 cannabinoid receptors promote oxidative stress and cell death in murine models of doxorubicin-induced cardiomyopathy and in human cardiomyocytes

Aims Here we investigated the mechanisms by which cardiovascular CB1 cannabinoid receptors may modulate the cardiac dysfunction, oxidative stress, and interrelated cell death pathways associated with acute/chronic cardiomyopathy induced by the widely used anti-tumour compound doxorubicin (DOX). Methods and results Both load-dependent and -independent indices of left-ventricular function were measured by the Millar pressure-volume conductance system. Mitogen-activated protein kinase (MAPK) activation, cell-death markers, and oxidative/nitrosative stress were measured by molecular biology/biochemical methods and flow cytometry. DOX induced left-ventricular dysfunction, oxidative/nitrosative stress coupled with impaired antioxidant defense, activation of MAPK (p38 and JNK), and cell death and/or fibrosis in hearts of wide-type mice (CB1+/+), and these effects were markedly attenuated in CB1 knockouts (CB1−/−). In human primary cardiomyocytes expressing CB1 receptors (demonstrated by RT-PCR, western immunoblot, and flow cytometry) DOX, likewise the CB1 receptor agonist HU210 and the endocannabinoid anandamide (AEA), induced MAPK activation and cell death. The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210. Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX ± AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs. Furthermore, AEA or HU210 in primary human cardiomyocytes triggered increased reactive oxygen species generation. Conclusion CB1 activation in cardiomyocytes may amplify the reactive oxygen/nitrogen species-MAPK activation-cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress, which may contribute to the pathophysiology of various cardiovascular disease

Interacting spinor and scalar fields in Bianchi type-I Universe filled with viscous fluid: exact and numerical solutions

We consider a self-consistent system of spinor and scalar fields within the framework of a Bianchi type I gravitational field filled with viscous fluid in presence of a $\Lambda$ term. Exact self-consistent solutions to the corresponding spinor, scalar and BI gravitational field equations are obtained in terms of $\tau$, where $\tau$ is the volume scale of BI universe. System of equations for $\tau$ and \ve, where \ve is the energy of the viscous fluid, is deduced. Some special cases allowing exact solutions are thoroughly studied.Comment: 18 pages, 6 figure

Attacks on quantum key distribution protocols that employ non-ITS authentication

We demonstrate how adversaries with unbounded computing resources can break Quantum Key Distribution (QKD) protocols which employ a particular message authentication code suggested previously. This authentication code, featuring low key consumption, is not Information-Theoretically Secure (ITS) since for each message the eavesdropper has intercepted she is able to send a different message from a set of messages that she can calculate by finding collisions of a cryptographic hash function. However, when this authentication code was introduced it was shown to prevent straightforward Man-In-The-Middle (MITM) attacks against QKD protocols. In this paper, we prove that the set of messages that collide with any given message under this authentication code contains with high probability a message that has small Hamming distance to any other given message. Based on this fact we present extended MITM attacks against different versions of BB84 QKD protocols using the addressed authentication code; for three protocols we describe every single action taken by the adversary. For all protocols the adversary can obtain complete knowledge of the key, and for most protocols her success probability in doing so approaches unity. Since the attacks work against all authentication methods which allow to calculate colliding messages, the underlying building blocks of the presented attacks expose the potential pitfalls arising as a consequence of non-ITS authentication in QKD-postprocessing. We propose countermeasures, increasing the eavesdroppers demand for computational power, and also prove necessary and sufficient conditions for upgrading the discussed authentication code to the ITS level.Comment: 34 page

Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathy

Diabetes is a recognized risk factor for cardiovascular diseases and heart failure. Diabetic cardiovascular dysfunction also underscores the development of diabetic retinopathy, nephropathy and neuropathy. Despite the broad availability of antidiabetic therapy, glycaemic control still remains a major challenge in the management of diabetic patients. Hyperglycaemia triggers formation of advanced glycosylation end products(AGEs), activates protein kinase C, enhances polyol pathway, glucose autoxidation, which coupled with elevated levels of free fatty acids, and leptin have been implicated in increased generation of superoxide anion by mitochondria, NADPH oxidases and xanthine oxidoreductase in diabetic vasculature and myocardium. Superoxide anion interacts with nitric oxide forming the potent toxin peroxynitrite via diffusion limited reaction, which in concert with other oxidants triggers activation of stress kinases, endoplasmic reticulum stress, mitochondrial and poly(ADP-ribose) polymerase 1-dependent cell death, dysregulates autophagy/mitophagy, inactivates key proteins involved in myocardial calcium handling/contractility and antioxidant defense, activates matrix metalloproteinases and redox-dependent pro-inflammatory transcription factors (e.g. nuclear factor kappaB) promoting inflammation, AGEs formation, eventually culminating in myocardial dysfunction, remodeling and heart failure. Understanding the complex interplay of oxidative/nitrosative stress with pro-inflammatory, metabolic and cell death pathways is critical to devise novel targeted therapies for diabetic cardiomyopathy, which will be overviewed in this brief synopsis. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases