Gluons at finite temperature

The gluon propagator is investigated at finite temperature via lattice simulations. In particular, we discuss its interpretation as a massive-type bosonic propagator. Moreover, we compute the corresponding spectral density and study the violation of spectral positivity. Finally, we explore the dependence of the gluon propagator on the phase of the Polyakov loop

Mitochondria: role in ischemia, reperfusion and cell death

Recent advances in the knowledge of the biochemical basis of myocardial ischemia have enabled a better understanding of the complex sequence of events occurring in ischemic cardiomyopathy, whatever its manifestations. This has clearly highlighted the important role played by cardiac mitochondria in these events. At first only associated with energy production, mitochondria have been clearly shown to have other important functions, like the maintenance of calcium homeostasis, as well as ischemic and non-ischemic preconditioning, and also modulation of cellular life and death. The aims of this review are twofold: firstly, to review the current knowledge on mitochondrial morphology and structure, and how these can be affected by ischemia and ischemia-reperfusion; and secondly, to summarize the role of cardiac mitochondria in cardioprotection and modulation of cell death mechanisms

Quantification of Maceration Changes using Post Mortem MRI in Fetuses

BACKGROUND: Post mortem imaging is playing an increasingly important role in perinatal autopsy, and correct interpretation of imaging changes is paramount. This is particularly important following intra-uterine fetal death, where there may be fetal maceration. The aim of this study was to investigate whether any changes seen on a whole body fetal post mortem magnetic resonance imaging (PMMR) correspond to maceration at conventional autopsy. METHODS: We performed pre-autopsy PMMR in 75 fetuses using a 1.5 Tesla Siemens Avanto MR scanner (Erlangen, Germany). PMMR images were reported blinded to the clinical history and autopsy data using a numerical severity scale (0 = no maceration changes to 2 = severe maceration changes) for 6 different visceral organs (total 12). The degree of maceration at autopsy was categorized according to severity on a numerical scale (1 = no maceration to 4 = severe maceration). We also generated quantitative maps to measure the liver and lung T2. RESULTS: The mean PMMR maceration score correlated well with the autopsy maceration score (R(2) = 0.93). A PMMR score of ≥4.5 had a sensitivity of 91%, specificity of 64%, for detecting moderate or severe maceration at autopsy. Liver and lung T2 were increased in fetuses with maceration scores of 3-4 in comparison to those with 1-2 (liver p = 0.03, lung p = 0.02). CONCLUSIONS: There was a good correlation between PMMR maceration score and the extent of maceration seen at conventional autopsy. This score may be useful in interpretation of fetal PMMR

Microchannels analogues for the study of viscoelastic fluid flows through porous media

This paper was presented at the 3rd Micro and Nano Flows Conference (MNF2011), which was held at the Makedonia Palace Hotel, Thessaloniki in Greece. The conference was organised by Brunel University and supported by the Italian Union of Thermofluiddynamics, Aristotle University of Thessaloniki, University of Thessaly, IPEM, the Process Intensification Network, the Institution of Mechanical Engineers, the Heat Transfer Society, HEXAG - the Heat Exchange Action Group, and the Energy Institute.This work studies the flow behavior and related pressure losses of viscoelastic polymer solutions in microchannels with two different sequences of contraction/expansion, disposed in a symmetric and an asymmetric arrangement, respectively. These microfluidic devices are proposed as simplified microchannel analogues for the flow of Newtonian and viscoelastic fluids through porous media. The results show that the symmetric configuration mimics the pressure gradient of these polymer solutions through a porous medium at low flow rates (below a critical Deborah number, Decr), while the asymmetric arrangement gives the asymptotic limit at high De values (above Decr) as a consequence of the intrinsic differences in the extensional rate profiles defined by each microgeometry.Fundação para a Ciência e a Tecnologia (FCT), COMPETE and FEDER through projects PTDC/ EQU-FTT/ 71800/ 2006, PTDC/EQUFTT/ 70727/ 2006, PTDC/ EME-MFE/ 99109/ 2008 and REEQ/ 262/ EME/ 2005

Simulations of extensional flow in microrheometric devices

We present a detailed numerical study of the flow of a Newtonian fluid through microrheometric devices featuring a sudden contraction–expansion. This flow configuration is typically used to generate extensional deformations and high strain rates. The excess pressure drop resulting from the converging and diverging flow is an important dynamic measure to quantify if the device is intended to be used as a microfluidic extensional rheometer. To explore this idea, we examine the effect of the contraction length, aspect ratio and Reynolds number on the flow kinematics and resulting pressure field. Analysis of the computed velocity and pressure fields show that, for typical experimental conditions used in microfluidic devices, the steady flow is highly three-dimensional with open spiraling vortical structures in the stagnant corner regions. The numerical simulations of the local kinematics and global pressure drop are in good agreement with experimental results. The device aspect ratio is shown to have a strong impact on the flow and consequently on the excess pressure drop, which is quantified in terms of the dimensionless Couette and Bagley correction factors. We suggest an approach for calculating the Bagley correction which may be especially appropriate for planar microchannels

A new viscoelastic benchmark flow: Stationary bifurcation in a cross-slot

AbstractIn this work we propose the cross-slot geometry as a candidate for a numerical benchmark flow problem for viscoelastic fluids. Extensive data of quantified accuracy is provided, obtained via Richardson extrapolation to the limit of infinite refinement using results for three different mesh resolutions, for the upper-convected Maxwell, Oldroyd-B and the linear form of the simplified Phan-Thien–Tanner constitutive models. Furthermore, we consider two types of flow geometry having either sharp or rounded corners, the latter with a radius of curvature equal to 5% of the channel’s width. We show that for all models the inertialess steady symmetric flow may undergo a bifurcation to a steady asymmetric configuration, followed by a second transition to time-dependent flow, which is in qualitative agreement with previous experimental observations for low Reynolds number flows. The critical Deborah number for both transitions is quantified and a set of standard parameters is proposed for benchmarking purposes

Influence of channel aspect ratio on the onset of purely-elastic flow instabilities in three-dimensional planar cross-slots

In this work, we perform creeping-flow simulations of upper-convected Maxwell and simplified Phan-Thien-Tanner fluids to study the purely-elastic steady bifurcation and transition to time-dependent flow in three-dimensional planar cross-slots. By analysing the flow in geometries with aspect ratios ranging from the near Hele-Shaw flow like limit, up to the very deep, two-dimensional limit, we are able to characterize the mechanism of the cross-slot bifurcation with significant detail. We conclude that the bifurcation mechanism is similar to a buckling instability, by which fluid is redirected via paths of least resistance, resulting in the emergence of peripheral stagnation points, above and below the central stagnation point. The intake of matter at the centre via the inlet axis is thus reduced, being compensated by fluid flowing through low resistance corridors along the central vertical axis, above and below the central point. Furthermore, we propose and locally compute a modified Pakdel-McKinley criterion, thereby producing a scalar stability field and suggesting emergent peripheral stagnation points also indirectly contribute to the onset of time-dependent flow. (c) 2015 The Authors. Published by Elsevier B.V

Impact of carvedilol on the mitochondrial damage induced by hypoxanthine and xantine oxidase: what role in myocardial ischemia and reperfusion?

OBJECTIVES: The cardioprotective effects of carvedilol (CV) may be explained in part by interactions with heart mitochondria. The objective of this work was to study the protection afforded by CV against oxidative stress induced in isolated heart mitochondria by hypoxanthine and xanthine oxidase (HX/XO), a well-known source of reactive oxygen species (ROS) in the cardiovascular system. METHODS: Mitochondria were isolated from Wistar rat hearts (n = 8) and incubated with HX/XO in the presence and in the absence of calcium. Several methods were used to assess the protection afforded by CV: evaluation of mitochondrial volume changes (by measuring changes in the optical density of the mitochondrial suspension), calcium uptake and release (with a fluorescent probe, Calcium Green 5-N) and mitochondrial respiration (with a Clark-type oxygen electrode). RESULTS: CV decreased mitochondrial damage associated with ROS production by HX and XO, as verified by the reduction of mitochondrial swelling and increase in mitochondrial calcium uptake. In the presence of HX and XO, CV also ameliorated mitochondrial respiration in the active phosphorylation state and prevented decrease in the respiratory control ratio (p < 0.05) and in mitochondrial phosphorylative efficiency (p < 0.001). CONCLUSIONS: The data indicate that CV partly protected heart mitochondria from oxidative damage induced by HX and XO, which may be useful during myocardial ischemia and reperfusion. It is also suggested that mitochondria may be a priority target for the protective action of some compounds

Residual brain injury after early discontinuation of cooling therapy in mild neonatal encephalopathy

We examined the brain injury and neurodevelopmental outcomes in a prospective cohort of 10 babies with mild encephalopathy who had early cessation of cooling therapy. All babies had MRI and spectroscopy within 2 weeks after birth and neurodevelopmental assessment at 2 years. Cooling was prematurely discontinued at a median age of 9 hours (IQR 5-13) due to rapid clinical improvement. Five (50%) had injury on MRI or spectroscopy, and two (20%) had an abnormal neurodevelopmental outcome at 2 years. Premature cessation of cooling therapy in babies with mild neonatal encephalopathy does not exclude residual brain injury and adverse long-term neurodevelopmental outcomes. This study refers to babies recruited into the MARBLE study (NCT01309711, pre-results stage)

Advantages in the use of carvedilol versus propranolol for the protection of cardiac mitochondrial function

BACKGROUND: Carvedilol is a neurohormonal antagonist of multiple action which is used in clinical practice for the treatment of congestive heart failure, mild to moderate hypertension and myocardial infarction. Previous results from our group have demonstrated that one of the main targets for the protective effect of carvedilol is the cardiac mitochondrial network. In-this work, we compare the effect of carvedilol with propranolol in different models of mitochondrial dysfunction and in the generation of transmembrane electric potential (EP). We further tested if carvedilol was able to inhibit the mitochondrial permeability transition (MPT) induced by doxorubicin and calcium-dependent cytochrome c release, a phenomenon frequently associated with apoptotic cell death. METHODS: Cardiac mitochondria were isolated by differential centrifugation. Oxygen consumption and mitochondrial EP were determined using an oxygen electrode and a tetraphenylphosphonium-sensitive electrode, respectively. Changes in mitochondrial volume and the release of cytochrome c were measured with spectrophotometric techniques. RESULTS: Propranolol, compared with carvedilol, had only a marginal effect, not only in protection against MPT induction, but also against oxygen consumption linked to the oxidation of external NADH, a process that is considered by several authors as key in the cardiotoxicity of doxorubicin. Regarding EP generation, propranolol had no effect, in contrast to carvedilol, which was confirmed to act as a protonophore. For the first time we also show that carvedilol inhibits the MPT induced by doxorubicin and calcium-dependent cytochrome c release. CONCLUSIONS: With this work, we further support the notion that carvedilol is effective in several models of mitochondrial dysfunction, particularly those involving oxidative stress. The results demonstrate that for some pathological conditions, carvedilol and propranolol have different mechanisms of action at the sub-cellular level, as propranolol seems to lack effectiveness in the protection of cardiac mitochondria