82 research outputs found
Analysis of motion of solid hydrogen tracer particles in oscillating superfluid flows
We have developed a relatively simple cryostat which allows us to image turbulent flows in superfluid helium at temperatures below 2 K, using frozen H2 particles. We analyze the statistics of the velocities of these solid tracers, which follow the turbulent flow generated by oscillating bodies. We have also studied one of the oscillators working in air at room temperature, and traced the flow with solid talcum particles for comparison. Images were recorded by a digital camera at 240 frames per second, while frequencies of the oscillators are between 20 to 45 Hz. The flow is characterized by a modified Reynolds number ReÎŽ based on the viscous penetration depth ÎŽ. Software in a dedicated particle tracking velocimetry code allows us to compute the trajectories and velocities of tens of thousands of particles. We have obtained the number of particles for equally spaced intervals of the velocity modulus. For the oscillators in the superfluid, the probability of finding particles at higher velocities has an exponential decay. Within our resolution the statistics in the superfluid for oscillating objects with sharp borders is largely independent of ReÎŽ, while the logarithmic decay at low velocities seems faster than for high velocities for rounded objects. On the other hand, for data taken in air the result is closer to a classical Gaussian distribution of velocities.Fil: Zemma, Elisa MarĂa. ComisiĂłn Nacional de EnergĂa AtĂłmica. Gerencia del Ărea de EnergĂa Nuclear. Instituto Balseiro; Argentina. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas; ArgentinaFil: Luzuriaga, J.. ComisiĂłn Nacional de EnergĂa AtĂłmica. Gerencia del Ărea de EnergĂa Nuclear. Instituto Balseiro; ArgentinaFil: Babuin, S.. Czech Academy of Sciences. Institute of Physics; RepĂșblica Chec
Fulminant myocarditis parvovirus B19 related in a young woman
We present the case of a 18-year-old female with fulminant lymphocytic myocarditis caused by Parvovirus B19 (PVB19), successfully treated using temporary LVAD. In the literature there is no consensus on the surgical strategy. While some surgeons prefer to use a single device supporting only the LV, others prefer to start immediately with a biventricular supporting. At pre-procedural ultrasound evaluation, her anatomical features were not suitable for a percutaneous device such as the Impella. Thus, a temporary paracorporeal continuous flow LVAD was inserted. The heart recovery allowed LVAD removal 9 days after the implant
Thermal counterflow in a periodic channel with solid boundaries
We perform numerical simulations of finite temperature quantum turbulence produced through thermal counterflow in superfluid 4He, using the vortex filament model. We investigate the effects of solid boundaries along one of the Cartesian directions, assuming a laminar normal fluid with a Poiseuille velocity profile, whilst varying the temperature and the normal fluid velocity. We analyze the distribution of the quantized vortices, reconnection rates, and quantized vorticity production as a function of the wall-normal direction. We find that the quantized vortex lines tend to concentrate close to the solid boundaries with their position depending only on temperature and not on the counterflow velocity. We offer an explanation of this phenomenon by considering the balance of two competing effects, namely the rate of turbulent diffusion of an isotropic tangle near the boundaries and the rate of quantized vorticity production at the center. Moreover, this yields the observed scaling of the position of the peak vortex line density with the mutual friction parameter. Finally, we provide evidence that upon the transition from laminar to turbulent normal fluid flow, there is a dramatic increase in the homogeneity of the tangle, which could be used as an indirect measure of the transition to turbulence in the normal fluid component for experiments
Rational Design and Characterization of D-Phe-Pro-D-Arg-Derived Direct Thrombin Inhibitors
The tremendous social and economic impact of thrombotic disorders, together with the considerable risks associated to the currently available therapies, prompt for the development of more efficient and safer anticoagulants. Novel peptide-based thrombin inhibitors were identified using in silico structure-based design and further validated in vitro. The best candidate compounds contained both l- and d-amino acids, with the general sequence d-Phe(P3)-Pro(P2)-d-Arg(P1)-P1âČ-CONH2. The P1âČ position was scanned with l- and d-isomers of natural or unnatural amino acids, covering the major chemical classes. The most potent non-covalent and proteolysis-resistant inhibitors contain small hydrophobic or polar amino acids (Gly, Ala, Ser, Cys, Thr) at the P1âČ position. The lead tetrapeptide, d-Phe-Pro-d-Arg-d-Thr-CONH2, competitively inhibits α-thrombin's cleavage of the S2238 chromogenic substrate with a Ki of 0.92 ”M. In order to understand the molecular details of their inhibitory action, the three-dimensional structure of three peptides (with P1âČ l-isoleucine (fPrI), l-cysteine (fPrC) or d-threonine (fPrt)) in complex with human α-thrombin were determined by X-ray crystallography. All the inhibitors bind in a substrate-like orientation to the active site of the enzyme. The contacts established between the d-Arg residue in position P1 and thrombin are similar to those observed for the l-isomer in other substrates and inhibitors. However, fPrC and fPrt disrupt the active site His57-Ser195 hydrogen bond, while the combination of a P1 d-Arg and a bulkier P1âČ residue in fPrI induce an unfavorable geometry for the nucleophilic attack of the scissile bond by the catalytic serine. The experimental models explain the observed relative potency of the inhibitors, as well as their stability to proteolysis. Moreover, the newly identified direct thrombin inhibitors provide a novel pharmacophore platform for developing antithrombotic agents by exploring the conformational constrains imposed by the d-stereochemistry of the residues at positions P1 and P1âČ
Troponin elevation in acute ischemic stroke (TRELAS) - protocol of a prospective observational trial
<p>Abstract</p> <p>Background</p> <p>Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.</p> <p>Methods/Design</p> <p>The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital CharitĂ© will be screened for cTnT elevations (i.e. >= 0.05 ÎŒg/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.</p> <p>Discussion</p> <p>TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.</p> <p>Trial registration</p> <p>clinicaltrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01263964">NCT01263964</a></p
The Heart Is an Early Target of Anthrax Lethal Toxin in Mice: A Protective Role for Neuronal Nitric Oxide Synthase (nNOS)
Anthrax lethal toxin (LT) induces vascular insufficiency in experimental animals through unknown mechanisms. In this study, we show that neuronal nitric oxide synthase (nNOS) deficiency in mice causes strikingly increased sensitivity to LT, while deficiencies in the two other NOS enzymes (iNOS and eNOS) have no effect on LT-mediated mortality. The increased sensitivity of nNOSâ/â mice was independent of macrophage sensitivity to toxin, or cytokine responses, and could be replicated in nNOS-sufficient wild-type (WT) mice through pharmacological inhibition of the enzyme with 7-nitroindazole. Histopathological analyses showed that LT induced architectural changes in heart morphology of nNOSâ/â mice, with rapid appearance of novel inter-fiber spaces but no associated apoptosis of cardiomyocytes. LT-treated WT mice had no histopathology observed at the light microscopy level. Electron microscopic analyses of LT-treated mice, however, revealed striking pathological changes in the hearts of both nNOSâ/â and WT mice, varying only in severity and timing. Endothelial/capillary necrosis and degeneration, inter-myocyte edema, myofilament and mitochondrial degeneration, and altered sarcoplasmic reticulum cisternae were observed in both LT-treated WT and nNOSâ/â mice. Furthermore, multiple biomarkers of cardiac injury (myoglobin, cardiac troponin-I, and heart fatty acid binding protein) were elevated in LT-treated mice very rapidly (by 6 h after LT injection) and reached concentrations rarely reported in mice. Cardiac protective nitrite therapy and allopurinol therapy did not have beneficial effects in LT-treated mice. Surprisingly, the potent nitric oxide scavenger, carboxy-PTIO, showed some protective effect against LT. Echocardiography on LT-treated mice indicated an average reduction in ejection fraction following LT treatment in both nNOSâ/â and WT mice, indicative of decreased contractile function in the heart. We report the heart as an early target of LT in mice and discuss a protective role for nNOS against LT-mediated cardiac damage
Avaliação dos valores de troponina I, eletrocardiograma e ecocardiograma em felinos sedados com cetamina e midazolam, suplementados ou nĂŁo com oxigĂȘnio
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