Acoustic black holes for relativistic fluids

We derive a new acoustic black hole metric from the Abelian Higgs model. In the non-relativistic limit, while the Abelian Higgs model becomes the Ginzburg-Landau model, the metric reduces to an ordinary Unruh type. We investigate the possibility of using (type I and II) superconductors as the acoustic black holes. We propose to realize experimental acoustic black holes by using spiral vortices solutions from the Navier-stokes equation in the non-relativistic classical fluids.Comment: 16 pages. typos corrected, contents expande

Acoustic Black Holes from Abelian Higgs Model with Lorentz Symmetry Breaking

In this paper we derive acoustic black hole metrics in the (3+1) and (2+1)-dimensional Abelian Higgs model with Lorentz symmetry breaking. In this set up the sound waves lose the Lorentz boost invariance and suffer a 'birefringence' effect. We have found acoustic black holes and respective Hawking temperatures depending on the Lorentz violating parameter. Furthermore, we obtain an acoustic Kerr-like black hole metric with the Lorentz violating term affecting its rate of loss of mass. We also have shown that for suitable values of the Lorentz violating parameter a wider spectrum of particle wave function can be scattered with increased amplitude by the acoustic black hole.Comment: 12 pages, Latex, no figures, version accepted to Phys. Lett.

Superresonance effect from a rotating acoustic black hole and Lorentz symmetry breaking

We investigate the possibility of the acoustic superresonance phenomenon (analog to the superradiance in black hole physics), i.e., the amplification of a sound wave by reflection from the ergoregion of a rotating acoustic black hole with Lorentz symmetry breaking. For rotating black holes the effect of superradiance corresponds to the situation where the incident waves has reflection coefficient greater than one, and energy is extracted from them. For an acoustic Kerr-like black hole its rate of loss of mass is affected by the Lorentz symmetry breaking. We also have shown that for suitable values of the Lorentz violating parameter a wider spectrum of particle wave function can be scattered with increased amplitude by the acoustic black hole.Comment: 9 pages, version to appear in PL

Mechanisms of Mycotoxin-Induced Neurotoxicity through Oxidative Stress-Associated Pathways

Among many mycotoxins, T-2 toxin, macrocyclic trichothecenes, fumonisin B1 (FB1) and ochratochin A (OTA) are known to have the potential to induce neurotoxicity in rodent models. T-2 toxin induces neuronal cell apoptosis in the fetal and adult brain. Macrocyclic trichothecenes bring about neuronal cell apoptosis and inflammation in the olfactory epithelium and olfactory bulb. FB1 induces neuronal degeneration in the cerebral cortex, concurrent with disruption of de novo ceramide synthesis. OTA causes acute depletion of striatal dopamine and its metabolites, accompanying evidence of neuronal cell apoptosis in the substantia nigra, striatum and hippocampus. This paper reviews the mechanisms of neurotoxicity induced by these mycotoxins especially from the viewpoint of oxidative stress-associated pathways

Doublecortin like kinase 1 regulates α-Synuclein levels and toxicity

α-Synuclein (α-Syn) accumulation is a pathological hallmark of Parkinson's disease. Duplications and triplications of SNCA, the gene coding for α-Syn, cause genetic forms of the disease, which suggests that increased α-Syn dosage can drive PD. To identify the proteins that regulate α-Syn we previously performed a screen of potentially druggable genes that led to the identification of 60 modifiers. Among them, Doublecortin like kinase 1 (DCLK1), a microtubule binding serine threonine kinase, emerged as a promising target due to its potent effect on α-Syn and potential druggability as a neuron-expressed kinase. In this study, we explore the relationship between DCLK1 and α-Syn in human cellular and mouse models of PD. First, we show that DCLK1 regulates α-Syn levels post-transcriptionally. Second, we demonstrate that knockdown of Dclk1 reduces phosphorylated species of α-Syn and α-Syn-induced neurotoxicity in the substantia nigra in two distinct mouse models of synucleinopathy. Lastly, silencing DCLK1 in human neurons derived from individuals with SNCA triplications reduces phosphorylated and total α-Syn, thereby highlighting DCLK1 as a potential therapeutic target to reduce pathological α-Syn in disease.SIGNIFICANCE STATEMENTDCLK1 regulates α-Syn protein levels and Dclk1 knockdown rescues α-Syn toxicity in mice. This study provides evidence for a novel function for DCLK1 in the mature brain, and for its potential as a new therapeutic target for synucleinopathies