Amplitude Modulation and Relaxation-Oscillation of Counterpropagating Rolls within a Broken-Symmetry Laser-Induced Electroconvection Strip

We report a liquid-crystal pattern-formation experiment in which we break the lateral (translational) symmetry of a nematic medium with a laser-induced thermal gradient. The work is motivated by an improved measurement (reported here) of the temperature dependence of the electroconvection threshold voltage in planar-nematic 4-methoxybenzylidene-4-butylaniline (MBBA). In contrast with other broken-symmetry-pattern studies that report a uniform drift, we observe a strip of counterpropagating rolls that collide at a sink point, and a strong temporally periodic amplitude modulation within a width of 3-4 rolls about the sink point. The time dependence of the amplitude at a fixed position is periodic but displays a nonsinusoidal relaxation-oscillation profile. After reporting experimental results based on spacetime contours and wavenumber profiles, along with a measurement of the change in the drift frequency with applied voltage at a fixed control parameter, we propose some potential guidelines for a theoretical model based on saddle-point solutions for Eckhaus-unstable states and coupled complex Ginzburg-Landau equations. Published in PRE 73, 036317 (2006).Comment: Published in Physical Review E in March 200

Estimation probabiliste de la complexité de circuits VLSI pour le traitement du signal

Afin de raccourcir le cycle de conception d'un système VLSI, il est nécessaire de pouvoir estimer les performances (temps, coût, consommation) de différentes solutions architecturales et algorithmiques au niveau d'abstraction le plus élevé. Nous présentons une nouvelle approche d'estimation dynamique de la complexité matérielle, appliquée aux architectures pipelines sous contrainte de temps. Elle se situe au niveau algorithmique, tout en restant indépendante de la méthode de synthèse qui sera choisie ultérieurement. Nous employons une méthode probabiliste prenant en compte réellement les contraintes entre opérations, dans le but de guider le choix des transformations et des algorithmes impliqués dans la spécification. Enfin, nous présentons des résultats d'estimation, et les comparons avec des résultats de synthèse architecturale

Algorithm-architecture matching metrics

The high level synthesis question is too wide to be optimaly addressed by a single and general CAD tool. So, interactive transfers of information are required between the tool and the designer, in order to make tractable the optimization of the synthesis task in a reasonnable time . This paper introduces an appoach which aims to provide the designer with information to quantify the hardware complexity in order to guide him in during his transformation choices . The method is based on probabilities, focuse the whole set of ressources and takes into account the real dependencies between operations . The method is characterized by a high level of abstraction. It firstly enables to combine the estimation with the most powerful algorithmic-transformations and secondly to be easily independent from the architectural model .Le champ d'action de la synthèse d'architecture s'avère trop vaste pour qu'un outil puisse offrir une solution optimale quelque soit l'algorithme cible. C'est pourquoi l'étude préalable de l'algorithme spécifié apparaît comme incontournable. Nous présentons ici, une nouvelle approche d'estimation dynamique des ressources, appliquée aux architectures pipelines sous contrainte de Latence. Nous employons une méthode probabiliste prenant en compte réellement les contraintes entre opérations, dans le but de guider le choix des transformations et des algorithmes impliqués dans la spécification. Les propriétés analysées sont la concurrence dans le temps des opérateurs, bus, registres et interconnexions et les statistiques de liens entre opérateurs. Des métriques sont également proposées pour l'interprétation des courbes d'estimation obtenues

A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin.

Huntington's disease (HD) is a neurodegenerative disorder caused by an abnormal expansion of a CAG repeat encoding a polyglutamine tract in the huntingtin (Htt) protein. The mutation leads to neuronal death through mechanisms which are still unknown. One hypothesis is that mitochondrial defects may play a key role. In support of this, the activity of mitochondrial complex II (C-II) is preferentially reduced in the striatum of HD patients. Here, we studied C-II expression in different genetic models of HD expressing N-terminal fragments of mutant Htt (mHtt). Western blot analysis showed that the expression of the 30 kDa Iron-Sulfur (Ip) subunit of C-II was significantly reduced in the striatum of the R6/1 transgenic mice, while the levels of the FAD containing catalytic 70 kDa subunit (Fp) were not significantly changed. Blue native gel analysis showed that the assembly of C-II in mitochondria was altered early in N171-82Q transgenic mice. Early loco-regional reduction in C-II activity and Ip protein expression was also demonstrated in a rat model of HD using intrastriatal injection of lentiviral vectors encoding mHtt. Infection of the rat striatum with a lentiviral vector coding the C-II Ip or Fp subunits induced a significant overexpression of these proteins that led to significant neuroprotection of striatal neurons against mHtt neurotoxicity. These results obtained in vivo support the hypothesis that structural and functional alterations of C-II induced by mHtt may play a critical role in the degeneration of striatal neurons in HD and that mitochondrial-targeted therapies may be useful in its treatment

Proton Magnetic Resonance Spectroscopy Reveals Neuroprotection by Oral Minocycline in a Nonhuman Primate Model of Accelerated NeuroAIDS

Background: Despite the advent of highly active anti-retroviral therapy (HAART), HIV-associated neurocognitive disorders continue to be a significant problem. In efforts to understand and alleviate neurocognitive deficits associated with HIV, we used an accelerated simian immunodeficiency virus (SIV) macaque model of NeuroAIDS to test whether minocycline is neuroprotective against lentiviral-induced neuronal injury. Methodology/Principal Findings: Eleven rhesus macaques were infected with SIV, depleted of CD8+ lymphocytes, and studied until eight weeks post inoculation (wpi). Seven animals received daily minocycline orally beginning at 4 wpi. Neuronal integrity was monitored in vivo by proton magnetic resonance spectroscopy and post-mortem by immunohistochemistry for synaptophysin (SYN), microtubule-associated protein 2 (MAP2), and neuronal counts. Astrogliosis and microglial activation were quantified by measuring glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (IBA-1), respectively. SIV infection followed by CD8+ cell depletion induced a progressive decline in neuronal integrity evidenced by declining N-acetylaspartate/creatine (NAA/Cr), which was arrested with minocycline treatment. The recovery of this ratio was due to increases in NAA, indicating neuronal recovery, and decreases in Cr, likely reflecting downregulation of glial cell activation. SYN, MAP2, and neuronal counts were found to be higher in minocycline-treated animals compared to untreated animals while GFAP and IBA-1 expression were decreased compared to controls. CSF and plasma viral loads were lower in MN-treated animals. Conclusions/Significance: In conclusion, oral minocycline alleviates neuronal damage induced by the AIDS virus

Pelazoneuron puberulum

Pteridophyte

Solanum elaeagnifolium

Angiosperm

Echinopterys eglandulosa

Angiosperm