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

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

APPLICATIONS DES PROPRIÉTÉS D'ÉLECTROLUMINESCENCE DES COMPOSÉS III-V

On décrit les propriétés des diodes électroluminescentes et dispositifs d'affichage élaborés en GaAs, GaP et GaAsP. On précise dans chaque cas la nature des recombinaisons radiatives utilisées, les valeurs des efficacités quantiques internes et externes, la nature des limitations, les critères de choix relatifs à la structure des dispositifs. Enfin on dégage les progrès attendus ainsi que les perspectives offertes par les matériaux d'introduction plus récente tels que GaInP, GaAlAs et GaN.The electroluminescence properties of GaAs, GaP and GaAsP diodes and displays are described. In each case, the nature of radiative recombinations, the internal and external quantum efficiency values, the limitations, the choice criteria dealing with the device structure are precized. In conclusion, the expected improvements and the possibilities offered by more recently introduced materials such as GaInP, GaAlAs and GaN are presented