Hydrogen Peroxide Upregulates TNF-Related Apoptosis-Inducing Ligand (TRAIL) Expression in Human Astroglial Cells, and Augments Apoptosis of T Cells

The brain is particularly vulnerable to oxygen free radicals, and these radicals have been implicated in the pathology of several neurological disorders. In this study, the modulation of TNF-related apoptosis-inducing ligand (TRAIL) expression by oxidative stress was shown in LN215 cells, an astroglioma cell line. Hydrogen peroxide (H2O2) treatment increased TRAIL expression in LN215 cells and H2O2-induced TRAIL augmented apoptosis in Peer cells, a cell line sensitive to TRAIL-mediated cell death. Our findings suggest that the upregulation of TRAIL in astroglial cells may abrogate immune cell effector functions

Human Brain Astrocytes Mediate TRAIL-mediated Apoptosis after Treatment with IFN-γ

TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1β, TNF-α or IFN-γ, TRAIL was induced in cultured fetal astrocytes. In particular, IFN-γ induced the highest levels of TRAIL in cultured astrocytes. When astrocytes were prereated with IFN-γ, they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-γ modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain

Advanced Technologies for Large-Sized OLED Display

Five years have passed, since the first 55″ full high-definition (FHD) OLED TV fabricated on Gen 8.5 glass was successfully launched into the TV market. For the time being, the size of OLED TV became diverse from 55″ to 77″, and the resolution was doubled into ultrahigh definition (UHD). The brightness and color gamut were enhanced, while the lower power consumption was realized. Utmost picture quality and slim form factor of OLED TV as well as the improved performance have made OLED TV recognized as the best premium TV. In this chapter, we describe the recent progress in three key technologies, which enable such an enhancement of performance in OLED TV, i.e., oxide thin-film transistor (TFT) and white organic light-emitting diode (WOLED), compensation circuit, and method to compensate the nonuniformity of oxide TFTs, OLED devices, and luminance

Burst Packet Loss Concealment Using Multiple Codebooks and Comfort Noise for CELP-Type Speech Coders in Wireless Sensor Networks

In this paper, a packet loss concealment (PLC) algorithm for CELP-type speech coders is proposed in order to improve the quality of decoded speech under burst packet loss conditions in a wireless sensor network. Conventional receiver-based PLC algorithms in the G.729 speech codec are usually based on speech correlation to reconstruct the decoded speech of lost frames by using parameter information obtained from the previous correctly received frames. However, this approach has difficulty in reconstructing voice onset signals since the parameters such as pitch, linear predictive coding coefficient, and adaptive/fixed codebooks of the previous frames are mostly related to silence frames. Thus, in order to reconstruct speech signals in the voice onset intervals, we propose a multiple codebook-based approach that includes a traditional adaptive codebook and a new random codebook composed of comfort noise. The proposed PLC algorithm is designed as a PLC algorithm for G.729 and its performance is then compared with that of the PLC algorithm currently employed in G.729 via a perceptual evaluation of speech quality, a waveform comparison, and a preference test under different random and burst packet loss conditions. It is shown from the experiments that the proposed PLC algorithm provides significantly better speech quality than the PLC algorithm employed in G.729 under all the test conditions

The orphan nuclear receptor SHP is a positive regulator of osteoblastic bone formation

The orphan nuclear receptor small heterodimer partner (SHP; NR0B2) interacts with a diverse array of transcription factors and regulates a variety of cellular events such as cell proliferation, differentiation, and metabolism. However, the role of SHP in bone formation has not yet been elucidated. SHP expression is significantly increased during osteoblast differentiation, and its expression is partially regulated by bone morphogenetic protein 2 (BMP-2), which plays an important role in bone formation. In our study, inhibition of SHP expression significantly repressed BMP-2-induced osteoblast differentiation and ectopic bone formation. In accordance with these in vitro and in vivo results, osteoblast differentiation in SHP −/− mice primary osteoblasts was significantly repressed, and the mice showed decreased bone mass resulting from decreased numbers of osteoblasts. Finally, SHP physically interacts and forms a complex with runt-related transcription factor 2 (Runx2) on the osteocalcin gene promoter, and overexpression of SHP increased Runx2 transactivity via competition with histone deacetylase 4 (HDAC4), an enzyme that inhibits DNA binding of Runx2 to its target genes. Taken together, these results indicate that SHP acts as a novel positive regulator of bone formation by augmenting osteoblast differentiation through regulation of the transcriptional activity of Runx2. © 2010 American Society for Bone and Mineral ResearchPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65055/1/90718_ftp.pd

Two novel mutations of Wiskott–Aldrich syndrome: the molecular prediction of interaction between the mutated WASP L101P with WASP-interacting protein by molecular modeling

AbstractWiskott–Aldrich syndrome (WAS) is an X-linked disorder characterized by eczema, thrombocytopenia and increased susceptibility of infections, with mutations of the WAS gene being responsible for WAS and X-linked thrombocytopenia. Herein, two novel mutations of WAS at T336C on exon 3, and at 1326–1329, a G deletion on exon 10, resulting in L101P missense mutation and frameshift mutation 444 stop, respectively, are reported. The affected patients with either mutation showed severe suppression of WAS protein (WASP) levels, T cell proliferation, and CFSE-labeled T cells division. Because WASP L101 have not shown direct nuclear Overhauser effect (NOE) contact with the WASP-interacting protein (WIP) in NMR spectroscopy, molecular modeling was performed to evaluate the molecular effect of WASP P101 to WIP peptide. It is presumed that P101 induced a conformational change in the Q99 residue of WASP and made the side chain of Q99 move away from the WIP peptide, resulting in disruption of the hydrogen bond between Q99 WASP and Y475 WIP. A possible model for the molecular pathogenesis of WAS has been proposed by analyzing the interactions of WASP and WIP using a molecular modeling study

Supersymmetric quantum mechanics with nonlocal potentials

We consider supersymmetric quantum mechanical models with both local and nonlocal potentials. We present a nonlocal deformation of exactly solvable local models. Its energy eigenfunctions and eigenvalues are determined exactly. We observe that both our model Hamiltonian and its supersymmetric partner may have normalizable zero-energy ground states, in contrast to local models with nonperiodic or periodic potentials.Comment: 4 pages, REVTeX, Minor revisions for clarificatio

Calcium-binding Protein Calretinin Immunoreactivity in the Dog Superior Colliculus

We studied calretinin-immunoreactive (IR) fibers and cells in the canine superior colliculus (SC) and studied the distribution and effect of enucleation on the distribution of this protein. Localization of calretinin was immunocytochemically observed. A dense plexus of anti-­calretinin-IR fibers was found within the upper part of the superficial gray layer (SGL). Almost all of the labeled fibers were small in diameter with few varicosities. The intermediate and deep layers contained many calretinin-IR neurons. Labeled neurons within the intermediate gray layer (IGL) formed clusters in many sections. By contrast, labeled neurons in the deep gray layer (DGL) did not form clusters. Calretinin-IR neurons in the IGL and DGL varied in morphology and included round/oval, vertical fusiform, stellate, and horizontal neurons. Neurons with varicose dendrites were also labeled in the IGL. Most of the labeled neurons were small to medium in size. Monocular enucleation produced an almost complete reduction of calretinin-IR fibers in the SC contralateral to the enucleation. However, many calretinin-IR cells appeared in the contralateral superficial SC. Enucleation appeared to have no effect on the distribution of calretinin-IR neurons in the contralateral intermediate and deep layers of the SC. The calretinin-IR neurons in the superficial dog SC were heterogeneous small- to medium-sized neurons including round/oval, vertical fusiform, stellate, pyriform, and ­horizontal in shape. Two-color immunofluorescence revealed that no cells in the dog SC ­expressed both calretinin and GABA. Many horseradish peroxidase (HRP)-labeled retinal ganglion cells were seen after injections into the superficial layers. The vast majority of the double-labeled cells (HRP and calretinin) were small cells. The present results indicate that antibody to calretinin labels subpopulations of neurons in the dog SC, which do not express GABA. The results also suggest that the calretinin-IR afferents in the superficial layers of the dog SC originate from small class retinal ganglion cells. The expression of calretinin might be changed by the cellular activity of selective superficial collicular neurons. These results are valuable in delineating the basic neurochemical architecture of the dog visual system