Dithered Color Quantization

Image quantization and digital halftoning are fundamental problems in computer graphics, which arise when displaying high-color images on non-truecolor devices. Both steps are generally performed sequentially and, in most cases, independent of each other. Color quantization with a pixel-wise defined distortion measure and the dithering process with its local neighborhood optimize different quality criteria or, frequently, follow a heuristic without reference to any quality measure. In this paper we propose a new method to simultaneously quantize and dither color images. The method is based on a rigorous cost–function approach which optimizes a quality criterion derived from a generic model of human perception. A highly efficient algorithm for optimization based on a multiscale method is developed for the dithered color quantization cost function. The quality criterion and the optimization algorithms are evaluated on a representative set of artificial and real–world images as well as on a collection of icons. A significant image quality improvement is observed compared to standard color reduction approaches

Development of a Synthetic Earth Gravity Model by 3D mass optimisation based on forward modelling

Several previous Synthetic Earth Gravity Model (SEGM) simulations are based on existing information about the Earth’s internal mass distribution. However, currently available information is insufficient to model the Earth’s anomalous gravity field on a global scale. The low-frequency information is missing when modelling only topography, bathymetry and crust (including the Mohorovičić discontinuity), but the inclusion of information on the mantle and core does not seem to significantly improve this situation. This paper presents a method to determine a more realistic SEGM by considering simulated 3D mass distributions within the upper mantle as a proxy for all unmodelled masses within the Earth.The aim is to improve an initial SEGM based on forward gravity modelling of the topography, bathymetry and crust such that the missing low-frequency information is now included. The simulated 3D mass distribution has been derived through an interactive and iterative mass model optimisation algorithm, which minimises geoid height differences with respect to a degree-360 spherical harmonic expansion of the EGM2008 global external gravity field model. We present the developed optimisation algorithm by applying it to the development of a global SEGM that gives a reasonably close fit to EGM2008, and certainly closer than a SEGM based only on the topography, bathymetry and crust

Regulation of Fission Yeast Morphogenesis by PP2A Activator pta2

Cell polarization is key for the function of most eukaryotic cells, and regulates cell shape, migration and tissue architecture. Fission yeast, Schizosaccharomyces pombe cells are cylindrical and polarize cell growth to one or both cell tips dependent on the cell cycle stage. Whereas microtubule cytoskeleton contributes to the positioning of the growth sites by delivering polarity factors to the cell ends, the Cdc42 GTPase polarizes secretion via actin-dependent delivery and tethering of secretory vesicles to plasma membrane. How growth is restricted to cell tips and how re-initiation of tip growth is regulated in the cell cycle remains poorly understood. In this work we investigated the function of protein phosphatase type 2A (PP2A) in S. pombe morphogenesis by deleting the evolutionary conserved PTPA-type regulatory subunit that we named pta2. pta2-deleted cells showed morphological defects and altered growth pattern. Consistent with this, actin patches and active Cdc42 were mislocalized in the pta2 deletion. These defects were additive to the lack of Cdc42-GAP Rga4. pta2Δ cells show upregulated Cdc42 activity and pta2 interacts genetically with polarisome components Tea1, Tea4 and For3 leading to complete loss of cell polarity and rounded morphology. Thus, regulation of polarity by PP2A requires the polarisome and involves Pta2-dependent control of Cdc42 activity

Systemic proteasome inhibition triggers neurodegeneration in a transgenic mouse model expressing human α-synuclein under oligodendrocyte promoter: implications for multiple system atrophy

Multiple system atrophy (MSA) is a progressive late onset neurodegenerative α-synucleinopathy with unclear pathogenesis. Recent genetic and pathological studies support a central role of α-synuclein (αSYN) in MSA pathogenesis. Oligodendroglial cytoplasmic inclusions of fibrillar αSYN and dysfunction of the ubiquitin–proteasome system are suggestive of proteolytic stress in this disorder. To address the possible pathogenic role of oligodendroglial αSYN accumulation and proteolytic failure in MSA we applied systemic proteasome inhibition (PSI) in transgenic mice with oligodendroglial human αSYN expression and determined the presence of MSA-like neurodegeneration in this model as compared to wild-type mice. PSI induced open field motor disability in transgenic αSYN mice but not in wild-type mice. The motor phenotype corresponded to progressive and selective neuronal loss in the striatonigral and olivopontocerebellar systems of PSI-treated transgenic αSYN mice. In contrast no neurodegeneration was detected in PSI-treated wild-type controls. PSI treatment of transgenic αSYN mice was associated with significant ultrastructural alterations including accumulation of fibrillar human αSYN in the cytoplasm of oligodendroglia, which resulted in myelin disruption and demyelination characterized by increased g-ratio. The oligodendroglial and myelin pathology was accompanied by axonal degeneration evidenced by signs of mitochondrial stress and dysfunctional axonal transport in the affected neurites. In summary, we provide new evidence supporting a primary role of proteolytic failure and suggesting a neurodegenerative pathomechanism related to disturbed oligodendroglial/myelin trophic support in the pathogenesis of MSA

Inositol 1,4,5- Trisphosphate Receptor Function in Drosophila Insulin Producing Cells

The Inositol 1,4,5- trisphosphate receptor (InsP3R) is an intracellular ligand gated channel that releases calcium from intracellular stores in response to extracellular signals. To identify and understand physiological processes and behavior that depends on the InsP3 signaling pathway at a systemic level, we are studying Drosophila mutants for the InsP3R (itpr) gene. Here, we show that growth defects precede larval lethality and both are a consequence of the inability to feed normally. Moreover, restoring InsP3R function in insulin producing cells (IPCs) in the larval brain rescues the feeding deficit, growth and lethality in the itpr mutants to a significant extent. We have previously demonstrated a critical requirement for InsP3R activity in neuronal cells, specifically in aminergic interneurons, for larval viability. Processes from the IPCs and aminergic domain are closely apposed in the third instar larval brain with no visible cellular overlap. Ubiquitous depletion of itpr by dsRNA results in feeding deficits leading to larval lethality similar to the itpr mutant phenotype. However, when itpr is depleted specifically in IPCs or aminergic neurons, the larvae are viable. These data support a model where InsP3R activity in non-overlapping neuronal domains independently rescues larval itpr phenotypes by non-cell autonomous mechanisms