MECHANISM OF CATIONIC LACTAM POLYMERIZATION

The authors suggested a new mechanism for the interpretation of cationic lactam polymerization according to which in the chain propagation reaction. through the appropriate intermediates. compounds belonging to various polymer homologous series are formed and additional polymerization processes are superimposed onto the original ones. On the basis of the new mechanism a kinetic model has been developed by the computer simulation of which rate and equilibrium constants could be determined. The latter enabled. a good quantitative description of polymerization

The E3 ubiquitin ligase IDOL regulates synaptic ApoER2 levels and is important for plasticity and learning.

Neuronal ApoE receptors are linked to learning and memory, but the pathways governing their abundance, and the mechanisms by which they affect the function of neural circuits are incompletely understood. Here we demonstrate that the E3 ubiquitin ligase IDOL determines synaptic ApoER2 protein levels in response to neuronal activation and regulates dendritic spine morphogenesis and plasticity. IDOL-dependent changes in ApoER2 abundance modulate dendritic filopodia initiation and synapse maturation. Loss of IDOL in neurons results in constitutive overexpression of ApoER2 and is associated with impaired activity-dependent structural remodeling of spines and defective LTP in primary neuron cultures and hippocampal slices. IDOL-deficient mice show profound impairment in experience-dependent reorganization of synaptic circuits in the barrel cortex, as well as diminished spatial and associative learning. These results identify control of lipoprotein receptor abundance by IDOL as a post-transcriptional mechanism underlying the structural and functional plasticity of synapses and neural circuits

ENABLING GENERIC DISTRIBUTED COMPUTING INFRASTRUCTURE COMPATIBILITY FOR WORKFLOW MANAGEMENT SYSTEMS

Solving workflow management system’s Distributed Computing Infrastructure (DCI) incompatibility and their workflow interoperability issues are very challenging and complex tasks. Workflow management systems (and therefore their workflows, workflow developers and also their end-users) are bounded tightly to some limited number of supported DCIs, and efforts required to allow additional DCI support. In this paper we are specifying a concept how to enable generic DCI compatibility for grid workflow management systems (such as ASKALON, MOTEUR, gUSE/WS-PGRADE, etc.) on job and indirectly on workflow level. To enable DCI compatibility among the different workflow management systems we have developed the DCI Bridge software solution. In this paper we will describe its internal architecture, provide usage scenarios to show how the developed service resolve the DCI interoperability issues between various middleware types. The generic DCI Bridge service enables the execution of jobs onto the existing major DCI platforms (such as Service Grids (Globus Toolkit 2 and 4, gLite, ARC, UNICORE), Desktop Grids, Web services, or even cloud based DCIs)

Chromosome 7 gain and DNA hypermethylation at the HOXA10 locus are associated with expression of a stem cell related HOX-signature in glioblastoma.

BACKGROUND: HOX genes are a family of developmental genes that are expressed neither in the developing forebrain nor in the normal brain. Aberrant expression of a HOX-gene dominated stem-cell signature in glioblastoma has been linked with increased resistance to chemo-radiotherapy and sustained proliferation of glioma initiating cells. Here we describe the epigenetic and genetic alterations and their interactions associated with the expression of this signature in glioblastoma. RESULTS: We observe prominent hypermethylation of the HOXA locus 7p15.2 in glioblastoma in contrast to non-tumoral brain. Hypermethylation is associated with a gain of chromosome 7, a hallmark of glioblastoma, and may compensate for tumor-driven enhanced gene dosage as a rescue mechanism by preventing undue gene expression. We identify the CpG island of the HOXA10 alternative promoter that appears to escape hypermethylation in the HOX-high glioblastoma. An additive effect of gene copy gain at 7p15.2 and DNA methylation at key regulatory CpGs in HOXA10 is significantly associated with HOX-signature expression. Additionally, we show concordance between methylation status and presence of active or inactive chromatin marks in glioblastoma-derived spheres that are HOX-high or HOX-low, respectively. CONCLUSIONS: Based on these findings, we propose co-evolution and interaction between gene copy gain, associated with a gain of chromosome 7, and additional epigenetic alterations as key mechanisms triggering a coordinated, but inappropriate, HOX transcriptional program in glioblastoma

EDGeS: a bridge between desktop grids and service grids

Desktop grids and service grids widely used by their different users communities as efficient solutions for making full use of computing power and achieving loads balances across Intranet or Internet. Nevertheless,little work has been done to combine these two grids technologies together to establish a seamless and vast grid resources pool. In this paper we will present a new European FP7 infrastructure project:EDGeS (enabling desktop grids for e-science), which aim to build technological bridges to facilitate interoperability between desktop grid and service grid. We give also a taxonomy of existing grid systems: desktop grids such as BONIC and XtremWeb, service grids such as EGEE. Then we describe furtherly our solution for identifying translation technologies for porting applications between desktop grids and service grids, and vice versa. There are three themes in our solution, which discuss actual popular bridging technologies, user access issues, and distributed data issues about deployment and application development