Exp[licit]-A Robot modeling Software based on Exponential Maps

$$Deriving a robot's equation of motion typically requires placing multiple coordinate frames, commonly using the Denavit-Hartenberg convention to express the kinematic and dynamic relationships between segments. This paper presents an alternative using the differential geometric method of Exponential Maps, which reduces the number of coordinate frame choices to two. The traditional and differential geometric methods are compared, and the conceptual and practical differences are detailed. The open-source software, Exp[licit], based on the differential geometric method, is introduced. It is intended for use by researchers and engineers with basic knowledge of geometry and robotics. Code snippets and an example application are provided to demonstrate the benefits of the differential geometric method and assist users to get started with the software.Comment: 8 pages, 5 figure

First Measurement of the 64Ni(gamma,n)63Ni Cross Section

Copyright owned by the author(s) under the terms of the Creative Commons Attribution-Non Commercial-ShareAlike LicenceIn the past 10 years new and more accurate stellar neutron capture cross section measurements have changed and improved the abundance predictions of the weak s process. Among other elements in the region between iron and strontium, most of the copper abundance observed today in the solar system distribution was produced by the s process in massive stars. However, experimental data for the stellar 63Ni(n,gamma)64Ni cross section are still missing, but is strongly required for a reliable prediction of the copper abundances. 63Ni (t1/2 =101.2 a) is a branching point and also bottleneck in the weak s process flow, and abehaves differently during core He and shell C burning. During core He burning the reaction flow proceeds via beta-decay to 63Cu, and a change of the 63Ni(n,gamma)64Ni cross section would have no influence. However, this behavior changes at higher temperatures and neutron densities during the shell C burning phase. Under these conditions, a significant amount of the s process nucleosynthesis flow is passing through the channel 62Ni(n,gamma)63Ni(n,gamma)64Ni. At present only theoretical estimates are available for the 63Ni(n,gamma)64Ni cross section. The corresponding uncertainty affects the production of 63Cu in present s process nucleosynthesis calculations and propagates to the abundances of the heavier species up to A=70. So far, experimental information is also missing for the inverse 64Ni(gamma,n) channel. We have measured for the first time the 64Ni(gamma,n)63Ni cross section and also combined for the first time successfully the photoactivation technique with subsequent Accelerator Mass Spectrometry (AMS). The activations at the ELBE facility in Dresden-Rossendorf were followed by the 63Ni/64Ni determination with AMS at the MLL accelerator laboratory in Garching. First results indicate that theoretical predictions have overestimated this cross section up to now. If this also holds for the inverse channel 63Ni(n,gamma)64Ni, more 63Ni is accumulated during the high neutron density regime of the C shell that will contribute to the final abundance of 63Cu by radiogenic decay. In this case, also a lower s process efficiency is expected for the heavier species along the neutron capture path up to the Ga-Ge regio

Epigenetics as a mechanism driving polygenic clinical drug resistance

Aberrant methylation of CpG islands located at or near gene promoters is associated with inactivation of gene expression during tumour development. It is increasingly recognised that such epimutations may occur at a much higher frequency than gene mutation and therefore have a greater impact on selection of subpopulations of cells during tumour progression or acquisition of resistance to anticancer drugs. Although laboratory-based models of acquired resistance to anticancer agents tend to focus on specific genes or biochemical pathways, such 'one gene : one outcome' models may be an oversimplification of acquired resistance to treatment of cancer patients. Instead, clinical drug resistance may be due to changes in expression of a large number of genes that have a cumulative impact on chemosensitivity. Aberrant CpG island methylation of multiple genes occurring in a nonrandom manner during tumour development and during the acquisition of drug resistance provides a mechanism whereby expression of multiple genes could be affected simultaneously resulting in polygenic clinical drug resistance. If simultaneous epigenetic regulation of multiple genes is indeed a major driving force behind acquired resistance of patients' tumour to anticancer agents, this has important implications for biomarker studies of clinical outcome following chemotherapy and for clinical approaches designed to circumvent or modulate drug resistance

Measurement of the strong interaction induced shift and width of the 1s state of kaonic deuterium at J-PARC

The antikaon-nucleon interaction close to threshold provides crucial information on the interplay between spontaneous and explicit chiral symmetry breaking in low-energy QCD. In this context the importance of kaonic deuterium X-ray spectroscopy has been well recognized, but no experimental results have yet been obtained due to the difficulty of the measurement. We propose to measure the shift and width of the kaonic deuterium 1s state with an accuracy of 60 eV and 140 eV respectively at J-PARC. These results together with the kaonic hydrogen data (KpX at KEK, DEAR and SIDDHARTA at DAFNE) will then permit the determination of values of both the isospin I=0 and I=1 antikaon-nucleon scattering lengths and will provide the most stringent constraints on the antikaon-nucleon interaction, promising a breakthrough. Refined Monte Carlo studies were performed, including the investigation of background suppression factors for the described setup. These studies have demonstrated the feasibility of determining the shift and width of the kaonic deuterium atom 1s state with the desired accuracy of 60 eV and 140 eV.Comment: 12 pages, 9 figure

Roles for H2A.Z and Its Acetylation in GAL1 Transcription and Gene Induction, but Not GAL1-Transcriptional Memory

H2A.Z does not appear to have a role in GAL1 transcriptional memory, but it does have both acetylation-dependent and acetylation-independent roles in GAL1 induction and expression

Tumor Suppressor Protein p53 Recruits Human Sin3B/HDAC1 Complex for Down-Regulation of Its Target Promoters in Response to Genotoxic Stress

Master regulator protein p53, popularly known as the “guardian of genome” is the hub for regulation of diverse cellular pathways. Depending on the cell type and severity of DNA damage, p53 protein mediates cell cycle arrest or apoptosis, besides activating DNA repair, which is apparently achieved by regulation of its target genes, as well as direct interaction with other proteins. p53 is known to repress target genes via multiple mechanisms one of which is via recruitment of chromatin remodelling Sin3/HDAC1/2 complex. Sin3 proteins (Sin3A and Sin3B) regulate gene expression at the chromatin-level by serving as an anchor onto which the core Sin3/HDAC complex is assembled. The Sin3/HDAC co-repressor complex can be recruited by a large number of DNA-binding transcription factors. Sin3A has been closely linked to p53 while Sin3B is considered to be a close associate of E2Fs. The theme of this study was to establish the role of Sin3B in p53-mediated gene repression. We demonstrate a direct protein-protein interaction between human p53 and Sin3B (hSin3B). Amino acids 1–399 of hSin3B protein are involved in its interaction with N-terminal region (amino acids 1–108) of p53. Genotoxic stress induced by Adriamycin treatment increases the levels of hSin3B that is recruited to the promoters of p53-target genes (HSPA8, MAD1 and CRYZ). More importantly recruitment of hSin3B and repression of the three p53-target promoters upon Adriamycin treatment were observed only in p53+/+ cell lines. Additionally an increased tri-methylation of the H3K9 residue at the promoters of HSPA8 and CRYZ was also observed following Adriamycin treatment. The present study highlights for the first time the essential role of Sin3B as an important associate of p53 in mediating the cellular responses to stress and in the transcriptional repression of genes encoding for heat shock proteins or proteins involved in regulation of cell cycle and apoptosis

Structural Biology of Human H3K9 Methyltransferases

SET domain methyltransferases deposit methyl marks on specific histone tail lysine residues and play a major role in epigenetic regulation of gene transcription. We solved the structures of the catalytic domains of GLP, G9a, Suv39H2 and PRDM2, four of the eight known human H3K9 methyltransferases in their apo conformation or in complex with the methyl donating cofactor, and peptide substrates. We analyzed the structural determinants for methylation state specificity, and designed a G9a mutant able to tri-methylate H3K9. We show that the I-SET domain acts as a rigid docking platform, while induced-fit of the Post-SET domain is necessary to achieve a catalytically competent conformation. We also propose a model where long-range electrostatics bring enzyme and histone substrate together, while the presence of an arginine upstream of the target lysine is critical for binding and specificity. Enhanced version: This article can also be viewed as an enhanced version in which the text of the article is integrated with interactive 3D representations and animated transitions. Please note that a web plugin is required to access this enhanced functionality. Instructions for the installation and use of the web plugin are available i