Neutron structure function and inclusive DIS from H-3 and He-3 at large Bjorken-x

A detailed study of inclusive deep inelastic scattering (DIS) from mirror A = 3 nuclei at large values of the Bjorken variable x is presented. The main purpose is to estimate the theoretical uncertainties on the extraction of the neutron DIS structure function from such nuclear measurements. On one hand, within models in which no modification of the bound nucleon structure functions is taken into account, we have investigated the possible uncertainties arising from: i) charge symmetry breaking terms in the nucleon-nucleon interaction, ii) finite Q**2 effects neglected in the Bjorken limit, iii) the role of different prescriptions for the nucleon Spectral Function normalization providing baryon number conservation, and iv) the differences between the virtual nucleon and light cone formalisms. Although these effects have been not yet considered in existing analyses, our conclusion is that all these effects cancel at the level of ~ 1% for x < 0.75 in overall agreement with previous findings. On the other hand we have considered several models in which the modification of the bound nucleon structure functions is accounted for to describe the EMC effect in DIS scattering from nuclei. It turns out that within these models the cancellation of nuclear effects is expected to occur only at a level of ~ 3%, leading to an accuracy of ~ 12 % in the extraction of the neutron to proton structure function ratio at x ~ 0.7 -0.8$. Another consequence of considering a broad range of models of the EMC effect is that the previously suggested iteration procedure does not improve the accuracy of the extraction of the neutron to proton structure function ratio.Comment: revised version to appear in Phys. Rev. C; main modifications in Section 4; no change in the conclusion

IBD risk loci are enriched in multigenic regulatory modules encompassing putative causative genes.

GWAS have identified >200 risk loci for Inflammatory Bowel Disease (IBD). The majority of disease associations are known to be driven by regulatory variants. To identify the putative causative genes that are perturbed by these variants, we generate a large transcriptome data set (nine disease-relevant cell types) and identify 23,650 cis-eQTL. We show that these are determined by ∼9720 regulatory modules, of which ∼3000 operate in multiple tissues and ∼970 on multiple genes. We identify regulatory modules that drive the disease association for 63 of the 200 risk loci, and show that these are enriched in multigenic modules. Based on these analyses, we resequence 45 of the corresponding 100 candidate genes in 6600 Crohn disease (CD) cases and 5500 controls, and show with burden tests that they include likely causative genes. Our analyses indicate that ≥10-fold larger sample sizes will be required to demonstrate the causality of individual genes using this approach

A five-year follow-up study of schizophrenia in Singapore

Singapore Medical Journal262171-177SIMJ

Molecular analysis of the pRA2 partitioning region: ParB autoregulates parAB transcription and forms a nucleoprotein complex with the plasmid partition site, parS

10.1046/j.1365-2958.2001.02405.xMolecular Microbiology403621-633MOMI

An optimisation framework for yard planning in a container terminal: Case with automated rail-mounted gantry cranes

10.1007/s00291-010-0200-9OR Spectrum323519-54