Electromagnetic Polarizabilities and Charge Radii of the Nucleons in the Diquark-model

The diquark model is used to calculate the electromagnetic polarizabilities and charge radii of the nucleons for three different potentials. Making the scalar diquark lower in mass introduces a mixing angle $\theta$ between the $\left| 56\right\rangle$ and $\left| 70\right\rangle$ states ,which allows an improvement in value of all 6 properties. Generalizing the Gamov-Teller matrix and the magnetic moment operator to the diquark model gives constraints on this mixing. We obtain for the Richardson potential $\theta =23.2^{\circ },$ $\overline{\alpha }_p=7.9_{-0.9}^{+1.0}\times 10^{-4}fm^3,$ $\overline{\alpha }_n=7.7_{-0.6}^{+0.3}\times 10^{-4}fm^3,$ $\overline{\beta }_p=5.4_{-0.4}^{+1.6}\times 10^{-4}fm^3,$ $\overline{\beta }_n=6.7_{-0.7}^{+1.3}\times 10^{-4}fm^3,$ $\left\langle r^2\right\rangle _p=0.37_{-0.03}^{+0.02}fm^2,$ $\left\langle r^2\right\rangle _n=-0.07_{-0.02}^{+0.03}fm^2.$ Additional pion cloud contributions could improve on all six results.Comment: 15 Pages, Latex, Figs on request, to be published Phys.Lett.B. Minor errors corrected and eqn 5,6,8,9 correcte

DNA Display Selection of Peptide Ligands for a Full-Length Human G Protein-Coupled Receptor on CHO-K1 Cells

The G protein-coupled receptors (GPCRs), which form the largest group of transmembrane proteins involved in signal transduction, are major targets of currently available drugs. Thus, the search for cognate and surrogate peptide ligands for GPCRs is of both basic and therapeutic interest. Here we describe the application of an in vitro DNA display technology to screening libraries of peptide ligands for full-length GPCRs expressed on whole cells. We used human angiotensin II (Ang II) type-1 receptor (hAT1R) as a model GPCR. Under improved selection conditions using hAT1R-expressing Chinese hamster ovary (CHO)-K1 cells as bait, we confirmed that Ang II gene could be enriched more than 10,000-fold after four rounds of selection. Further, we successfully selected diverse Ang II-like peptides from randomized peptide libraries. The results provide more precise information on the sequence-function relationships of hAT1R ligands than can be obtained by conventional alanine-scanning mutagenesis. Completely in vitro DNA display can overcome the limitations of current display technologies and is expected to prove widely useful for screening diverse libraries of mutant peptide and protein ligands for receptors that can be expressed functionally on the surface of CHO-K1 cells

Feather pecking in chickens is genetically related to behavioural and developmental traits

International audienc

A database generator for human brain imaging

Sharing scientific data containing complex information requires new concepts and new technology. NEUROGENERATOR is a database generator for the neuroimaging community. A database generator is a database that generates new databases. The scientists submit raw PET and fMRI data to NEUROGENERATOR, which then processes the data in a uniform way to create databases of homogenous data suitable for data sharing, met-analysis and modelling the human brain at the systems level. These databases are then distributed to the scientists

Diclofenac inhibits tumor necrosis factor-a-induced nuclear factor-kB activation causing synergic hepatocyte apoptosis

Drug-induced liver injury (DILI) is an important clinical problem. It involves crosstalk between drug toxicity and the immune system, but the exact mechanism at the cellular hepatocyte level is not well understood. Here we studied the mechanism of crosstalk in hepatocyte apoptosis caused by diclofenac and the proinflammatory cytokine tumor necrosis factor α (TNF-α). HepG2 cells were treated with diclofenac followed by TNF-α challenge and subsequent evaluation of necrosis and apoptosis. Diclofenac caused a mild apoptosis of HepG2 cells, which was strongly potentiated by TNF-α. A focused apoptosis machinery short interference RNA (siRNA) library screen identified that this TNF-α-mediated enhancement involved activation of caspase-3 through a caspase-8/Bid/APAF1 pathway. Diclofenac itself induced sustained activation of c-Jun N-terminal kinase (JNK) and inhibition of JNK decreased both diclofenac and diclofenac/TNF-α-induced apoptosis. Live cell imaging of GFPp65/RelA showed that diclofenac dampened the TNF-α-mediated nuclear factor kappaB (NF-κB) translocation oscillation in association with reduced NF-κB transcriptional activity. This was associated with inhibition by diclofenac of the TNF-α-induced phosphorylation of the inhibitor of NF-κB alpha (IκBα). Finally, inhibition of IκB kinase β (IKKβ) with BMS-345541 as well as stable lentiviral short hairpin RNA (shRNA)-based knockdown of p65/RelA sensitized hepatocytes towards diclofenac/TNF-α-induced cytotoxicity. Conclusion: Together, our data suggest a model whereby diclofenac-mediated stress signaling suppresses TNF-α-induced survival signaling routes and sensitizes cells to apoptosis. Copyright © 2011 American Association for the Study of Liver Diseases