Dissociation of virtual photons in events with a leading proton at HERA

The ZEUS detector has been used to study dissociation of virtual photons in events with a leading proton, gamma^* p -> X p, in e^+p collisions at HERA. The data cover photon virtualities in two ranges, 0.03<Q^2<0.60 GeV^2 and 2<Q^2<100 GeV^2, with M_X>1.5 GeV, where M_X is the mass of the hadronic final state, X. Events were required to have a leading proton, detected in the ZEUS leading proton spectrometer, carrying at least 90% of the incoming proton energy. The cross section is presented as a function of t, the squared four-momentum transfer at the proton vertex, Phi, the azimuthal angle between the positron scattering plane and the proton scattering plane, and Q^2. The data are presented in terms of the diffractive structure function, F_2^D(3). A next-to-leading-order QCD fit to the higher-Q^2 data set and to previously published diffractive charm production data is presented

Abstract 4404: Variation in the 4q25 Chromosomal Locus Predicts New-Onset Atrial Fibrillation after Cardiac Surgery

Atrial fibrillation (AF) is the most common adverse event following cardiac surgery. A recent genome wide association study identified SNPs associated with AF on chromosome 4q25 adjacent to PITX2, a cardiac transcription factor. However, the role of these genetic variants in post-CABG AF remains unknown. We used clinical and genomic data from 3 major cardiovascular surgical programs to determine the role of 4q25 variants in new-onset postoperative AF. We conducted a prospective observational study of 1,551 consecutive patients undergoing CABG surgery within 3 US centers. Haplotype tagging SNPs encompassing ~300kbp of PITX2 genic region were genotyped. In a discovery cohort of 566 patients, the previously identified SNPs associated with clinical and genomic multivariate predictors of postoperative AF were identified and then assessed in a validation cohort of 985 patients. In the discovery and replication cohorts, 31.4% and 30.0% of patients developed postoperative AF, respectively. A multivariable logistic model of the occurrence of postoperative AF confirmed older age and prior AF to be risk factors for the development of AF. 4q25 SNPs previously associated with ambulatory AF, and other SNPs in linkage disequilibrium described a haplotype that was significantly associated with new-onset postoperative AF. Odds ratio for the associated SNPs ranged between 1.50 and 1.87 (P&lt;10 – 6) in the validation cohort, after accounting for clinical covariates. No SNP within 90kbp of the PITX2 coding region was associated with AF. We have shown in discovery and validation cohorts that non-coding 4q25 SNPs associated with ambulatory AF are also strongly associated with postoperative AF. </jats:p

New Organochalcogen Multitarget Drug: Synthesis and Antioxidant and Antitumoral Activities of Chalcogenozidovudine Derivatives

In this article we present the synthesis, characterization, and in vitro biological and biochemical activities of new chalcogenozidovudine derivatives as antioxidant (inhibition of TBARS in brain membranes and thiol peroxidase-like activity) as well as antitumoral agents in bladder carcinoma 5637. A prominent response was obtained for the selected chalcogenonucleosides, showing effective antioxidant and antitumoral activities

Unbiased screen for interactors of leucine-rich repeat kinase 2 supports a common pathway for sporadic and familial Parkinson disease

Mutations in leucine-rich repeat kinase 2 (LRRK2) cause inherited Parkinson disease (PD), and common variants around LRRK2 are a risk factor for sporadic PD. Using protein-protein interaction arrays, we identified BCL2-associated athanogene 5, Rab7L1 (RAB7, member RAS oncogene family-like 1), and Cyclin-G-associated kinase as binding partners of LRRK2. The latter two genes are candidate genes for risk for sporadic PD identified by genome-wide association studies. These proteins form a complex that promotes clearance of Golgi-derived vesicles through the autophagy-lysosome system both in vitro and in vivo. We propose that three different genes for PD have a common biological function. More generally, data integration from multiple unbiased screens can provide insight into human disease mechanisms