Deoxyribonucleic acid damage in human lymphocytes after percutaneous transluminal coronary angioplasty

AbstractObjectivesWe investigated the presence of oxidative deoxyribonucleic acid (DNA) damage in the peripheral lymphocytes of patients undergoing percutaneous transluminal coronary angioplasty (PTCA) by using the micronucleus test and comet assay, which are sensitive biomarkers of DNA damage.BackgroundAlthough it has recognized that ischemia-reperfusion can induce oxidative DNA damage, its occurrence in patients undergoing PTCA has not yet been demonstrated.MethodsThree groups of patients were enrolled: 30 patients with documented coronary heart disease who underwent elective PTCA (group I); 25 patients who underwent elective coronary angiography for diagnostic purpose (group II); and 27 healthy, age- and gender-matched subjects (group III). For each subject, the frequency of micronucleated binucleated (MNBN) cells, DNA single-strand breaks (SSBs), endonuclease III-sensitive sites, and sites sensitive to formamidopyrimidine glycosylase (FPG) were analyzed before and after diagnostic procedures.ResultsThe mean basal values of MNBN cells (p = 0.04), DNA-SSBs (p = 0.001), endonuclease III-sensitive sites (p = 0.002), and FPG sites (p < 0.0001) were significantly higher in groups I and II than in group III. A high significant increase of MNBN cell frequency was observed in group I after the PTCA procedure (11.0 ± 1.3 vs. 19.8 ± 1.6, p < 0.0001), whereas no significant difference was observed in group II (10.2 ± 1.3 vs. 12.9 ± 1.4, p = 0.18). A significant positive correlation was observed between the increase in the MNBN cell rate and total inflation time during PTCA (R = 0.549, p = 0.0017). The levels of DNA-SSBs (11.7 ± 1.4 vs. 26.5 ± 3.0, p = 0.0003) and FPG sites (13.8 ± 1.8 vs. 22.5 ± 2.4, p = 0.01) were also higher after PTCA.ConclusionsOur results provide evidence for oxidative DNA damage after PTCA, likely related to ischemia-reperfusion injury

First observation of forward Z→bbˉZ \rightarrow b \bar{b} production in pppp collisions at s=8\sqrt{s}=8 TeV

The decay Z→bb¯ is reconstructed in pp collision data, corresponding to 2 fb −1 of integrated luminosity, collected by the LHCb experiment at a centre-of-mass energy of s=8 TeV. The product of the Z production cross-section and the Z→bb¯ branching fraction is measured for candidates in the fiducial region defined by two particle-level b -quark jets with pseudorapidities in the range 2.220 GeV and dijet invariant mass in the range 4520$GeV and dijet invariant mass in the range$45 < m_{jj} < 165$GeV. From a signal yield of$5462 \pm 763$$Z \rightarrow b \bar{b}$events, where the uncertainty is statistical, a production cross-section times branching fraction of$332 \pm 46 \pm 59$pb is obtained, where the first uncertainty is statistical and the second systematic. The measured significance of the signal yield is 6.0 standard deviations. This measurement represents the first observation of the$Z \rightarrow b \bar{b}$production in the forward region of$pp$ collisions

Study of the lineshape of the chi(c1) (3872) state

A study of the lineshape of the chi(c1) (3872) state is made using a data sample corresponding to an integrated luminosity of 3 fb(-1) collected in pp collisions at center-of-mass energies of 7 and 8 TeV with the LHCb detector. Candidate chi(c1)(3872) and psi(2S) mesons from b-hadron decays are selected in the J/psi pi(+)pi(-) decay mode. Describing the lineshape with a Breit-Wigner function, the mass splitting between the chi(c1 )(3872) and psi(2S) states, Delta m, and the width of the chi(c1 )(3872) state, Gamma(Bw), are determined to be (Delta m=185.598 +/- 0.067 +/- 0.068 Mev,)(Gamma BW=1.39 +/- 0.24 +/- 0.10 Mev,) where the first uncertainty is statistical and the second systematic. Using a Flatte-inspired model, the mode and full width at half maximum of the lineshape are determined to be (mode=3871.69+0.00+0.05 MeV.)(FWHM=0.22-0.04+0.13+0.07+0.11-0.06-0.13 MeV, ) An investigation of the analytic structure of the Flatte amplitude reveals a pole structure, which is compatible with a quasibound D-0(D) over bar*(0) state but a quasivirtual state is still allowed at the level of 2 standard deviations

Genetics of bicuspid aortic valve aortopathy

Purpose of review The incidence of aortic dilation and acute complications (rupture and dissection) is higher in patients with a bicuspid aortic valve (BAV), the most frequent congenital heart defect. The present review focuses on the current knowledge in the genetics of BAV, emphasizing the clinical implications for early detection and personalized care. Recent findings BAV is a highly heritable trait, but the genetic causes remain largely elusive. NOTCH1 is the only proven candidate gene to be associated with both familial and sporadic BAV. Other genes have been reported to be associated with BAV, but some of these associations may result from coexisting disease. The application of modern high-throughput technologies (next generation sequencing, genome-wide copy number and genome-wide methylation arrays) have begun to dissect the genetic heterogeneity underlying BAV as well as the diverse molecular pathways involved in the progression of BAV aortopathy. Summary The clinical variability seen in BAV aortopathy, in terms of phenotype and natural/clinical history, suggests complex interactions between primary genetic defects, other modifier genes, epigenetic factors (DNA methylation or histone modifications, microRNA) and environmental factors (disturbed flow). Integrated, more comprehensive studies are needed for elucidating these connections to develop more individualized and accurate risk assessment methods