Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.

BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362

Kinematic Evidence For Top-quark Pair Production In W Plus Multijet Events In P(p)over-bar Collisions At Root-s=1.8 Tev

We present a study of W+multijet events that compares the kinematics of the observed events with expectations from direct QCD W+jet production and from production and decay of top quark pairs. The data were collected in the 1992-93 run with the Collider Detector at Fermilab (CDF) from 19.3 pb-1 of proton-antiproton collisions at s =1.8 TeV. A W+2 jet sample and a W+3 jet sample are selected with the requirement that at least the two or three jets have energy transverse with respect to the beam axis in excess of 20 GeV. The jet energy distributions for the W+2 jet sample agree well with the predictions of direct QCD W production. From the W+3 jet events, a "signal sample" with an improved ratio of tt̄ to QCD produced W events is selected by requiring each jet to be emitted centrally in the event center of mass frame. This sample contains 14 events with unusually hard jet ET distributions not well described by expectations for jets from direct QCD W production and other background processes. Using expected jet ET distributions, a relative likelihood is defined and used to determine if an event is more consistent with the decay of tt̄ pairs, with Mtop=170 GeV/c2, than with direct QCD W production. Eight of the 14 signal sample events are found to be more consistent with top-quark than direct QCD W production, while only 1.7 such top-quark-like events are expected in the absence of tt̄. The probability that the observation is due to an upward fluctuation of the number of background events is found to be 0.8%. The robustness of the result was tested by varying the cuts defining the signal sample, and the largest probability for such a fluctuation found was 1.9%. Good agreement in the jet spectra is obtained if jet production from tt̄ pair decays is included. For those events kinematically more consistent with tt̄ we find evidence for a b-quark content in their jets to the extent expected from top quark decay, and larger than expected for background processes. For events with four or more jets, the discrepancy with the predicted jet distributions from direct QCD W production, and the associated excess of b-quark content, is more pronounced. © 1995 The American Physical Societ

Inclusive jet cross section in p\u304p collisions at 1as = 1.8 TeV

The inclusive jet differential cross section has been measured for jet transverse energies, ET, from 15 to 440 GeV, in the pseudorapidity region 0.1 64|\u3b7| 640.7. The results are based on 19.5pb 121 of data collected by the CDF Collaboration at the Fermilab Tevatron collider. The data are compared with QCD predictions for various sets of parton distribution functions. The cross section for jets with ET>200GeV is significantly higher than current predictions based on O(\u3b13s) perturbative QCD calculations. Various possible explanations for the high- ET excess are discussed

Properties of jets in Z boson events from 1.8 TeV p\u304p collisions

We present a study of events with Z bosons and hadronic jets produced in p\uafp collisions at a center-of-mass energy of 1.8 TeV. The data consist of 6708 Z\u2192e+e 12 decays from 106pb 121 of integrated luminosity collected using the CDF detector at the Fermilab Tevatron Collider. The Z+ 65n jet cross sections and jet production properties have been measured for n=1 to 4. The data are compared to predictions of leading-order QCD matrix element calculations with added gluon radiation and simulated parton fragmentation

Measurement of the \u3b3 + D*\ub1 cross section in p\u304p collisions at 1as = 1.8 TeV

We have measured the cross section of gamma + D-*+/- production in &lt;(p)over bar p&gt; collisions at root s = 1.8 TeV using the Collider Detector at Fermilab. In this kinematic region, the Compton scattering process (g(c) --&gt; gamma(c)) is expected to dominate and thus provide a direct link to the charm quark density in the proton. From the 45 +/- 18 gamma + D-*+/- candidates in a 16.4 pb(-1) data sample, we have determined the production cross section to be 0.38 +/- 0.15(stat) +/- 0.11(syst) nb for the rapidity range y(D-*+/-) &lt; 1.2 and y(gamma) &lt; 0.9, and for the transverse momentum range p(T)(D-*+/-) &gt; 6 GeV/c and 16 &lt; p(T)(gamma) &lt; 40 GeV/c. The measured cross section is compared to a theoretical prediction

DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis*

Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving “sensor” proteins that sense the damage, and transmit signals to “transducer” proteins, which, in turn, convey the signals to numerous “effector” proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among the most crucial regulators of apoptosis and performs vital functions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation