Carnegie Supernova Project-I and -II: Measurements of H0H_0 using Cepheid, TRGB, and SBF Distance Calibration to Type Ia Supernovae

We present an analysis of Type Ia Supernovae (SNe~Ia) from both the Carnegie Supernova Project~I (CSP-I) and II (CSP-II), and extend the Hubble diagram from the optical to the near-infrared wavelengths ($uBgVriYJH$). We calculate the Hubble constant, $H_0$, using various distance calibrators: Cepheids, Tip of the Red Giant Branch (TRGB), and Surface Brightness Fluctuations (SBF). Combining all methods of calibrations, we derive $\rm H_0=71.76 \pm 0.58 \ (stat) \pm 1.19 \ (sys) \ km \ s^{-1} \ Mpc^{-1}$from$B$-band, and$\rm H_0=73.22 \pm 0.68 \ (stat) \pm 1.28 \ (sys) \ km \ s^{-1} \ Mpc^{-1}$from$H$-band. By assigning equal weight to the Cepheid, TRGB, and SBF calibrators, we derive the systematic errors required for consistency in the first rung of the distance ladder, resulting in a systematic error of$1.2\sim 1.3 \rm \ km \ s^{-1} \ Mpc^{-1}$in$H_0$. As a result, relative to the statistics-only uncertainty, the tension between the late-time$H_0$we derive by combining the various distance calibrators and the early-time$H_0$from the Cosmic Microwave Background is reduced. The highest precision in SN~Ia luminosity is found in the$Y$band ($0.12\pm0.01$mag), as defined by the intrinsic scatter ($\sigma_{int}$). We revisit SN~Ia Hubble residual-host mass correlations and recover previous results that these correlations do not change significantly between the optical and the near-infrared wavelengths. Finally, SNe~Ia that explode beyond 10 kpc from their host centers exhibit smaller dispersion in their luminosity, confirming our earlier findings. Reduced effect of dust in the outskirt of hosts may be responsible for this effect.Comment: Revised calculations are made. Will be resubmitted to Ap

Development and testing of innovative patient resources for the management of coronary heart disease (CHD): a descriptive study

BACKGROUND: Although heart disease is a major cause of morbidity and mortality the majority of patients do not access existing rehabilitation programs and patient resources are not designed to facilitate patient choice and decision-making. The objective of this study was to develop and test a series of risk factor modules and corresponding patient information leaflets for secondary prevention of CHD. METHODS: In phase one, a series of risk factor modules and management options were developed following analysis of literature and interviews with health professionals. In phase two, module information leaflets were developed using published guidelines and interviews of people with CHD. In phase three, the leaflets were tested for quality (DISCERN), readability (Flesch) and suitability (SAM) and were compared to the existing cardiac rehabilitation (CR) information leaflet. Finally, the patients assessed the leaflets for content and relevance. RESULTS: Four key risk factors identified were cholesterol, blood pressure, smoking and physical inactivity. Choice management options were selected for each risk factor and included medical consultation, intensive health professional led program, home program and self direction. Patient information needs were then identified and leaflets were developed. DISCERN quality scores were high for cholesterol (62/80), blood pressure (59/80), smoking (62/80) and physical activity (62/80), all scoring 4/5 for overall rating. The mean Flesch readability score was 75, representing "fairly easy to read", all leaflets scored in the superior category for suitability and were reported to be easy to understand, useful and motivating by persons with CHD risk factors. The developed leaflets scored higher on each assessment than the existing CR leaflets. CONCLUSION: Using a progressive three phase approach, a series of risk factor modules and information leaflets were successfully developed and tested. The leaflets will contribute to shared-decision making and empowerment for persons with CHD

iPhone ECG application for community screening to detect silent atrial fibrillation: a novel technology to prevent stroke.

Atrial fibrillation (AF) is the most common sustained arrhythmia, and its prevalence increases with age. In those aged 65 or older, screening studies reveal the prevalence (in AF at time of screening) to be 4.4%, with 1.4% of those having previously undiagnosed AF [1]. In our own study of ambulant patients, 6.7% of those ? 65 years were in AF and in 10% of these, AF was incidentally detected, most without symptoms of palpitations or the elevation of resting heart rate [2].AF is associated with increased morbidity and mortality including a 5-fold increased risk of stroke. Since many with AF are asymptomatic, presentation with a complication such as stroke may be the first manifestation of this arrhythmia. In up to one quarter of cases of ischemic stroke, a cause is not found and subclinical AF is a likely aetiological factor. A recent pacemaker study revealed a significant association between device-detected silent AF and the risk of stroke or systemic embolization [3].With temporal trends showing an increasing AF incidence, in part due to the aging population, a community screening program to detect silent AF could have a significant impact on stroke prevention. However, until now, community screening with ECGs has not been thought cost-effective for AF detection [4].The development of new technology, such as an iPhone application which records a high quality single lead ECG (Fig. 1), makes mass ECG screening feasible. We assessed the accuracy of the iPhone ECG as a diagnostic screening tool for the detection of AF by comparing it with a contemporaneous 12-lead ECG interpreted by a cardiologist

Pre-treatment with the synthetic antioxidant T-butyl bisphenol protects cerebral tissues from experimental ischemia reperfusion injury

Treatments to inhibit or repair neuronal cell damage sustained during focal ischemia/reperfusion injury in stroke are largely unavailable. We demonstrate that dietary supplementation with the antioxidant di-tert-butyl-bisphenol (BP) before injury decreases infarction and vascular complications in experimental stroke in an animal model. We confirm that BP, a synthetic polyphenol with superior radical-scavenging activity than vitamin E, crosses the blood-brain barrier and accumulates in rat brain. Supplementation with BP did not affect blood pressure or endogenous vitamin E levels in plasma or cerebral tissue. Pre-treatment with BP significantly lowered lipid, protein and thiol oxidation and decreased infarct size in animals subjected to middle cerebral artery occlusion (2 h) and reperfusion (24 h) injury. This neuroprotective action was accompanied by down-regulation of hypoxia inducible factor-1α and glucose transporter-1 mRNA levels, maintenance of neuronal tissue ATP concentration and inhibition of pro-apoptotic factors that together enhanced cerebral tissue viability after injury. That pre-treatment with BP ameliorates oxidative damage and preserves cerebral tissue during focal ischemic insult indicates that oxidative stress plays at least some causal role in promoting tissue damage in experimental stroke. The data strongly suggest that inhibition of oxidative stress through BP scavenging free radicals in vivo contributes significantly to neuroprotection. We demonstrate that pre-treatment with ditert-butyl bisphenol(Di-t-Bu-BP) inhibits lipid, protein, and total thiol oxidation and decreases caspase activation and infarct size in rats subjected to middle cerebral artery occlusion (2 h) and reperfusion (24 h) injury. These data suggest that inhibition of oxidative stress contributes significantly to neuroprotection. We demonstrate that pre-treatment with ditert-butyl bisphenol(Di-t-Bu-BP) inhibits lipid, protein, and total thiol oxidation and decreases caspase activation and infarct size in rats subjected to middle cerebral artery occlusion (2 h) and reperfusion (24 h) injury. These data suggest that inhibition of oxidative stress contributes significantly to neuroprotection.15 page(s

Incidence and determinants of myocardial infarction following percutaneous coronary interventions according to the revised Joint Task Force definition of troponin T elevation

Background: Elevations in troponin T (TnT) occur frequently following percutaneous coronary intervention (PCI) and are associated with an adverse prognosis. The Joint ESC/ACC/AHA/WHF Task Force have released a proposal for a universal definition of myocardial infarction (MI), including diagnostic criteria for PCI associated MI. This is based on a TnT cut-point of more than three times the 99th percentile (0.03 ng/ml), which better reflects the precision of the assay. Our study investigated the incidence and predictive factors of a PCI associated MI, using the revised definition. Methods: 325 patients were studied following PCI with stenting. TnT was collected at both 8 and 18 h following PCI in patients with either stable or unstable angina and normal baseline TnT levels. Comparison was made of both clinical and procedural characteristics of patients with and without a rise in TnT following intervention, using cut points of 0.01 and 0.03 ng/ml. Results: TnT was elevated ≥ 0.03 ng/ml in 27% and ≥ 0.01 ng/ml in 39% of patients following PCI. Troponin elevation was significantly more likely in those patients who experienced peri-procedural ischemic symptoms or EKG changes, or in whom abciximab was used. The variables associated with a troponin rise showed a greater difference between TnT positive and negative patients when using 0.03 ng/ml compared to 0.01 ng/ml, suggesting that this may be a better definition of PCI-related MI. Conclusions: Approximately one-quarter of low risk patients experience a procedural MI according to the revised definition. Rises in troponin were significantly associated with peri-procedural ischemic symptoms and EKG changes, and abciximab use, consistent with this level of TnT reflecting true myocardial necrosis.7 page(s

Serum Amyloid A Receptor Blockade and Incorporation into High-Density Lipoprotein Modulates Its Pro-Inflammatory and Pro-Thrombotic Activities on Vascular Endothelial Cells

The acute phase protein serum amyloid A (SAA), a marker of inflammation, induces expression of pro-inflammatory and pro-thrombotic mediators including ICAM-1, VCAM-1, IL-6, IL-8, MCP-1 and tissue factor (TF) in both monocytes/macrophages and endothelial cells, and induces endothelial dysfunction—a precursor to atherosclerosis. In this study, we determined the effect of pharmacological inhibition of known SAA receptors on pro-inflammatory and pro-thrombotic activities of SAA in human carotid artery endothelial cells (HCtAEC). HCtAEC were pre-treated with inhibitors of formyl peptide receptor-like-1 (FPRL-1), WRW4; receptor for advanced glycation-endproducts (RAGE), (endogenous secretory RAGE; esRAGE) and toll-like receptors-2/4 (TLR2/4) (OxPapC), before stimulation by added SAA. Inhibitor activity was also compared to high-density lipoprotein (HDL), a known inhibitor of SAA-induced effects on endothelial cells. SAA significantly increased gene expression of TF, NFκB and TNF and protein levels of TF and VEGF in HCtAEC. These effects were inhibited to variable extents by WRW4, esRAGE and OxPapC either alone or in combination, suggesting involvement of endothelial cell SAA receptors in pro-atherogenic gene expression. In contrast, HDL consistently showed the greatest inhibitory action, and often abrogated SAA-mediated responses. Increasing HDL levels relative to circulating free SAA may prevent SAA-mediated endothelial dysfunction and ameliorate atherogenesis