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Objective: To investigate changes in quality of life (QoL), cognition and functional status according to arrhythmia recurrence after atrial fibrillation (AF) ablation.Methods: We compared QoL, cognition and functional status in patients with recurrent atrial tachycardia (AT)/AF versus those without recurrent AT/AF in the AXAFA-AFNET 5 clinical trial. We also sought to identify factors associated with improvement in QoL and functional status following AF ablation by overall change scores with and without analysis of covariance (ANCOVA).Results: Among 518 patients who underwent AF ablation, 154 (29.7%) experienced recurrent AT/AF at 3 months. Patients with recurrent AT/AF had higher mean CHA2DS2-VASc scores (2.8 vs 2.3, p<0.001) and more persistent forms of AF (51 vs 39%, p=0.012). Median changes in the SF-12 physical (3 (25th, 75th: -1, 8) vs 1 (-5, 8), p=0.026) and mental scores (2 (-3, 9) vs 0 (-4, 5), p=0.004), EQ-5D (0 (0,2) vs 0 (-0.1, 0.1), p=0.027) and Karnofsky functional status scores (10 (0, 10) vs 0 (0, 10), p=0.001) were more favourable in patients without recurrent AT/AF. In the overall cohort, the proportion with at least mild cognitive impairment (Montreal Cognitive Assessment <26) declined from 30.3% (n=157) at baseline to 21.8% (n=113) at follow-up. ANCOVA identified greater improvement in Karnofsky functional status (p<0.001) but not SF-12 physical (p=0.238) or mental scores (p=0.065) in those without recurrent AT/AF compared with patients with recurrent AT/AF.Conclusions: Patients without recurrent AT/AF appear to experience greater improvement in functional status but similar QoL as those with recurrent AT/AF after AF ablation. [ABSTRACT FROM AUTHOR]

Introduction: Altered lipid metabolism is implicated in Alzheimer's disease (AD), but the mechanisms remain obscure. Aging‐related declines in circulating plasmalogens containing omega‐3 fatty acids may increase AD risk by reducing plasmalogen availability. Methods: We measured four ethanolamine plasmalogens (PlsEtns) and four closely related phosphatidylethanolamines (PtdEtns) from the Alzheimer's Disease Neuroimaging Initiative (ADNI; n = 1547 serum) and University of Pennsylvania (UPenn; n = 112 plasma) cohorts, and derived indices reflecting PlsEtn and PtdEtn metabolism: PL‐PX (PlsEtns), PL/PE (PlsEtn/PtdEtn ratios), and PBV (plasmalogen biosynthesis value; a composite index). We tested associations with baseline diagnosis, cognition, and cerebrospinal fluid (CSF) AD biomarkers. Results: Results revealed statistically significant negative relationships in ADNI between AD versus CN with PL‐PX (P = 0.007) and PBV (P = 0.005), late mild cognitive impairment (LMCI) versus cognitively normal (CN) with PL‐PX (P = 2.89 × 10−5) and PBV (P = 1.99 × 10−4), and AD versus LMCI with PL/PE (P = 1.85 × 10−4). In the UPenn cohort, AD versus CN diagnosis associated negatively with PL/PE (P = 0.0191) and PBV (P = 0.0296). In ADNI, cognition was negatively associated with plasmalogen indices, including Alzheimer's Disease Assessment Scale 13‐item cognitive subscale (ADAS‐Cog13; PL‐PX: P = 3.24 × 10−6; PBV: P = 6.92 × 10−5) and Mini‐Mental State Examination (MMSE; PL‐PX: P = 1.28 × 10−9; PBV: P = 6.50 × 10−9). In the UPenn cohort, there was a trend toward a similar relationship of MMSE with PL/PE (P = 0.0949). In ADNI, CSF total‐tau was negatively associated with PL‐PX (P = 5.55 × 10−6) and PBV (P = 7.77 × 10−6). Additionally, CSF t‐tau/Aβ1‐42 ratio was negatively associated with these same indices (PL‐PX, P = 2.73 × 10−6; PBV, P = 4.39 × 10−6). In the UPenn cohort, PL/PE was negatively associated with CSF total‐tau (P = 0.031) and t‐tau/Aβ1‐42 (P = 0.021). CSF Aβ1‐42 was not significantly associated with any of these indices in either cohort. Discussion: These data extend previous studies by showing an association of decreased plasmalogen indices with AD, mild cognitive impairment (MCI), cognition, and CSF tau. Future studies are needed to better define mechanistic relationships, and to test the effects of interventions designed to replete serum plasmalogens. [ABSTRACT FROM AUTHOR]

This study uses county-level surveillance data to systematically analyze geographic variation and clustering of persons living with diagnosed HIV (PLWH) in the southern United States in 2011. Clusters corresponding to large metropolitan areas – including Miami, Atlanta, and Baltimore – had HIV prevalence rates higher (p < .001) than the regional rate. Regression analysis within the counties included in these clusters determined that race was a significant indicator for PLWH. These results provide a general picture of the distribution of PLWH in the southern United States at the county level and provide insights for identifying local geographic areas with a high number of PLWH, as well as subpopulations that may have an increased risk of infection. [ABSTRACT FROM PUBLISHER]

Use of enzyme-linked immunosorbent assay (ELISA) is recommended for control of Johne's disease (JD) in the cattle industry. A recent report showed that prevalence of JD in dairy farms could be reduced by applying an ELISA-based control strategy, even though the sensitivity of the current ELISA has been reported to be lower than 30%. We previously developed a more sensitive ELISA test (EVELISA; Ethanol Vortex ELISA) for diagnosis of JD and, in this report, aimed to evaluate cost-effectiveness of the EVELISA in JD control compared to that of a current ELISA test. For simulation of population dynamics, we developed a deterministic, discrete-time mathematical model incorporating contact structure, possibility of adult infection and the concept of order of events. In our model, the number of animals infected with the causative agent of JD, Mycobacterium avium subsp. paratuberculosis (MAP), increases in a 10-year simulation if no JD control measure is applied. When test results of ELISA or EVELISA are used for JD control, the increase in MAP-infected animals is less significant. According to our model, EVELISA-based control measures increase the annual per capita revenue of US dairy farms when compared to no JD control and ELISA-based JD control, respectively. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common cause of dementia. The mechanism of disease development and progression is not well understood, but increasing evidence suggests multifactorial etiology, with a number of genetic, environmental, and aging-related factors. There is a growing body of evidence that metabolic defects may contribute to this complex disease. To interrogate the relationship between system level metabolites and disease susceptibility and progression, the AD Metabolomics Consortium (ADMC) in partnership with AD Neuroimaging Initiative (ADNI) is creating a comprehensive biochemical database for patients in the ADNI1 cohort. We used the Biocrates Bile Acids platform to evaluate the association of metabolic levels with disease risk and progression. We detail the quantitative metabolomics data generated on the baseline samples from ADNI1 and ADNIGO/2 (370 cognitively normal, 887 mild cognitive impairment, and 305 AD). Similar to our previous reports on ADNI1, we present the tools for data quality control and initial analysis. This data descriptor represents the third in a series of comprehensive metabolomics datasets from the ADMC on the ADNI. Measurement(s) bile acid • Medication Technology Type(s) ultra high performance liquid chromatography with mass spectrometer • Resource Informatics Factor Type(s) age • biological sex • cognitive state Sample Characteristic - Organism Homo sapiens Machine-accessible metadata file describing the reported data: 10.6084/m9.figshare.9724652 [ABSTRACT FROM AUTHOR]

Background: Appropriate antithrombotic regimens for patients with atrial fibrillation who have an acute coronary syndrome or have undergone percutaneous coronary intervention (PCI) are unclear.Methods: In an international trial with a two-by-two factorial design, we randomly assigned patients with atrial fibrillation who had an acute coronary syndrome or had undergone PCI and were planning to take a P2Y12 inhibitor to receive apixaban or a vitamin K antagonist and to receive aspirin or matching placebo for 6 months. The primary outcome was major or clinically relevant nonmajor bleeding. Secondary outcomes included death or hospitalization and a composite of ischemic events.Results: Enrollment included 4614 patients from 33 countries. There were no significant interactions between the two randomization factors on the primary or secondary outcomes. Major or clinically relevant nonmajor bleeding was noted in 10.5% of the patients receiving apixaban, as compared with 14.7% of those receiving a vitamin K antagonist (hazard ratio, 0.69; 95% confidence interval [CI], 0.58 to 0.81; P<0.001 for both noninferiority and superiority), and in 16.1% of the patients receiving aspirin, as compared with 9.0% of those receiving placebo (hazard ratio, 1.89; 95% CI, 1.59 to 2.24; P<0.001). Patients in the apixaban group had a lower incidence of death or hospitalization than those in the vitamin K antagonist group (23.5% vs. 27.4%; hazard ratio, 0.83; 95% CI, 0.74 to 0.93; P = 0.002) and a similar incidence of ischemic events. Patients in the aspirin group had an incidence of death or hospitalization and of ischemic events that was similar to that in the placebo group.Conclusions: In patients with atrial fibrillation and a recent acute coronary syndrome or PCI treated with a P2Y12 inhibitor, an antithrombotic regimen that included apixaban, without aspirin, resulted in less bleeding and fewer hospitalizations without significant differences in the incidence of ischemic events than regimens that included a vitamin K antagonist, aspirin, or both. (Funded by Bristol-Myers Squibb and Pfizer; AUGUSTUS ClinicalTrials.gov number, NCT02415400.). [ABSTRACT FROM AUTHOR]