Enveloping algebras of Malcev algebras

We first discuss the construction by Perez-Izquierdo and Shestakov of universal nonassociative enveloping algebras of Malcev algebras. We then describe recent results on explicit structure constants for the universal enveloping algebras (both nonassociative and alternative) of the 4-dimensional solvable Malcev algebra and the 5-dimensional nilpotent Malcev algebra. We include a proof (due to Shestakov) that the universal alternative enveloping algebra of the real 7-dimensional simple Malcev algebra is isomorphic to the 8-dimensional division algebra of real octonions. We conclude with some brief remarks on tangent algebras of analytic Bol loops and monoassociative loops. This is a revised and expanded version of the survey talk given by the first author at the Second Mile High Conference on Nonassociative Mathematics at the University of Denver (Denver, Colorado, USA, June 22 to 26, 2009).Comment: 15 page

Dimension formulas for the free nonassociative algebra

The free nonassociative algebra contains two subspaces closed under both the commutator and the associator: the Akivis elements and the primitive elements. Every Akivis element is primitive, but there are primitive elements which are not Akivis

Sickle cell trait and risk of cognitive impairment in African-Americans: The REGARDS cohort

Background: Sickle cell anemia may be associated with cognitive dysfunction, and some complications of sickle cell anemia might affect those with sickle cell trait (SCT), so we hypothesized that SCT is a risk factor for cognitive impairment. Methods: The Reasons for Geographic and Racial Differences in Stroke (REGARDS) study enrolled a national cohort of 30,239 white and black Americans from 2003 to 7, who are followed every 6 months. Baseline and annual global cognitive function testing used the Six-Item Screener (SIS), a validated instrument (scores range 0-6; ≤ 4 indicates cognitive impairment). Participants with baseline cognitive impairment and whites were excluded. Logistic regression was used to calculate the association of SCT with incident cognitive impairment, adjusted for risk factors. Linear mixed models assessed multivariable-adjusted change in test scores on a biennially administered 3-test battery measuring learning, memory, and semantic and phonemic fluency. Findings: Among 7743 participants followed for a median of 7·1 years, 85 of 583 participants with SCT (14·6%) developed incident cognitive impairment compared to 902 of 7160 (12·6%) without SCT. In univariate analysis, the odds ratio (OR) of incident cognitive impairment was 1·18 (95% CI: 0·93, 1·51) for those with SCT vs. those without. Adjustment did not impact the OR. There was no difference in change on 3-test battery scores by SCT status (all p > 0·11). Interpretation: In this prospective cohort study of black Americans, SCT was not associated with incident cognitive impairment or decline in test scores of learning, memory and executive function. Funding: National Institutes of Health, American Society of Hematology

Catalysts for long-life closed-cycle CO2 lasers

Long-life, closed-cycle operation of pulsed CO2 lasers requires catalytic CO-O2 recombination both to remove O2, which is formed by discharge-induced CO2 decomposition, and to regenerate CO2. Platinum metal on a tin (IV) oxide substrate (Pt/SnO2) has been found to be an effective catalyst for such recombination in the desired temperature range of 25 to 100 C. This paper presents a description of ongoing research at NASA-LaRC on Pt/SnO2 catalyzed CO-O2 recombination. Included are studies with rare-isotope gases since rare-isotope CO2 is desirable as a laser gas for enhanced atmospheric transmission. Results presented include: (1) achievement of 98% to 100% conversion of a stoichiometric mixture of CO and O2 to CO2 for 318 hours (greater than 1 x 10 to the 6th power seconds), continuous, at a catalyst temperature of 60 C, and (2) development of a technique verified in a 30-hour test, to prevent isotopic scrambling when CO-18 and O-18(2) are reacted in the presence of a common-isotope Pt/Sn O-16(2) catalyst

Age and Sex Are Associated with the Plasma Lipidome: Findings from the GOLDN Study

Background Developing an understanding of the biochemistry of aging in both sexes is critical for managing disease throughout the lifespan. Lipidomic associations with age and sex have been reported, but prior studies are limited by measurements in serum rather than plasma or by participants taking lipid-lowering medications. Methods Our study included lipidomic data from 980 participants aged 18–87 years old from the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN). Participants were off lipid-lowering medications for at least 4 weeks, and signal intensities of 413 known lipid species were measured in plasma. We examined linear age and sex associations with signal intensity of (a) 413 lipid species; (b) 6 lipid classes (glycerolipids, glycerophospholipids, sphingolipids, sterol lipids, fatty acids, and acylcarnitines); and (c) 15 lipid subclasses; as well as with the particle sizes of three lipoproteins. Results Significant age associations were identified in 4 classes, 11 subclasses, 147 species, and particle size of one lipoprotein while significant sex differences were identified in 5 classes, 12 subclasses, 248 species, and particle sizes of two lipoproteins. For many lipid species (n = 97), age-related associations were significantly different between males and females. Age*sex interaction effects were most prevalent among phosphatidylcholines, sphingomyelins, and triglycerides. Conclusion We identified several lipid species, subclasses, and classes that differ by age and sex; these lipid phenotypes may serve as useful biomarkers for lipid changes and associated cardiovascular risk with aging in the future. Future studies of age-related changes throughout the adult lifespan of both sexes are warranted. Trial registration ClinicalTrials.gov NCT00083369; May 21, 2004

Ethical Approaches to Mandating Influenza Vaccinations for Local Health Department Workforce in Georgia

Background: The seasonal influenza illness occurs every year in the United States during the cooler months from October to April, sometimes lasting longer. Although certain populations are more susceptible to this condition, data have shown that otherwise healthy individuals have experienced alarming rates of morbidity and mortality associated with these infections. Despite the CDC’s recommendation for influenza vaccination for all HCWs, compliance have been lagging among local health departments’ workforce. This practice arguably exposes a wide cross section of the U.S. population to the flu, while being served in these facilities. The utilitarian approach provides a framework to examine the ethical implications to the public of mandating influenza vaccination for these employees. Methods: A systematic review of peer-reviewed literature was conducted to address the following research questions: 1) Do local public health departments in Georgia mandate annual influenza vaccinations?  2) What are the ethical considerations for mandating influenza vaccinations for public health employees? and 3) What are the ethical considerations for mandating influenza vaccinations for the community? Twenty-five articles were included in the review. Results: Descriptive analysis shows that there is no mandatory vaccination policy in place for state or local departments in health in the state of Georgia. Most of the literature available relates to policy implementation within acute or long-term care facilities. A systematic review of mandatory influenza vaccination for public health workers focused on four areas: theoretical approaches to increase influenza vaccination coverage and support of, opposition to, and alternative strategies for influenza vaccinations. Conclusions: The utilitarian approach is sufficient for the influenza vaccination policy- making strategies and in the ethical approaches of mandating influenza vaccinations for local health department workforce in Georgia if need be, for vaccination targets are to be achieved

Whole-exome Sequencing and an iPSC-Derived Cardiomyocyte Model Provides a Powerful Platform for Gene Discovery in Left Ventricular Hypertrophy

Rationale: Left ventricular hypertrophy (LVH) is a heritable predictor of cardiovascular disease, particularly in blacks. Objective: Determine the feasibility of combining evidence from two distinct but complementary experimental approaches to identify novel genetic predictors of increased LV mass. Methods: Whole-exome sequencing (WES) was conducted in seven African-American sibling trios ascertained on high average familial LV mass indexed to height (LVMHT) using Illumina HiSeq technology. Identified missense or nonsense (MS/NS) mutations were examined for association with LVMHT using linear mixed models adjusted for age, sex, body weight, and familial relationship. To functionally assess WES findings, human induced pluripotent stem cell-derived cardiomyocytes (induced pluripotent stem cell-CM) were stimulated to induce hypertrophy; mRNA sequencing (RNA-seq) was used to determine gene expression differences associated with hypertrophy onset. Statistically significant findings under both experimental approaches identified LVH candidate genes. Candidate genes were further prioritized by seven supportive criteria that included additional association tests (two criteria), regional linkage evidence in the larger HyperGEN cohort (one criterion), and publically available gene and variant based annotations (four criteria). Results: WES reads covered 91% of the target capture region (of size 37.2 MB) with an average coverage of 65×. WES identified 31,426 MS/NS mutations among the 21 individuals. A total of 295 MS/NS variants in 265 genes were associated with LVMHT with q-value <0.25. Of the 265 WES genes, 44 were differentially expressed (P < 0.05) in hypertrophied cells. Among the 44 candidate genes identified, 5, including HLA-B, HTT, MTSS1, SLC5A12, and THBS1, met 3 of 7 supporting criteria. THBS1 encodes an adhesive glycoprotein that promotes matrix preservation in pressure-overload LVH. THBS1 gene expression was 34% higher in hypertrophied cells (P = 0.0003) and a predicted conserved and damaging NS variant in exon 13 (A2099G) was significantly associated with LVHMT (P = 4 × 10−6). Conclusion: Combining evidence from cutting-edge genetic and cellular experiments can enable identification of novel LVH risk loci

SNPs located at CpG sites modulate genome-epigenome interaction

DNA methylation is an important molecular-level phenotype that links genotypes and complex disease traits. Previous studies have found local correlation between genetic variants and DNA methylation levels (cis-meQTLs). However, general mechanisms underlying cis-meQTLs are unclear. We conducted a cis-meQTL analysis of the Genetics of Lipid Lowering Drugs and Diet Network data (n = 593). We found that over 80% of genetic variants at CpG sites (meSNPs) are meQTL loci (P-value < 10(−9)), and meSNPs account for over two thirds of the strongest meQTL signals (P-value < 10(−200)). Beyond direct effects on the methylation of the meSNP site, the CpG-disrupting allele of meSNPs were associated with lowered methylation of CpG sites located within 45 bp. The effect of meSNPs extends to as far as 10 kb and can contribute to the observed meQTL signals in the surrounding region, likely through correlated methylation patterns and linkage disequilibrium. Therefore, meSNPs are behind a large portion of observed meQTL signals and play a crucial role in the biological process linking genetic variation to epigenetic changes