4f spin density in the reentrant ferromagnet SmMn2Ge2

The spin contribution to the magnetic moment in SmMn2Ge2 has been measured by magnetic Compton scattering in both the low and high temperature ferromagnetic phases. At low temperature, the Sm site is shown to possess a large 4f spin moment of 3.4 +/- 0.1 Bohr magnetons, aligned antiparallel to the total magnetic moment. At high temperature, the data show conclusively that ordered magnetic moments are present on the samarium site.Comment: 5 pages, 2 figures, transferred from PRL to PRB (Rapid Comm.

Marine diatoms grown in chemostats under silicate or ammonium limitation. III. Cellular chemical composition and morphology of Chaetoceros debilis, Skeletonema costatum , and Thalassiosira gravida

Three marine diatoms, Skeletonema costatum, Chaetoceros debilis , and Thalassiosira gravida were grown under no limitation and ammonium or silicate limitation or starvation. Changes in cell morphology were documented with photomicrographs of ammonium and silicate-limited and non-limited cells, and correlated with observed changes in chemical composition. Cultures grown under silicate starvation or limitation showed an increase in particulate carbon, nitrogen and phosporus and chlorophyll a per unit cell volume compared to non-limited cells; particulate silica per cell volume decreased. Si-starved cells were different from Si-limited cells in that the former contained more particulate carbon and silica per cell volume. The most sensitive indicator of silicate limitation or starvation was the ratio C:Si, being 3 to 5 times higher than the values for non-limited cells. The ratios Si:chlorophyll a and S:P were lower and N:Si was higher than non-limited cells by a factor of 2 to 3. The other ratios, C:N, C:P, C:chlorophyll a , N:chlorophyll a , P:chlorophyll a and N:P were considered not to be sensitive indicators of silicate limitation or starvation. Chlorophyll a , and particulate nitrogen per unit cell volume decreased under ammonium limitation and starvation. NH 4 -starved cells contained more chlorophyll a , carbon, nitrogen, silica, and phosphorus per cell volume than NH 4 -limited cells. N:Si was the most sensitive ratio to ammonium limitation or starvation, being 2 to 3 times lower than non-limited cells. Si:chlorophyll a , P:chlorophyll a and N:P were less sensitive, while the ratios C:N, C:chlorophyll a , N:chlorophyll a , C:Si, C:P and Si:P were the least sensitive. Limited cells had less of the limiting nutrient per unit cell volume than starved cells and more of the non-limiting nutrients (i.e., silica and phosphorus for NH 4 -limited cells). This suggests that nutrient-limited cells rather than nutrient-starved cells should be used along with non-limited cells to measure the full range of potential change in cellular chemical composition for one species under nutrient limitation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46631/1/227_2004_Article_BF00392568.pd

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Multi-ancestry GWAS of the electrocardiographic PR interval identifies 202 loci underlying cardiac conduction

The electrocardiographic PR interval reflects atrioventricular conduction, and is associated with conduction abnormalities, pacemaker implantation, atrial fibrillation (AF), and cardiovascular mortality. Here we report a multi-ancestry (N = 293,051) genome-wide association meta-analysis for the PR interval, discovering 202 loci of which 141 have not previously been reported. Variants at identified loci increase the percentage of heritability explained, from 33.5% to 62.6%. We observe enrichment for cardiac muscle developmental/contractile and cytoskeletal genes, highlighting key regulation processes for atrioventricular conduction. Additionally, 8 loci not previously reported harbor genes underlying inherited arrhythmic syndromes and/or cardiomyopathies suggesting a role for these genes in cardiovascular pathology in the general population. We show that polygenic predisposition to PR interval duration is an endophenotype for cardiovascular disease, including distal conduction disease, AF, and atrioventricular pre-excitation. These findings advance our understanding of the polygenic basis of cardiac conduction, and the genetic relationship between PR interval duration and cardiovascular disease

Genetic insights into resting heart rate and its role in cardiovascular disease.

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development