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Surface heat flux estimates from NCAR electra data over the pacific warm pool during TOGA COARE
The warm pool region of the western tropical Pacific is of particular interest to atmospheric dynamics because it represents a significant source of energy to the atmosphere. A better understanding of heat transfer driven by mesoscale and turbulent circulations within this region could lead to improved global circulation models, and therefore to improved prediction of global weather patterns. A first step to this understanding is to evaluate empirical data as well as the methods used to estimate heat transfer, or heat flux, at the surface. Of specific interest here are latent heat flux, the heat transfer associated with evaporation, and sensible heat flux, the heat transfer associated with convection and conduction. In this paper, two different methods of turbulent flux calculation, eddy correlation and the bulk aerodynamic method are compared. Eddy correlation directly uses turbulence measurements to estimate heat flux whereas the bulk aerodynamic method relies on similarity theory to relate heat flux to mean flow quantities. A brief discussion of selection of averaging length based on flight altitude is included, as well as a comparison of errors introduced in averaging velocity as a scalar or as a vector. Errors introduced by averaging, including mesoscale flux enhancement, are evaluated for strong and weak wind cases during relatively light convection in the region. Finally, month to month variability in heat flux is evaluated in an effort to further understand the accuracy of various approximations used in flux calculation
Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization.
The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD
Human Muscle Satellite Cells as Targets of Chikungunya Virus Infection
BACKGROUND: Chikungunya (CHIK) virus is a mosquito-transmitted alphavirus that causes in humans an acute infection characterised by fever, polyarthralgia, head-ache, and myalgia. Since 2005, the emergence of CHIK virus was associated with an unprecedented magnitude outbreak of CHIK disease in the Indian Ocean. Clinically, this outbreak was characterized by invalidating poly-arthralgia, with myalgia being reported in 97.7% of cases. Since the cellular targets of CHIK virus in humans are unknown, we studied the pathogenic events and targets of CHIK infection in skeletal muscle. METHODOLOGY/PRINCIPAL FINDINGS: Immunohistology on muscle biopsies from two CHIK virus-infected patients with myositic syndrome showed that viral antigens were found exclusively inside skeletal muscle progenitor cells (designed as satelllite cells), and not in muscle fibers. To evaluate the ability of CHIK virus to replicate in human satellite cells, we assessed virus infection on primary human muscle cells; viral growth was observed in CHIK virus-infected satellite cells with a cytopathic effect, whereas myotubes were essentially refractory to infection. CONCLUSIONS/SIGNIFICANCE: This report provides new insights into CHIK virus pathogenesis, since it is the first to identify a cellular target of CHIK virus in humans and to report a selective infection of muscle satellite cells by a viral agent in humans
Smoking, Sex, and Non–Small Cell Lung Cancer: Steroid Hormone Receptors in Tumor Tissue (S0424)
Genetic loci associated with heart rate variability and their effects on cardiac disease risk
Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate (-0.74<r g <-0.55) and blood pressure (-0.35<r g <-0.20). These findings provide clinically relevant biological insight into heritable variation in vagal heart rhythm regulation, with a key role for genetic variants (GNG11, RGS6) that influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization
Erratum : Genetic loci associated with heart rate variability and their effects on cardiac disease risk
This corrects the article DOI: 10.1038/ncomms15805
Erratum : Genetic loci associated with heart rate variability and their effects on cardiac disease risk
This corrects the article DOI: 10.1038/ncomms15805
Genetic loci associated with heart rate variability and their effects on cardiac disease risk (vol 8, pg 15805, 2017)
status: publishe
Erratum: Genetic loci associated with heart rate variability and their effects on cardiac disease risk
This corrects the article DOI: 10.1038/ncomms15805.status: publishe