A 100-Element MODFET Grid Amplifier

A 100-element quasi-optical amplifier is presented. The active devices are custom-fabricated modulation-doped field-effect transistors (MODFETs). Common-mode oscillations were suppressed using resistors in the input gate leads. The grid has 9 dB of gain at 10.1 GHz. The 3-dB bandwidth is 1.2 GHz. We present a model for the gain of the grid versus frequency and compare measurement with theory

Gain and Stability Models for HBT Grid Amplifiers

A 16-element heterojunction bipolar transistor (HBT) grid amplifier has been fabricated with a peak gain of 11 dB at 9.9 GHz with a 3-dB bandwidth of 350 MHz. We report a gain analysis model for the grid and give a comparison of the measurement and theory. The measured patterns show the evidence of a common-mode oscillation. A stability model for the common-mode oscillation is developed. Based on the stability model, a lumped capacitor gives suitable phase shift of the circular function, thus stabilizing the grid. A second 18-element grid was fabricated, using this theory, with improved stability

Pattern Classification with a Partitioned Training Set

Coordinated Science Laboratory was formerly known as Control Systems LaboratoryJoint Services Electronics Program / DAAB 07-67-C-0199OE C-1-071213-455

Modeling and performance of a 100-element pHEMT grid amplifier

A 100-element hybrid grid amplifier has been fabricated, The active devices in the grid are custom-made pseudomorphic high electron mobility transistor (pHEMT) differential-pair chips. We present a model for gain analysis and compare measurements with theory. The grid includes stabilizing resistors in the gate. Measurements show the grid has a peak gain of 10 db when tuned for 10 GHz and a gain of 12 dB when tuned for 9 GHz. The maximum 3-dB bandwidth is 15% at 9 GHz. The minimum noise figure is 3 dB. The maximum saturated output power is 3.7 W, with a peak power-added efficiency of 12%. These results area significant improvement over previous grid amplifiers based on heterojunction bipolar transistors (HBT's)

Genome-wide association with bone mass and geometry in the Framingham Heart Study

© 2007 Kiel et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution Licens

Genome-wide association study identifies a variant in HDAC9 associated with large vessel ischemic stroke

Genetic factors have been implicated in stroke risk but few replicated associations have been reported. We conducted a genome-wide association study (GWAS) in ischemic stroke and its subtypes in 3,548 cases and 5,972 controls, all of European ancestry. Replication of potential signals was performed in 5,859 cases and 6,281 controls. We replicated reported associations between variants close to PITX2 and ZFHX3 with cardioembolic stroke, and a 9p21 locus with large vessel stroke. We identified a novel association for a SNP within the histone deacetylase 9(HDAC9) gene on chromosome 7p21.1 which was associated with large vessel stroke including additional replication in a further 735 cases and 28583 controls (rs11984041, combined P = 1.87×10−11, OR=1.42 (95% CI) 1.28-1.57). All four loci exhibit evidence for heterogeneity of effect across the stroke subtypes, with some, and possibly all, affecting risk for only one subtype. This suggests differing genetic architectures for different stroke subtypes

Common Genetic Variation at the IL1RL1 Locus Regulates IL-33/ST2 Signaling

The suppression of tumorigenicity 2/IL-33 (ST2/IL-33) pathway has been implicated in several immune and inflammatory diseases. ST2 is produced as 2 isoforms. The membrane-bound isoform (ST2L) induces an immune response when bound to its ligand, IL-33. The other isoform is a soluble protein (sST2) that is thought to be a decoy receptor for IL-33 signaling. Elevated sST2 levels in serum are associated with an increased risk for cardiovascular disease. We investigated the determinants of sST2 plasma concentrations in 2,991 Framingham Offspring Cohort participants. While clinical and environmental factors explained some variation in sST2 levels, much of the variation in sST2 production was driven by genetic factors. In a genome-wide association study (GWAS), multiple SNPs within IL1RL1 (the gene encoding ST2) demonstrated associations with sST2 concentrations. Five missense variants of IL1RL1 correlated with higher sST2 levels in the GWAS and mapped to the intracellular domain of ST2, which is absent in sST2. In a cell culture model, IL1RL1 missense variants increased sST2 expression by inducing IL-33 expression and enhancing IL-33 responsiveness (via ST2L). Our data suggest that genetic variation in IL1RL1 can result in increased levels of sST2 and alter immune and inflammatory signaling through the ST2/IL-33 pathway.Stem Cell and Regenerative Biolog

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

Burden of Rare Sarcomere Gene Variants in the Framingham and Jackson Heart Study Cohorts

Rare sarcomere protein variants cause dominant hypertrophic and dilated cardiomyopathies. To evaluate whether allelic variants in eight sarcomere genes are associated with cardiac morphology and function in the community, we sequenced 3,600 individuals from the Framingham Heart Study (FHS) and Jackson Heart Study (JHS) cohorts. Out of the total, 11.2% of individuals had one or more rare nonsynonymous sarcomere variants. The prevalence of likely pathogenic sarcomere variants was 0.6%, twice the previous estimates; however, only four of the 22 individuals had clinical manifestations of hypertrophic cardiomyopathy. Rare sarcomere variants were associated with an increased risk for adverse cardiovascular events (hazard ratio: 2.3) in the FHS cohort, suggesting that cardiovascular risk assessment in the general population can benefit from rare variant analysis