Ramsey interferometry with generalized one-axis twisting echoes

We consider a large class of Ramsey interferometry protocols which are enhanced by squeezing and un-squeezing operations before and after a phase signal is imprinted on the collective spin of $N$ particles. We report an analytical optimization for any given particle number and strengths of (un-)squeezing. These results can be applied even when experimentally relevant decoherence processes during the squeezing and un-squeezing interactions are included. Noise between the two interactions is however not considered in this work. This provides a generalized characterization of squeezing echo protocols, recovering a number of known quantum metrological protocols as local sensitivity maxima, thereby proving their optimality. We discover a single new protocol. Its sensitivity enhancement relies on a double inversion of squeezing. In the general class of echo protocols, the newly found over-un-twisting protocol is singled out due to its Heisenberg scaling even at strong collective dephasing.Comment: 11+8 pages, 7 figures, comments welcome! ; accepted versio

Optimal Ramsey interferometry with echo protocols based on one-axis twisting

We study a variational class of generalised Ramsey protocols that include two one-axis twisting (OAT) operations, one performed before the phase imprint and the other after. In this framework, we optimise the axes of the signal imprint, the OAT interactions, and the direction of the final projective measurement. We distinguish between protocols that exhibit symmetric or antisymmetric dependencies of the spin projection signal on the measured phase. Our results show that the quantum Fisher information, which sets the limits on the sensitivity achievable with a given uniaxially twisted input state, can be saturated within our class of variational protocols for almost all initial twist strengths. By incorporating numerous protocols previously documented in the literature, our approach creates a unified framework for Ramsey echo protocols with OAT states and measurements

RANTES/CCL5 and risk for coronary events: Results from the MONICA/KORA Augsburg case-cohort, Athero-express and CARDIoGRAM studies

Background: The chemokine RANTES (regulated on activation, normal T-cell expressed and secreted)/CCL5 is involved in the pathogenesis of cardiovascular disease in mice, whereas less is known in humans. We hypothesised that its relevance for atherosclerosis should be reflected by associations between CCL5 gene variants, RANTES serum concentrations and protein levels in atherosclerotic plaques and risk for coronary events. Methods and Findings: We conducted a case-cohort study within the population-based MONICA/KORA Augsburg studies. Baseline RANTES serum levels were measured in 363 individuals with incident coronary events and 1,908 non-cases (mean follow-up: 10.2±

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways

Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways