Casimir-Lifshitz force out of thermal equilibrium

We study the Casimir-Lifshitz interaction out of thermal equilibrium, with particular attention devoted to the surface-surface and surface-atom configurations. A systematic investigation of the contributions to the force coming from the propagating and evanescent components of the electromagnetic radiation is performed. The large distance behaviors of such interactions is discussed, and both analytical and numerical results are compared with the equilibrium ones. A detailed analysis of the crossing between the surface-surface and the surface-rarefied body, and finally the surface-atom force is shown, and a complete derivation and discussion of the recently predicted non-additivity effects and new asymptotic behaviors is presented.Comment: 26 pages, 11 figures. Published version, revised and more detaile

Effect of the Casimir-Polder force on the collective oscillations of a trapped Bose-Einstein condensate

We calculate the effect of the interaction between an optically active material and a Bose-Einstein condensate on the collective oscillations of the condensate. We provide explicit expressions for the frequency shift of the center of mass oscillation in terms of the potential generated by the substrate and of the density profile of the gas. The form of the potential is discussed in details and various regimes (van der Waals-London, Casimir-Polder and thermal regimes) are identified as a function of the distance of atoms from the surface. Numerical results for the frequency shifts are given for the case of a sapphire dielectric substrate interacting with a harmonically trapped condensate of $^{87}$Rb atoms. We find that at distances of $4-8 \mu m$, where thermal effects become visible, the relative frequency shifts produced by the substrate are of the order $10^{-4}$ and hence accessible experimentally. The effects of non linearities due to the finite amplitude of the oscillation are explicitly discussed. Predictions are also given for the radial breathing mode.Comment: 28 pages, 10 figures. Submitted to PR

Effect of amlodipine on the circulating renin-angiotensin-aldosterone system in healthy cats

Background: Systemic hypertension (SH) is a common cardiovascular disease in older cats that is treated primarily with the calcium channel blocker amlodipine besylate (AML). The systemic effect of AML on the classical and alterative arms of the renin-angiotensin-aldosterone system (RAAS) in cats is incompletely characterized.Hypothesis/Objectives: To determine the effect of AML compared to placebo on circulating RAAS biomarkers in healthy cats using RAAS fingerprinting. Animals: Twenty healthy client-owned cats. Methods: Cats were administered amlodipine besylate (0.625 mg in toto) or placebo by mouth once daily for 14 days in a crossover design with a 4-week washout period. Plasma AML concentrations and RAAS biomarker concentrations were measured at multiple timepoints after the final dose in each treatment period. Time-weighted averages for RAAS biomarkers over 24 hours after dosing were compared between treatment groups using Wilcoxon rank-sum testing. Results: Compared to placebo, AML treatment was associated with increases in markers of plasma renin concentration (median 44% increase; interquartile range [IQR] 19%-86%; P = .009), angiotensin I (59% increase; IQR 27-101%; P = .006), angiotensin II (56% increase; IQR 5-70%; P = .023), angiotensin IV (42% increase; −19% to 89%; P = .013); and angiotensin 1-7 (38% increase; IQR 9-118%; P = .015). Conclusions and Clinical Importance: In healthy cats, administration of AML resulted in nonspecific activation of both classical and alternative RAAS pathways.This article is published as Garcia Marrero, Tatiana M., Jessica L. Ward, Melissa A. Tropf, Agnes Bourgois‐Mochel, Emilie Guillot, Oliver Domenig, Lingnan Yuan, Debosmita Kundu, and Jonathan P. Mochel. "Effect of amlodipine on the circulating renin‐angiotensin‐aldosterone system in healthy cats." Journal of Veterinary Internal Medicine (2024). doi: https://doi.org/10.1111/jvim.17006. © 2024 The Authors. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs

Hidden heritability due to heterogeneity across seven populations

Meta-analyses of genome-wide association studies, which dominate genetic discovery, are based on data from diverse historical time periods and populations. Genetic scores derived from genome-wide association studies explain only a fraction of the heritability estimates obtained from whole-genome studies on single populations, known as the ‘hidden heritability’ puzzle. Using seven sampling populations (n = 35,062), we test whether hidden heritability is attributed to heterogeneity across sampling populations and time, showing that estimates are substantially smaller across populations compared with within populations. We show that the hidden heritability varies substantially: from zero for height to 20% for body mass index, 37% for education, 40% for age at first birth and up to 75% for number of children. Simulations demonstrate that our results are more likely to reflect heterogeneity in phenotypic measurement or gene–environment interactions than genetic heterogeneity. These findings have substantial implications for genetic discovery, suggesting that large homogenous datasets are required for behavioural phenotypes and that gene–environment interaction may be a central challenge for genetic discovery

Miniature Schnauzers under primary veterinary care in the UK in 2013: demography, mortality and disorders

Individual dog breeds are often reported as predisposed to specific breed-related disorders but reliable epidemiological data on disease prevalence are sparse. The Miniature Schnauzer in the UK is a popular small breed dog that is often considered as relatively healthy and long-lived, but is this really true? This study aimed to use data from the VetCompass™ Programme at the Royal Veterinary College to characterise the demography, mortality and common disorders of the general population of Miniature Schnauzers under veterinary care in the UK

Evidence for Genetic Overlap Between Schizophrenia and Age at First Birth in Women

IMPORTANCE: A recently published study of national data by McGrath et al in 2014 showed increased risk of schizophrenia (SCZ) in offspring associated with both early and delayed parental age, consistent with a U-shaped relationship. However, it remains unclear if the risk to the child is due to psychosocial factors associated with parental age or if those at higher risk for SCZ tend to have children at an earlier or later age. OBJECTIVE: To determine if there is a genetic association between SCZ and age at first birth (AFB) using genetically informative but independently ascertained data sets. DESIGN, SETTING, AND PARTICIPANTS: This investigation used multiple independent genome-wide association study data sets. The SCZ sample comprised 18 957 SCZ cases and 22 673 controls in a genome-wide association study from the second phase of the Psychiatric Genomics Consortium, and the AFB sample comprised 12 247 genotyped women measured for AFB from the following 4 community cohorts: Estonia (Estonian Genome Center Biobank, University of Tartu), the Netherlands (LifeLines Cohort Study), Sweden (Swedish Twin Registry), and the United Kingdom (TwinsUK). Schizophrenia genetic risk for each woman in the AFB community sample was estimated using genetic effects inferred from the SCZ genome-wide association study. MAIN OUTCOMES AND MEASURES: We tested if SCZ genetic risk was a significant predictor of response variables based on published polynomial functions that described the relationship between maternal age and SCZ risk in offspring in Denmark. We substituted AFB for maternal age in these functions, one of which was corrected for the age of the father, and found that the fit was superior for the model without adjustment for the father's age. RESULTS: We observed a U-shaped relationship between SCZ risk and AFB in the community cohorts, consistent with the previously reported relationship between SCZ risk in offspring and maternal age when not adjusted for the age of the father. We confirmed that SCZ risk profile scores significantly predicted the response variables (coefficient of determination R2 = 1.1E-03, P = 4.1E-04), reflecting the published relationship between maternal age and SCZ risk in offspring by McGrath et al in 2014. CONCLUSIONS AND RELEVANCE: This study provides evidence for a significant overlap between genetic factors associated with risk of SCZ and genetic factors associated with AFB. It has been reported that SCZ risk associated with increased maternal age is explained by the age of the father and that de novo mutations that occur more frequently in the germline of older men are the underlying causal mechanism. This explanation may need to be revised if, as suggested herein and if replicated in future studies, there is also increased genetic risk of SCZ in older mothers