Generalized Misner-Sharp Energy in f(R) Gravity

We study generalized Misner-Sharp energy in $f(R)$ gravity in a spherically symmetric spacetime. We find that unlike the cases of Einstein gravity and Gauss-Bonnet gravity, the existence of the generalized Misner-Sharp energy depends on a constraint condition in the $f(R)$ gravity. When the constraint condition is satisfied, one can define a generalized Misner-Sharp energy, but it cannot always be written in an explicit quasi-local form. However, such a form can be obtained in a FRW universe and for static spherically symmetric solutions with constant scalar curvature. In the FRW universe, the generalized Misner-Sharp energy is nothing but the total matter energy inside a sphere with radius $r$, which acts as the boundary of a finite region under consideration. The case of scalar-tensor gravity is also briefly discussed.Comment: Revtex, 17 pages, v2: some references added, to appear in PR

Shear Viscosity from Effective Couplings of Gravitons

We calculate the shear viscosity of field theories with gravity duals using Kubo-formula by calculating the Green function of dual transverse gravitons and confirm that the value of the shear viscosity is fully determined by the effective coupling of transverse gravitons on the horizon. We calculate the effective coupling of transverse gravitons for Einstein and Gauss-Bonnet gravities coupled with matter fields, respectively. Then we apply the resulting formula to the case of AdS Gauss-Bonnet gravity with $F^4$ term corrections of Maxwell field and discuss the effect of $F^4$ terms on the ratio of the shear viscosity to entropy density.Comment: 18 pages, 1 figure; references added, to appear in PR

More on QCD Ghost Dark Energy

The difference between vacuum energy of quantum fields in Minkowski space and in Friedmann-Robterson-Walker universe might be related to the observed dark energy. The vacuum energy of the Veneziano ghost field introduced to solve the $U(1)_A$ problem in QCD is of the form, $H+ {\cal O}(H^2)$. Based on this, we study the dynamical evolution of a phenomenological dark energy model whose energy density is of the form $\alpha H+\beta H^2$. In this model, the universe approaches to a de Sitter phase at late times. We fit the model with current observational data including SnIa, BAO, CMB, BBN, Hubble parameter and growth rate of matter perturbation. It shows that the universe begins to accelerate at redshift $z\sim 0.75$ and this model is consistent with current data. In particular, this model fits the data of growth factor well as the $\Lambda CDM$ model.Comment: 14 pages, 4 figures, 2 table

Hawking-Page Phase Transition of black Dp-branes and R-charged black holes with an IR Cutoff

We show that the confinement-deconfinement phase transition of supersymmetric Yang-Mills theories with 16 supercharges in various dimensions can be realized through the Hawking-Page phase transition between the near horizon geometries of black Dp-branes and BPS Dp-branes by removing a small radius region in the geometry in order to realize a confinement phase, which generalizes the Herzog's discussion for the holographic hard-wall AdS/QCD model. Removing a small radius region in the gravitational dual corresponds to introducing an IR cutoff in the dual field theory. We also discuss the Hawking-Page phase transition between thermal $AdS_5$, $AdS_4$, $AdS_7$ spaces and R-charged AdS black holes coming from the spherical reduction of the decoupling limit of rotating D3-, M2-, and M5- branes in type IIB supergravity and 11 dimensional supergravity in grand canonical ensembles, where the IR cutoff also plays a crucial role in the existence of the phase transition.Comment: 34 pages, 18 figures, JHEP3, v2, references added, v3, some explanations adde

A Lifshitz Black Hole in Four Dimensional R^2 Gravity

We consider a higher derivative gravity theory in four dimensions with a negative cosmological constant and show that vacuum solutions of both Lifshitz type and Schr\"{o}dinger type with arbitrary dynamical exponent z exist in this system. Then we find an analytic black hole solution which asymptotes to the vacuum Lifshitz solution with z=3/2 at a specific value of the coupling constant. We analyze the thermodynamic behavior of this black hole and find that the black hole has zero entropy while non-zero temperature, which is very similar to the case of BTZ black holes in new massive gravity at a specific coupling. In addition, we find that the three dimensional Lifshitz black hole recently found by E. Ayon-Beato et al. has a negative entropy and mass when the Newton constant is taken to be positive.Comment: 11 pages, no figure; v2, a minor error correcte

Modeling Light Adaptation in Circadian Clock: Prediction of the Response That Stabilizes Entrainment

Periods of biological clocks are close to but often different from the rotation period of the earth. Thus, the clocks of organisms must be adjusted to synchronize with day-night cycles. The primary signal that adjusts the clocks is light. In Neurospora, light transiently up-regulates the expression of specific clock genes. This molecular response to light is called light adaptation. Does light adaptation occur in other organisms? Using published experimental data, we first estimated the time course of the up-regulation rate of gene expression by light. Intriguingly, the estimated up-regulation rate was transient during light period in mice as well as Neurospora. Next, we constructed a computational model to consider how light adaptation had an effect on the entrainment of circadian oscillation to 24-h light-dark cycles. We found that cellular oscillations are more likely to be destabilized without light adaption especially when light intensity is very high. From the present results, we predict that the instability of circadian oscillations under 24-h light-dark cycles can be experimentally observed if light adaptation is altered. We conclude that the functional consequence of light adaptation is to increase the adjustability to 24-h light-dark cycles and then adapt to fluctuating environments in nature

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD