Radiative falloff of a scalar field in a weakly curved spacetime without symmetries

We consider a massless scalar field propagating in a weakly curved spacetime whose metric is a solution to the linearized Einstein field equations. The spacetime is assumed to be stationary and asymptotically flat, but no other symmetries are imposed -- the spacetime can rotate and deviate strongly from spherical symmetry. We prove that the late-time behavior of the scalar field is identical to what it would be in a spherically-symmetric spacetime: it decays in time according to an inverse power-law, with a power determined by the angular profile of the initial wave packet (Price falloff theorem). The field's late-time dynamics is insensitive to the nonspherical aspects of the metric, and it is governed entirely by the spacetime's total gravitational mass; other multipole moments, and in particular the spacetime's total angular momentum, do not enter in the description of the field's late-time behavior. This extended formulation of Price's falloff theorem appears to be at odds with previous studies of radiative decay in the spacetime of a Kerr black hole. We show, however, that the contradiction is only apparent, and that it is largely an artifact of the Boyer-Lindquist coordinates adopted in these studies.Comment: 17 pages, RevTeX

Computing gravitational waves from slightly nonspherical stellar collapse to black hole: Odd-parity perturbation

Nonspherical stellar collapse to a black hole is one of the most promising gravitational wave sources for gravitational wave detectors. We numerically study gravitational waves from a slightly nonspherical stellar collapse to a black hole in linearized Einstein theory. We adopt a spherically collapsing star as the zeroth-order solution and gravitational waves are computed using perturbation theory on the spherical background. In this paper we focus on the perturbation of odd-parity modes. Using the polytropic equations of state with polytropic indices $n_p=1$ and 3, we qualitatively study gravitational waves emitted during the collapse of neutron stars and supermassive stars to black holes from a marginally stable equilibrium configuration. Since the matter perturbation profiles can be chosen arbitrarily, we provide a few types for them. For $n_p=1$, the gravitational waveforms are mainly characterized by a black hole quasinormal mode ringing, irrespective of perturbation profiles given initially. However, for $n_p=3$, the waveforms depend strongly on the initial perturbation profiles. In other words, the gravitational waveforms strongly depend on the stellar configuration and, in turn, on the ad hoc choice of the functional form of the perturbation in the case of supermassive stars.Comment: 31 pages, accepted for publication in Phys. Rev. D, typos and minor errors correcte

Influence of Dietary Oil Content and Conjugated Linoleic Acid (CLA) on Lipid Metabolism Enzyme Activities and Gene Expression in Tissues of Atlantic Salmon (Salmo salar L.)

The overall objective is to test the hypothesis that conjugated linoleic acid (CLA) has beneficial effects in Atlantic salmon through affecting lipid and fatty acid metabolism. The specific aims of the present study were to determine the effects of CLA on some key pathways of fatty acid metabolism including fatty acid oxidation and highly unsaturated fatty acid (HUFA) synthesis. Salmon smolts were fed diets containing two levels of fish oil (low, ~18% and high, ~34%) containing three levels of CLA (a 1:1 mixture of 9-cis,trans-11 and trans-10,cis-12 at 0, 1 and 2% of diet) for 3 months. The effects of dietary CLA on HUFA synthesis and β-oxidation were measured and the expression of key genes in the fatty acid oxidation and HUFA synthesis pathways, and potentially important transcription factors, peroxisome proliferators activated receptors (PPARs), determined in selected tissues. Liver HUFA synthesis and desaturase gene expression was increased by dietary CLA and decreased by high dietary oil content. Carnitine palmitoyltransferase-I (CPT-I) activity and gene expression were generally increased by CLA in muscle tissues although dietary oil content had relatively little effect. In general CPT-I activity or gene expression was not correlated with β-oxidation. Dietary CLA tended to increase PPARα and β gene expression in both liver and muscle tissues, and PPARγ in liver. In summary, gene expression and activity of the fatty acid pathways were altered in response to dietary CLA and/or oil content, with data suggesting that PPARs are also regulated in response to CLA. Correlations were observed between dietary CLA, liver HUFA synthesis and desaturase gene expression, and liver PPARα expression, and also between dietary CLA, CPT-I expression and activity, and PPARα expression in muscle tissues. In conclusion, this study suggests that dietary CLA has effects on fatty acid metabolism in Atlantic salmon and on PPAR transcription factors. However, further work is required to assess the potential of CLA as a dietary supplement, and the role of PPARs in the regulation of lipid metabolism in fish

Effects of dietary vegetable oil on atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions

Fatty acyl desaturase activities, involved in the conversion of the C18 EFA, 18:2n-6 and 18:3n-3, to the highly unsaturated fatty acids (HUFA) 20:4n-6, 20:5n-3 and 22:6n-3, are known to be under nutritional regulation. Specifically, the activity of the desaturation/elongation pathway is depressed when animals, including fish, are fed fish oils rich in n-3HUFA compared to animals fed vegetable oils rich in C18 EFA. The primary aims of the present study were a) to establish the relative importance of product inhibition (n-3HUFA) versus increased substrate concentration (C18 EFA) and, b) to determine whether 18:2n-6 and 18:3n-3 differ in their effects, on the hepatic fatty acyl desaturation/elongation pathway in Atlantic salmon (Salmo salar). Smolts were fed ten experimental diets containing blends of two vegetable oils, linseed (LO) and rapeseed oil (RO), and fish oil (FO) in a triangular mixture design for 50 weeks. Fish were sampled after 32 and 50 weeks, lipid and fatty acid composition of liver determined, fatty acyl desaturation/elongation activity estimated in hepatocytes using [1-14C]18:3n-3 as substrate, and the data subjected to regression analyses. Dietary 18:2n-6 was positively correlated, and n-3HUFA negatively correlated, with lipid content of liver. Dietary 20:5n-3 and 22:6n-3 were positively correlated with liver fatty acids with a slope greater than unity suggesting relative retention and deposition of these HUFA. In contrast, dietary 18:2n-6 and 18:3n-3 were positively correlated with liver fatty acids with a slope of less than unity suggesting metabolism via β-oxidation and/or desaturation/elongation. Consistent with this, fatty acyl desaturation/elongation in hepatocytes was significantly increased by feeding diets containing vegetable oils. Dietary 20:5n-3 and 22:6n-3 levels were negatively correlated with hepatocyte fatty acyl desaturation. At 32 weeks, 18:2n-6 but not 18:3n-3, was positively correlated with hepatocyte fatty acyl desaturation activity whereas the reverse was true at 50 weeks. The data indicate that both feedback inhibition through increased n-3HUFA and decreased C18 fatty acyl substrate concentration are probably important in determining hepatocyte fatty acyl desaturation activities, and that 18:2n-6 and 18:3n-3 may differ in their effects on this pathway

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Regulation of lipid homeostasis in fish: isolation of multiple PPAR subtypes from Atlantic salmon

International audienc

Multiple peroxisome proliferator-activated receptor β subtypes from Atlantic salmon (Salmo salar)

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily that function as critical regulators of lipid and energy homeostasis. Although intensively studied in mammals, their basic biological functions are still poorly understood. The objective of this work was to characterise PPARβ subtypes in a fish the Atlantic salmon (Salmo salar) in order to address PPAR function and the regulation of lipid homeostasis in lower vertebrates. The screening of an Atlantic salmon genomic library revealed the presence of four genes for PPARβ subtypes. Based on comparisons of exons and exon-flanking regions, these genes were assigned into two families, ssPPARβ1 and ssPPARβ2, each family containing two isotypes; ssPPARβ1A and β1B and ssPPARβ2A and β2B. Two full-length cDNAs for ssPPARβ1A and ssPPPARβ2A were isolated. Transcripts for ssPPARβ1A and ssPPARβ2A have distinct tissue expression profiles, with ssPPARβ1A predominating in liver and ssPPARβ2A predominating in gill. Expression levels of mRNA of either isotype were up to ten fold lower in kidney, heart, spleen, muscle, and brain.. In cellular transfection assays ssPPARβ1A is activated by monounsaturated fatty acids, 2-bromopalmitate and by the mammalian PPARβ-specific ligand GW501516. In contrast, PPARβ2A was not activated by any of the compounds tested. Furthermore, ssPPARβ2A repressed both basal reporter gene activity and the GW501516-induced activity of ssPPARβ1A. The results indicate unexpected levels of variety and complexity in PPAR subtype and mechanism of action in lower vertebrates

Does an online psychological intervention improve self-efficacy and disability in people also receiving Multimodal Manual Therapy for chronic low back pain compared to Multimodal Manual Therapy alone? Design of a randomized controlled trial

Background: Various interventions are available for the treatment of chronic low back pain (LBP), including Manual Therapy and Cognitive Behavioural Therapy (CBT). The purpose of this study is to evaluate whether the addition of an internet-based CBT program leads to better outcomes in patients who are treated with multimodal manual therapy for chronic LBP. Methods/Design: A randomized controlled trial comparing a combined intervention, consisting of internet-based CBT utilising MoodGYM plus multimodal manual therapy, to multimodal manual therapy alone for patients with chronic LBP. Multimodal manual therapy will be delivered by experienced chiropractors and physiotherapists. Treatment sessions will consist of a combination of joint and soft tissue mobilisation; spinal manipulation as well as muscle and fascia massage; education and reassurance; and rehabilitative exercise prescription. In total, 108 adult participants will be recruited from multiple chiropractic and physiotherapy private practices in Australia. Participants older than 18 years of age and diagnosed with chronic non-specific LBP will be included in the trial, where chronic LBP is defined as continuous or fluctuating pain for a minimum of three months. The Keele STarT Back screening tool will be used to screen for potential participants who are in the medium risk category. The primary outcomes are self efficacy and disability measured by the Patient Self-Efficacy Questionnaire (PSEQ) and Roland Morris Disability Questionnaire (RMDQ) respectively. Secondary outcome measures will assess pain, catastrophising, depression, anxiety, stress and work ability. Participants will be randomly allocated into one of two groups. Both groups will receive an upper limit of 12 multimodal manual therapy sessions over a period of 8 weeks. The intervention group will also receive five weeks of MoodGYM covering five modules in total. Assessment will be conducted at pre-treatment, post-treatment 8- and follow-up at 26- and 52 weeks. In addition, a verbal pain measure will be completed by the treating practitioner at time of treatments on an 11-point VAS. The primary data analysis will be by intention to treat using a linear mixed model for each outcome. Discussion: This paper outlines the design of a randomised controlled trial that investigates the potential benefits of adding a widely available and inexpensive internet-based psychological intervention to standard multimodal manual therapy for the management of chronic low back pain. Trial registration:ACTRN1261500026953