An analysis of the fluctuations of the geomagnetic dipole

The time evolution of the strength of the Earth's virtual axial dipole moment (VADM) is analyzed by relating it to the Fokker-Planck equation, which describes a random walk with VADM-dependent drift and diffusion coefficients. We demonstrate first that our method is able to retrieve the correct shape of the drift and diffusion coefficients from a time series generated by a test model. Analysis of the Sint-2000 data shows that the geomagnetic dipole mode has a linear growth time of 13 to 33 kyr, and that the nonlinear quenching of the growth rate follows a quadratic function of the type [1-(x/x0)^2]. On theoretical grounds, the diffusive motion of the VADM is expected to be driven by multiplicative noise, and the corresponding diffusion coefficient to scale quadratically with dipole strength. However, analysis of the Sint-2000 VADM data reveals a diffusion which depends only very weakly on the dipole strength. This may indicate that the magnetic field quenches the amplitude of the turbulent velocity in the Earth's outer core.Comment: 11 pages, 6 figure

Timing of supplementation of selenium and isoflavones determines prostate cancer risk factor reduction in rats

<p>Abstract</p> <p>Background</p> <p>High dietary intake of selenium or isoflavones reduces risk factors for prostate cancer. We tested whether combined supplementation of these two dietary components would reduce prostate cancer risk factors in rats more than supplementation of each component individually.</p> <p>Methods</p> <p>Male Noble rat pups were exposed from conception to diets containing an adequate (0.33–0.45 mg/kg diet) or high (3.33–3.45 mg/kg) concentration of selenium as Se-methylselenocysteine and a low (10 mg/kg) or high (600 mg/kg) level of isoflavones in a 2 × 2 factorial design. Pups consumed their respective diets until sacrifice at 35, 100, or 200 days. Male Noble rat breeders, whose exposure to the diets began after puberty, were sacrificed at 336 days. Rats were weighed biweekly. Blood was collected at the time of sacrifice and body fat and prostates were dissected and weighed. Serum levels of leptin, IGF-1, and testosterone were determined using ELISA kits. Serum levels of isoflavones were assayed by GC/MS. Liver activity of selenium-dependent glutathione peroxidase 1 was measured as an indicator of selenium status.</p> <p>Results</p> <p>Serum isoflavone concentrations were nearly 100-fold higher at 35 days of age (1187.1 vs. 14.4 ng/mL, mean ± SD) in pups fed the high vs. low isoflavone diets, and remained so at 100 and 200 days, and in breeders. There were no dietary differences in liver glutathione peroxidase activity in pups or breeders. High isoflavone intake significantly (p = 0.001–0.047) reduced body weight in rat pups from 35 days onward, but not in breeders. Body fat and leptin were likewise significantly reduced by high isoflavones in pups while effects in breeders were less pronounced but still significant. High intake of Se and isoflavones each decreased serum IGF-1 in pups at 100 and 200 days, but not in breeders. No consistent dietary effects were observed on serum testosterone or relative weights of prostates. In pups, the combination of high isoflavones and high selenium produced the lowest weight gain, the lowest serum leptin, and the lowest serum IGF-1 concentrations of all four diets.</p> <p>Conclusion</p> <p>Combined intake of high selenium and high isoflavones may achieve greater chemopreventive effects than either compound individually. The timing of supplementation may determine the significance of its effects.</p

Timing of supplementation of selenium and isoflavones determines prostate cancer risk factor reduction in rats

<p>Abstract</p> <p>Background</p> <p>High dietary intake of selenium or isoflavones reduces risk factors for prostate cancer. We tested whether combined supplementation of these two dietary components would reduce prostate cancer risk factors in rats more than supplementation of each component individually.</p> <p>Methods</p> <p>Male Noble rat pups were exposed from conception to diets containing an adequate (0.33–0.45 mg/kg diet) or high (3.33–3.45 mg/kg) concentration of selenium as Se-methylselenocysteine and a low (10 mg/kg) or high (600 mg/kg) level of isoflavones in a 2 × 2 factorial design. Pups consumed their respective diets until sacrifice at 35, 100, or 200 days. Male Noble rat breeders, whose exposure to the diets began after puberty, were sacrificed at 336 days. Rats were weighed biweekly. Blood was collected at the time of sacrifice and body fat and prostates were dissected and weighed. Serum levels of leptin, IGF-1, and testosterone were determined using ELISA kits. Serum levels of isoflavones were assayed by GC/MS. Liver activity of selenium-dependent glutathione peroxidase 1 was measured as an indicator of selenium status.</p> <p>Results</p> <p>Serum isoflavone concentrations were nearly 100-fold higher at 35 days of age (1187.1 vs. 14.4 ng/mL, mean ± SD) in pups fed the high vs. low isoflavone diets, and remained so at 100 and 200 days, and in breeders. There were no dietary differences in liver glutathione peroxidase activity in pups or breeders. High isoflavone intake significantly (p = 0.001–0.047) reduced body weight in rat pups from 35 days onward, but not in breeders. Body fat and leptin were likewise significantly reduced by high isoflavones in pups while effects in breeders were less pronounced but still significant. High intake of Se and isoflavones each decreased serum IGF-1 in pups at 100 and 200 days, but not in breeders. No consistent dietary effects were observed on serum testosterone or relative weights of prostates. In pups, the combination of high isoflavones and high selenium produced the lowest weight gain, the lowest serum leptin, and the lowest serum IGF-1 concentrations of all four diets.</p> <p>Conclusion</p> <p>Combined intake of high selenium and high isoflavones may achieve greater chemopreventive effects than either compound individually. The timing of supplementation may determine the significance of its effects.</p

Diets high in selenium and isoflavones decrease androgen-regulated gene expression in healthy rat dorsolateral prostate

<p>Abstract</p> <p>Background</p> <p>High dietary intake of selenium or soybean isoflavones reduces prostate cancer risk. These components each affect androgen-regulated gene expression. The objective of this work was to determine the combined effects of selenium and isoflavones on androgen-regulated gene expression in rat prostate.</p> <p>Methods</p> <p>Male Noble rats were exposed from conception until 200 days of age to diets containing an adequate (0.33-0.45 mg/kg diet) or high (3.33-3.45 mg/kg) concentration of selenium as Se-methylselenocysteine and a low (10 mg/kg) or high (600 mg/kg) level of isoflavones in a 2 × 2 factorial design. Gene expression in the dorsolateral prostate was determined for the androgen receptor, for androgen-regulated genes, and for Akr1c9, whose product catalyzes the reduction of dihydrotestosterone to 5alpha-androstane-3alpha, 17beta-diol. Activity of hepatic glutathione peroxidise 1 and of prostatic 5alpha reductase were also assayed.</p> <p>Results</p> <p>There were no differences due to diet in activity of liver glutathione peroxidase activity. Total activity of 5alpha reductase in prostate was significantly lower (<it>p </it>= 0.007) in rats fed high selenium/high isoflavones than in rats consuming adequate selenium/low isoflavones. High selenium intake reduced expression of the androgen receptor, Dhcr24 (24-dehydrocholesterol reductase), and Abcc4 (ATP-binding cassette sub-family C member 4). High isoflavone intake decreased expression of Facl3 (fatty acid CoA ligase 3), Gucy1a3 (guanylate cyclase alpha 3), and Akr1c9. For Abcc4 the combination of high selenium/high isoflavones had a greater inhibitory effect than either treatment alone. The effects of selenium on gene expression were always in the direction of chemoprevention</p> <p>Conclusion</p> <p>These results suggest that combined intake of high selenium and high isoflavones may achieve a greater chemopreventive effect than either compound supplemented individually.</p

Statistical dynamo theory: Mode excitation

We compute statistical properties of the lowest-order multipole coefficients of the magnetic field generated by a dynamo of arbitrary shape. To this end we expand the field in a complete biorthogonal set of base functions, viz. B = sum_k a^k(t) b^k(r). We consider a linear problem and the statistical properties of the fluid flow are supposed to be given. The turbulent convection may have an arbitrary distribution of spatial scales. The time evolution of the expansion coefficients a^k(t) is governed by a stochastic differential equation from which we infer their averages , autocorrelation functions <a^k(t) a^{k*}(t+tau)>, and an equation for the cross correlations . The eigenfunctions of the dynamo equation (with eigenvalues lambda_k) turn out to be a preferred set in terms of which our results assume their simplest form. The magnetic field of the dynamo is shown to consist of transiently excited eigenmodes whose frequency and coherence time is given by Im(lambda_k) and -1/(Re lambda_k), respectively. The relative r.m.s. excitation level of the eigenmodes, and hence the distribution of magnetic energy over spatial scales, is determined by linear theory. An expression is derived for / in case the fundamental mode b^0 has a dominant amplitude, and we outline how this expression may be evaluated. It is estimated that / ~ 1/N where N is the number of convective cells in the dynamo. We show that the old problem of a short correlation time (or FOSA) has been partially eliminated. Finally we prove that for a simple statistically steady dynamo with finite resistivity all eigenvalues obey Re(lambda_k) < 0.Comment: 14 pages, 2 figures. Accepted for publication in Physical Review

B cells and monocytes from patients with active multiple sclerosis exhibit increased surface expression of both HERV-H Env and HERV-W Env, accompanied by increased seroreactivity

<p>Abstract</p> <p>Background</p> <p>The etiology of the neurogenerative disease multiple sclerosis (MS) is unknown. The leading hypotheses suggest that MS is the result of exposure of genetically susceptible individuals to certain environmental factor(s). Herpesviruses and human endogenous retroviruses (HERVs) represent potentially important factors in MS development. Herpesviruses can activate HERVs, and HERVs are activated in MS patients.</p> <p>Results</p> <p>Using flow cytometry, we have analyzed HERV-H Env and HERV-W Env epitope expression on the surface of PBMCs from MS patients with active and stable disease, and from control individuals. We have also analyzed serum antibody levels to the expressed HERV-H and HERV-W Env epitopes. We found a significantly higher expression of HERV-H and HERV-W Env epitopes on B cells and monocytes from patients with active MS compared with patients with stable MS or control individuals. Furthermore, patients with active disease had relatively higher numbers of B cells in the PBMC population, and higher antibody reactivities towards HERV-H Env and HERV-W Env epitopes. The higher antibody reactivities in sera from patients with active MS correlate with the higher levels of HERV-H Env and HERV-W Env expression on B cells and monocytes. We did not find such correlations for stable MS patients or for controls.</p> <p>Conclusion</p> <p>These findings indicate that both HERV-H Env and HERV-W Env are expressed in higher quantities on the surface of B cells and monocytes in patients with active MS, and that the expression of these proteins may be associated with exacerbation of the disease.</p

Fertility History and Physical and Mental Health Changes in European Older Adults

Previous studies have shown that aspects of reproductive history, such as earlier parenthood and high parity, are associated with poorer health in mid and later life. However, it is unclear which dimensions of health are most affected by reproductive history, and whether the pattern of associations varies for measures of physical, psychological and cognitive health. Such variation might provide more insight into possible underlying mechanisms. We use longitudinal data for men and women aged 50–79 years in ten European countries from the Survey of Health, Ageing and Retirement in Europe to analyse associations between completed fertility history and self-reported and observed health indicators measured 2–3 years apart (functional limitations, chronic diseases, grip strength, depression and cognition), adjusting for socio-demographic, and health factors at baseline. Using multiple imputation and pattern mixture modelling, we tested the robustness of estimates to missing data mechanisms. The results are partly consistent with previous studies and show that women who became mothers before age 20 had worse functional health at baseline and were more likely to suffer functional health declines. Parents of 4 or more children had worse physical, psychological and cognitive health at baseline and were more likely to develop circulatory disease over the follow-up period. Men who delayed fatherhood until age 35 or later had better health at baseline but did not experience significantly different health declines. This study improves our understanding of linkages between fertility histories and later life health and possible implications of changes in fertility patterns for population health. However, research ideally using prospective life course data is needed to further elucidate possible mechanisms, considering interactions with partnership histories, health behaviour patterns and socio-economic trajectories

Regulating STING in health and disease.

The presence of cytosolic double-stranded DNA molecules can trigger multiple innate immune signalling pathways which converge on the activation of an ER-resident innate immune adaptor named "STimulator of INterferon Genes (STING)". STING has been found to mediate type I interferon response downstream of cyclic dinucleotides and a number of DNA and RNA inducing signalling pathway. In addition to its physiological function, a rapidly increasing body of literature highlights the role for STING in human disease where variants of the STING proteins, as well as dysregulated STING signalling, have been implicated in a number of inflammatory diseases. This review will summarise the recent structural and functional findings of STING, and discuss how STING research has promoted the development of novel therapeutic approaches and experimental tools to improve treatment of tumour and autoimmune diseases