10 research outputs found
Rotational modes of relativistic stars: analytical results
No full textWe study the r modes and rotational "hybrid" modes (inertial modes) of relativistic stars. As in Newtonian gravity, the spectrum of low-frequency rotational modes is highly sensitive to the stellar equation of state. If the star and its perturbations obey the same one-parameter equation of state (as with barotropic stars), there exist no pure r modes at all—no modes whose limit, for a star with zero angular velocity, is an axial-parity perturbation. Rotating stars of this kind similarly have no pure g modes, no modes whose spherical limit is a perturbation with polar parity and vanishing perturbed pressure and density. In spherical stars of this kind, the r modes and g modes form a degenerate zero-frequency subspace. We find that rotation splits the degeneracy to zeroth order in the star's angular velocity Omega, and the resulting modes are generically hybrids, whose limit as Omega-->0 is a stationary current with both axial and polar parts. Because each mode has definite parity, its axial and polar parts have alternating values of l. We show that each mode belongs to one of two classes, axial-led or polar-led, depending on whether the spherical harmonic with the lowest value of l that contributes to its velocity field is axial or polar. Newtonian barotropic stars retain a vestigial set of purely axial modes (those with l = m); however, for relativistic barotropic stars, we show that these modes must also be replaced by axial-led hybrids. We compute the post-Newtonian corrections to the l = m modes for uniform density stars. On the other hand, if the star is nonbarotropic (that is, if the perturbed star obeys an equation of state that differs from that of the unperturbed star), the r modes alone span the degenerate zero-frequency subspace of the spherical star. In Newtonian stars, this degeneracy is split only by the order-Omega2 rotational corrections. However, when relativistic effects are included, the degeneracy is again broken at zeroth order. We compute the r modes of a nonbarotropic, uniform density model to first post-Newtonian order
Regularizing the r-mode problem for non-barotropic relativistic stars
No full textWe present results for r-modes of relativistic nonbarotropic stars. We show that the main differential equation, which is formally singular at lowest order in the slow-rotation expansion, can be regularized if one considers the initial value problem rather than the normal mode problem. However, a more physically motivated way to regularize the problem is to include higher order terms. This allows us to develop a practical approach for solving the problem and we provide results that support earlier conclusions obtained for uniform density stars. In particular, we show that there will exist a single r-mode for each permissible combination of l and m. We discuss these results and provide some caveats regarding their usefulness for estimates of gravitational-radiation reaction timescales. The close connection between the seemingly singular relativistic r-mode problem and issues arising because of the presence of corotation points in differentially rotating stars is also clarified
Rotational modes of relativistic stars: numerical results
No full textWe study the inertial modes of slowly rotating, fully relativistic compact stars. The equations that govern perturbations of both barotropic and nonbarotropic models are discussed, but we present numerical results only for the barotropic case. For barotropic stars all inertial modes are a hybrid of axial and polar perturbations. We use a spectral method to solve for such modes of various polytropic models. Our main attention is on modes that can be driven unstable by the emission of gravitational waves. Hence, we calculate the gravitational-wave growth time scale for these unstable modes and compare the results to previous estimates obtained in Newtonian gravity (i.e. using post-Newtonian radiation formulas). We find that the inertial modes are slightly stabilized by relativistic effects, but that previous conclusions concerning, e.g., the unstable r modes remain essentially unaltered when the problem is studied in full general relativity
Differential rotation of the unstable nonlinear r-modes
No full textAt second order in perturbation theory, the r-modes of uniformly rotating stars include an axisymmetric part that can be identified with differential rotation of the background star. If one does not include radiation reaction, the differential rotation is constant in time and has been computed by Sá. It has a gauge dependence associated with the family of time-independent perturbations that add differential rotation to the unperturbed equilibrium star: For stars with a barotropic equation of state, one can add to the time-independent second-order solution arbitrary differential rotation that is stratified on cylinders (that is a function of distance ϖ to the axis of rotation). We show here that the gravitational radiation-reaction force that drives the r-mode instability removes this gauge freedom; the exponentially growing differential rotation of the unstable second-order r-mode is unique. We derive a general expression for this rotation law for Newtonian models and evaluate it explicitly for slowly rotating models with polytropic equations of state
Short- and long-term safety of weekly high-dose vitamin D3 supplementation in school children
No full textBackground: Hypovitaminosis D is prevalent in youth worldwide, but the safety of vitamin D at doses exceeding 200 IU-d is unknown in this age group. We assessed the safety of high doses of vitamin D3 administered to apparently healthy schoolchildren. Methods: To assess short-term safety, 25 subjects randomly received placebo or vitamin D3 at doses of 14,000 IU-wk for 8 wk. To assess long-term safety, 340 subjects randomly received placebo, vitamin D3 as 1,400 IU-wk or 14,000 IU-wk for 1 yr. Biochemical variables were monitored at 0, 2, 4, 6, and 8 wk and 8 wk off therapy in the short-term study and at 0, 6, and 12 months in the long-term study. Results: In both the short- and long-term studies, mean serum calcium and 1,25-hydroxyvitamin levels did not change in any group. In the short-term study, mean 25-hydroxyvitamin concentrations increased from 44 (± 11) to 54 (± 19) ng-ml in the treated groups (P = 0.033). In the long-term study, mean 25-hydroxyvitamin D levels increased from 15 ± 8 to 19 ± 7 ng-ml (P andlt; 0.0001) in subjects receiving 1,400 IU-wk and from 15 ± 7 to 36 ± 22 ng-ml (P andlt; 0.0001) in the group receiving 14,000 IU-wk. No subject developed vitamin D intoxication. Conclusion: Vitamin D 3 at doses equivalent to 2000 IU-d for 1 yr is safe in adolescents and results in desirable vitamin D levels. Copyright © 2008 by The Endocrine Society.AKSNES L, 1982, J CLIN ENDOCR METAB, V55, P94; Armas LAG, 2004, J CLIN ENDOCR METAB, V89, P5387, DOI 10.1210-jc.2004-0360; Binkley N, 2004, J CLIN ENDOCR METAB, V89, P3152, DOI 10.1210-jc.2003-031979; Chel V, 2008, OSTEOPOROSIS INT, V19, P663, DOI 10.1007-s00198-007-0465-2; *COMM SCI EV DIET, 1997, DIET REF INT CAL PHO; *COMM SCI EV DIET, 1999, DIET REF INT CALC PH; Baker SS, 1999, PEDIATRICS, V104, P1152; Dahifar Hossein, 2006, J Med Invest, V53, P204, DOI 10.2152-jmi.53.204; Dawson-Hughes B, 2005, OSTEOPOROSIS INT, V16, P713, DOI 10.1007-s00198-005-1867-7; Docio S, 1998, J BONE MINER RES, V13, P544, DOI 10.1359-jbmr.1998.13.4.544; El-Hajj Fuleihan G, 2001, PEDIATRICS, V107, P1; Fuleihan GE, 2006, J CLIN ENDOCR METAB, V91, P405, DOI 10.1210-jc.2005-1436; FULEIHAN GEH, 2007, NUTR ASPECTS OSTEOPO, V1297, P91; Gartner LM, 2003, PEDIATRICS, V111, P908, DOI 10.1542-peds.111.4.908; GLASTRE C, 1990, J CLIN ENDOCR METAB, V70, P1330; Gordon CM, 2004, ARCH PEDIAT ADOL MED, V158, P531, DOI 10.1001-archpedi.158.6.531; Guillemant J, 1999, OSTEOPOROSIS INT, V10, P222, DOI 10.1007-s001980050219; Guillemant J, 1995, BONE, V17, P513, DOI 10.1016-8756-3282(95)00401-7; Guillemant J, 2001, OSTEOPOROSIS INT, V12, P875, DOI 10.1007-s001980170040; Hathcock JN, 2007, AM J CLIN NUTR, V85, P6; Heaney RP, 2003, AM J CLIN NUTR, V78, P912; Holick MF, 2007, NEW ENGL J MED, V357, P266, DOI 10.1056-NEJMra070553; Holick MF, 2006, MAYO CLIN PROC, V81, P353; Hollis BW, 2004, J CLIN ENDOCR METAB, V89, P3149, DOI 10.1210-jc.2004-0682; Houghton LA, 2006, AM J CLIN NUTR, V84, P694; ILICH JZ, 1997, CALCIFIED TISSUE INT, P61104; Knight JA, 2007, CANCER EPIDEM BIOMAR, V16, P422, DOI 10.1158-1055-9965.EPI-06-0865; Lips P, 1999, OSTEOPOROSIS INT, V9, P394, DOI 10.1007-s001980050162; Lips P, 2004, J STEROID BIOCHEM, V89-90, P611, DOI 10.1016-j.jsbmb.2004.03.040; LOCKITCH G, 1988, CLIN CHEM, V34, P1622; Luscombe CJ, 2001, LANCET, V358, P641, DOI 10.1016-S0140-6736(01)05788-9; MAALOUF J, 2005, BONE S1, V36, pS50; Maalouf J, 2006, J BONE MINER RES, V21, pS29; Matkovic Velimir, 2005, American Journal of Clinical Nutrition, V81, P175; Oliveri B, 1996, EUR J CLIN NUTR, V50, P807; OLIVERI MB, 1993, BONE MINER, V20, P99, DOI 10.1016-S0169-6009(08)80041-4; Pittas AG, 2006, DIABETES CARE, V29, P650, DOI 10.2337-diacare.29.03.06.dc05-1961; Trang HM, 1998, AM J CLIN NUTR, V68, P854; VIETH R, 1990, AM J PHYSIOL, V258, pE780; Vieth R, 1999, AM J CLIN NUTR, V69, P842; Vieth Reinhold, 2004, Nutr J, V3, P8, DOI 10.1186-1475-2891-3-8; Vieth R, 2001, AM J CLIN NUTR, V73, P288; Vieth R, 2004, J STEROID BIOCHEM, V89-90, P575, DOI 10.1016-j.jsbmb.2004.03.038; Vieth R, 2007, AM J CLIN NUTR, V85, P649; Viljakainen HT, 2006, J BONE MINER RES, V21, P836, DOI 10.1359-JBMR.060302; Weaver CM, 1999, J CLIN ENDOCR METAB, V84, P1839, DOI 10.1210-jc.84.6.183962545
Crushed rock and clay amelioration of a nutrient decifient, sandy soil of Maputaland
No full textBibliography: leaves 57-62.Various studies have suggested the possibility that food derived through subsistence agriculture in the Mseleni region of Maputaland contributes to malnutrition within the local community, particularfy within the high proportion of the population which suffers from a severe, disabling form of osteoarthritis. This study was conducted to determine if the application of local crushed rock or black clay to these nutrient deficient, sandy soils would increase available nutrient concentrations and improve the growth of plants in the ameliorated soil
Regulation of hepcidin and hemojuvelin expression and their role in iron homeostasis
No full textHepcidin is the key regulator of iron homeostasis acting as a negative regulator of intestinal iron absorption. Several proteins have recently been identified to act as upstream regulators of hepcidin expression, such as HFE and hemojuvelin (HJV). Although hepcidin is regulated by iron, the molecules involved in this regulation and whether HFE is involved in this regulation remain to be clarified. The aims of this study were to investigate the molecules involved in hepcidin regulation by iron and the role played by HFE in this regulation, to understand the regulation of hepcidin and HJV expression during inflammation, and finally to investigate the possible role of upstream stimulatory factors (USFs) in the regulation of HJV expression.
Wild type and HFE KO animal models were used to investigate the regulation of hepcidin by iron in vivo; the same animal models and in vitro studies were conducted to study the regulation of hepcidin and HJV expression during inflammation. A possible regulation of HJV by USFs was also examined in vitro and in vivo using ChIP assay.
In this study, it was found that iron regulates the expression of BMP-6, for which HJV acts as a co-receptor, and phosphorylation of SMADs 1/5/8 in the liver which in turn may regulate hepcidin gene expression in response to different iron status. Moreover, HFE seems to be involved in the regulation of downstream signalling of BMP-6 that regulates hepcidin expression in response to iron loading.
It was also found that the pro-inflammatory cytokines regulate hepcidin and HJV expression differently during inflammation. TNF-alpha seems to act directly on HJV to suppress its transcription possibly via a TNFRE within the HJV promoter, while IL-6 induces hepcidin expression via STAT3 signalling. In addition, acute inflammation studies in mice showed that although hepcidin expression is upregulated as a result of inflammation, HJV and BMP expression is selectively repressed in the liver suggesting a crucial requirement for the downregulation of these genes in order to induce hepcidin during inflammation in vivo. However, this response seems to be HFE-independent.
Finally, the study showed an interaction between USFs and the HJV promoter both in vitro and in vivo suggesting that USFs are important for the regulation of hemojuvelin expression, and further strengthen the link between these transcription factors and iron metabolism
