Nonandrogenic Anabolic Hormones Predict Risk of Frailty: European Male Ageing Study Prospective Data

Context: Low levels of nonandrogenic anabolic hormones have been linked with frailty, but evidence is conflicting and prospective data are largely lacking.Objective: To determine associations between nonandrogenic anabolic hormones and prospective changes in frailty status.Design/Setting: A 4.3-year prospective observational study of community-dwelling men participating in the European Male Ageing Study.Participants: Men (n = 3369) aged 40 to 79 years from eight European centers.Main Outcome Measures: Frailty status was determined using frailty phenotype (FP; n = 2114) and frailty index (FI; n = 2444).Analysis: Regression models assessed relationships between baseline levels of insulinlike growth factor 1 (IGF-1), its binding protein 3 (IGFBP-3), dehydroepiandrosterone sulfate (DHEA-S), 25-hydroxyvitamin D (25OHD), and parathyroid hormone (PTH), with changes in frailty status (worsening or improving frailty).Results: The risk of worsening FP and FI decreased with 1 standard deviation higher IGF-1, IGFBP-3, and 25OHD in models adjusted for age, body mass index, center, and baseline frailty [IGF-1: odds ratio (OR) for worsening FP, 0.82 (0.73, 0.93), percentage change in FI, -3.7% (-6.0, -1.5); IGFBP-3: 0.84 (0.75, 0.95), -4.2% (-6.4, -2.0); 25OHD: 0.84 (0.75, 0.95); -4.4%, (-6.7, -2.0)]. Relationships between IGF-1 and FI were attenuated after adjusting for IGFBP-3. Higher DHEA-S was associated with a lower risk of worsening FP only in men >70 years old [OR, 0.57 (0.35, 0.92)]. PTH was unrelated to change in frailty status.Conclusions: These longitudinal data confirm the associations between nonandrogenic anabolic hormones and the changes in frailty status. Interventional studies are needed to establish causality and determine therapeutic implications

25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 exert distinct effects on human skeletal muscle function and gene expression

Age-associated decline in muscle function represents a significant public health burden. Vitamin D-deficiency is also prevalent in aging subjects, and has been linked to loss of muscle mass and strength (sarcopenia), but the precise role of specific vitamin D metabolites in determining muscle phenotype and function is still unclear. To address this we quantified serum concentrations of multiple vitamin D metabolites, and assessed the impact of these metabolites on body composition/muscle function parameters, and muscle biopsy gene expression in a retrospective study of a cohort of healthy volunteers. Active serum 1,25-dihydroxyvitamin D3 (1α,25(OH)2D3), but not inactive 25-hydroxyvitamin D3 (25OHD3), correlated positively with measures of lower limb strength including power (rho = 0.42, p = 0.02), velocity (Vmax, rho = 0.40, p = 0.02) and jump height (rho = 0.36, p = 0.04). Lean mass correlated positively with 1α,25(OH)2D3 (rho = 0.47, p = 0.02), in women. Serum 25OHD3 and inactive 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) had an inverse relationship with body fat (rho = -0.30, p = 0.02 and rho = -0.33, p = 0.01, respectively). Serum 25OHD3 and 24,25(OH)2D3 were also correlated with urinary steroid metabolites, suggesting a link with glucocorticoid metabolism. PCR array analysis of 92 muscle genes identified vitamin D receptor (VDR) mRNA in all muscle biopsies, with this expression being negatively correlated with serum 25OHD3, and Vmax, and positively correlated with fat mass. Of the other 91 muscle genes analysed by PCR array, 24 were positively correlated with 25OHD3, but only 4 were correlated with active 1α,25(OH)2D3. These data show that although 25OHD3 has potent actions on muscle gene expression, the circulating concentrations of this metabolite are more closely linked to body fat mass, suggesting that 25OHD3 can influence muscle function via indirect effects on adipose tissue. By contrast, serum 1α,25(OH)2D3 has limited effects on muscle gene expression, but is associated with increased muscle strength and lean mass in women. These pleiotropic effects of the vitamin D ‘metabolome’ on muscle function indicate that future supplementation studies should not be restricted to conventional analysis of the major circulating form of vitamin D, 25OHD3

Measurement of the branching fraction for B−→D0K∗−B^- \to D^0 K^{*-}

We present a measurement of the branching fraction for the decay B- --> D0 K*- using a sample of approximately 86 million BBbar pairs collected by the BaBar detector from e+e- collisions near the Y(4S) resonance. The D0 is detected through its decays to K- pi+, K- pi+ pi0 and K- pi+ pi- pi+, and the K*- through its decay to K0S pi-. We measure the branching fraction to be B.F.(B- --> D0 K*-)= (6.3 +/- 0.7(stat.) +/- 0.5(syst.)) x 10^{-4}

Observation of a significant excess of π0π0\pi^{0}\pi^{0} events in B meson decays

We present an observation of the decay $B^{0} \to \pi^{0} \pi^{0}$ based on a sample of 124 million $B\bar{B}$ pairs recorded by the BABAR detector at the PEP-II asymmetric-energy $B$ Factory at SLAC. We observe $46 \pm 13 \pm 3$ events, where the first error is statistical and the second is systematic, corresponding to a significance of 4.2 standard deviations including systematic uncertainties. We measure the branching fraction \BR(B^{0} \to \pi^{0} \pi^{0}) = (2.1 \pm 0.6 \pm 0.3) \times 10^{-6}, averaged over $B^{0}$ and $\bar{B}^{0}$ decays

Measurements of branching fractions and CP-violating asymmetries in B meson decays to charmless two-body states containing a K-0

We present measurements of branching fractions and CP-violating asymmetries in decays of B mesons to two-body final states containing a K-0. The results are based on a data sample of approximately 88x10(6) Y(4S)-->B (B) over bar decays collected with the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. We measure B(B+-->K(0)pi(+))=(22.3+/-1.7+/-1.1)x10(-6), B(B-0-->K(0)pi(0))=(11.4+/-1.7+/-0.8)x10(-6), B(B+-->(K) over bar K-0(+))K-0(K) over bar (0))K(0)pi(+))=-0.05+/-0.08+/-0.01 and A(CP)(B-0-->K(0)pi(0))=0.03+/-0.36+/-0.11

Measurement of the branching fractions and CP asymmetry of B- -> (D(CP)K-)-K-0 decays with the BaBar detector

We present a study of B--->(DCPK-)-K-0 decays, where D-CP(0) is reconstructed in CP-even channels, based on a sample of 88.8x10(6) Y(4S)-->B (B) over bar decays collected with the BABAR detector at the PEP-II e(+)e(-) storage ring. We measure the ratio of Cabibbo-suppressed to Cabibbo-favored branching fractions B(B--->(DCPK-)-K-0)/B(B--->D(CP)(0)pi(-))=[8.8+/-1.6(stat)+/-0.5(syst)]x10(-2) and the CP asymmetry A(CP)=0.07+/-0.17(stat)+/-0.06(syst). We also measure B(B--->(DK-)-K-0)/B(B--->D(0)pi(-))=[8.31+/-0.35(stat)+/-0.20(syst)]x10(-2) using a sample of 61.0x10(6) B (B) over bar pairs

Measurement of the branching fraction for B±→χc0K±

We present preliminary results for the measurement of the branching fraction of the decay B+- -> chi_c0 K+- from a sample of 75 million BB pairs collected by the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. The chi_c0 meson is reconstructed through its two-body decays to pi+ pi- and K+ K-. We measure BR(B+- -> chi_c0 K+-) * BR(chi_c0 -> pi+ pi-) = (1.08 +- 0.35 (stat) +- 0.10 (syst))*10^-6 and BR(B+- -> chi_c0 K+-) * BR(chi_c0 -> K+ K-) = (1.48 +- 0.44 (stat) +- 0.17 (syst)) * 10^-6. Using the known values for the chi_c0 decays branching fractions, we combined these results to obtain BR(B+- -> chi_c0 K+-) = (2.4 +- 0.7) * 10^-4

Measurement of the branching fractions and CP asymmetry of B- -> (D(CP)K-)-K-0 decays with the BaBar detector

We present a study of B--->(DCPK-)-K-0 decays, where D-CP(0) is reconstructed in CP-even channels, based on a sample of 88.8x10(6) Y(4S)-->B (B) over bar decays collected with the BABAR detector at the PEP-II e(+)e(-) storage ring. We measure the ratio of Cabibbo-suppressed to Cabibbo-favored branching fractions B(B--->(DCPK-)-K-0)/B(B--->D(CP)(0)pi(-))=[8.8+/-1.6(stat)+/-0.5(syst)]x10(-2) and the CP asymmetry A(CP)=0.07+/-0.17(stat)+/-0.06(syst). We also measure B(B--->(DK-)-K-0)/B(B--->D(0)pi(-))=[8.31+/-0.35(stat)+/-0.20(syst)]x10(-2) using a sample of 61.0x10(6) B (B) over bar pairs.The Particle Physics and Astronomy Research Council (United Kingdom); A. P. Sloan Foundation; the Research Corporation; and the Alexander von Humboldt Foundation