Positive correlations of leptin with %Fat and FM were found in both sexes, while positive associations of %Fat with OC and insulin were found only in boys. Bone Z-score and SOS positively correlated with OC in boys but negatively correlated with 25(OH)D in girls. When classifying the obese group using %Fat ≥25, the positive correlations between %Fat and insulin and the negative associations between %Fat and adiponectin in girls were more pronounced. These results suggest that the associations of body fat and bone parameters with OC, adiponectin, 25(OH)D, and insulin were sex-specific, with greater clarity when %Fat was used instead of BMI to classify obesity.

Lipocalin 2 (LCN2) is an adipokine involved in many physiological functions, including bone metabolism. We previously demonstrated its implication in mouse models of mechanical unloading-induced osteoporosis and in a cohort of bed rest volunteers. We therefore aimed at studying its involvement in postmenopausal osteoporosis.

We measured serum LCN2 and correlated its levels to Dickkopf WNT Signaling Pathway Inhibitor 1 (DKK1), Tartrate Resistant Acid Phosphatase 5B (TRAcP5B), sclerostin, urinary N-terminal telopeptide of type I collagen (NTX), serum C-terminal telopeptide of type I collagen (CTX), parathyroid hormone and vitamin K by ELISA performed in a cohort of younger (50-65years) and older (66-90years) osteoporotic women in comparison to healthy subjects. A cohort of male healthy and osteoarthritic patients was also included. Sobel mediation analysis was used to test indirect associations among age, LCN2 and DKK1 or NTX.

LCN2 levels were unchanged in osteoporotic and in osteoarthritis patients when compared to healthy subjects and did not correlate with BMD. However, serum LCN2 correlated with age in healthy women (

=0.44;

=0.003) and men (

=0.5;

=0.001) and serum concentrations of DKK1 (

=0.47; P=0.003) and urinary NTX (

=0.34;

=0.04). Sobel mediation analysis showed that LCN2 mediates an indirect relationship between age and DKK1 (

=0.02), but not with NTX, in healthy subjects.

Taken together, the results suggest a hitherto unknown association between LCN2, DKK1 and age in healthy individuals, but not in postmenopausal osteoporotic women.

Taken together, the results suggest a hitherto unknown association between LCN2, DKK1 and age in healthy individuals, but not in postmenopausal osteoporotic women.We live in a world that changes on many timescales. To learn and make decisions appropriately, the human brain has evolved to integrate various types of information, such as sensory evidence and reward feedback, on multiple timescales. This is reflected in cortical hierarchies of timescales consisting of heterogeneous neuronal activities and expression of genes related to neurotransmitters critical for learning. We review the recent findings on how timescales of sensory and reward integration are affected by the temporal properties of sensory and reward signals in the environment. Despite existing evidence linking behavioral and neuronal timescales, future studies must examine how neural computations at multiple timescales are adjusted and combined to influence behavior flexibly.Perception is often described as probabilistic inference requiring an internal representation of uncertainty. However, it is unknown whether uncertainty is represented in a task-dependent manner, solely at the level of decisions, or in a fully Bayesian manner, across the entire perceptual pathway. To address this question, we first codify and evaluate the possible strategies the brain might use to represent uncertainty, and highlight the normative advantages of fully Bayesian representations. In such representations, uncertainty information is explicitly represented at all stages of processing, including early sensory areas, allowing for flexible and efficient computations in a wide variety of situations. Next, we critically review neural and behavioral evidence about the representation of uncertainty in the brain agreeing with fully Bayesian representations. We argue that sufficient behavioral evidence for fully Bayesian representations is lacking and suggest experimental approaches for demonstrating the existence of multivariate posterior distributions along the perceptual pathway.

The study sought to determine the rate of aortic expansion and correlation with somatic growth in patients with repaired tetralogy of Fallot (rTOF), and predictors for determining the annual growth rate of the aorta (Ao-AGR).

Ninety-four rTOF patients (mean age 14.5 ± 4.4 years) with two cardiac magnetic resonance tests (CMR) (median duration 52 months, interquartile range, IQR 24-71) were analyzed for aortic diameter (AoD) at the annulus, the sinus of Valsalva (SoV), the sinotubular junction, and the ascending aorta (AAo), and compared with the normal limit AoD (NL-AoD) values. The median age-at-repair was 60 months (IQR 36-84). Ao-AGR and its index (Ao-AGRI) were derived from changes of the AoD and AoD-index, respectively, divided by the duration between the two studies. Three potential predictors (baseline AoD, sex, and age-at-repair) for the progression of Ao-AGR were analyzed.

There was a significant larger AoD than NL-AoD (

 < 0.001). Slow aortic growth was encountered in 78-85 % of patients. The Ao-AGR was slow, the median AGR ranged from 0.37 mm (IQR 0.13-0.72) at annulus to 0.56 mm (IQR 0.22-0.91) at AAo. There was a regression in Ao-AGRI, ranged from -1.41 mm (IQR -1.94, -0.87) at annulus to -2.36 mm (IQR -3.09, -1.63) at SoV. The three predictors were not correlated with severity of Ao-AGR.

Most adolescents with rTOF show significant aortic dilatation. There is a slow Ao-AGR with regression of Ao-AGRI, which may suggest that the rate of aortic growth is slower than the somatic growth. P7C3 nmr There are no significant predictors of the progression of Ao-AGR.

Most adolescents with rTOF show significant aortic dilatation. There is a slow Ao-AGR with regression of Ao-AGRI, which may suggest that the rate of aortic growth is slower than the somatic growth. There are no significant predictors of the progression of Ao-AGR.