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Starting from ClSbRF2 (RF = C2F5, 3,5-(CF3)2C6H3) and H(E)P(tBu)2 (E = O, S), we prepared the oxy- and sulphanediyl-bridged adducts RF2Sb(Cl)–E–(H)P(tBu)2, which are stable against the elimination of HCl. The different electron-withdrawing substituents and chalcogen bridging units influence the size of the Sb–E–P angle. ClSb(C2F5)2 and nBu3SnH react to give HSb(C2F5)2, which seems to interact weakly with H(O)P(tBu)2 in solution as observed via NMR. All products were characterised by NMR spectroscopy and all the stable ones were additionally characterised by X-ray diffraction and elemental analyses. [ABSTRACT FROM AUTHOR]

We investigated the development of the HPA axis in group-living rhesus monkeys. Forty-three infants were studied from birth through their third year of life; 22 infants were physically abused by their mothers, while 21 infants were not abused. Plasma cortisol levels in basal conditions and in response to a novel environment test were assessed at 6-month intervals. Both basal and stress cortisol increased steadily from 6 to 24 months of age and then dropped. Across all ages, stress cortisol levels were significantly higher than the basal levels. The cortisol responses to stress at 30 and 36 months of age were significantly lower than the responses at all other ages. At most ages there was an inverse relationship between basal and stress cortisol levels. Individual differences in basal cortisol levels were generally stable in the first 2 years and more variable in the third year while the opposite for true for cortisol responses to stress. At the end of the first year, but not later in life, abused infants had higher cortisol levels than controls across the basal and stress conditions. Rates of social interactions with the mother and other group members were positively correlated with basal cortisol levels early in life, and with cortisol responses to stress later in life. Altogether, these results indicate that there are strong individual differences in HPA function, that there is a relationship between basal activity and stress reactivity, and that early abuse has the short-term effect of increasing both basal activity and stress reactivity. © 2012 Wiley Periodicals, Inc. Dev Psychobiol 56: 86-95, 2014. [ABSTRACT FROM AUTHOR]

Insufficient sleep (short sleep duration and poor sleep quality) is associated with obesity risk. Emerging adults (ages 18-28 years) have a greater risk of excess weight gain and insufficient sleep, and these risks are higher in Black individuals. Using a measurement burst design, we assessed associations between sleep with energy balance components and obesity marker changes over 6 months in 15 Black emerging adults (12 females; age 21±2.5 years; body mass index 25.7±4.5 kg/m2; body fat 25.8±11.9%). Since our sample was predominantly female (80%), we repeated our analyses for females only. Participants completed the following measurements at baseline (BLN) and 6 months later (6MO): 7 days of actigraphy-based sleep and physical activity energy expenditure (EE) and 2 nights of in-home polysomnography-based sleep; resting EE and thermic effect of food with indirect calorimetry; ad libitum energy intake (EI) via self-reported methods over 4 days and directly measured over 3 days with provided meals. Body weight (2.6 kg, p=0.01) and waist circumference (2.4 cm, p=0.03) increased from BLN to 6MO. Changes in actigraphy-based sleep duration were associated with changes in body weight (β=0.03, Standard error (SE)=0.02, p=0.04) and fat mass (β=0.07, SE=0.03 p=0.03) in females only. Greater rapid eye movement sleep duration was associated with increases in resting EE (β=2.24, SE=0.84, p=0.02). Greater slow-wave sleep was associated with increases in self-reported EI (β=18.34, SE=4.7, p<0.01). Sleep may impact components of energy balance and risk of weight gain in Black emerging adults. Additional research is needed to confirm our pilot findings.