Oxytocin and Vasopressin Are Dysregulated in Williams Syndrome, a Genetic Disorder Affecting Social Behavior

The molecular and neural mechanisms regulating human social-emotional behaviors are fundamentally important but largely unknown; unraveling these requires a genetic systems neuroscience analysis of human models. Williams Syndrome (WS), a condition caused by deletion of ∼28 genes, is associated with a gregarious personality, strong drive to approach strangers, difficult peer interactions, and attraction to music. WS provides a unique opportunity to identify endogenous human gene-behavior mechanisms. Social neuropeptides including oxytocin (OT) and arginine vasopressin (AVP) regulate reproductive and social behaviors in mammals, and we reasoned that these might mediate the features of WS. Here we established blood levels of OT and AVP in WS and controls at baseline, and at multiple timepoints following a positive emotional intervention (music), and a negative physical stressor (cold). We also related these levels to standardized indices of social behavior. Results revealed significantly higher median levels of OT in WS versus controls at baseline, with a less marked increase in AVP. Further, in WS, OT and AVP increased in response to music and to cold, with greater variability and an amplified peak release compared to controls. In WS, baseline OT but not AVP, was correlated positively with approach, but negatively with adaptive social behaviors. These results indicate that WS deleted genes perturb hypothalamic-pituitary release not only of OT but also of AVP, implicating more complex neuropeptide circuitry for WS features and providing evidence for their roles in endogenous regulation of human social behavior. The data suggest a possible biological basis for amygdalar involvement, for increased anxiety, and for the paradox of increased approach but poor social relationships in WS. They also offer insight for translating genetic and neuroendocrine knowledge into treatments for disorders of social behavior

Mesure de la diffusivité de l’oxygène par inhibition de fluorescence de sondes pyréniques dans la membrane d’érythrocyte enrichie en cholestérol

L’influence du cholestérol sur la diffusibilité de l’oxygène dans les membranes biologiques a été étudiée par inhibition de la fluorescence des acides pyrènebutyrique (PBA) et dodécanoïque (PDA). La « fluidité membranaire », mesurée par polarisation de fluorescence avec des sondes spécifiques de différentes régions membranaires (6, 12-AS, DPH, TMA- DPH), évolue inversement au rapport cholestérol/protéine (C/Pt) et varie en fonction de la région étudiée. La durée de vie du monomère du PDA, mesurée par fluorescence résolue dans le temps, croît avec le rapport C/Pt en absence d’O2. En présence d’O2, les valeurs des constantes d’inhibition dynamique du PDA augmentent avec le rapport C/Pt (diffusivité apparente d’02 accrue). La diffusion d’O, augmenterait uniquement dans la région centrale de la membrane, caractérisée par le PDA. La variation de la solubilité d’O2 dans des domaines restreints de polarité différente pourrait expliquer l’inhibition de fluorescence du PDA

Characterization of a boro-silicon oxynitride prepared by thermal nitridation of a polyborosiloxane

Fine physicochemical characterization has allowed proposing of a mechanism for the nitridation pathway of a polyborosiloxane polymer into a new ceramic material in the SiBON system. A polyborosiloxane, a polymer consisting of Si-O-B linkages, was synthesized by the condensation reaction between tetrachlorosilane SiCl4 and boric acid B(OH)(3). The polymer was then thermally nitridated under flowing ammonia into an oxynitride of boron and silicon. This conversion was observed using various structural techniques: chemical analysis, X-ray diffraction, infrared spectroscopy and X-ray photoelectron spectroscopy. The nitridation process can be divided in two main stages: (i) between 400 and 800 degrees C, B-N bonds are formed by B-O bond cleavage; (ii) above 1000 degrees C, Si-N bonds are formed by Si-O bond cleavage, The oxynitride remains amorphous even at 1300 degrees C. Pyrolysis up to 1700 degrees C led to a partial crystallization of hexagonal boron nitride