Measurement of illumination exposure in postpartum women

BACKGROUND: Low levels of light exposure at critical times are thought to cause seasonal affective disorder. Investigators, in studies demonstrating the usefulness of bright light therapy, also have implicated light's role in non-seasonal depression. The precise cause of postpartum depression has not been delineated, but it seemed possible that new mothers would spend reduced time in daylight. The goal of this study was to examine the levels of illumination experienced by postpartum mothers and to discover any relationship between light exposure and mood levels experienced during the postpartum period. METHODS: Fifteen postpartum women, who did not have any baseline indication of depression, wore a wrist device (Actillume) for 72 hours to measure their exposure to light. At the end of the recording period, they completed a self-reported measure of mood. The mean light exposure of these postpartum women (expressed as the 24-hour average logarithm of illumination in lux) was compared with that of a representative sample of women of comparable age, residence, and seasonal months of recording. Mood levels were then rank-ordered and tested for correlation with light exposure levels. RESULTS: There was no significant difference between the amount of light [log(10)lux] experienced by postpartum (1.01 SD 0.236) and control women (1.06 SD 0.285). Mood was not correlated with illumination in the postpartum sample. CONCLUSIONS: Postpartum women in San Diego did not receive reduced light, nor was low mood related to low illumination

Calculation of molecular thermochemical data and their availability in databases

Thermodynamic properties of molecules can be obtained by experiment, by statistical mechanics in conjunction with electronic structure theory and by empirical rules like group additivity. The latter two methods are briefly re-viewed in this chapter. The overview of electronic structure methods is intended for readers less experienced in electronic structure theory and focuses on concepts without going into mathematical details. This is followed by a brief description of group additivity schemes; finally, an overview of databases listing reliable thermochemical data is given

Copy number elevation of 22q11.2 genes arrests the developmental maturation of working memory capacity and adult hippocampal neurogenesis

Working memory capacity, a critical component of executive function, expands developmentally from childhood through adulthood. Anomalies in this developmental process are seen in individuals with autism spectrum disorder (ASD), schizophrenia and intellectual disabilities (ID), implicating this atypical process in the trajectory of developmental neuropsychiatric disorders. However, the cellular and neuronal substrates underlying this process are not understood. Duplication and triplication of copy number variants of 22q11.2 are consistently and robustly associated with cognitive deficits of ASD and ID in humans, and overexpression of small 22q11.2 segments recapitulates dimensional aspects of developmental neuropsychiatric disorders in mice. We capitalized on these two lines of evidence to delve into the cellular substrates for this atypical development of working memory. Using a region- and cell-type-selective gene expression approach, we demonstrated that copy number elevations of catechol-O-methyl-transferase (COMT) or Tbx1, two genes encoded in the two small 22q11.2 segments, in adult neural stem/progenitor cells in the hippocampus prevents the developmental maturation of working memory capacity in mice. Moreover, copy number elevations of COMT or Tbx1 reduced the proliferation of adult neural stem/progenitor cells in a cell-autonomous manner in vitro and migration of their progenies in the hippocampus granular layer in vivo. Our data provide evidence for the novel hypothesis that copy number elevations of these 22q11.2 genes alter the developmental trajectory of working memory capacity via suboptimal adult neurogenesis in the hippocampus.Peer reviewe