Molecular Regulation of Fetal Brain Development in Inbred and Congenic Mouse Strains Differing in Longevity.

The objective of this study was to investigate gene regulation of the developing fetal brain from congenic or inbred mice strains that differed in longevity. Gene expression and alternative splice variants were analyzed in a genome-wide manner in the fetal brain of C57BL/6J mice (long-lived) in comparison to B6.Cg-/J (congenic, short-lived) and AKR/J (inbred, short-lived) mice on day(d) 12, 15, and 17 of gestation.

Single-Cell Transcriptional Response of the Placenta to the Ablation of Caveolin-1: Insights into the Adaptive Regulation of Brain-Placental Axis in Mice.

Caveolin-1 () is a major plasma membrane protein that plays important functions in cellular metabolism, proliferation, and senescence. Mice lacking show abnormal gene expression in the fetal brain. Though evidence for placental influence on brain development is emerging, whether the ablation of affects the regulation of the brain-placental axis remains unexamined.

Role of paralogs in the sex-bias transcriptional and metabolic regulation of the brain-placental axis in mice.

Introduction: Duplicated genes or paralogs play important roles in the adaptive function of eukaryotic genomes. Animal studies have shown evidence for the functional role of paralogs in pregnancy, but our knowledge about the role of paralogs in the fetoplacental regulation remains limited. In particular, if fetoplacental metabolic regulation is modulated by differential expression of paralogs remains unexamined.

Ablation of placental REST deregulates fetal brain metabolism and impacts gene expression of the offspring brain at the postnatal and adult stages.

In this study, the transcriptional repressor REST (Repressor Element 1 Silencing Transcription factor) was ablated in the mouse placenta to investigate molecular and cellular impacts on the offspring brain at different life stages. Ablation of placental REST deregulated several brain metabolites, including glucose and lactate that fuel brain energy, vitamin C (ascorbic acid) that functions in the epigenetic programming of the brain during postnatal development, and glutamate and creatine that help the brain to respond to stress conditions during adult life. Bulk RNA-seq analysis showed that a lack of placental REST persistently altered multiple transport genes, including those related to oxygen transportation in the offspring brain.

Role of caveolin-1 in metabolic programming of fetal brain.

Mice lacking caveolin-1 (), a key protein of plasma membrane, exhibit brain aging at an early adult stage. Here, integrative analyses of metabolomics, transcriptomics, epigenetics, and single-cell data were performed to test the hypothesis that metabolic deregulation of fetal brain due to the ablation of is linked to brain aging in these mice. The results of this study show that lack of caused deregulation in the lipid and amino acid metabolism in the fetal brain, and genes associated with these deregulated metabolites were significantly altered in the brain upon aging.

Efficiency improvement of thin film solar cell using silver pyramids array and antireflective layer.

In recent years, plasmonics has been widely employed to improve light trapping in solar cells. Silver nanospheres have been used in several research works to improve the capability of solar absorption. In this paper, we use silver pyramid-shaped nanoparticles, a noble plasmonic nanoparticle, inside thin-film silicon and InP solar cells to increase light absorption compared to previously published topologies.

Fetal origin of sex-bias brain aging.

DNA methylation plays crucial roles during fetal development as well as aging. Whether the aging of the brain is programmed at the fetal stage remains untested. To test this hypothesis, mouse epigenetic clock (epiclock) was profiled in fetal (gestation day 15), postnatal (day 5), and aging (week 70) brain of male and female C57BL/6J inbred mice.