In optical and near-infrared background light, excess brightness and fluctuation over the known backgrounds have been reported. To delineate their origin, a fluctuation analysis of the deepest optical images was performed, leading to the detection of a flat fluctuation down to 0.2 arcsec, which is much larger than that expected for galaxies. The sky brightness obtained from the detected fluctuation is a few-times brighter than the integrated light of the galaxies. These findings require some new objects. As a candidate, faint compact objects (FCOs) whose surface number density rapidly increases to the faint end were proposed. FCOs are very compact and show peculiar spectra with infrared excess. If FCOs cause the excess brightness and fluctuation, the surface number density reaches 2.6 × 10³ arcsec⁻². γ-ray observations require the redshift of FCOs to be less than 0.1 with FCOs consisting of missing baryons. A very low M/L indicates that FCOs are powered by gravitational energy associated with black holes.

Neural stem cells (NSCs) actively proliferate and generate neurons and glial cells (active state) in the embryonic brain, whereas they are mostly dormant (quiescent state) in the adult brain. The expression dynamics of Hes1 are different between active and quiescent NSCs. In active NSCs, Hes1 expression oscillates and periodically represses the expression of proneural genes such as Ascl1, thereby driving their oscillations. By contrast, in quiescent NSCs, Hes1 oscillations maintain expression at higher levels even at trough phases (thus continuous), thereby continuously suppressing proneural gene expression. High levels of Hes1 expression and the resultant suppression of Ascl1 promote the quiescent state of NSCs, whereas oscillatory Hes1 expression and the resultant oscillatory Ascl1 expression regulate their active state. Furthermore, in other developmental contexts, high, continuous Hes1 expression induces astrocyte differentiation or the formation of boundaries, which function as signaling centers. Thus, the expression dynamics of Hes1 are a key regulatory mechanism generating and maintaining various cell types in the nervous system.

Adiponectin is an adipokine that can exert a regulatory function on bone metabolism. However, there are many contradictions between clinical and pre-clinical studies on adiponectin. APPL1 is an adaptor protein that can interact with adiponectin receptors. In the current study, we found that knockout of the Appl1 gene in male mice was associated with higher bone volume and numbers of trabeculae than in females or controls. The trabecular thickness, cortical thickness, ratio of bone volume/trabecular volume, cross-sectional bone area, and mean polar moment of inertia increased in Appl1 KO mice compared with wild-type mice. The number of osteoblasts increased but the number of adipocytes decreased in Appl1 KO mice. Knockdown of Appl1 impaired adipogenesis in bone marrow-derived mesenchymal stem cells. Mineralization was increased by knockdown of Appl1 during osteoblast differentiation. Data from differentiation-related genes showed results consistent with the in vivo effects. In summary, this study provides further clarification of the effect of the adiponectin signaling pathway on bone metabolism.