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Epigenetic silencing of fragile X mental retardation 1 (FMR1) causes fragile X syndrome (FXS), a common inherited form of intellectual disability and autism. FXS correlates with abnormal synapse and dendritic spine development, but the molecular link between the absence of the FMR1 product FMRP, an RNA binding protein, and the neuropathology is unclear. We found that the messenger RNA encoding bone morphogenetic protein type II receptor (BMPR2) is a target of FMRP. Depletion of FMRP increased BMPR2 abundance, especially that of the full-length isoform that bound and activated LIM domain kinase 1 (LIMK1), a component of the noncanonical BMP signal transduction pathway that stimulates actin reorganization to promote neurite outgrowth and synapse formation. Heterozygosity for BMPR2 rescued the morphological abnormalities in neurons both in Drosophila and in mouse models of FXS, as did the postnatal pharmacological inhibition of LIMK1 activity. Compared with postmortem prefrontal cortex tissue from healthy subjects, the amount of full-length BMPR2 and of a marker of LIMK1 activity was increased in this brain region from FXS patients. These findings suggest that increased BMPR2 signal transduction is linked to FXS and that the BMPR2-LIMK1 pathway is a putative therapeutic target in patients with FXS and possibly other forms of autism.

In this article, we propose a simple photochemical method to synthesize pure La2Ti2O7 films and La2Ti2O7 films doped with silver at 1.0, 3.0, and 5.0 mol%. After annealing the photo-deposited films at 900 °C, XRD, SEM, and XPS analyses showed the formation of a monoclinic La2Ti2O7 phase and the presence of Ag and AgO in doped samples. Photocatalytic tests for Congo red degradation demonstrated that pure La2Ti2O7 achieved 25.4% degradation, while doped samples reached a maximum of 92.7% degradation. Moreover, increasing silver doping on La2Ti2O7 films significantly reduced the growth of Staphylococcus aureus, indicating potential antibacterial properties. The enhanced photoactivity was attributed to the formation of a type I heterojunction between La2Ti2O7 and AgO, and a degradation mechanism was proposed based on Congo red degradation. [ABSTRACT FROM AUTHOR]

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In the present work, the synthesis, electropolymerization and polymer characterization of 2,6-di(4-butylphenyl)-4,8-dithiophenylbenzobisoxazole are reported. The synthesis involves several steps from 1,4-benzoquinone to form 2,5-diamine-3,6-dibromohydroquinone, which is condensed with 4-butylbenzoyl chloride and later with thiophen-2-ylmagnesium bromide through Kumada coupling reactions. This monomer is polymerized by potentiodynamic cyclic voltammetry. The voltammograms show a dependency on the range of applied potential, and three different processes of thermodynamically reversible oxidation and reduction occur on a platinum surface. Theoretical calculations are used to characterize these redox processes. The distribution of the frontier orbital density for the monomer and trimer forms show the participation of the thiophene ring in the polymerization processes and partial oxidation of the benzoxazole fragment. The characterization of the polymeric deposit was carried out by scanning electron microscopy and Raman spectroscopy. A dependence of both the morphology and vibrational state of the polymer on the potential range applied exists. This is attributed to the different conformations and dihedral angles of the macromolecule. Finally, the optical properties of the material indicate the existence of intramolecular charge transfer through the system's thiophene and benzobisoxazole (donor and acceptor). [ABSTRACT FROM AUTHOR]