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Combining BiOCl with TiO2 nanomaterials is beneficial to enhance the photocatalytic activity and optoelectronic activity. In this paper, BiOCl nanosheet–TiO2 nanotube array composites were synthesized to enhance the photocatalytic degradation performance for methyl orange (MO) of TiO2 under ultraviolet light irradiation. BiOCl nanosheets were deposited on TiO2 nanotube arrays by the straightforward impregnation method. X-ray diffraction, scanning electron microscopy, energy dispersive x-ray spectroscopy, transmission electron microscopy, x-ray photoelectron spectroscopy, and photocurrent (i–t) were used to evaluate the composites of BiOCl nanosheets–TiO2 nanotube arrays. The results showed that the tetragonal BiOCl nanosheets clustered together on the surface of the TiO2 nanotubes and grew along the (110) crystal plane. The composites outperformed pure TiO2 regarding outstanding structure and overall photocatalytic performance, and the MO photocatalytic degradation rate was 98.5%. For the 30-BiOCl–TiO2, its photocurrent intensity (58 µA) was 4.5 higher than TiO2 (13 µA). The degradation rate of 87% can still be reached after three cycles.

Filamin B (FLNB) plays an important role in skeletal development. Mutations in FLNB can lead to skeletal malformation such as an abnormal number of ossification centers, indicating that the skeletal segmentation in the embryonic period may be interfered with. We established a mouse model with the pathogenic point mutation FLNB NM_001081427.1: c.4756G > A (p.Gly1586Arg) using CRISPR-Cas9 technology. Micro-CT, HE staining and whole skeletal preparation were performed to examine the skeletal malformation. In situ hybridization of embryos was performed to examine the transcription of HOX genes during embryonic development. The expression of FLNB was downregulated in FLNBG1586R/G1586R and FLNBWT/G1586R mice, compared to FLNBWT/WT mice. Fusions in tarsal bones were found in FLNBG1586R/G1586R and FLNBWT/G1586R mice, indicating that the skeletal segmentation was interfered with. In the embryo of FLNBG1586R/G1586R mice (E12.5), the transcription levels of HOXD10 and HOXB2 were downregulated in the carpal region and cervical spine region, respectively. This study indicated that the loss-of-function mutation G1586R in FLNB may lead to abnormal skeletal segmentation, and the mechanism was possibly associated with the downregulation of HOX gene transcription during the embryonic period.