Acid-induced tubular g-C3N4 for the selective generation of singlet oxygen by energy transfer: Implications for the photocatalytic degradation of parabens in real water environments.

Parabens are widely present in aquatic environments and pose potential health risk. Although great progress has been made in the field of the photocatalytic degradation of parabens, the powerful Coulomb interactions between electrons and holes are the major limitations to photocatalytic performance. Hence, acid-induced tubular g-C3N4 (AcTCN) was prepared and applied for the removal of parabens from a real water environment. AcTCN not only increased the specific surface area and light absorption capacity, but also selectively generated 1O2 via an energy transfer-mediated oxygen activation pathway. The 1O2 yield of AcTCN was 11.8 times higher than that of g-C3N4. AcTCN exhibited remarkable removal efficiencies for parabens depending on the length of the alkyl group. Furthermore, the rate constants (k values) of parabens in ultrapure water were higher than those in tap and river water because of the presence of organic and inorganic species in real water environments. Two possible pathways for the photocatalytic degradation of parabens are proposed based on the identification of intermediates and theoretical calculations. In summary, this study offers theoretical support for the efficient enhancement of the photocatalytic performance of g-C3N4 for the removal of parabens in real water environments.

Triple-gene deletion for osteocalcin significantly impairs the alignment of hydroxyapatite crystals and collagen in mice.

Osteocalcin (Ocn), also known as bone Gla protein, is synthesized by osteoblasts and thought to regulate energy metabolism, testosterone synthesis and brain development. However, its function in bone is not fully understood. Mice have three Ocn genes: Bglap, Bglap2 and Bglap3. Due to the long span of these genes in the mouse genome and the low expression of Bglap3 in bone, researchers commonly use Bglap and Bglap2 knockout mice to investigate the function of Ocn. However, it is unclear whether Bglap3 has any compensatory mechanisms when Bglap and Bglap2 are knocked out. Considering the controversy surrounding the role of Ocn in bone, we constructed an Ocn-deficient mouse model by knocking out all three genes (Ocn-/-) and analyzed bone quality by Raman spectroscopy (RS), Scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FTIR) and MicroCT (µCT). The RS test showed that the alignment of hydroxyapatite crystals and collagen fibers was significantly poorer in Ocn-/- mice than in wild-type (WT) mice. Ocn deficiency resulted in a looser surface structure of bone particles and a larger gap area proportion. FTIR analysis showed few differences in bone mineral index between WT and Ocn-/- mice, while µCT analysis showed no significant difference in cortical and trabecular regions. However, under tail-suspension simulating bone loss condition, the disorder of hydroxyapatite and collagen fiber alignment in Ocn-/- mice led to more obvious changes in bone mineral composition. Collectively, our results revealed that Ocn is necessary for regulating the alignment of minerals parallel to collagen fibrils.