Photocatalytic transfer of aqueous nitrogen into ammonia using nickel-titanium-layered double hydroxide.

The development of solar-driven transfer of atmospheric nitrogen into ammonia is one of the green and sustainable strategies in industrial ammonia production. Nickel-titanium-layered double hydroxide (NiTi-LDH) was synthesised using the soft-chemical process for atmospheric nitrogen fixation application under photocatalysis in an aqueous system. NiTi-LDH was investigated using advanced characterisation techniques and confirmed the potential oxygen vacancies and/or surface defects owing to better photocatalytic activity under the solar spectrum. It also exhibited a bandgap of 2.8 eV that revealed its promising visible-light catalytic activities. A maximum of 33.52 µmol L-1 aqueous NH3 was obtained by continuous nitrogen (99.9% purity) supply into the photoreactor under an LED light source. Atmospheric nitrogen supply (≈78%) yielded 14.67 µmol L-1 aqueous NH3 within 60 min but gradually reduced to 3.6 µmol L-1 at 330 min. Interestingly, in weak acidic pH, 20.90 µmol L-1 NH3 was produced compared to 11.51 µmol L-1 NH3 in basic pH. The application of NiTi-LDH for visible-light harvesting capability and photoreduction of atmospheric N2 into NH3 thereby opens a new horizon of eco-friendly NH3 production using natural sunlight as alternative driving energy

SIGN-R1, a C-type lectin, enhances apoptotic cell clearance through the complement deposition pathway by interacting with C1q in the spleen

Complements, such as C1q and C3, and macrophages in the splenic marginal zone (MZMs) play pivotal roles in the efficient uptake and processing of circulating apoptotic cells. SIGN-R1, a C-type lectin that is highly expressed in a subpopulation of MZMs, regulates the complement fixation pathway by interacting with C1q, to fight blood-borne Streptococcus pneumoniae. Therefore, we examined whether the SIGN-R1-mediated classical complement pathway plays a role in apoptotic cell clearance and immune tolerance. SIGN-R1 first-bound apoptotic cells and this binding was significantly enhanced in the presence of C1q. SIGN-R1-C1q complex then immediately mediated C3 deposition on circulating apoptotic cells in the MZ, leading to the efficient clearance of them. SIGN-R1-mediated C3 deposition was completely abolished in the spleen of SIGN-R1 knockout (KO) mice. Given that SIGN-R1 is not expressed in the liver, we were struck by the finding that C3-deposited apoptotic cells were still found in the liver of wild-type mice, and dramatically reduced in the SIGN-R1 KO liver. In particular, SIGN-R1 deficiency caused delayed clearance of apoptotic cells and aberrant secretion of cytokines, such as TNF-alpha, IL-6, and TGF-beta in the spleen as well as in the liver. In addition, anti-double-and single-stranded DNA antibody level was significantly increased in SIGN-R1-depleted mice compared with control mice. These findings suggest a novel mechanism of apoptotic cell clearance which is initiated by SIGN-R1 in the MZ and identify an integrated role of SIGN-R1 in the systemic clearance of apoptotic cells, linking the recognition of apoptotic cells, the opsonization of complements, and the induction of immune tolerance.close