ABSTRACT
A thorough comprehension of the mechanism underlying the methanol oxidation reaction (MOR) on Ni-based catalysts is critical for future electrocatalytic design and development. However, the mechanism of MOR on these materials remains a matter of controversy. Herein, we combine in situ surface-enhanced infrared absorption spectroscopy (SEIRAS) and density functional theory (DFT) calculations to identify the active sites and determine the mechanism of MOR on monometallic Ni-based catalysts in alkaline media. The SEIRAS results show that formate and (bi)carbonate are formed after the commencement of the MOR with potential-dependent relative distributions. These spectroscopic results are in good agreement with the DFT-computed reaction profiles over an oxygen vacancy, suggesting that the MOR mainly proceeds through the formate-involving pathway, in which the early consumption of methanol yields formate as the major product, while increasing potential drives further oxidation of formate to (bi)carbonate. We also find a parallel pathway for the generation of (bi)carbonate at high potentials that bypasses the formation of formate. The two main pathways are thermodynamically more feasible than the one predominantly reported in the literature for MOR on NiOOH that involves CHO and/or CO as key intermediates. These DFT results are supported by spectroscopic evidence showing that no band associated with CHO or CO can be detected by SEIRAS, which is attributed to the nature of the oxygen vacancies as the active sites, suppressing deep dehydrogenation of CH2O to CHO. This work thus shows the promising role of defect engineering in promoting the electrocatalytic MOR activity and selectivity.
ABSTRACT
Cholangiopathies are characterized by dysregulation of the balance between biliary growth and loss. We have shown that histamine (HA) stimulates biliary growth via autocrine mechanisms. To evaluate the paracrine effects of mast cell (MC) stabilization on biliary proliferation, sham or BDL rats were treated by IP-implanted osmotic pumps filled with saline or cromolyn sodium (24 mg/kg BW/day (inhibits MC histamine release)) for 1 week. Serum, liver blocks and cholangiocytes were collected. Histidine decarboxylase (HDC) expression was measured using real-time PCR in cholangiocytes. Intrahepatic bile duct mass (IBDM) was evaluated by IHC for CK-19. MC number was determined using toluidine blue staining and correlated to IBDM. Proliferation was evaluated by PCNA expression in liver sections and purified cholangiocytes. We assessed apoptosis using real-time PCR and IHC for BAX. Expression of MC stem factor receptor, c-kit, and the proteases chymase and tryptase were measured by real-time PCR. HA levels were measured in serum by EIA. In vitro, MCs and cholangiocytes were treated with 0.1% BSA (basal) or cromolyn (25 µM) for up to 48 h prior to assessing HDC expression, HA levels and chymase and tryptase expression. Supernatants from MCs treated with or without cromolyn were added to cholangiocytes before measuring (i) proliferation by MTT assays, (ii) HDC gene expression by real-time PCR and (iii) HA release by EIA. In vivo, cromolyn treatment decreased BDL-induced: (i) IBDM, MC number, and biliary proliferation; (ii) HDC and MC marker expression; and (iii) HA levels. Cromolyn treatment increased cholangiocyte apoptosis. In vitro, cromolyn decreased HA release and chymase and tryptase expression in MCs but not in cholangiocytes. Cromolyn-treated MC supernatants decreased biliary proliferation and HA release. These studies provide evidence that MC histamine is key to biliary proliferation and may be a therapeutic target for the treatment of cholangiopathies.
