Hokkaido University

About: Hokkaido University is a education organization based out in Sapporo, Hokkaidô, Japan. It is known for research contribution in the topics: Catalysis & Population. The organization has 53925 authors who have published 115403 publications receiving 2651647 citations. The organization is also known as: Hokudai & Hokkaidō daigaku.

Alkali‐Metal‐Promoted Pt/TiO2 Opens a More Efficient Pathway to Formaldehyde Oxidation at Ambient Temperatures

Abstract: Formaldehyde is emitted from building and furnishing materials and consumer products, and is known to cause irritation of eyes and respiratory tract, headache, pneumonia, and even cancer. It is a dominant indoor air pollutant, especially in developing countries, and significant efforts have gone into indoor HCHO purification to meet environmental regulations and human health needs. Removal of HCHO by adsorbents has been investigated extensively using potassium permanganate, activated carbon, aluminum oxide, and some ceramic materials. Sorbent effectiveness is typically limited by low adsorption capacities. Catalytic oxidation is the most effective technology for volatile organic compound (VOC) abatement because VOCs can be oxidized to CO2 over certain catalysts at much lower temperatures than in thermal oxidation. Supported noble metal catalysts (Pt, Pd, Rh, Au, Ag) or metal oxide catalysts (Ni, Cu, Cr, Mn) have been used for the catalytic oxidation of VOCs. Complete oxidation of HCHO over catalysts occurs above 150 8C on clean and oxidized films of Ni, Pd, and Al and over silver–cerium composite oxide, above 100 8C over Ag/MnOx-CeO2 [18] and Au/CeO2, [19] and above 85 8C over Pd-Mn/Al2O3 [17] and Au/FeOx. As catalytic oxidation at even lower temperatures is desirable for indoor air purification, the development of a catalyst for total HCHOoxidation at room temperature is of great interest. In our recent study, 1% Pt/TiO2 catalyst was shown to be effective for HCHO oxidation at room temperature, achieving 100% conversion of d= 100 ppm HCHO to CO2 and H2O at a gas hourly space velocity (GHSV) of 50000 h . However, we also observed that this type catalyst is not as active as needed for practical applications, and deactivates with time-on-stream. Herein, we report a novel alkali-metal-promoted Pt/TiO2 catalyst for the ambient destruction of HCHO. We show that the addition of alkali-metal ions (such as Li, Na, and K) to Pt/TiO2 catalyst stabilized an atomically dispersed PtO(OH)x–alkali-metal species on the catalyst surface and also opened a new low-temperature reaction pathway, significantly promoting the activity for the HCHO oxidation by activating H2O and catalyzing the facile reaction between surface OH and formate species to total oxidation products. Figure 1a shows the HCHO conversion to CO2 as a function of temperature over the x% Na-1% Pt/TiO2 (x= 0, 1, and 2) samples at a GHSVof 120000 h 1 andHCHO inlet of d= 600 ppm. All gas streams were humidified to a RH of around 50%. Before each activity test, the samples were reduced in H2 at 300 8C for 30 min. The sodium-free catalyst had low activity for the HCHO oxidation reaction, with HCHO conversion being only about 19% at 15 8C. With 1% Na addition, the HCHO conversion reached 96% at 15 8C and 100% at 40 8C. With 2% Na addition, 100% HCHO conversion to CO2 and H2O was measured at 15 8C. The effect of Na addition on the surface reducibility was examined by H2 temperature-programmed reduction (TPR; Figure 1b). The amounts of H2 consumption were about the same over all the samples, but the addition of Na shifted the reduction peak to lower temperatures, that is, from 2 8C for 1% Pt/TiO2 to 6 8C for 1% Na-1% Pt/TiO2 and 11 8C for 2% Na-1% Pt/ TiO2. Thus, the sample reducibility correlates with the sample activity. The most active 2% Na-promoted sample had excellent stability as checked by long isothermal tests. For example, at a GHSV of 300000 h 1 and with the same other reaction conditions, approximately 80% HCHO conversion was maintained over a 72 h-long test (Figure 1a, inset). Li and K were equally effective promoters to Na and imparted the same high activity and stability to the Pt species (Supporting Information, Figure S1). Water vapor and oxygen effects on the activity of Na-Pt/TiO2 are important (Supporting Information, Figures S2,S3). Deionized-water washing of the samples was performed to check the alkali-metal and Pt interaction.While most of the Na was removed from the Nacontaining catalysts, a residual amount remained (Supporting Information, Table S1). Activity test results (Supporting Information, Figure S1) showed that the washed catalyst had identical activity for HCHO [*] C. Zhang, F. Liu, Y. Liu, Prof. H. He Research Center for Eco-Environmental Sciences Chinese Academy of Sciences Shuangqing Road 18, Beijing, 100085 (China) E-mail: honghe@rcees.ac.cn

Mutations in the TRKA /NGF receptor gene in patients with congenital insensitivity to pain with anhidrosis

Abstract: Congenital insensitivity to pain with anhidrosis (CIPA; MIM 256800) is an autosomal-recessive disorder characterized by recurrent episodes of unexplained fever, anhidrosis (absence of sweating) and absence of reaction to noxious stimuli, self-mutilating behaviour and mental retardation. The genetic basis for CIPA is unknown. Nerve growth factor (NGF) induces neurite outgrowth and promotes survival of embryonic sensory and sympathetic neurons. Mice lacking the gene for TrkA, a receptor tyrosine kinase for NGF, share dramatic phenotypic features of CIPA, including loss of responses to painful stimuli, although anhidrosis is not apparent in these animals. We therefore considered the human TRKA homologue as a candidate for the CIPA gene. The mRNA and genomic DNA encoding TRKA were analysed in three unrelated CIPA patients who had consanguineous parents. We detected a deletion-, splice- and missense-mutation in the tyrosine kinase domain in these three patients. Our findings strongly suggest that defects in TRKA cause CIPA and that the NGF-TRKA system has a crucial role in the development and function of the nociceptive reception as well as establishment of thermoregulation via sweating in humans. These results also implicate genes encoding other TRK and neurotrophin family members as candidates for developmental defect(s) of the nervous system.