Reaction Characteristics of Monolithic Catalysts with Different Size of Channels for NOₓ Reduction

The NOₓ reduction with carbon and NH₃ on various monolithic catalysts was investigated over a wide range of space velocity. A three-component composite catalyst, Co-La₂O₃-Pt, supported on active carbon (DIAHOPE 008) was used. It was pulverized into fine powder, and after mixing with hydrogel of aluminum hydroxide, this was molded into cylindrical forms with an inner channel of three sizes along the axial direction. The maximum limit of space velocity (SVₘₐₓ) to achieve a 100% NO conversion was mainly discussed. The same catalyst components were extensively supported on substrates having various channel structures of ceramic honeycomb. For these substrates, the effects of alumina sol-precoating and thermal treatment on the NO-NH₃ reaction were studied. The 0.93% Co-0.51% La₂O₃-1.6% Pt catalyst supported on the honeycomb precoated with 9.2% AI₂O₃ and calcined at 600°C for 1 hour gave the best performance among the various catalyst components. It also showed the best performance among the various structures from the viewpoint of SVₘₐₓ for achieving a 100% NO conversion

Altered interaction between plasminogen activator inhibitor type 1 activity and sympathetic nerve activity with aging

取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1917号 , 学位授与年月日 : 平成20年3月22日, 学位授与大学 : 金沢大学, 主査教授 : 山岸 正和, 副査教授 : 中尾 眞二 , 多久和

Fabrication and characterization of high-T/sub c/ SQUID magnetometer with damping resistance

Effects of damping resistance on current versus voltage (I-V) characteristics for high-T/sub c/ superconducting quantum interference devices (SQUIDs) were studied. In the transverse-type SQUID with coplanar strip lines, parasitic capacitance originating from the large dielectric constant of SrTiO/sub 3/ substrates can induce resonance structures on I-V curves and degrade the modulation voltage. In our simulations, it is shown that the modulation voltage is much improved by using damping resistance. However, the obtained experimental results for our SQUIDs with Au damping do not agree well with those in the simulations. The discrepancy is likely due to existence of the large contact resistance between Au and YBa/sub 2/Cu/sub 3/O/sub 7-/spl delta// films

Oxytocin receptor gene variations predict neural and behavioral response to oxytocin in autism

Oxytocin appears beneficial for autism spectrum disorder (ASD), and more than 20 single-nucleotide polymorphisms (SNPs) in oxytocin receptor (OXTR) are relevant to ASD. However, neither biological functions of OXTR SNPs in ASD nor critical OXTR SNPs that determine oxytocin's effects on ASD remain unknown. Here, using a machine-learning algorithm that was designed to evaluate collective effects of multiple SNPs and automatically identify most informative SNPs, we examined relationships between 27 representative OXTR SNPs and six types of behavioral/neural response to oxytocin in ASD individuals. The oxytocin effects were extracted from our previous placebo-controlled within-participant clinical trial administering single-dose intranasal oxytocin to 38 high-functioning adult Japanese ASD males. Consequently, we identified six different SNP sets that could accurately predict the six different oxytocin efficacies, and confirmed the robustness of these SNP selections against variations of the datasets and analysis parameters. Moreover, major alleles of several prominent OXTR SNPs-including rs53576 and rs2254298-were found to have dissociable effects on the oxytocin efficacies. These findings suggest biological functions of the OXTR SNP variants on autistic oxytocin responses, and implied that clinical oxytocin efficacy may be genetically predicted before its actual administration, which would contribute to establishment of future precision medicines for ASD

The underpotential deposition that should not be : Cu(1x1) on Au(111)

Peer reviewedPostprin

Concordance of genetic variation that increases risk for anxiety disorders and posttraumatic stress disorders and that influences their underlying neurocircuitry

Background There have been considerable recent advances in understanding the genetic architecture of anxiety disorders and posttraumatic stress disorder (PTSD), as well as the underlying neurocircuitry of these disorders. However, there is little work on the concordance of genetic variations that increase risk for these conditions, and that influence subcortical brain structures. We undertook a genome-wide investigation of the overlap between the genetic influences from single nucleotide polymorphisms (SNPs) on volumes of subcortical brain structures and genetic risk for anxiety disorders and PTSD. Method We obtained summary statistics of genome-wide association studies (GWAS) of anxiety disorders (Ncases=?7016, Ncontrols=?14,745), PTSD (European sample; Ncases=?2424, Ncontrols=?7113) and of subcortical brain structures (N?=?13,171). SNP Effect Concordance Analysis (SECA) and Linkage Disequilibrium (LD) Score Regression were used to examine genetic pleiotropy, concordance, and genome-wide correlations respectively. SECAs conditional false discovery was used to identify specific risk variants associated with anxiety disorders or PTSD when conditioning on brain related traits. Results For anxiety disorders, we found evidence of significant concordance between increased anxiety risk variants and variants associated with smaller amygdala volume. Further, by conditioning on brain volume GWAS, we identified novel variants that associate with smaller brain volumes and increase risk for disorders: rs56242606 was found to increase risk for anxiety disorders, while two variants (rs6470292 and rs683250) increase risk for PTSD, when conditioning on the GWAS of putamen volume. Limitations Despite using the largest available GWAS summary statistics, the analyses were limited by sample size. Conclusions These preliminary data indicate that there is genome wide concordance between genetic risk factors for anxiety disorders and those for smaller amygdala volume, which is consistent with research that supports the involvement of the amygdala in anxiety disorders. It is notable that a genetic variant that contributes to both reduced putamen volume and PTSD plays a key role in the glutamatergic system. Further work with GWAS summary statistics from larger samples, and a more extensive look at the genetics underlying brain circuits, is needed to fully delineate the genetic architecture of these disorders and their underlying neurocircuitry

Flt1/VEGFR1 heterozygosity causes transient embryonic edema

Vascular endothelial growth factor-A is a major player in vascular development and a potent vascular permeability factor under physiological and pathological conditions by binding to a decoy receptor Flt1 and its primary receptor Flk1. In this study, we show that Flt1 heterozygous (Flt1+/−) mouse embryos grow up to adult without life-threatening abnormalities but exhibit a transient embryonic edema around the nuchal and back regions, which is reminiscent of increased nuchal translucency in human fetuses. Vascular permeability is enhanced and an intricate infolding of the plasma membrane and huge vesicle-like structures are seen in Flt1+/− capillary endothelial cells. Flk1 tyrosine phosphorylation is elevated in Flt1+/− embryos, but Flk1 heterozygosity does not suppress embryonic edema caused by Flt1 heterozygosity. When Flt1 mutants are crossed with Aspp1−/− mice which exhibit a transient embryonic edema with delayed formation and dysfunction of lymphatic vessels, only 5.7% of Flt1+/−; Aspp1−/− mice survive, compared to expected ratio (25%). Our results demonstrate that Flt1 heterozygosity causes a transient embryonic edema and can be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype