Photocatalytic Activity Enhancement of Anatase/Rutile-Mixed Phase TiO2 Nanoparticles Annealed with Low-Temperature O2 Plasma

Photodecomposition and photobactericidal activities of anatase/rutile-mixed phase TiO2 nanoparticles annealed with low-temperature O2 plasma were clarified by comparing them with those annealed in ambient air. The photocatalytic activities of plasma-assisted-annealed sample greatly enhanced as compared with the untreated sample, under not only ultraviolet irradiation but also visible-light irradiation. The photocatalytic activities of air-annealed samples did not enhance under ultraviolet irradiation but enhanced under visible-light irradiation. The enhanced photocatalytic activities due to the plasma-assisted annealing (PAA) originated from the increased photoexcited carrier concentration. This enhancement was discussed from PAA-induced characteristic factors. PAA facilitated the phase transformation to anatase, contributing directly to extending the photoexcited carrier lifetime. PAA introduced more oxygen vacancies, contributing to trapping more photogenerated electrons. PAA also introduced more bridging/terminal oxygen groups adsorbed on the surface, increasing the upward band-bending, the depletion layer width at the surface, and the charge transfer from rutile to anatase. These two introductions contributed to facilitating the separation of photoexcited carriers. Furthermore, PAA reduced the aggregate size of TiO2 nanoparticles formed on the surface, contributing to increasing optical absorptions. More reactive oxygen species produced from the bridging/terminal oxygen groups by the photoexcited carriers would also enhance the photocatalytic activities

Effects of nonequilibrium atmospheric-pressure O2 plasma-assisted annealing on anatase TiO2 nanoparticles

Anatase TiO2 nanoparticles (NPs) immobilized on glass substrates were annealed with the assistance of nonequilibrium atmospheric-pressure O2 plasma. The plasma-assisted annealing greatly enhanced the photodecomposition and photobactericidal activity as compared with electric-furnace annealing. The plasma-assisted annealing reduced the TiO2 NP agglomerate size and increased the optical absorption, the photoinduced electrical conductivity, the amounts of bridging and terminal oxygen groups, and the (112)/(101) plane intensity ratio, causing the lattice oxygen deficiency that formed partially Ti-rich surface portions. The enhanced photobactericidal activity would arise from the bridging and terminal oxygen groups. The enhanced photodecomposition would arise from the increased concentration of photogenerated carriers due to the following three factors. The first is the optical absorption increased by the agglomerate size reduction and the (112) plane growth or appearance, which exert scattering more incident photons. The second is the charge separation of photogenerated carriers facilitated by the bridging and terminal oxygen groups, which originate from oxygen vacancies via oxygen ion impact from the plasma. The third is the charge transfer of plasmon-excited electrons from the partially Ti-rich portions to TiO2. The enhanced photodecomposition would also arise from more reactive oxygen species generated from the bridging and terminal oxygen groups by the photogenerated carriers

高等植物における細胞分裂と生理機能の制御機構の分子遺伝学的解析

生き物は成長するために細胞分裂し細胞増殖しなければならない。しかしそれも植物の場合にはその時期が適切でなければならない。移動能力のある動物の場合は受精と同時に発生を開始し、できるだけ速やかに成長することが生き残るためにもっとも大事なことといえる。しかし移動能力のない植物の場合は適切な時期に発生や成長をしなければ、枯死する運命が待ち受けている。成長に不利な時期を耐え、生き残るために、植物は発生や成長の時期を制御したり、種子を形成して休眠する。そして適当な時期が到来すると発芽し発生を開始する。生殖を行うために花を形成するのにも時期が大切である。さらに植物に特有な現象であるがセネッセンスと呼ばれる現象がある。これは環境がその植物の成長に不適切で個体を維持するのが困難であったり不利であったりする場合に、その個体の一部あるいは大部分の生理機能を低下させたり枯死させたりし、環境が回復するのを待つというものである。このように植物はその生活環の様々な場面で細胞分裂や生理機能の調節を行っている。我々は i) 種子の発芽の誘導機構、ii) 栄養成長から生殖成長への転換(花器官形成)の誘導機構、iii) 緑葉におけるセネッセンスの誘導機構の 3 つの現象に着目し分子遺伝学の手法を用いて解析を行う

Predictive factors of efficacy of combination therapy with basal insulin and liraglutide in type 2 diabetes when switched from longstanding basal-bolus insulin: Association between the responses of β- and α-cells to GLP-1 stimulation and the glycaemic control at 6?months after switching therapy

Aims: To evaluate the glycaemic control of combination therapy with basal insulin and liraglutide, and to explore the factors predictive of efficacy in patients with type 2 diabetes when switched from longstanding basal-bolus insulin therapy. Methods: We studied 41 patients who switched from basal-bolus insulin therapy of more than 3 years to basal insulin/liraglutide combination therapy. Glycaemic control was evaluated at 6 months after switching therapy and used to subdivide the patients into good-responders (HbA1c <7.0% or 1.0% decrease) and poor-responders (the rest of participants). To evaluate the glucose-dependent insulin/glucagon responses without/with liraglutide, a 75-g oral glucose tolerance test (OGTT) was performed twice, before (1st-OGTT) and 2-days after (2nd-OGTT) liraglutide administration. Results: Twenty-eight patients (68.3%) were identified as good-responders. No differences were found in baseline characteristics including insulin/glucagon responses during 1st-OGTT between the groups. 2nd-OGTT revealed that paradoxical hyperglucagonemia were significantly improved in both groups, but significant increases in insulin secretory response were observed only in good-responders. Logistic regression analyses revealed that the improvement of the insulin-response during 2nd-OGTT compared to that during 1st-OGTT is associated with the good-responder. Conclusions: Enhancement of glucose-dependent insulin-response under liraglutide administration is a potential predictor of long-term glycaemic control after switching the therapies

Impaired early-phase suppression of glucagon secretion after glucose load is associated with insulin requirement during pregnancy in gestational diabetes

Aims/Introduction: The role of glucagon abnormality has recently been reported in type 2 diabetes; however, its role in gestational diabetes mellitus (GDM) is still unknown. The glucose intolerance in GDM is heterogeneous, and not all patients require insulin treatment during pregnancy. Here, we investigated whether glucagon abnormality is associated with the requirement for insulin treatment during pregnancy. Materials and Methods: A total of 49 pregnant women diagnosed with GDM were enrolled. They underwent a 75-g oral glucose tolerance test during mid-gestation, and we measured their plasma glucagon levels (by a new sandwich enzyme-linked immunosorbent assay) at fasting (0 min), and at 30, 60 and 120 min after glucose load in addition to the levels of plasma glucose and serum insulin. All participants underwent another oral glucose tolerance test at postpartum. Results: Of the 49 patients, 15 required insulin treatment (Insulin group) and 34 were treated with diet therapy alone until delivery (Diet group). The early-phase glucagon secretion after glucose load, as determined by the changes in glucagon from the baseline to 30 min, was paradoxically augmented during mid-gestation in the Insulin group, but not in the Diet group. The impaired glucagon suppression during mid-gestation in the Insulin group was not associated with insulin secretory/sensitivity indexes studied, and was ameliorated postpartum, although the plasma glucose levels remained higher in the Insulin group versus the Diet group. Conclusions: Impaired early-phase suppression of glucagon could be associated with the requirement for insulin treatment during pregnancy in patients with GDM

DNA Methylation of Colon Mucosa in Ulcerative Colitis Patients: Correlation with Inflammatory Status

Background: Although DNA methylation of colonic mucosa in ulcerative colitis (UC) has been suggested, the majority of published reports indicate the correlation between methylation of colon mucosa and occurrence of UC-related dysplasia or cancer without considering the mucosal inflammatory status. The aim of this study was to verify whether mucosal inflammation-specific DNA methylation occurs in the colon of UC. Methods: Of 15 gene loci initially screened, six loci (ABCB1, CDH1. ESR1, GDNF, HPP1, and MYOD1) methylated in colon mucosa of UC were analyzed according to inflammatory status using samples from 28 surgically resected UC patients. Results: Four of six regions (CDH1, GDNF, HPP1, and MYOD1) were more highly methylated in the active inflamed mucosa than in the quiescent mucosa in each UC patient (P = 0.003, 0.0002, 0.02, and 0.048, respectively). In addition, when the methylation status of all samples taken from examined patients was stratified according to inflammatory status, methylation of CDHI and GDNF loci was significantly higher in active inflamed mucosa than in quiescent mucosa (P = 0.045 and 0.002, respectively). Multiple linear regression analysis revealed that active inflammation was an independent factor of methylation for CDHI and GDNF. DNA methyltransferase 1 and 3b were highly expressed in colon epithelial cells with active mucosa] inflammation, suggesting their involvement in inflammation-dependent methylation. Conclusions: Methylation in colonic mucosa of UC was correlated with mucosal inflammatory status, suggesting the involvement of methylation due to chronic active inflammation in UC carcinogenesis