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This paper considers an emergency communication system controlling multiple unmanned aerial vehicles (UAVs) in the sky over a large-scale disaster-affected area. This system is based on delay-tolerant networking, and information from ground users is relayed by the UAVs through wireless transmission and the movement of UAVs in a store-and-forward manner. Each UAV moves autonomously according to a predetermined flight method, which uses the positions of other UAVs through communication. In this paper, we propose a new method for UAV flight considering the non-uniformity of user distributions. The method is based on the Voronoi cell using the predicted locations of other UAVs. We evaluate the performance of the proposed method through computer simulations with a non-uniform user distribution generated by a general cluster point process. The simulation results demonstrate the effectiveness of the proposed method.

Permethrin has been shown to increase lung adenomas in female CD-1 mice, but not in male mice or Wistar rats. The proposed mode of action (MOA) for permethrin-induced female mouse lung tumor formation involves morphological changes in Club cells; increased Club cell proliferation; increased Club cell hyperplasia, and lung tumor formation. In this study, the treatment of female CD-1 mice with tumorigenic doses (2500 and 5000 ppm) of permethrin, but not with a nontumorigenic dose (20 ppm), for 14 and/or 28 days increased Club cell replicative DNA synthesis. Global gene expression analysis of female mouse lung samples demonstrated that permethrin treatment up-regulated 3 genes associated with cell proliferation, namely aldehyde dehydrogenase 3a1 (Aldh3a1), oxidative stress-induced growth inhibitor 1, and thioredoxin reductase 1. Treatment with 2500 and 5000 ppm, but not 20 ppm, permethrin for 7 days produced significant increases in mRNA levels of these 3 genes. Immunohistochemical analysis demonstrated that Club cell secretory protein, CYP2F2, and ALDH3A1 colocalized in Club cells; confirmed by flow cytometry analysis of lung cells employing KI67 as a cell proliferation marker. Overall, the present data extend the proposed MOA by demonstrating that Club cells are the primary initial target of permethrin administration in female mouse lungs. As humans are quantitatively much less sensitive to agents that increase Club cell proliferation and lung tumor formation in mice, it is most likely that permethrin could not produce lung tumors in humans. This conclusion is supported by available negative epidemiological data from several studies.

Porphyrinogenic compounds are known to induce porphyria-mediated hepatocellular injury and subsequent regenerative proliferation in rodents, ultimately leading to hepatocellular tumor induction. However, an appropriate in vivo experimental model to evaluate an effect of porphyrinogenic compounds on human liver has not been fully established. Recently, the chimeric mouse with humanized liver (PXB mice) became widely used as a humanized model in which human hepatocytes are transplanted. In the present study, we examined the utility of PXB mice as an in vivo experimental model to evaluate the key events of the porphyria-mediated cytotoxicity mode of action (MOA) in humans. The treatment of PXB mice with 5-aminolevulinic acid, a representative porphyrinogenic compound, for 28 days caused protoporphyrin IX accumulation, followed by hepatocyte necrosis, increased mitosis, and an increase in replicative DNA synthesis in human hepatocytes, indicative of cellular injury and regenerative proliferation, similar to findings in patients with porphyria or experimental porphyria models and corresponding to the key events of the MOA for porphyria-mediated hepatocellular carcinogenesis. We conclude that the PXB mouse is a useful model to evaluate the key events of the porphyria-mediated cytotoxicity MOA in humans and suggest the utility of PXB mice for clarifying the human relevancy of findings in mice.

Epyrifenacil (trademark name: Rapidicil®), a novel protoporphyrinogen oxidase (PPO)-inhibiting herbicide, induces hepatocellular adenomas and carcinomas in male CD-1 mice after 78 weeks treatment. The mode of action (MOA) of these mouse liver tumors and their relevance to humans was assessed based on the 2006 International Programme on Chemical Safety (IPCS) Human Relevance Framework. Epyrifenacil is not genotoxic and induced liver tumors via the postulated porphyria-mediated cytotoxicity MOA with the following key events: (#1) PPO inhibition; (#2) porphyrin accumulation; (#3) hepatocellular injury; with (#4) subsequent regenerative cell proliferation; and ultimately (#5) development of liver tumors. This article evaluates the weight of evidence for this MOA based on the modified Bradford Hill criteria. The MOA data were aligned with the dose and temporal concordance, biological plausibility, coherence, strength, consistency, and specificity for a porphyria-mediated cytotoxicity MOA while excluding other alternative MOAs. Although the postulated MOA could qualitatively potentially occur in humans, we demonstrate that it is unlikely to occur in humans because of quantitative toxicodynamic and toxicokinetic differences between mice and humans. Therefore, this MOA is considered not relevant to humans, utilizing the IPCS Human Relevance Framework; consequently, a nonlinear, threshold dose response would be appropriate for human risk assessment.

Introduction: Recently, the sodium-glucose cotransporter2 (SGLT2) inhibitor empagliflozin has been shown to lower cardiovascular risk among diabetic patients. It is intriguing that some SGLT2 inhibitors have been found to increase low-density lipoprotein (LDL) cholesterol levels, while the relevance to high-density lipoprotein (HDL) cholesterol is unknown. Although the inhibitory effect of SGLT2 inhibitors on glucose reabsorption may accelerate compensatory lipid metabolism and subsequently reduce body weight and affect the lipid profile, much remains unclear about this mechanism. Therefore, we conducted this study to investigate in detail how canagliflozin affects lipoprotein fractions including LDL and HDL subclasses. Materials and Methods: This study is a multicenter prospective study. The participants were patients with 22 type 2 diabetes (60.7 ± 11.6 years, 59.1% of men) who had HbA1c ⩾ 7.0% and consented to participate in the study. They were administered 100 mg canagliflozin orally once per day. Biochemistry test and cholesterol levels of 20 lipoprotein fractions (G1-G20) using high performance liquid chromatography methods were examined before and after 12 weeks of treatment period. Results: Significant decreases were observed in the participants’ body weight (69.7 to 67.9 kg, P < .001), systolic blood pressure (129.3 to 119.5 mm Hg, P < .01), and HbA1c (8.5% to 7.4%, P < .001). Cholesterol levels in the 20 lipoprotein fractions increased for very large HDL (G14, G15) and large HDL (G16) ( P < .05). Conclusions: Reduction in body weight, improvement of blood glucose levels, and increases in very large HDL and large HDL subclasses were observed after canagliflozin treatment. These beneficial changes might contribute to subsequent suppression of cardiovascular outcomes.

The carcinogenic potential of a non-genotoxic pyrethroid imiprothrin was examined in rats and mice. There was no carcinogenicity in rats up to a maximum dose of 5000 ppm of the diet. There was a higher (p = 0.03) incidence of lung adenocarcinomas at 7000 ppm in males, and females showed an increasing (p 0.01) trend in the incidence of lung adenomas and combined lung adenoma/adenocarcinomas. Additional step sections of lung demonstrated no significant increases in any tumor at p 0.05, although an increasing trend with dose was observed among females. We argue that, the 7000 ppm dose exceeded the Maximum Tolerated Dose (MTD) for both sexes, based on systemic toxicity as evidenced by body weight gain reduction (both sexes) and high mortality (females). If the 7000 ppm dose is therefore removed from consideration, there are not significant (p 0.05) increases in tumor formation. Moreover, a consideration of multiple comparisons reveals that the lung tumor increases observed are totally consistent with what would be expected by chance alone. Based on high susceptibility of this mouse strain for the appearance of lung tumors and the lack of a statistically significant increase in tumors by appropriate analysis, the mouse study does not indicate a carcinogenic effect of imiprothrin, and thus no classification for carcinogenicity is warranted.

In the mouse carcinogenicity study, an apparent increase in lung adenocarcinoma was observed in male mice at 7000 ppm. Based on the overall evaluation of toxicology, oncology, pathology and statistics, we concluded that the apparent increase in lung tumors is not relevant for evaluation of carcinogenicity of imiprothrin (Regul Toxicol Pharmacol, 105, 1–14, 2019). To investigate whether imiprothrin has any mitogenic effect on mouse Club cells, the present study examined its effects on replicative DNA synthesis of Club cells and lung histopathology in male mice treated with imiprothrin for 7 days at 3500 and 7000 ppm in the diet. Isoniazid, a known mouse lung mitogen and tumor inducer, was also examined at 1000 ppm in the diet as a positive control of Club cell mitogenesis and morphological changes. Neither imiprothrin nor isoniazid caused any necrotic changes in lung by light or electron microscopy. There were no increases observed in the bromodeoxyuridine (BrdU) labeling index in the imiprothrin groups, while there was a statistically significant increase in the BrdU labeling index in the isoniazid group. These findings demonstrate that imiprothrin does not induce mouse Club cell proliferation or morphologic changes, supporting our previous conclusion described above. Thus, imiprothrin should not be classified as a carcinogen. Furthermore, this study indicates that short-term studies focusing on cell proliferation can be reliable for predicting a lack of carcinogenic potential of test chemicals.

To investigate epigenetic regulation of the plasma concentration of resistin, we performed an epigenome-wide association study for this variable and DNA methylation (DNAm) in an elderly Japanese cohort and then assessed the relation of single nucleotide polymorphisms (SNPs) associated with the plasma resistin concentration to DNAm level at identified sites.The association of plasma resistin level with DNAm status was examined in 191 nondiabetic elderly men with the Illumina Infinium HumanMethylation450 BeadChip array. The association between DNAm status at specific sites in the flanking region of the resistin gene (RETN) and RETN mRNA abundance was then evaluated with a public data set for 1202 monocyte samples from a multi-ethnic cohort. Finally, the association of DNAm status and SNPs in the promoter region of RETN was assessed in two cohorts comprising a total of 478 Japanese individuals.DNAm status at cg02346997 located in the RETN promoter region showed a negative genome-wide significant association with the plasma resistin level (p = 6.02 × 10(-10)). Four DNAm sites in the RETN promoter region including cg02346997 (p = 4.23 × 10(-70)) showed a negative genome-wide significant association with RETN mRNA abundance in monocytes. Furthermore, the number of minor alleles of the RETN promoter SNPs rs34861192 and rs3219175 was negatively associated with DNAm level at cg02346997 (p = 4.43 × 10(-17)).Our results suggest that RETN promoter SNPs might influence the circulating resistin level through an effect on DNAm at cg02346997 and on RETN mRNA abundance in monocytes.

To determine miRNAs and their predicted target proteins regulatory networks which are potentially involved in onset of pulmonary fibrosis in the bleomycin rat model, we conducted integrative miRNA microarray and iTRAQ-coupled LC-MS/MS proteomic analyses, and evaluated the significance of altered biological functions and pathways. We observed that alterations of miRNAs and proteins are associated with the early phase of bleomycin-induced pulmonary fibrosis, and identified potential target pairs by using ingenuity pathway analysis. Using the data set of these alterations, it was demonstrated that those miRNAs, in association with their predicted target proteins, are potentially involved in canonical pathways reflective of initial epithelial injury and fibrogenic processes, and biofunctions related to induction of cellular development, movement, growth, and proliferation. Prediction of activated functions suggested that lung cells acquire proliferative, migratory, and invasive capabilities, and resistance to cell death especially in the very early phase of bleomycin-induced pulmonary fibrosis. The present study will provide new insights for understanding the molecular pathogenesis of idiopathic pulmonary fibrosis.

Annular-ring coupled structures (ACSs) will increase the beam energy of the Japan proton accelerator research complex (J-PARC) linac from 181 to 400 MeV to achieve a beam power of 1 MW for a materials and life science experimental facility. The mass production of the ACS cavities commenced in March 2009. Before the installation, all cavities require power testing. High-power testing is essential not only for confirming the cavity’s design performance but also for preventing delays in cavity conditioning schedule. However, the 2011 Tohoku earthquake damaged J-PARC facilities, including the ACS power-test area, and cavity conditioning was interrupted for two years. After the facility’s restoration, two ACS cavities (M01 and M11) were conditioned. They performed 15–20% above the designed accelerating field of 4.2 MV/m. As M01 was initially conditioned six years ago, the most recent conditioning time required for M01 was drastically reduced. From this result, we confirmed that long-term stored ACS cavities purged with nitrogen gas do not produce critical cavity performance issues. During high-power operation of M11, which is a unique cavity equipped with a capacitive iris in a waveguide, no significant increases in the temperature and the discharge rate around the capacitive iris were observed. Even considering beam loss due to residual gas scattering, the vacuum pressure was sufficiently low (4 × 10−6 Pa). More stable operation can be expected following a month-long conditioning process before the beam is commissioned. M11’s conditioning successfully demonstrated an auto-conditioning program, and we established the conditioning scheme using this auto-conditioning program for all ACS cavities in a limited time and with limited manpower.

Background Development of cardiovascular disease (CVD), including coronary artery disease, arrhythmia, and ischemic stroke, depends on environmental and genetic factors. To investigate the epigenetic basis of myocardial infarction (MI), we performed an epigenome-wide association study for this condition in elderly Japanese subjects. A total of 192 case subjects with MI and 192 control subjects were recruited from hospital attendees and the general population, respectively. Genome-wide DNA methylation (DNAm) profiles for DNA isolated from whole blood were obtained by analysis with an Infinium HumanMethylation450 BeadChip. The relation of DNAm sites found to be significantly associated with MI to nearby single nucleotide polymorphisms (SNPs) previously shown to be associated with CVD was assessed in the control group. Findings Three DNAm sites (cg06642177, cg07786668, cg17218495) showed genome-wide significant associations with MI (p = 4.33 × 10−8, 3.96 × 10−10, and 3.77 × 10−8, respectively). Two of these sites (cg07786668, cg17218495) still showed such associations after adjustment for classical risk factors of MI (p = 1.04 × 10−7 and 6.60 × 10−8, respectively). The DNAm sites cg07786668 and cg17218495 are located in ZFHX3 (zinc finger homeobox 3) and SMARCA4 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 4) genes, respectively. SNPs in ZFHX3 or SMARCA4 that were previously found to be associated with CVD were not significantly associated with these DNAm sites in our control subjects. Conclusions We identified two DNAm sites—cg07786668 in ZFHX3 and cg17218495 in SMARCA4— that are independently and significantly associated with MI. Our results suggest that the development of MI might be influenced by changes in DNAm at these sites via a pathway that differs from that affected by CVD-associated SNPs in these genes. The Kita-Nagoya Genomic Epidemiology (KING) study, which was the source of control samples in the present study, was registered in ClinicalTrials.gov (NCT00262691) on 6 December 2005.

Impedance matching of RF windows that minimizes the RF reflection is necessary to prevent localized standing waves between an RF window and a cavity, which may cause thermal and/or multipactoring issues. It has been observed that the impedance matching condition of the pillbox-type RF window, checked by voltage standing wave ratio (VSWR) measurement, depends on the manufacturing lot of the window ceramic disk made of 95% purity Al2O3. The present report proposes new procedures for impedance matching as follows: (i) The relative dielectric constant of the ceramic window is directly measured using the resonant frequency of a cavity made by temporarily combining the pillbox part of the RF window and two short-circuiting plates. (ii) The dimensions of the pillbox section including the ceramic disk are fixed on the basis of the measured relative dielectric constant. To confirm this procedure, three RF windows were fabricated using the same type of ceramic material, and successful impedance matching of these windows was performed ( VSWR 1.05 ). The measured results also suggest that the relative dielectric constant increases linearly with increasing density and that the impedance matching condition is mainly affected by variations of the relative dielectric constant due to shrinkage of the alumina during sintering.

Oligodendroglioma is a rare tumor originating from oligodendrocytes found mainly in the cerebrum in aged rats. Only a few reports have shown spontaneous occurrence of this tumor in the spinal cord, and no report has mentioned its occurrence in young rats. We encountered a case of spontaneous oligodendroglioma in the lumbar portion of the spinal cord in a young (9 weeks old) female BrlHan:WIST@Jcl (GALAS) rat. Here we report the detailed histopathological and immunohistochemical characteristics of this case. No clinical signs, no gross lesions at necropsy, and no specific changes in hematology or blood biochemistry were observed. The tumor was located in the dorsal funiculus in the lumbar portion of the spinal cord and widely spread to the dorsal root nerve. The neoplastic cells showed a sheet-like growth pattern and had small round nuclei, clear cytoplasm and distinct cell borders that resulted in a honeycomb pattern. No mitotic figures or other histological lesions were observed. The neoplastic cells were positively stained for Olig2 and PCNA. The present case was considered to be a low-grade oligodendroglioma based on the histological and immunohistochemical features. To our knowledge, our case is considered to be extremely rare and the first report in a young rat.

Background— Myocardial infarction (MI) is a leading cause of death worldwide. Given that a family history is an independent risk factor for coronary artery disease, genetic variants are thought to contribute directly to the development of this condition. The identification of susceptibility genes for coronary artery disease or MI may thus help to identify high-risk individuals and offer the opportunity for disease prevention. Methods and Results— We designed a 5-step protocol, consisting of a genome-wide linkage study followed by association analysis, to identify novel genetic variants that confer susceptibility to coronary artery disease or MI. A genome-wide affected sib-pair linkage study with 221 Japanese families with coronary artery disease yielded a statistically significant logarithm of the odds score of 3.44 for chromosome 2p13 and MI. Further association analysis implicated Alström syndrome 1 gene ( ALMS1 ) as a candidate gene within the linkage region. Validation association analysis revealed that representative single-nucleotide polymorphisms of the ALMS1 promoter region were significantly associated with early-onset MI in both Japanese and Korean populations. Moreover, direct sequencing of the ALMS1 coding region identified a glutamic acid repeat polymorphism in exon 1, which was subsequently found to be associated with early-onset MI. Conclusions— The glutamic acid repeat polymorphism of ALMS1 identified in the present study may provide insight into the pathogenesis of early-onset MI.

The cyanobacterium Synechococcus elongatus PCC 7942 is a major model species for studies of photosynthesis. It is are also a potential cell factory for the production of renewable biofuels and valuable chemicals. We employed engineered riboswitches to control translational initiation of target genes in this cyanobacterium. A firefly luciferase reporter assay revealed that three theophylline riboswitches performed as expected in the cyanobacterium. Riboswitch-E* exhibited very low leaky expression of luciferase and superior and dose-dependent on/off regulation of protein expression by theophylline. The maximum magnitude of the induction vs. basal level was ∼190-fold. Furthermore, the induction level was responsive to a wide range of theophylline concentrations in the medium, from 0 to 2 mM, facilitating the fine-tuning of luciferase expression. We adapted this riboswitch to another gene regulation system, in which expression of the circadian clock kaiC gene product is controlled by the theophylline concentration in the culture medium. The results demonstrated that the adequately adjusted expression level of KaiC restored complete circadian rhythm in the kaiC-deficient arrhythmic mutant. This theophylline-dependent riboswitch system has potential for various applications as a useful genetic tool in cyanobacteria.

Although over 30 common genetic susceptibility loci have been identified to be independently associated with coronary artery disease (CAD) risk through genome-wide association studies (GWAS), genetic risk variants reported to date explain only a small fraction of heritability. To identify novel susceptibility variants for CAD and confirm those previously identified in European population, GWAS and a replication study were performed in the Koreans and Japanese. In the discovery stage, we genotyped 2123 cases and 3591 controls with 521 786 SNPs using the Affymetrix SNP Array 6.0 chips in Korean. In the replication, direct genotyping was performed using 3052 cases and 4976 controls from the KItaNagoya Genome study of Japan with 14 selected SNPs. To maximize the coverage of the genome, imputation was performed based on 1000 Genome JPT+CHB and 5.1 million SNPs were retained. CAD association was replicated for three GWAS-identified loci (1p13.3/SORT1 (rs599839), 9p21.3/CDKN2A/2B (rs4977574), and 11q22.3/ PDGFD (rs974819)) in Koreans. From GWAS and a replication, SNP rs3782889 showed a strong association (combined P=3.95 × 10(-14)), although the association of SNP rs3782889 doesn't remain statistically significant after adjusting for SNP rs11066015 (proxy SNP with BRAP (r(2)=1)). But new possible CAD-associated variant was observed for rs9508025 (FLT1), even though its statistical significance did marginally reach at the genome-wide a significance level (combined P=6.07 × 10(-7)). This study shows that three CAD susceptibility loci, which were previously identified in European can be directly replicated in Koreans and also provides additional evidences implicating suggestive loci as risk variants for CAD in East Asian.

A new understanding of the genetic basis of coronary artery disease (CAD) has recently emerged from genome-wide association (GWA) studies of common single-nucleotide polymorphisms (SNPs), thus far performed mostly in European-descent populations. To identify novel susceptibility gene variants for CAD and confirm those previously identified mostly in populations of European descent, a multistage GWA study was performed in the Japanese. In the discovery phase, we first genotyped 806 cases and 1337 controls with 451 382 SNP markers and subsequently assessed 34 selected SNPs with direct genotyping (541 additional cases) and in silico comparison (964 healthy controls). In the replication phase, involving 3052 cases and 6335 controls, 12 SNPs were tested; CAD association was replicated and/or verified for 4 (of 12) SNPs from 3 loci: near BRAP and ALDH2 on 12q24 (P=1.6 × 10(-34)), HLA-DQB1 on 6p21 (P=4.7 × 10(-7)), and CDKN2A/B on 9p21 (P=6.1 × 10(-16)). On 12q24, we identified the strongest association signal with the strength of association substantially pronounced for a subgroup of myocardial infarction cases (P=1.4 × 10(-40)). On 6p21, an HLA allele, DQB1(*)0604, could show one of the most prominent association signals in an ∼8-Mb interval that encompasses the LTA gene, where an association with myocardial infarction had been reported in another Japanese study. CAD association was also identified at CDKN2A/B, as previously reported in different populations of European descent and Asians. Thus, three loci confirmed in the Japanese GWA study highlight the likely presence of risk alleles with two types of genetic effects - population specific and common - on susceptibility to CAD.

Apoptosis controls erythroid homeostasis by balancing survival and death of erythroid cells. The mitochondrial pathway of apoptosis involves regulation of apoptotic events caused by the Bcl-2 family proteins, including the anti-apoptotic and pro-apoptotic members. However, little has been reported on the role of the anti-apoptotic Bcl-2 family members in rat late-stage erythroblasts that are no longer erythropoietin (EPO)-dependent. In the present study, to investigate this we analyzed changes in apoptosis-related factors that occurred in vitro. EPO stimulation resulted in reduced apoptotic cell death of the late-stage erythroblasts accompanied by decreased caspase-3 and caspase-9 activities, which is indicative of the induction of apoptosis through the mitochondrial pathway. Analysis of mRNA expression of the Bcl-2 family proteins demonstrated that EPO stimulation up-regulated the Bcl-xL mRNA, resulting in decreases in the mRNA ratios of Bak, Bax, and Bad to Bcl-xL. Also, the mRNA ratios of Bak and Noxa to Mcl-1 were decreased, mainly due to up-regulation of Mcl-1 mRNA. These results showed a close association between reduced apoptotic cell death and increased mRNA levels of Bcl-xL and Mcl-1 in the presence of EPO. Thus, the present study suggests that Bcl-xL may be an important anti-apoptotic factor of rat late-stage erythroblasts as has been reported in murine erythroblasts. Moreover, the results also indicate the possibility that Mcl-1 may act on the rat late-stage erythroblasts as an anti-apoptotic factor.

Titanium dioxide ( TiO 2) thin films are prepared on glass substrates by metal-organic chemical vapor deposition (MOCVD) method using the different organic solvents, e.g. ethanol or cyclohexane, in nitrogen carrier gas with different their concentrations. We reported the effects of the each organic solvent in the carrier gas for MOCVD method on the morphology of the composed particles, the thickness, the surface roughness, and the transparency of the prepared TiO 2 thin films with changing the deposition temperature. The morphology of the particles which compose the thin films, and the surface roughness of the prepared TiO 2 thin films are observed and measured by atomic force microscope (AFM) and field emission scanning electron microscopy (FE-SEM). The film thickness is measured by fluorescent X-ray spectroscopy (XRF), and the transparency of the films is confirmed by UV-vis spectroscopy. The transparencies of the TiO 2 thin films differ depending on the MOCVD conditions, e.g. the organic solvents species, the concentration of the container in the carrier gas and the deposition temperatures. We have found that the species and the concentration of the organic solvents in the carrier gas are very important factor to prepare homogeneous TiO 2 thin films by MOCVD method; cyclohexane inhibits to aggregate of the TiO 2 nanoparticles on the glass substrate during the MOCVD process.

According to machinery statistics of the Ministry of Economy, Trade and Industry, the quantity of electric lamps produced in Japan was 613,000,000 (68.1% compared to the previous year). Of these, 73,000,000 were general lamps (88.1% compared to the previous year) and 32,000,000 were halogen lamps (79.3% compared to the previous year). The number of fluorescent lamps produced was 627,000,000 (72.9% compared to the previous year), and the number of general fluorescent lamps excluding backlights was 240,000,000 (86.0% compared to the previous year). Furthermore, the number of HID lamps produced was 7,600,000 (75.6% compared to the previous year). On the other hand, when looking at the sales amounts compared to the previous year, the results for general lighting electric lamps, halogen lamps, general fluorescent lamps, backlights, and HID lamps were 88.5%, 87.7%, 91.6%, 49.1%, and 76.4%, respectively. For compact fluorescent lamps, which are included within the numbers for general fluorescent lamps, sales amounts were 92.7% compared to the previous year, which was a large drop from 137.3% in 2008. The main causes mentioned for the decreases in production numbers and sales volume for these mainstream lamps are generally the economic recession and the rise of LEDs, a new light source that is now being used in the general lighting field. The main exhibition domestically was Lighting Fair 2009 held in March at Tokyo Big Sight. Internationally, it was Light Fair held in New York City in May. Although some new types of and research results for incandescent electric lamps are seen, their use and production continues to be stopped worldwide due to their low luminescence efficiency. In particular, the EUP directive (a directive related to energy using products and now named the ERP directive) was enacted in Europe in September. The sales of white diffused and clear types of incandescent electric lamps of 100 W or more and halogen lamps are prohibited. In Japan as well, major manufacturers continue to stop or reduce production of incandescent electric lamps. With fluorescent lamps, development into energy efficiency and longer life is healthy and new product releases of compact fluorescent lamps and ring fluorescent lamps are seen. Furthermore, the issue of reducing the amount of enclosed mercury remains and the IEC is continuing validity investigations of measurement methods. For light emitting diode (LED) light sources, 2009 was the year they saw full-fledged commercial viability and it may be remembered as the year that LEDs started to receive attention from average consumers. The luminescence efficiency of individual chips was reported to have reached 250 lm/W at the research level. In the Japanese production industry, the current market price of LED light bulbs quickly dropped to almost a third between the beginning and the end of the year. This drop is believed to be due to competition between the main existing light source manufacturers and manufacturers newly entering the market, the development and market introduction of LED products, and the flow of manufacturing processes to developing countries with cheap labor costs. In high-intensity discharge (HID) lamp field, product development and technological research related to ceramic metal halide lamps is as popular as ever. With increased emphasis on environmental conservation, mercury-free ceramic metal halide lamps are also being announced as reference exhibits at exhibitions. While reports regarding HID lamps cover fundamental research, reports of applications for growing plants are also being seen. There are also many reports about other types discharge lamps, including electrodeless lamps that use inductively-coupled mercury, microwave discharge lamps, and excimer discharge lamps. Furthermore, there are many reports about application examples of the nanotechnology as a new light source. With regard to lighting circuits, (…)

Aims/hypothesis Resistin is a cytokine derived from adipose tissue and is implicated in obesity-related insulin resistance and type 2 diabetes mellitus. Polymorphisms of the resistin gene (RETN) have been shown to affect the plasma resistin concentration. The aims of this study were to identify polymorphisms of RETN that influence plasma resistin concentration and to clarify the relation between plasma resistin level and metabolic disorders in an aged Japanese cohort.

Preparations and reactions of a series of 2-trifluoromethylketenimines are described. Trifluoromethylketenimines were prepared from trifluoropropanoic acids via corresponding imidoyl chlorides in good yields. 2-Trifluoromethylketenimine was functionalized at its β-position by electrophilic addition of halide, followed by dehydrohalogenation. Addition of nucleophile at α-position gave trifluoroethylated β-amino acid derivative via 1,3-proton shift.

Objectives We performed dobutamine stress testing for evaluation of myocardial contractile reserve in asymptomatic or mildly symptomatic patients with dilated cardiomyopathy (DCM). Background Catecholamine sensitivity is reduced in failing hearts as a result of myocardial abnormalities in the beta-adrenergic receptor signaling pathway. However, little is known about adrenergic myocardial contractile reserve in asymptomatic or mildly symptomatic patients with DCM. Methods The maximal first derivative of left ventricular pressure (LV dP/dtmax) was determined during infusion of dobutamine (10 μg kg−1 min−1) in 46 asymptomatic or mildly symptomatic (New York Heart Association functional class I or II) patients with DCM. The expression of messenger ribonucleic acid (mRNA) for contractile regulatory proteins in endomyocardial biopsy specimens was quantified by reverse transcription and real-time polymerase chain reaction analysis. Plasma norepinephrine levels were measured in all patients and [123I]metaiodobenzylguanidine (MIBG) scintigraphy performed. Results Patients were classified into 3 groups based on the percentage increase in LV dP/dtmax induced by dobutamine (ΔLV dP/dtmax) and on LV ejection fraction (LVEF) at baseline: group I (n = 18): ΔLV dP/dtmax >100% and LVEF >25%; group IIa (n = 17): ΔLV dP/dtmax ≤100% and LVEF > 25%; and group IIb (n = 11): ΔLV dP/dtmax ≤100% and LVEF ≤25%. The amounts of beta1-adrenergic receptor, sarcoplasmic reticulum Ca2+-adenosine triphosphatase, and phospholamban mRNA were significantly smaller in groups IIa and IIb than in group I. The plasma norepinephrine level was increased and the delayed heart/mediastinum count ratio in MIBG scintigraphy was decreased in both groups IIa and IIb. Conclusions Dobutamine stress testing is a useful diagnostic tool for identifying reduced adrenergic myocardial contractile reserve related to altered myocardial expression of beta1-adrenergic receptor, sarcoplasmic reticulum Ca2+-adenosine triphosphatase, and phospholamban genes even in asymptomatic or mildly symptomatic patients with DCM.

We newly developed self-expandable covered stents by combining two of our original technologies. Of these, the first is the dip-coating covering method that was developed previously for balloon-expandable stents; the other is the newly developed self-expandable Nitinol stents, namely, Sendai stents. The three types of covered stents with the expansion diameter of 4.5, 5.0, or 6.0 mm thus obtained had a laser-processed microporous elastomeric cover film (pore diameter: 100 microm, interpore distance: 250 microm). Although the film was extremely thin (approximately 15 microm), the film could be expanded without causing any damage, the strut was completely embedded within the film, and the luminal surface of the film was smooth and flat. Mechanical properties such as ideal flexibility to follow the shapes of arteries were almost retained even after covering. As appropriate drugs, the blood-contacting inner and tissue-contacting outer surfaces of the film were differentially coated with argatroban for antithrombogenicity or FK506 for anti-inflammation, respectively. The preliminary in vivo study indicated that the covered stents mounted in the delivery catheter were navigated and placed to appropriate position in the arteries, and permissible neointimal thickening after 1-month implantation was observed similarly in noncovered stents.

The correlation between major disease factors and sample size remains an important question in clinical investigations. A small sample size results in the selection of falsely significant risk factors that are not derived from population data. This problem is more serious in studies on multifactorial diseases based on polymorphisms and environmental factors because these studies require combination analysis. In the present study, we defined threshold lines to identify risk factors comprising complex interactions based on sample size. These threshold lines were constructed by a simulation study based on a resampling method that comprised a large data set (1441 case subjects with myocardial infarction and 979 control subjects). Finally, we demonstrated that these threshold lines could be used to identify risk factors for different data sets. In conclusion, these threshold lines enable us to design an association study of multifactorial diseases based on combination analysis.

Multifactorial diseases, such as lifestyle-related diseases, for example, cancer, diabetes mellitus, and myocardial infarction, are believed to be caused by the complex interactions between various environmental factors on a polygenic basis. In addition, it is believed that genetic risk factors for the same disease differ on an individual basis according to their susceptible environmental factors. In the present study, to predict the development of myocardial infarction (MI) and classify the subjects into personally optimum development patterns, we have extracted risk factor candidates (RFCs) that comprised a state that is a derivative form of polymorphisms and environmental factors using a statistical test. We then selected the risk factors using a criterion for detecting personal group (CDPG), which is defined in the present study. By using CDPG, we could predict the development of MI in blinded subjects with an accuracy greater than 75%. In addition, the risk percentage for MI was higher with an increase in the number of selected risk factors in the blinded data. Since sensitivity using the CDPG was high, it can be an effective and useful tool in preventive medicine and its use may provide a high quality of life and reduce medical costs.

Porphyromonas gingivalis is one of the major microbial pathogens associated with chronic periodontitis. To eradicate such pathogens by periodontal therapy, it is essential to clarify the source of infection. Recent findings suggest that the genotype of the fimbriae is one of the important factors in infection by P. gingivalis. The objectives of the present study were to investigate the transmission of P. gingivalis between spouses and to determine the relationship between P. gingivalis fimA type and colonization.A total of 14 couples were selected to investigate the transmission of P. gingivalis and its association with the fimA types. To examine the distribution of fimA type in the general population, 32 subgingival plaque samples from 47 patients with periodontitis were also tested. The transmission of P. gingivalis strains was determined by using pulsed field gel electrophoresis (PFGE). P. gingivalis strains isolated from the couples and subgingival dental plaque samples were studied for fimA classification.The PFGE patterns of P. gingivalis strains from matched husbands and wives were identical for six of the 14 couples. In five of these six couples (83.3%), P. gingivalis strains harboring the type II fimA gene were present. The proportion of type II fimA in the strains isolated from couples with probable intrafamilial transmission was significantly higher than that in patients with periodontitis or in the group of samples isolated from one member of a couple.This study suggests that fimA type II, even though widely distributed in patients with periodontitis, may be an important factor in the transmission of P. gingivalis between spouses.

点電極プローブを用いて気泡塔模擬装置における気相体積率の三次元分布を測定した．さらに，著者らが開発した(N+2)-field model（NP2モデル）を用いて気泡－液相間運動量輸送項および乱流渦粘性に関する各種相関式の感度解析を実施した．実験と計算の比較により，（1）気泡径依存性を考慮した揚力係数，および大きさに基づく気泡の分類が非均質気泡流の数値予測に不可欠であること，（2）仮想質量係数および気泡誘起渦粘性係数は計算結果にほとんど影響を及ぼさないこと，（3）液相渦粘性係数評価にせん断誘起乱れを考慮すると乱流エネルギーを過大評価することを確認した．また，気泡誘起乱れが乱流分散力に及ぼす影響と気泡クラスターへの後続気泡の加速接近によるみかけの抗力係数低減のモデル化が予測精度向上のためにとくに重要な課題であることを確認した．

This paper provides a part of series of “Development of an Evaluation Method for Seismic Isolation Systems of Nuclear Power Facilities”. This part shows an evaluation of seismic isolator design established in this project where several methods are newly developed. The major four accomplishments are as follows. One: establishment of design earthquake specially considered for seismically isolated nuclear power facilities. The design earthquakes are made to fit multiple target spectra with different damping factors considering a building, equipment and seismic isolators for more precise response analyses. Two: design and development of a high-performance seismic isolator. Against the large design earthquakes, a seismic isolator is newly developed which has a large diameter lead plug for more damping; the isolators were actually manufactured and tested. Three: seismic response analyses for seismically isolated nuclear power plants. Light water reactors are designed where the structural characteristics of the seismic isolation system is reflected. Four: evaluation of thermal effects on seismic isolators by a long-duration earthquake. Considering a long-duration earthquake, the heat generation phenomenon in the lead plug is analytically evaluated to ensure the lead plug’s damping performance. By introducing these accomplishments, the realistic design of a seismically isolated nuclear power plant is achieved.