ファジィニューラルネットワークを用いた手書き曲線同定法FSCIの学習最適化

This paper demonstrates effectiveness of training of Fuzzy Spline Curve Identifier (FSCI) using a fuzzy neural network. FSCI was proposed as a primitive curve identification system designed to establish a general-purpose freehand interface for computer aided drawing (CAD) systems. It succeeded in distinguishing a freehand drawing into seven kinds of primitive curves which are indispensable for use in CAD. The key was the introduction of a fuzzy reasoning which embodied a strategy to try to find the simplest primitive curves in drawing. A trainable version of FSCI was then proposed, by introducing a structured fuzzy neural network, in order that it would acquire learning ability to adapt itself to individual drawing manner. This paper sets up some experiment on FSCI and demonstrates the effectiveness of the training by evaluating curve class recognition rates. Furthermore, through some considerations on a concrete example of the training, it shows that the introduced fuzzy neural network is informative for us to analyze users\u27 drawing manner and also the identification characteristics of FSCI.特集 : 「産業におけるソフトコンピューティングに関する国際会議\u2799」発表論文選

High-Resolution X-Ray Spectroscopy of the Galactic Supernova Remnant Puppis A with the XMM-Newton RGS

We present high-resolution X-ray spectra of cloud-shock interaction regions in the eastern and northern rims of the Galactic supernova remnant Puppis A, using the Reflection Grating Spectrometer onboard the XMM-Newton satellite. A number of emission lines including K(alpha) triplets of He-like N, O , and Ne are clearly resolved for the first time. Intensity ratios of forbidden to resonance lines in the triplets are found to be higher than predictions by thermal emission models having plausible plasma parameters. The anomalous line ratios cannot be reproduced by effects of resonance scattering, recombination, or inner-shell ionization processes, but could be explained by charge-exchange emission that should arise at interfaces between the cold/warm clouds and the hot plasma. Our observations thus provide observational support for charge-exchange X-ray emission in supernova remnants

自閉症スペクトラム障害における近赤外線スペクトロスコピーを用いた表情認知機能の評価

One of the characteristics of Autism Spectrum Disorder (ASD) is social disorder. The specificity of facial and expression recognition for people with ASD is gathering attention as a factor of this social disorder. The study examined the hemodynamic activities in the prefrontal cortex using near-infrared spectroscopy (NIRS) when a person with ASD performed an expression recognition task. The subjects were twenty males (18 - 22 years old) with ASD and without intellectual disabilities. Forty-five healthy males matched for age and sex were included as a control group. In both groups, the degree of autistic tendencies was evaluated using the Autism-Spectrum Quotient (AQ). Using eight standard emotional expressions of Japanese people, two expression recognition tasks were set. An NIRS was used to measure the prefrontal cortex blood mobilization during the expression-processing process. The AQ was significantly higher in the ASD group, while the rate of overall correct expression response was significantly lower (p < 0.001). A negative correlation was found when the relationship between the AQ and the rate of overall correct expression response was evaluated by combining the results of the control group with those of the ASD group (ρ = −0.40 p < 0.001). In the automatic expression-processing task, no activation in the prefrontal cortex was found in either the ASD or the control group. In the conscious expression-processing task, the activation of the left and right lateral prefrontal cortex was weaker in the ASD group compared to the control group. Unlike in the control group, a mild activation of posterior prefrontal cortex was found in the ASD group. The expression-processing process of the ASD group was found to be different from that of the control group. NIRS was effective in detecting a brain function disorder in people with ASD during an expression-processing process

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1977年にベロ細胞傷害性の毒素を産生する大腸菌の存在が報告され, 1982年に米国でベロ毒素産生大腸菌(VTEC)による食中毒が発生してこの菌のヒトにおける病原性が確認された。その後, 世界各地でこの菌による食中毒が報告され, 最近ではその散発的あるいは集団発生が日本各地で報告されている。腸管出血性大腸菌ともいわれるこの菌による感染症の症状としては出血性の下痢と, 続発する溶血性尿毒症症候群および中枢神経系異常が挙げられる。VTECによる発症の過程は, 1)大腸菌が腸管壁に付着し, コロニーを形成して増殖する, 2)ベロ毒素を産生・遊離する, ついで, 3)ベロ毒素が局所的に腸管上皮細胞を傷害し, 全身的には腎細胞傷害, 溶血, 中枢神経系障害を引き起こすの各ステップがある。さらに, 腸管ではattaching and effacing lesionといわれる腸管上皮細胞の病変が観察され, これにはベロ毒素以外にいくつかの因子が関与する。本稿では主としてVTECのビルレンスに関する因子について最近の知見を紹介する。Verotoxin-producing Escherichia coli (VTEC) was first reported in 1977,and was recognized as a human pathogen in 1982 by an outbreak of the disease in the USA. Thereafter, the food-borne diseases by the bacteria, enterohemorrhagic E.coli, have been reported in many countries. The VTEC infection is responsible for a heterogeneous group of diseases, including diarrhea, hemorrhagic colitis, homolytic uremic syndrome, and central nervous system abnormalities. The process for the development of the complex diseases is considered as follows; 1) adherence of the bacteria to intestinal mucosa, and enteric colonization, 2) production and release of verotoxin, 3) local injury of intestinal epithelial cells, and causing systemic disorders such as hemolytic uremic syndrome and central nervous system complications. In the present paper, we review the literature concerning VTEC, and its virulence factor in particular

Low replicative fitness of neuraminidase inhibitor-resistant H7N9 avian influenza a virus with R292K substitution in neuraminidase in cynomolgus macaques compared with I222T substitution.

Human cases of H7N9 influenza A virus infection have been increasing since 2013. The first choice of treatment for influenza is neuraminidase (NA) inhibitors (NAIs), but there is a concern that NAI-resistant viruses are selected in the presence of NAIs. In our previous study, an H7N9 virus carrying AA substitution of threonine (T) for isoleucine (I) at residue 222 in NA (NA222T, N2 numbering) and an H7N9 virus carrying AA substitution of lysine (K) for arginine (R) at residue 292 in NA (NA292K, N2 numbering) were found in different macaques that had been infected with A/Anhui/1/2013 (H7N9) and treated with NAIs. In the present study, the variant with NA292K showed not only resistance to NAIs but also lower replication activity in MDCK cells than did the virus with wild-type NA, whereas the variant with NA222T, which was less resistant to NAIs, showed replication activity similar to that of the wild-type virus. Next, we examined the pathogenicity of these H7N9 NAI-resistant viruses in macaques. The variants caused clinical signs similar to those caused by the wild-type virus with similar replication potency. However, the virus with NA292K was replaced within 7 days by that with NA292R (same as the wild-type) in nasal samples from macaques infected with the virus with NA292K, i.e. the so-called revertant (wild-type virus) became dominant in the population in the absence of an NAI. These results suggest that the clinical signs observed in macaques infected with the NA292K virus are caused by the NA292K virus and the NA292R virus and that the virus with NA292K may not replicate continuously in the upper respiratory tract of patients without treatment as effectively as the wild-type virus