著者

加藤 昌彦 Masahiko Kato

出版者

関西外国語大学

雑誌

人権を考える = Thinking about Human Rights (ISSN:2189177X)

巻号頁・発行日

vol.19, pp.68-94, 2016-03

著者

Yoshiharu Kinugasa Masahiko Kato Shinobu Sugihara Masayuki Hirai Kensaku Yamada Kiyotaka Yanagihara Kazuhiro Yamamoto

出版者

The Japanese Circulation Society

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

vol.77, no.3, pp.705-711, 2013 (Released:2013-02-25)

参考文献数

32

被引用文献数

92 208 15

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Background: The clinical significance of nutritional risk assessment in patients with heart failure with preserved ejection fraction (HFpEF) remains undefined. Geriatric nutritional risk index (GNRI) is a simple nutritional assessment tool for elderly subjects. Its predictive value was evaluated in patients with HFpEF, a common HF phenotype in the elderly population. Methods and Results: The present study enrolled 152 consecutive patients (mean age, 77±11 years; male, 53.9%) who were hospitalized with HFpEF at the authors’ institution. GNRI on admission was calculated as follows: 14.89×serum albumin (g/dl)+41.7×body mass index/22. Characteristics and mortality (median follow-up of 2.1 years) were compared between 2 groups: low GNRI (<92) with moderate or severe nutritional risk; and high GNRI (≥92) with no or low nutritional risk. Patients in the low-GNRI group were more often female, and had lower serum hemoglobin and sodium, but higher serum blood urea nitrogen (BUN), C-reactive protein, and B-type natriuretic peptide (BNP) compared to those in the high-GNRI group (P<0.05, respectively). Physical activity at discharge measured by Barthel index was significantly lower in the low-GNRI group than the high-GNRI group (P<0.05). On Cox hazard analysis, lower GNRI predicted increased mortality independent of age, gender, prior HF hospitalization, and higher BUN and BNP (P<0.01). Conclusions: GNRI may be useful for predicting functional dependency and mortality in patients with HFpEF.  (Circ J 2013; 77: 705–711)

著者

Shinobu Sugihara Ichiro Hisatome Masanari Kuwabara Koichiro Niwa Nani Maharani Masahiko Kato Kazuhide Ogino Toshihiro Hamada Haruaki Ninomiya Yukihito Higashi Kimiyoshi Ichida Kazuhiro Yamamoto

出版者

The Japanese Circulation Society

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

vol.79, no.5, pp.1125-1132, 2015-04-24 (Released:2015-04-24)

参考文献数

41

被引用文献数

24 82

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Background:Uric acid (UA) serves as an antioxidant in vascular endothelial cells. UA transporter 1 (URAT1) encoded by SLC22A12 is expressed in the kidney and vessels and its loss of function causes hypouricemia. The purpose of this study was to examine whether there is any endothelial dysfunction in patients with hypouricemia.Methods and Results:Twenty-six patients with hypouricemia (<2.5 mg/dl) and 13 healthy control subjects were enrolled. Endothelial function was evaluated using flow-mediated dilation (FMD). mRNA of UA transporters expressed in cultured human umbilical endothelial cells (HUVEC) was detected on RT-PCR. There was a positive correlation between FMD and serum UA in the hypouricemia group. URAT1 loss-of-function mutations were found in the genome of 21 of 26 patients with hypouricemia, and not in the other 5. In the hypouricemia groups, serum UA in homozygous and compound heterozygous patients was significantly lower than in other groups, suggesting that severity of URAT1 dysfunction may influence the severity of hypouricemia. Thirteen of 16 hypouricemia subjects with homozygous and compound heterozygote mutations had SUA <0.8 mg/dl and their FMD was lower than in other groups. HUVEC do not express mRNA of URAT1, suggesting the null role of URAT1 in endothelial function.Conclusions:Depletion of UA due to SLC22A12/URAT1 loss-of-function mutations causes endothelial dysfunction in hypouricemia patients. (Circ J 2015; 79: 1125–1132)

著者

Mizuki Watanabe Ryotaro Kobayashi Masahiko Kato

出版者

Information Processing Society of Japan

雑誌

Journal of Information Processing (ISSN:18826652)

巻号頁・発行日

vol.23, no.5, pp.655-663, 2015 (Released:2015-09-15)

参考文献数

15

被引用文献数

1 1

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Currently, Web services are widely utilized to disclose company information, and offer online services and e-commerce. As these services have become an essential part of our everyday lives, the public is greatly inconvenienced when they are disrupted. Denial of service (DoS) attacks exert adverse influences on Web services. We focus on HTTP-GET Flood attacks, which are manually operable DoS attacks. It is possible to simply block manually operable DoS attacks such as F5 attacks on the server side; however, such measures could be noticed by the attackers. Therefore, to prevent the attacker changing their method of attack, it is possible to overcome the attack by redirecting the attack to another system, for which a previous study has proposed a feasible technique located in the service provider. The previous study assumes a correlation between the CPU resource and the request error rate. However, the Web Server actually has multiple resources. Therefore, it is important to be able to control the server resources rather than the CPU and the memory. The operational implementation of the proposed method and the evaluation experiments confirm the effectiveness of the proposed method.

著者

加藤 昌彦 Masahiko Kato

雑誌

関西外国語大学人権教育思想研究 = The Study of Human Rights Education

巻号頁・発行日

vol.15, pp.149-167, 2012-03

著者

Yuya Takeuchi Takuro Yoshida Ryotaro Kobayashi Masahiko Kato Hiroyuki Kishimoto

雑誌

情報処理学会論文誌 (ISSN:18827764)

巻号頁・発行日

vol.57, no.9, 2016-09-15

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The Domain Name System (DNS), whose major function is to manage associations between domain names and IP addresses, plays a major role in managing the Internet. Thus, a DNS impairment would significantly impact society. A major cause of DNS impairment is Distributed Denial of Service (DDoS) attack on authoritative DNS servers. Our study focuses on the recently emerging DDoS attack known as the DNS Water Torture Attack. This attack causes open resolvers, which are improperly configured cache DNS servers that accept requests from both LAN and WAN, to send many queries to resolve domains managed by target servers. Domain names for resolving sent in this attack include varying random subdomains. Cache servers certainly will not have cached data for these queries, and so a huge volume of queries converges to the target authoritative servers via cache servers. In this paper, we propose a detection method for this attack using the Naive Bayes Classifier. Experimental results show that our method is capable of detecting this attack with a 95.59% detection rate. Moreover, the results of performance simulation show that our method is fast enough to process more than 2.3Gbps of traffic on the fly.------------------------------This is a preprint of an article intended for publication Journal ofInformation Processing(JIP). This preprint should not be cited. Thisarticle should be cited as: Journal of Information Processing Vol.24(2016) No.5 (online)DOI http://dx.doi.org/10.2197/ipsjjip.24.793------------------------------

著者

Shinobu Sugihara Ichiro Hisatome Masanari Kuwabara Koichiro Niwa Nani Maharani Masahiko Kato Kazuhide Ogino Toshihiro Hamada Haruaki Ninomiya Yukihito Higashi Kimiyoshi Ichida Kazuhiro Yamamoto

出版者

日本循環器学会

雑誌

Circulation Journal (ISSN:13469843)

巻号頁・発行日

pp.CJ-14-1267, (Released:2015-02-23)

参考文献数

41

被引用文献数

10 82

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Background:Uric acid (UA) serves as an antioxidant in vascular endothelial cells. UA transporter 1 (URAT1) encoded by SLC22A12 is expressed in the kidney and vessels and its loss of function causes hypouricemia. The purpose of this study was to examine whether there is any endothelial dysfunction in patients with hypouricemia.Methods and Results:Twenty-six patients with hypouricemia (<2.5 mg/dl) and 13 healthy control subjects were enrolled. Endothelial function was evaluated using flow-mediated dilation (FMD). mRNA of UA transporters expressed in cultured human umbilical endothelial cells (HUVEC) was detected on RT-PCR. There was a positive correlation between FMD and serum UA in the hypouricemia group. URAT1 loss-of-function mutations were found in the genome of 21 of 26 patients with hypouricemia, and not in the other 5. In the hypouricemia groups, serum UA in homozygous and compound heterozygous patients was significantly lower than in other groups, suggesting that severity of URAT1 dysfunction may influence the severity of hypouricemia. Thirteen of 16 hypouricemia subjects with homozygous and compound heterozygote mutations had SUA <0.8 mg/dl and their FMD was lower than in other groups. HUVEC do not express mRNA of URAT1, suggesting the null role of URAT1 in endothelial function.Conclusions:Depletion of UA due to SLC22A12/URAT1 loss-of-function mutations causes endothelial dysfunction in hypouricemia patients.