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YASUDA Hisafumi
Graduate School of Health Sciences / Faculty of Health Sciences
Professor
Medicine
Last Updated :2022/04/15

Researcher Profile and Settings

Affiliation

  • ＜Faculty / Graduate School / Others＞

    Graduate School of Health Sciences / Faculty of Health Sciences

  • ＜Related Faculty / Graduate School / Others＞

    School of Medicine / Faculty of Health Sciences, Center for Mathematical and Data Sciences

Teaching

Research Activities

Research Interests

  • 生活習慣病
  • 老年医学
  • １型糖尿病

Research Areas

  • Life sciences / Internal medicine - General

Committee Memberships

  • 日本老年医学会, 総会代議員、近畿支部世話人
  • 日本糖尿病学会, 学術評議員
  • 日本内科学会, 近畿支部評議員
  • 日本糖尿病療養指導士認定機構, 理事
  • 日本糖尿病学会, １型糖尿病調査研究委員会委員
  • 日本糖尿病動物学会, 評議員

Awards

  • Jan. 2000 神戸大学医学部, 神戸大学医学部優秀学術論文賞, Local expression of immunoregulatopry IL-12p40 gene prolonged syngeneic islet graft survival in diabetic NOD mice

    YASUDA HISAFUMI

    Others

Published Papers

  • 1型糖尿病におけるIA-2抗体RIA法とELISA法の比較検討 1型糖尿病の成因・病態に関する調査研究委員会報告

    川崎 英二, 島田 朗, 今川 彰久, 阿比留 教生, 粟田 卓也, 及川 洋一, 大澤 春彦, 梶尾 裕, 川畑 由美子, 小澤 純二, 小林 哲郎, 高橋 和眞, 中條 大輔, 福井 智康, 三浦 順之助, 安田 和基, 安田 尚史, 花房 俊昭, 池上 博司

    (一社)日本糖尿病学会, May 2021, 糖尿病, 64 (Suppl.1), I - 6, Japanese

  • Japanese Type 1 Diabetes Database Study (TIDE‑J): rationale and study design

    Daisuke Chujo, Akihisa Imagawa, Kazuki Yasuda, Norio Abiru, Takuya Awata, Tomoyasu Fukui, Hiroshi Ikegami, Eiji Kawasaki, Takeshi Katsuki, Tetsuro Kobayashi, Junji Kozawa, Kan Nagasawa, Hiroshi Ohtsu, Yoichi Oikawa, Haruhiko Osawa, Akira Shimada, Masayuki Shimoda, Kazuma Takahashi, Kyoichiro Tsuchiya, Tetsuro Tsujimoto, Hisafumi Yasuda, Toshiaki Hanafusa, Hiroshi Kajio

    2021, Diabetology International, English

    [Refereed]

  • Effect of a Combined Exercise and Cognitive Activity Intervention on Cognitive Function in Community-dwelling Older Adults: A Pilot Randomized Controlled Trial

    Shunsuke Murata, Rei Ono, Hisafumi Yasuda, Rumi Tanemura, Yoshiaki Kido, Hisatomo Kowa

    2021, Phys Ther Res ., 24 (2), 112 - 119, English

    [Refereed]

    Scientific journal

  • 地域在住高齢がんサバイバーにおける運動機能と精神機能、生化学データの特徴

    小野 玲, 牧浦 大祐, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

    (NPO)日本緩和医療学会, Aug. 2020, Palliative Care Research, 15 (Suppl.), S241 - S241, Japanese

  • 急性発症1型糖尿病における発症後内因性インスリン分泌低下関連因子 甲状腺自己免疫との関連(TIDE-J研究)

    戎野 朋子, 橘 恵, 金綱 規夫, 寺前 純吾, 今川 彰久, 阿比留 教生, 粟田 卓也, 池上 博司, 及川 洋一, 大澤 春彦, 香月 健志, 川崎 英二, 小澤 純二, 小林 哲郎, 島田 朗, 高橋 和眞, 中條 大輔, 土屋 恭一郎, 長澤 幹, 福井 智康, 安田 和基, 安田 尚史, 梶尾 裕, 花房 俊昭

    (一社)日本糖尿病学会, Aug. 2020, 糖尿病, 63 (Suppl.1), S - 146, Japanese

  • 地域在住高齢者における自己記入によるDASC-21の特性

    小野 玲, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

    (一社)日本老年医学会, Jul. 2020, 日本老年医学会雑誌, 57 (Suppl.), 81 - 81, Japanese

  • 地域在住高齢者における自己記入によるDASC-21の特性

    小野 玲, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

    (一社)日本老年医学会, Jul. 2020, 日本老年医学会雑誌, 57 (Suppl.), 81 - 81, Japanese

  • Yumiko Kawabata, Nao Nishida, Takuya Awata, Eiji Kawasaki, Akihisa Imagawa, Akira Shimada, Haruhiko Osawa, Shoichiro Tanaka, Kazuma Takahashi, Masao Nagata, Hisafumi Yasuda, Yasuko Uchigata, Hiroshi Kajio, Hideichi Makino, Kazuki Yasuda, Tetsuro Kobayashi, Toshiaki Hanafusa, Katsushi Tokunaga, Hiroshi Ikegami

    The first genome-wide association study of fulminant type 1 diabetes was performed in Japanese individuals. As previously reported using a candidate gene approach, a strong association was observed with multiple single nucleotide polymorphisms (SNPs) in the HLA region, and the strongest association was observed with rs9268853 in the class II DR region (P = 1.56 × 10-23, odds ratio [OR] 3.18). In addition, rs11170445 in CSAD/lnc-ITGB7-1 on chromosome 12q13.13 showed an association at a genome-wide significance level (P = 7.58 × 10-9, OR 1.96). Fine mapping of the region revealed that rs3782151 in CSAD/lnc-ITGB7-1 showed the lowest P value (P = 4.60 × 10-9, OR 1.97 [95% CI 1.57-2.48]). The risk allele of rs3782151 is a cis expression quantitative trait locus for ITGB7 that significantly increases the expression of this gene. CSAD/lnc-ITGB7-1 was found to be strongly associated with susceptibility to fulminant, but not classical, autoimmune type 1 diabetes, implicating this locus in the distinct phenotype of fulminant type 1 diabetes.

    Mar. 2019, Diabetes, 68 (3), 665 - 675, English, International magazine

    [Refereed]

    Scientific journal

  • 抗PD-1抗体投与後に発症する1型糖尿病の特徴および臨床経過に関する調査報告

    馬殿 恵, 今川 彰久, 阿比留 教生, 粟田 卓也, 池上 博司, 内潟 安子, 及川 洋一, 大澤 春彦, 梶尾 裕, 川崎 英二, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 中條 大輔, 福井 智康, 三浦 順之助, 安田 和基, 安田 尚史, 小林 哲郎, 花房 俊昭

    抗PD-1抗体投与後に発症する1型糖尿病について、日本糖尿病学会員への調査と文献検索を行い22症例を検討した。初回の薬剤投与日から発症までの平均期間は155日、発症時の平均年齢63歳、平均血糖値617mg/dL、平均HbA1c8.1%、尿中C-ペプチド4.1μg/日(中央値)、空腹時血中C-ペプチド0.46ng/mL(中央値)であった。31.6%に消化器症状、27.8%に感冒様症状、16.7%に意識障害を認め、85.0%でケトーシス、38.9%で糖尿病性ケトアシドーシスを発症した。50.0%が劇症1型糖尿病、50.0%が急性発症1型糖尿病と診断された。膵外分泌酵素は52.6%で発症時に、28.6%で発症前に上昇した。1例でGAD抗体陽性であった。抗PD-1抗体投与後に発症する1型糖尿病は、劇症1型糖尿病から急性発症1型糖尿病まで幅広い臨床病型を呈し、高頻度に糖尿病性ケトアシドーシスを発症するため、適切な診断と治療が不可欠である。(著者抄録)

    (一社)日本糖尿病学会, Jan. 2019, 糖尿病, 62 (1), 37 - 46, Japanese

    [Refereed]

  • Megu Yamaguchi Baden, Akihisa Imagawa, Norio Abiru, Takuya Awata, Hiroshi Ikegami, Yasuko Uchigata, Yoichi Oikawa, Haruhiko Osawa, Hiroshi Kajio, Eiji Kawasaki, Yumiko Kawabata, Junji Kozawa, Akira Shimada, Kazuma Takahashi, Shoichiro Tanaka, Daisuke Chujo, Tomoyasu Fukui, Junnosuke Miura, Kazuki Yasuda, Hisafumi Yasuda, Tetsuro Kobayashi, Toshiaki Hanafusa

    Aims: We conducted a national survey to clarify the characteristics and clinical course of type 1 diabetes related to anti-programmed cell death-1 therapy. Methods: We analyzed the detailed data of 22 patients that were collected using a Japan Diabetes Society survey and a literature database search. Results: Among the 22 patients, 11 (50.0%) met the criteria for fulminant type 1 diabetes and 11 (50.0%) met the criteria for acute-onset type 1 diabetes. The average patient age was 63 years. The mean duration between the date of the first anti-PD-1 antibody injection and development of type 1 diabetes was 155 days and ranged from 13 to 504 days. Flu-like symptoms, abdominal symptoms, and drowsiness were observed in 27.8, 31.6, and 16.7% patients, respectively. Mean ± standard deviation or median (first quartile-third quartile) glucose levels, HbA1c levels, urinary C-peptide immunoreactivity levels, and fasting serum C-peptide immunoreactivity levels were 617 ± 248 mg/dl, 8.1 ± 1.3%, 4.1 (1.4-9.4) μg/day, and 0.46 (0.20-0.70) ng/ml, respectively. Seventeen of 20 patients (85.0%) developed ketosis, and 7 of 18 patients (38.9%) developed diabetic ketoacidosis. Ten of 19 patients (52.6%) showed at least one elevated pancreatic enzyme level at the onset and two of seven patients showed this elevation before diabetes onset. Only one of 21 patients was anti-glutamic acid decarboxylase antibody positive. Conclusions: Anti-programmed cell death-1 antibody-related type 1 diabetes varies from typical fulminant type 1 diabetes to acute-onset type 1 diabetes. However, diabetic ketoacidosis was frequently observed at the onset of diabetes. An appropriate diagnosis and treatment should be provided to avoid life-threatening metabolic alterations.

    Jan. 2019, Diabetology international, 10 (1), 58 - 66, English, Domestic magazine

    [Refereed]

    Scientific journal

  • 日本, 型糖尿病の成因, 診断,病態, 治療に関する調査研究委員会, 徳永あゆみ, 今川彰久, 西尾博, 早田敏, 下村伊一郎, 阿比留教生, 粟田卓也, 池上博司, 内潟安子, 及川洋一, 大澤春彦, 梶尾裕, 川﨑英二, 川畑由美子, 小澤純二, 島田朗, 高橋和眞, 田中昌一郎, 中條大輔, 福井智康, 三浦順之助, 安田和基, 安田尚史, 小林哲郎, 花房俊昭

    Dec. 2018, 糖尿病, 61 (12), 840 - 849, Japanese

    [Refereed]

    Scientific journal

  • Ayumi Tokunaga, Akihisa Imagawa, Hiroshi Nishio, Satoshi Hayata, Iichiro Shimomura, Norio Abiru, Takuya Awata, Hiroshi Ikegami, Yasuko Uchigata, Yoichi Oikawa, Haruhiko Osawa, Hiroshi Kajio, Eiji Kawasaki, Yumiko Kawabata, Junji Kozawa, Akira Shimada, Kazuma Takahashi, Shoichiro Tanaka, Daisuke Chujo, Tomoyasu Fukui, Junnosuke Miura, Kazuki Yasuda, Hisafumi Yasuda, Tetsuro Kobayashi, Toshiaki Hanafusa

    Abrupt disease onset and severe metabolic disorders are main characteristics of fulminant type 1 diabetes. Diffusion-weighted magnetic resonance imaging (DWI) is an imaging technique that reflects restricted diffusion in organs and can detect mononuclear cell infiltration into the pancreas at the onset of the disease. Fourteen patients with fulminant type 1 diabetes who underwent abdominal magnetic resonance imaging were recruited for the measurement of apparent diffusion coefficient (ADC) values of the pancreas that were compared with those of 21 non-diabetic controls. The ADC values of all parts of the pancreas were significantly lower in fulminant type 1 diabetes than in controls (head, 1.424 ± 0.382 × 10-3 vs. 1.675 ± 0.227 × 10-3 mm2/s; body, 1.399 ± 0.317 × 10-3 vs. 1.667 ± 0.170 × 10-3 mm2/s; tail, 1.336 ± 0.247 × 10-3 vs. 1.561 ± 0.191 × 10-3 mm2/s; mean, 1.386 ± 0.309 × 10-3 vs. 1.634 ± 0.175 × 10-3 mm2/s) (p < 0.01). The best cut-off value indicated that the sensitivity was 86% and the specificity was 71% when using DWI, which was also efficient in two atypical patients with fulminant type 1 diabetes without elevated levels of exocrine pancreatic enzymes or with high HbA1c levels due to the preexistence of type 2 diabetes. The ADC values were significantly correlated to plasma glucose levels and arterial pH, and tended to increase with the lapse of time. DWI may be an additional tool for making an efficient diagnosis of fulminant type 1 diabetes.

    Oct. 2018, Diabetology international, 9 (4), 257 - 265, English, Domestic magazine

    [Refereed]

    Scientific journal

  • 慢性閉塞性肺疾患患者における便通状態と身体・精神機能との関連性

    沖 侑大郎, 松本 真裕美, 藤本 由香里, 山口 卓巳, 山田 莞爾, 渡邊 佑, 金子 弘美, 大平 峰子, 安田 尚史, 石川 朗

    (一社)日本老年医学会, Oct. 2017, 日本老年医学会雑誌, 54 (4), 618 - 618, Japanese

  • Yoichi Oikawa, Akira Shimada, Takuya Awata, Tomoyasu Fukui, Hiroshi Ikegami, Akihisa Imagawa, Hiroshi Kajio, Yumiko Kawabata, Eiji Kawasaki, Junnosuke Miura, Haruhiko Osawa, Kazuma Takahashi, Shoichiro Tanaka, Yasuko Uchigata, Hisafumi Yasuda, Kazuki Yasuda, Toshiaki Hanafusa, Tetsuro Kobayashi

    The pathogenesis of type 1 diabetes is different from that of type 2 diabetes, and anti-glutamic acid decarboxylase antibody (GADA) helps to diagnose autoimmune type 1 diabetes. Some studies reported that GADA seroconversion occurs during the clinical course of type 2 diabetes, leading to development of "type 1 on type 2 diabetes". To clarify the clinical characteristics and triggers of GADA seroconversion, we performed a nationwide questionnaire survey for clinical cases identified by literature search, and obtained information on 38 cases (24 with insulin therapy and 14 without it). The diabetes duration up to determination of GADA seroconversion was significantly longer in the group with insulin therapy than that without it. This finding was particularly noted in insulin-treated non-obese patients with lower serum C-peptide levels. In these patients, insulin therapy could have masked sudden increases in plasma glucose and HbA1c levels, possibly leading to delayed determination of GADA seroconversion. In non-obese patients without insulin therapy, an abrupt rise in the plasma glucose and HbA1c levels was observed at immediately before the determination, a finding which may help to predict GADA seroconversion. From the results of the present survey, we could not determine apparent triggers of GADA seroconversion. Thus, physicians may need to consider the possibility of concurrent type 1 diabetes during the therapeutic course of type 2 diabetes; GADA measurement should be considered when non-obese type 2 diabetic patients not receiving insulin therapy experience unexpected abrupt hyperglycemia and when those receiving insulin therapy show low serum C-peptide levels.

    Aug. 2017, Diabetology international, 8 (3), 306 - 315, English, Domestic magazine

    [Refereed]

    Scientific journal

  • Yukari Fujimoto, Yutaro Oki, Masahiro Kaneko, Hideki Sakai, Shogo Misu, Takumi Yamaguchi, Yuji Mitani, Hisafumi Yasuda, Akira Ishikawa

    Purpose: A straightforward, noninvasive method is needed to assess emphysema and pulmonary hypertension (PH) in COPD patients. The desaturation-distance ratio (DDR) is an index derived from the distance traveled and level of desaturation during a six-minute walk test (6MWT); it has previously been shown to be associated with percentage of forced expiratory volume in the first second of expiration (%FEV1.0) and percentage of diffusion capacity of the lung for carbon monoxide (%DLCO). The aim of this study was to examine the associations between DDR and emphysema and PH. Patients and methods: We collected the following data for 74 stable COPD outpatients: lung function tests (%FEV1.0 and %DLCO), 6MWT distance and desaturation, and area of emphysema on computed tomography (percentage of low attenuation area). Enlargement of the pulmonary artery (PA) was assessed by the ratio of the diameter of the PA to that of the aorta (PA:A ratio) as an index of PH. DDR was calculated by the distance traveled and the degree of desaturation reached during a 6MWT. The relationships between study outcomes were assessed with Spearman's rank-correlation analysis. Receiver operating characteristic (ROC) curves were used to determine the threshold values with the optimum cutoff points for predicting severe or very severe airway obstruction, pulmonary diffusing capacity disorder, moderate or severe emphysema, and enlargement of the PA. Results: DDR correlated significantly with %FEV1.0, %DLCO, %LAA, and PA:A ratio. DDR showed high accuracy (area under the ROC curve>0.7) for predicting severe or very severe airway obstruction, pulmonary diffusing capacity disorder, moderate or severe emphysema, and enlargement of the PA. Conclusion: The results suggest that DDR is a good index of emphysema and PH in COPD patients. The 6MWT is widely used to assess COPD, and DDR could help with the early diagnosis of COPD.

    DOVE MEDICAL PRESS LTD, 2017, INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE, 12, 2669 - 2675, English

    [Refereed]

    Scientific journal

    Link to Kobe Univ. Repository (Kernel)

  • Megu Yamaguchi Baden, Akihisa Imagawa, Hiromi Iwahashi, Iichiro Shimomura, Takuya Awata, Hiroshi Ikegami, Yasuko Uchigata, Haruhiko Osawa, Hiroshi Kajio, Eiji Kawasaki, Yumiko Kawabata, Akira Shimada, Kazuma Takahashi, Shoichiro Tanaka, Kazuki Yasuda, Hisafumi Yasuda, Tetsuro Kobayashi, Toshiaki Hanafusa

    Aims: The onset of fulminant type 1 diabetes mellitus is sometimes accompanied by sudden death or cardiac arrest. The aim of this study was to determine the risk factors for the development of these conditions at the onset of fulminant type 1 diabetes mellitus. Methods: We conducted a search of the literature on fulminant type 1 diabetes and sudden death or cardiac arrest published up to 2012 in PubMed and Ichushi (a Japanese article database), and a questionnaire survey was administered to the authors of the articles and to diabetes specialists affiliated to the Japan Diabetes Society. We analyzed the clinical data at disease onset of 17 patients with fulminant type 1 diabetes mellitus who experienced sudden death or cardiac arrest, and those of 257 patients who did not develop these conditions. Results: Patients with sudden death or cardiac arrest were younger, had a higher rate of impaired consciousness, more severe acidosis, hyperglycemia, hyponatremia, hyperkalemia, and hypochloremia, a higher serum blood urea nitrogen level, a higher serum creatinine level, and a higher plasma osmolality level than the other patients. In multiple logistic regression analyses, plasma glucose level was positively associated with sudden death or cardiac arrest. Receiver operating characteristic curve analyses showed that patients with a plasma glucose level over 1000 mg/dl (55.5 mmol/l) were at a high risk of cardiac arrest. Conclusions: Severe metabolic derangement, especially a high plasma glucose level, is associated with sudden death or cardiac arrest at the onset of fulminant type 1 diabetes mellitus.

    Sep. 2016, Diabetology international, 7 (3), 281 - 288, English, Domestic magazine

    [Refereed]

    Scientific journal

  • Junichi Yasui, Eiji Kawasaki, Shoichiro Tanaka, Takuya Awata, Hiroshi Ikegami, Akihisa Imagawa, Yasuko Uchigata, Haruhiko Osawa, Hiroshi Kajio, Yumiko Kawabata, Akira Shimada, Kazuma Takahashi, Kazuki Yasuda, Hisafumi Yasuda, Toshiaki Hanafusa, Tetsuro Kobayashi

    Aims Glutamic acid decarboxylase autoantibodies (GADAb) differentiate slowly progressive insulin-dependent (type 1) diabetes mellitus (SPIDDM) from phenotypic type 2 diabetes, but many GADAb-positive patients with diabetes do not progress to insulin-requiring diabetes. To characterize GADAb-positive patients with adult-onset diabetes who do not require insulin therapy for >5 years (NIR-SPIDDM), we conducted a nationwide cross-sectional survey in Japan. Methods We collected 82 GADAb-positive patients who did not require insulin therapy for >5 years (NIR-SPIDDM) and compared them with 63 patients with insulin-requiring SPIDDM (IR-SPIDDM). Clinical and biochemical characteristics, HLA-DRB1-DQB1 haplotypes, and predictive markers for progression to insulin therapy were investigated. Results Compared with the IR-SPIDDM group, the NIR-SPIDDM patients showed later diabetes onset, higher body mass index, longer duration before diagnosis, and less frequent hyperglycemic symptoms at onset. In addition, C-peptide, LDL-cholesterol, and TG were significantly higher in the NIR-SPIDDM compared to IR-SPIDDM patients. The NIR-SPIDDM group had lower frequency of susceptible HLA-DRB1*04:05-DQB1*04:01 and a higher frequency of resistant HLA-DRB1*15:01-DQB1*06:02 haplotype compared to IR-SPIDDM. A multivariable analysis showed that age at diabetes onset (OR = 0.82), duration before diagnosis of GADAb-positive diabetes (OR = 0.82), higher GADAb level (>= 10.0 U/ml) (OR = 20.41), and fasting C-peptide at diagnosis (OR = 0.07) were independent predictive markers for progression to insulin-requiring diabetes. An ROC curve analysis showed that the optimal cut-off points for discriminating two groups was the GADAb level of 13.6 U/ml, age of diabetes onset of 47 years, duration before diagnosis of 5 years, and fasting C-peptide of 0.65 ng/ml. Conclusions Clinical, biochemical and genetic characteristics of patients with NIR-SPIDDM are different from those of IR-SPIDDM patients. Age of diabetes onset, duration before GADAb-positivity, GADAb level, and fasting C-peptide at diagnosis must be carefully considered in planning prevention trials for SPIDDM.

    PUBLIC LIBRARY SCIENCE, May 2016, PLOS ONE, 11 (5), e0155643, English

    [Refereed]

    Scientific journal

  • Hiroyuki Seto, Mitsushige Nishimura, Katsuhiro Minamiji, Sonoko Miyoshi, Hiroyuki Mori, Kenji Kanazawa, Hisafumi Yasuda

    We herein report the case of a 63-year-old man who presented with a 3-month history of a cutaneous nodular lesion of his jaw, low grade fever, lethargy and progressive cognitive impairment. He had a 30-year history of multiple sclerosis and had been treated with fingolimod for the previous 2 years. Laboratory data revealed CD4 lymphocytopenia and a tissue culture of the skin nodule was positive for Cryptococcus neoformans. Cerebrospinal fluid and serum cryptococcal antigen tests were also positive and we diagnosed him to have disseminated cryptococcosis. This dissemination might be associated with fingolimod-induced CD4 lymphocytopenia. The risk of an opportunistic infection should therefore be considered when encountering fingolimod-treated patients.

    JAPAN SOC INTERNAL MEDICINE, 2016, INTERNAL MEDICINE, 55 (22), 3383 - 3386, English

    [Refereed]

    Scientific journal

  • Yutaro Oki, Masahiro Kaneko, Yukari Fujimoto, Hideki Sakai, Shogo Misu, Yuji Mitani, Takumi Yamaguchi, Hisafumi Yasuda, Akira Ishikawa

    Purpose: Pulmonary hypertension and exercise-induced oxygen desaturation (EID) influence acute exacerbation of COPD. Computed tomography (CT)-detected pulmonary artery (PA) enlargement is independently associated with acute COPD exacerbations. Associations between PA to aorta (PA: A) ratio and EID in patients with COPD have not been reported. We hypothesized that the PA: A ratio correlated with EID and that results of the 6-minute walk test (6MWT) would be useful for predicting the risk associated with PA: A.1. Patients and methods: We retrospectively measured lung function, 6MWT, emphysema area, and PA enlargement on CT in 64 patients with COPD. The patients were classified into groups with PA: A <= 1 and <= 1. Receiver-operating characteristic curves were used to determine the threshold values with the best cutoff points to predict patients with PA: A.1. Results: The PA: A.1 group had lower forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1: FVC ratio, diffusion capacity of lung carbon monoxide, 6MW distance, and baseline peripheral oxygen saturation (SpO(2)), lowest SpO(2), highest modified Borg scale results, percentage low-attenuation area, and history of acute COPD exacerbations <1 year, and worse BODE (Body mass index, airflow Obstruction, Dyspnea, and Exercise) index results (P<0.05). Predicted PA: A>1 was determined for SpO(2) during 6MWT (best cutoff point 89%, area under the curve 0.94, 95% confidence interval 0.88-1). SpO(2) <90% during 6MWT showed a sensitivity of 93.1, specificity of 94.3, positive predictive value of 93.1, negative predictive value of 94.3, positive likelihood ratio of 16.2, and negative likelihood ratio of 0.07. Conclusion: Lowest SpO(2) during 6MWT may predict CT-measured PA: A, and lowest SpO(2),89% during 6MWT is excellent for detecting pulmonary hypertension in COPD.

    DOVE MEDICAL PRESS LTD, 2016, INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE, 11, 2869 - 2875, English

    [Refereed]

    Scientific journal

    Link to Kobe Univ. Repository (Kernel)
  • 汎下垂体機能低下症、橋本病および境界型耐糖能異常を呈した多腺性自己免疫症候群3型の一例

    竹内健人, 原賢太, 高吉倫史, 高橋利匡, 西山勝人, Yasuda Hisafumi, 横野浩一, 安友佳朗

    Jul. 2015, 日本内分泌学会雑誌, 91 (Suppl.), 7 - 9, Japanese

    [Refereed]

    Scientific journal

  • 腎周囲膿瘍から広範囲の腸腰筋膿瘍を来たした2型糖尿病患者の1例

    Toyokuni Takehiro, Arai Takashi, Kanazawa Kenji

    Dec. 2014, 糖尿病, 57 (12号), 934, Japanese

    Research society

  • Mami Shimizu, Hisafumi Yasuda, Kenta Hara, Kazuma Takahashi, Masao Nagata, Koichi Yokono

    Human type 1 diabetes is an autoimmune disease that results from the autoreactive destruction of pancreatic beta cells by T cells. Antigen presenting cells including dendritic cells and macrophages are required to activate and suppress antigen-specific T cells. It has been suggested that antigen uptake from live cells by dendritic cells via scavenger receptor class A (SR-A) may be important. However, the role of SR-A in autoimmune disease is unknown. In this study, SR-A(-/-) nonobese diabetic (NOD) mice showed significant attenuation of insulitis, lower levels of insulin autoantibodies, and suppression of diabetes development compared with NOD mice. We also found that diabetes progression in SR-A(-/-) NOD mice treated with low-dose polyinosinic-polycytidylic acid (poly(I:C)) was significantly accelerated compared with that in disease-resistant NOD mice treated with low-dose poly(I:C). In addition, injection of high-dose poly(I: C) to mimic an acute RNA virus infection significantly accelerated diabetes development in young SR-A 2/2 NOD mice compared with untreated SR-A(-/-) NOD mice. Pathogenic cells including CD4(+) CD25(+) activated T cells were increased more in SR-A(-/-) NOD mice treated with poly(I:C) than in untreated SR-A(-/-) NOD mice. These results suggested that viral infection might accelerate diabetes development even in diabetes-resistant subjects. In conclusion, our studies demonstrated that diabetes progression was suppressed in SR-A(-/-) NOD mice and that acceleration of diabetes development could be induced in young mice by poly(I:C) treatment even in SR-A(-/-) NOD mice. These results suggest that SR-A on antigen presenting cells such as dendritic cells may play an unfavorable role in the steady state and a protective role in a mild infection. Our findings imply that SR-A may be an important target for improving therapeutic strategies for type 1 diabetes.

    PUBLIC LIBRARY SCIENCE, Oct. 2014, PLOS ONE, 9 (10), :e109531, English

    [Refereed]

    Scientific journal

  • Mami Shimizu, Hisafumi Yasuda, Kenta Hara, Kazuma Takahashi, Masao Nagata, Koichi Yokono

    Human type 1 diabetes is an autoimmune disease that results from the autoreactive destruction of pancreatic beta cells by T cells. Antigen presenting cells including dendritic cells and macrophages are required to activate and suppress antigen-specific T cells. It has been suggested that antigen uptake from live cells by dendritic cells via scavenger receptor class A (SR-A) may be important. However, the role of SR-A in autoimmune disease is unknown. In this study, SR-A(-/-) nonobese diabetic (NOD) mice showed significant attenuation of insulitis, lower levels of insulin autoantibodies, and suppression of diabetes development compared with NOD mice. We also found that diabetes progression in SR-A(-/-) NOD mice treated with low-dose polyinosinic-polycytidylic acid (poly(I:C)) was significantly accelerated compared with that in disease-resistant NOD mice treated with low-dose poly(I:C). In addition, injection of high-dose poly(I: C) to mimic an acute RNA virus infection significantly accelerated diabetes development in young SR-A 2/2 NOD mice compared with untreated SR-A(-/-) NOD mice. Pathogenic cells including CD4(+) CD25(+) activated T cells were increased more in SR-A(-/-) NOD mice treated with poly(I:C) than in untreated SR-A(-/-) NOD mice. These results suggested that viral infection might accelerate diabetes development even in diabetes-resistant subjects. In conclusion, our studies demonstrated that diabetes progression was suppressed in SR-A(-/-) NOD mice and that acceleration of diabetes development could be induced in young mice by poly(I:C) treatment even in SR-A(-/-) NOD mice. These results suggest that SR-A on antigen presenting cells such as dendritic cells may play an unfavorable role in the steady state and a protective role in a mild infection. Our findings imply that SR-A may be an important target for improving therapeutic strategies for type 1 diabetes.

    PUBLIC LIBRARY SCIENCE, Oct. 2014, PLOS ONE, 9 (10), e109531, English

    [Refereed]

    Scientific journal

  • 竹内 健人, 安友 佳朗, 高吉 倫史, 高橋 利匡, 西山 勝人, 安田 尚史, 原 賢太, 横野 浩一

    (一社)日本内分泌学会, Oct. 2014, 日本内分泌学会雑誌, 90 (3), 958 - 958, Japanese

  • Hepatic and Brain Abscesses with Endophthalmitis, due to Klebsiella pneumoniae: An Emerging Infectious Disease.

    NISHIMURA MITSUSHIGE, YASUDA HISAFUMI, KANAZAWA KENJI

    Nov. 2013, Infectious Diseases in Clinical Practice, English

    [Refereed]

    Scientific journal

  • 高齢者に見られた猫咬傷が原因のPasturella multocidaの1例

    Kanazawa Kenji

    Sep. 2013, 日本老年医学会雑誌, 50 (5号), 688, Japanese

    Research society

  • クローン病加療中に発熱・皮疹・意識障害が出現、スイート病と診断された若年女性の１例

    NISHIMURA MITSUSHIGE, YASUDA HISAFUMI, KANAZAWA KENJI

    日本総合診療医学会, Jun. 2013, 日本総合診療医学会雑誌, Japanese

    [Refereed]

    Scientific journal

  • 広範囲にガス壊疽を伴う皮膚重症感染症を来たした血糖コントロール不良2型糖尿病の1例

    Kanazawa Kenji

    Feb. 2013, 糖尿病, 56 (2号), 128, Japanese

    Research society

  • 自己免疫性肝炎、Sjoegren症候群、CREST症候群の経過中に発症した1型糖尿病の1例

    Yasuda Hisafumi, Toyokuni Takehiro, Kanazawa Kenji, Hara Kenta

    Aug. 2012, 糖尿病, 55 (8号), 669, Japanese

    [Refereed]

    Research society

  • Akira Nakamura, Kenta Hara, Kazuhiro Yamamoto, Hisafumi Yasuda, Hiroaki Moriyama, Midori Hirai, Masao Nagata, Koichi Yokono

    Aim: Oral intake of nutrients is often compromised in elderly, multimorbid patients, but parenteral nutrition causes intestinal atrophy and impairs intestinal function. To uncover the molecular mechanisms by which amino acids are involved in intestinal atrophy and recovery, we studied whether the rapamycin-sensitive mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) pathway is involved in this process. Methods: C57BL/6N mice were fed a glucose solution alone, glucose solution with amino acids or normal chow diet for various lengths of time. Intestinal sections were prepared from these mice and the villus height and villus density were quantified. As a readout for the mTORC1 pathway, the phosphorylation of the ribosomal S6 protein (S6) was analyzed by immunostaining and immunoblotting. To confirm the role of the mTORC1 pathway, the inhibitory effect of a specific mTOR inhibitor, rapamycin, was examined. Results: Inducing fasting in mice fed only glucose caused time-dependent intestinal mucosal atrophy, whereas supplementation with amino acids protected the intestinal mucosa from atrophy. Phosphorylation of S6 decreased in the intestinal mucosa of mice fed only glucose, whereas supplementation with amino acids increased S6 phosphorylation. Importantly, intraperitoneal injection of rapamycin attenuated the protective effect of amino acids on the intestinal mucosa in a pattern consistent with the decrease of S6 phosphorylation. Conclusions: These results indicate that the mTORC1 pathway plays a crucial role in the in vivo maintenance of the intestinal mucosa by the oral intake of amino acids. Geriatr Gerontol Int 2012; 12: 131-139.

    WILEY-BLACKWELL, Jan. 2012, GERIATRICS & GERONTOLOGY INTERNATIONAL, 12 (1), 131 - 139, English

    [Refereed]

    Scientific journal

  • H. Yasuda, M. Nagata, H. Moriyama, H. Kobayashi, T. Akisaki, H. Ueda, K. Hara, K. Yokono

    Background Fulminant Type 1 diabetes was originally reported as idiopathic Type 1 diabetes. Involvement of viral infections in the pathogenesis of fulminant T1D has been suggested, but the development of fulminant Type 1 diabetes after influenza vaccination has not been reported. Case Report We report a case of fulminant Type 1 diabetes with thrombocytopenia following influenza vaccination. A 54-year-old man was admitted to hospital with hyperglycaemia and diabetic ketosis. Seven days before admission, he received a seasonal influenza vaccine for the prevention of influenza infection. On admission, blood glucose was 29 mmol/L and HbA1c 40 mmol/mol (5.9%). Fasting and 2-h C-peptide immunoreactivity were <0.0333 nmol/L and 0.0999 nmol/L, respectively. Anti-GAD and anti-IA-2 antibodies were negative, so no autoimmunity seemed to participate in the etiology. ELISPOT assay also showed no association with T cell-mediated autoimmunity. HLA genotypes were consistent with susceptibility to fulminant Type 1 diabetes. After the abrupt onset of diabetes, he showed mild thrombocytopenia, which has been observed for approximately 5 years after diabetes development. Conclusion This is the first description of fulminant Type 1 diabetes after influenza vaccination. Our observation raises the possibility that influenza vaccination might trigger this condition via the TLR7 pathway.

    WILEY-BLACKWELL, Jan. 2012, DIABETIC MEDICINE, 29 (1), 88 - 89, English

    [Refereed]

    Scientific journal

  • 傍神経節腫の肝転移に対し、経カテーテル的動脈塞栓が著効した一例

    Toyokuni Takehiro, Hiraoka Eiji, Nishimura Mitsushige, Mori Hiroyuki, Yasuda Hisafumi, Kanazawa Kenji, Hara Kenta

    2012, 日本病院総合診療医学会雑誌, 3 (2), 81 - 89, Japanese

    [Refereed]

    Scientific journal

  • Kenta Hara, Hisafumi Yasuda, Takashi Arai, Sonoko Miyoshi, Osamu Kubokawa, Hiroyuki Mori, Taichi Akisaki, Yoshiaki Kido, Koichi Yokono, Hozuka Akita

    A 72-year-old woman with slowly progressive type 1 diabetes (SPIDDM) was admitted to our hospital because of increasing abdominal pain and diarrhea. The patient was diagnosed with nonocclusive mesenteric ischemia (NOMI), and a subtotal colonectomy was performed successfully. The resected sample revealed transmural gangrenous necrosis of the colon and rectum. This case is interesting because the severe NOMI occurred in a SPIDDM patient without common predisposing events such as hypoperfusion. Prolonged generation of reactive oxygen species in SPIDDM, together with the decline in adaptive response to oxidative stress with aging, might be an exacerbating factor for ischemic injury in the elderly.

    JAPAN SOC INTERNAL MEDICINE, 2012, INTERNAL MEDICINE, 51 (9), 1065 - 1068, English

    [Refereed]

    Scientific journal

  • 急性膵炎に準じて治療した2型糖尿病の1例

    高橋 利匡, 小林 寛和, 河野 泰博, 安田 尚史, 森山 啓明, 原 賢太, 櫻井 孝, 永田 正男, 横野 浩一

    (一社)日本老年医学会, Jul. 2011, 日本老年医学会雑誌, 48 (4), 415 - 415, Japanese

  • Ningwen Tai, Hisafumi Yasuda, Yufei Xiang, Li Zhang, Daniel Rodriguez-Pinto, Koichi Yokono, Robert Sherwin, F. Susan Wong, Masao Nagata, Li Wen

    This study was to determine whether BMDCs cultured in the presence of IL-10 (G/10-DCs) could promote T cell tolerance and prevent autoimmune diabetes in two different animal models of T1D. Our results showed that G/10-DCs suppressed both insulitis and spontaneous diabetes in NOD and HLA-DQ8/RIP-B7.1 mice. The suppression was likely to be mediated by T cells, as we found that regulatory CD4(+)CD25(+)Foxp3(+) cells were significantly increased in G/10-DC treated animals. In vivo, the G/10-DCs inhibited diabetogenic T cell proliferation; in vitro, they had reduced expression of costimulatory molecules and produced little IL-12/23 p40 or IL-6 but a large amount of IL-10 when compared with DCs matured in the presence of IL-4 (G/4-DC). We conclude that IL-10-treated DCs are tolerogenic and induce islet-directed immune tolerance, which was likely to be mediated by T regulatory cells. This non-antigen-specific DC-based approach offers potential for a new therapeutic intervention in T1D. (C) 2011 Elsevier Inc. All rights reserved.

    ACADEMIC PRESS INC ELSEVIER SCIENCE, Jun. 2011, CLINICAL IMMUNOLOGY, 139 (3), 336 - 349, English

    [Refereed]

    Scientific journal

  • Hirotomo Sasaki, Hisafumi Yasuda, Hiroaki Moriyama, Akira Nakamura, Mami Shimizu, Takashi Arai, Masao Nagata, Kenta Hara, Koichi Yokono

    The protein Ras homolog enriched in brain (Rheb) is a Ras-like small GTPase that activates the mechanistic target of rapamycin complex 1 (mTORC1), which promotes cell growth. We previously generated transgenic C57BL/6 mice overexpressing Rheb in beta-cells (B6(Rheb)), which exhibited increased beta-cell size and improved glucose tolerance with higher insulin secretion than wild type C57BL/6 mice. The mice also showed resistance to obesity-induced hyperglycemia, a model of type 2 diabetes, and to multiple lowdose-streptozotocin (MLDS)-induced hyperglycemia, a model of type 1 diabetes (T1D). To investigate whether the effects of mTORC1 activation by Rheb in B6(Rheb) mice would also be evident in NOD mice, a spontaneous autoimmune T1D model, we created two NOD mouse lines overexpressing Rheb in their beta-cells (NOD(Rheb): R3 and R20). We verified Rheb overexpression in beta-cells, the relative activation of mTORC1 and beta-cell enlargement. By 35 weeks of age, diabetes incidence was significantly greater in the R3 line and tended to be greater in the R20 line than in NOD mice. Histological analysis demonstrated that insulitis was significantly accelerated in 12-week-old R3 NOD(Rheb) mice compared with NOD mice. Furthermore, serum insulin autoantibody (IAA) expression was significantly higher than that of NOD mice. We also examined whether complete Freund's adjuvant (CFA) treatment alone or with glucagon-like peptide-1 (GLP-1) analog would reverse the hyperglycemia of NOD(Rheb) mice; unexpectedly, almost none achieved normoglycemia. In summary, diabetes progression was significantly accelerated rather than prevented in NOD(Rheb) mice. Our results suggest that the beta-cell enlargement might merely enhance the autoimmunity of pathogenic T-cells against islets, leading to acceleration of autoimmune diabetes. We conclude that not only enlargement but also regeneration of beta-cells in addition to the prevention of beta-cell destruction will be required for the ideal therapy of autoimmune T1D. (C) 2011 Elsevier Inc. All rights reserved.

    ACADEMIC PRESS INC ELSEVIER SCIENCE, May 2011, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 408 (2), 306 - 311, English

    [Refereed]

    Scientific journal

  • Saeko Kushida, Taichi Akisaki, Hisafumi Yasuda, Hiroaki Moriyama, Kenta Hara, Masao Nagata, Miyako Taniguchi, Katsuya Urakami, Koichi Yokono, Takashi Sakurai

    It is often difficult to diagnose disease in elderly patients, in particular those with dementia, who do not present with typical symptoms. This report describes our experience of an elderly patient (an 83-year-old woman) who presented with a chief complaint of memory loss, showed a marked inflammatory response, and was diagnosed with large-vessel giant cell arteritis (GCA) on the basis of 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) findings. She had no symptoms typical of GCA including jaw claudication, visual field defect and heavy headed feeling. Corticosteroid therapy resulted in a trend toward improvement in the inflammatory response and then she first recognized that she might have experienced slight dull headache before treatment of GCA. This was probably because this patient had large-vessel GCA, which produces a few symptoms in the head and neck, and because she had Alzheimer's disease and could not accurately describe her symptoms. Our experience suggests the usefulness of FDG-PET for the diagnosis of GCA, particularly in elderly patients without typical symptoms. Geriatr Gerontol Int 2011; 11: 114-118.

    WILEY-BLACKWELL PUBLISHING, INC, Jan. 2011, GERIATRICS & GERONTOLOGY INTERNATIONAL, 11 (1), 114 - 118, English

    [Refereed]

    Scientific journal

  • Hiroshi Yoshino, Yasuyo Okumachi, Taichi Akisaki, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Hozuka Akita

    A 62-year-old man was admitted to our hospital because of melena. On admission physical examination revealed that he had typical features of Noonan syndrome (NS). Investigation via upper endoscopy with the single balloon demonstrated oozing from the small intestine. Bleeding sometimes occurs in patients with NS. We speculated that coagulation defects or vascular malformations might have been present at the first visit in this case. However, coagulation function was normal. By upper endoscopy with the single balloon we clearly revealed the angioectasia in the small intestine. This case documents the first association among NS, aortic regurgitation and angioectasia in the small intestine.

    JAPAN SOC INTERNAL MEDICINE, 2011, INTERNAL MEDICINE, 50 (21), 2611 - 2613, English

    [Refereed]

    Scientific journal

  • 1型糖尿病の経過中に食道アカラシアを合併した多腺性自己免疫症候群の一例

    Yasuda Hisafumi, Hara Kenta

    Dec. 2010, 糖尿病, 53巻, 12号, pp. 829-833, Japanese

    [Refereed]

    Scientific journal

  • 膵腎同時移植後に肺クリプトコッカス症を発症した1型糖尿病の1例

    Yasuda Hisafumi, Hara Kenta

    Aug. 2010, 糖尿病, 53巻, 8号, pp. 607-612, Japanese

    [Refereed]

    Scientific journal

  • Takashi Arai, Hiroaki Moriyama, Mami Shimizu, Hirotomo Sasaki, Minoru Kishi, Yasuyo Okumachi, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    Antigen-specific immunotherapy is expected to be an ideal strategy for treating type 1 diabetes (T1D). We investigated the therapeutic efficacy of a peptide in the leader sequence of preproinsulin, which was selected because of its binding affinity to the MHC I-A(g7) molecule. Preproinsulin-1 L7-24 peptide (L7-24) emulsified in Freund's incomplete adjuvant was administered subcutaneously to NOD mice. Administration of L7-24 increased the proportion of regulatory T cells in the spleen. Splenocytes of NOD mice immunized with this peptide secreted IL-4 and IL-10 in response to L7-24. This peptide also significantly prevented the development of diabetes and cured some newly diabetic NOD mice without recurrence. L7-24 peptide, which has a high affinity for pockets of I-A(g7), induced regulatory T cells and showed therapeutic effects. This peptide may provide a new approach for developing antigen-specific immunotherapy for autoimmune diabetes. (C) 2010 Elsevier Inc. All rights reserved.

    ACADEMIC PRESS INC ELSEVIER SCIENCE, Jul. 2010, CLINICAL IMMUNOLOGY, 136 (1), 74 - 82, English

    [Refereed]

    Scientific journal

  • Minoru Kishi, Hisafumi Yasuda, Yasuhisa Abe, Hirotomo Sasaki, Mami Shimizu, Takashi Arai, Yasuyo Okumachi, Hiroaki Moriyama, Kenta Hara, Koichi Yokono, Masao Nagata

    Antigen-specific regulatory CD4(+) T cells have been described but there are few reports on regulatory CD8(+) T cells. We generated islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-specific regulatory CD8(+) T cells from 8.3-NOD transgenic mice. CD8(+) T cells from 8.3-NOD splenocytes were cultured with IGRP, splenic dendritic cells (SpDCs), TGF-beta, and all-trans retinoic acid (ATRA) for 5 days. CD8(+). T cells cultured with either IGRP alone or IGRP and SpDCs in the absence of TGF-beta and ATRA had low Foxp3(+) expression (1.7 +/- 0.9% and 3.2 +/- 4.5%, respectively). In contrast, CD8(+) T cells induced by exposure to IGRP, SpDCs, TGF-beta, and ATRA showed the highest expression of Foxp3(+) in IGRP-reactive CDS+ T cells (36.1 +/- 10.6%), which was approximately 40-fold increase compared with that before induction culture. CD25 expression on CD8(+) T cells cultured with IGRP, SpDCs, TGF-beta, and ATRA was only 7.42%, whereas CD103 expression was greater than 90%. These CD8(+) T cells suppressed the proliferation of diabetogenic CD8(+) T cells from 8.3-NOD splenocytes in vitro and completely prevented diabetes onset in NOD-scid mice in cotransfer experiments with diabetogenic splenocytes from NOD mice in vivo. Here we show that exposure to ATRA and TGF-beta induces CD8(+)Foxp3(+) T cells ex vivo, which suppress diabetogenic T cells in vitro and in vivo. (C) 2010 Elsevier Inc. All rights reserved.

    ACADEMIC PRESS INC ELSEVIER SCIENCE, Mar. 2010, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 394 (1), 228 - 232, English

    [Refereed]

    Scientific journal

  • BIGUANIDE, BUT NOT THIAZOLIDINEDIONE, IMPROVED INSULIN RESISTANCE IN WERNER SYNDROME

    Hisafumi Yasuda, Masao Nagata, Kenta Hara, Hiroaki Moriyama, Koichi Yokono

    WILEY-BLACKWELL PUBLISHING, INC, Jan. 2010, JOURNAL OF THE AMERICAN GERIATRICS SOCIETY, 58 (1), 181 - 182, English

    [Refereed]

    Scientific journal

  • 脂質異常症治療薬の投与法

    Yasuda Hisafumi

    Dec. 2009, 日本医事新報, 巻, 4470号, pp. 74-76, Japanese

    Scientific journal

  • Suirin Hamada, Kenta Hara, Takeshi Hamada, Hisafumi Yasuda, Hiroaki Moriyama, Rika Nakayama, Masao Nagata, Koichi Yokono

    OBJECTIVE-Components of insulin/IGF-1 receptor-mediated signaling pathways in pancreatic beta-cells have been implicated in the development of diabetes, in part through the regulation of beta-cell mass. the protein Ras homolog in vivo. Studies in vitro have shown that, enriched in brain (Rheb) plays a key role as a positive upstream regulator of the mammalian target of rapamycin complex 1 (mTORC1) pathway in integrating inputs from nutrients and growth factors for cell growth. Our objective was to investigate the role of the mTORC1 pathway in the regulation of beta-cell mass in vivo. RESEARCH DESIGN AND METHODS-We generated transgenic mice that, overexpress Rheb in beta-cells. We examined the activation of the mTORC1 pathway and its effects on beta-cell mass, on glucose metabolism, and on protection against, hyperglycemia. RESULTS-Immunoblots of islet extracts revealed that the phosphorylation levels of ribosomal protein S6 and eukaryotic initiation factor 4E binding protein 1, downstream effectors for mTORC1, were upregulated in transgenic beta-cells. Immunostaining of the pancreatic sections with anti-phospho-S6 antibody confirmed upregulation of the mTORC1 pathway in beta-cells in vivo. The mice showed improved glucose tolerance with higher insulin secretion. This arose from increased beta-cell mass accompanied by increased cell size. The mice also exhibited resistance to hyperglycemia induced by streptozotocin and obesity. CONCLUSIONS-Activation of the mTORC1 pathway by Rheb led to increased beta-cell mass in this mouse model without producing obvious unfavorable effects, giving a potential approach for the treatment of beta-cell failure and diabetes. Diabetes 58:1321-1332, 2009

    AMER DIABETES ASSOC, Jun. 2009, DIABETES, 58 (6), 1321 - 1332, English

    [Refereed]

    Scientific journal

  • Hisafumi Yasuda, Zhenzi Jin, Maki Nakayama, Katsumi Yamada, Minoru Kishi, Yasuyo Okumachi, Takashi Arai, Hiroaki Moriyama, Koichi Yokono, Masao Nagata

    Type 1 diabetes (T1D) is caused mostly by autoimmune destruction of pancreatic p-cells, the precise mechanism of which remains unclear. Two major effector mechanisms have been proposed: direct cell-mediated and indirect cytokine-mediated cytotoxicity. Cytokine-mediated p-cell destruction is presumed mainly caused by NO production. To evaluate the role of iNOS expression in T1D, this study used a novel iNOS inhibitor ONO-1714. ONO-1714 significantly reduced cytokine-mediated cytotoxicity and NO production in both MIN6N9a cells and C57BL/6 islets in the presence of IL-1 beta, TNF-alpha, and IFN-gamma. To evaluate whether NO contributes to diabetes progression in vivo, ONO-1714 was administered to four different mouse models of autoimmune diabetes: multiple low-dose STZ (MLDS)-induced C57BL/6, CY-induced, adoptive transfer and spontaneous NOD diabetes. Exposure to STZ in vitro induced NO production in MIN6N9a cells and C57BL/6 islets, and in vivo injection of ONO-1714 to MLDS-treated mice significantly reduced hyperglycemia and interestingly, led to complete suppression of cellular infiltration of pancreatic islets. in contrast, when ONO-1714 was injected into spontaneous NOD mice and CY-induced and adoptive transfer models of NOD diabetes, overt diabetes could not be inhibited in these models. These findings suggest that NO-mediated cytotoxicity significantly contributes to MLDS-induced diabetes but not to NOD diabetes. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

    ELSEVIER IRELAND LTD, Feb. 2009, DIABETES RESEARCH AND CLINICAL PRACTICE, 83 (2), 200 - 207, English

    [Refereed]

    Scientific journal

  • Yasuyo Okumachi, Hiroaki Moriyama, Mami Kameno, Takashi Arai, Minoru Kishi, Midori Kurohara, Katsumi Yamada, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    InsulinB:9-23 peptide (insB:9-23) reactive T cells has been reported as crucial for type 1 diabetes. In this study, experimental autoimmune diabetes (EAD) mice, which subcutaneous immunization of ins1 or 2B:9-23 induced autoimmune diabetes in F1(B7.1B6 x BALB/c), was investigated for antigen specific therapy to delete pathogenic T cells. Intravenous injection of ins1 OF 213:9-23 significantly delayed the development of diabetes on the corresponding peptide-induced FAD (ins1EAD or ins2EAD) concomitant with reduced insulitis and insulin autoantibodies expression. Population of Foxp3(+) CD4(+) T cell was unchanged whereas the level of anti-insB:9-23 specific IgG(2a) but not IgG(1) were specifically decreased, Suggesting reduction of pathogenic insB:9-23 reactive T cells. Most interestingly, intravenous administration of ins2B:9-23, whose amino acid sequence had one amino acid difference at position 9 delayed the development of diabetes in both ins1EAD and ins2EAD whereas ins1B:9-23 administration delayed diabetes in the ins1EAD but not ins2EAD, suggesting that one amino acid difference gives critical influence on the effect of intravenous injection of antigenic peptide for type 1 diabetes. (C) 2008 Elsevier Inc. All rights reserved.

    ACADEMIC PRESS INC ELSEVIER SCIENCE, Sep. 2008, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 374 (3), 581 - 586, English

    [Refereed]

    Scientific journal

  • Muneaki Sakata, Hisafumi Yasuda, Hiroaki Moriyama, Katsumi Yamada, Reiko Kotani, Midori Kurohara, Yasuyo Okumachi, Minoru Kishi, Takashi Arai, Kenta Hara, Hirofumi Hamada, Koichi Yokono, Masao Nagata

    Pancreatic islet transplantation has the potential to maintain normoglycemia. in patients with established type 1 diabetes, thereby obviating the need for frequent insulin injections. our previous study showed that recombinant IL-12p40-producing islets prevented the recurrence of NOD diabetes. First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice. The immunomodulating molecules produced by these adenovirus-transfected islets in vitro were 74 +/- 19 ng, 50 +/- 4 ng, 821 +/- 31 ng, and 77 +/- 18 ng/100 islets, respectively. Transplantation of IL-12p40, TNF-alpha, and CTLA4-Ig but not TGF-beta-secreting islets displayed enhanced survival and delayed diabetes recurrence in recent-onset diabetic recipients. IL-12p40-producing islet grafts most powerfully prevented recurrent diabetes in NOD mice. in addition, local production of TNF-alpha and CTLA4-Ig significantly prolonged islet graft survival. in second series of experiment, these manipulated islets were transplanted under the renal capsule of 10-week-old NOD recipients and were also transplanted subcutaneously into 2-week-old NOD recipients. Transplantation of these islets into 2- or 10-week-old pre-diabetic mice failed to protect them from developing diabetes; in fact, transplantation of Ad.TNF-alpha-transfected islets into 2-week-old mice actually accelerated diabetes onset. Taken together, this approach was ineffectual as a prophylactic protocol. In conclusion, this study showed comparisons of the immunomodulating effects of 4 different adenoviral vectors in the same transplantation model and local production of IL-12p40, TNF-alpha and CTLA4-Ig significantly prevented recurrent diabetes in NOD mice. (c) 2008 Elsevier Ireland Ltd. All rights reserved.

    ELSEVIER IRELAND LTD, Jun. 2008, DIABETES RESEARCH AND CLINICAL PRACTICE, 80 (3), 352 - 359, English

    [Refereed]

    Scientific journal

  • Low-dose warfarin functions as an immunomodulator to prevent cyclophosphamide-induced NOD diabetes

    Yasuda H, Hara K, Yokono K

    May 2008, Kobe J Med Sci

    [Refereed]

    Scientific journal

    Link to Kobe Univ. Repository (Kernel)
  • Regulation of hypoxia-inducible factor 1 by glucose availability under hypoxic conditions

    Hara K, Yasuda H, Nagata M, Yokono K

    Feb. 2008, Kobe J Med Sci

    [Refereed]

    Scientific journal

    Link to Kobe Univ. Repository (Kernel)

  • Katsumi Yamada, Hiroaki Moriyama, Yasuyo Okumachi, Takashi Arai, Mami Kameno, Minoru Kishi, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    Insulin has been reported as a major autoantigen in both human and murine type 1 diabetes (T1D). Insulin1-knockout NOD mice with only insulin2 are protected against the development of autoimmune diabetes, suggesting that insulin1 has strong immunogenicity and insulin2 has weak immunogenicity or a possible protective role in the pathogenesis of type 1 diabetes. In this study, we have developed fiber-mutant adenovirus vectors that express murine proinsulin1 or proinsulin2 (named Ad.Pinsl-RGD/Ad.Pins2-RGD) and administered those virus vectors to the NOD mouse to evaluate modulation of autoimmune responses. The intravenous administration of either Ad.Pinsl-RGD or Ad.Pins2-RGD at 3 and 5 weeks of age strongly suppressed the development of overt diabetes, accompanied by a significant reduction of insulin autoantibody (IAA), and suppression of disease was similar between administration of Ad.Pinsl-RGD and that of Ad.Pins2-RGD. Our study suggests that systemic administration of fiber-mutant adenovirus vectors, which induce transient expression of proinsulin, may be applicable to a gene therapy inducing tolerance to insulin.

    BLACKWELL PUBLISHING, 2008, Immunology of Diabetes V: From Bench to Bedside, 1150, 183 - 186, English

    [Refereed]

    Scientific journal

  • Hiroaki Moriyama, Reiko Kotani, Atsumi Katsuta, Mami Kameno, Takashi Arai, Yasuyo Okumachi, Minoru Kishi, Katsumi Yamada, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    CD4(+)CD25(+) T cells (Tregs) play a critical role in maintaining dominant peripheral tolerance, and pathogenic autoreactive T cells may be frequent in the CD25-negative fraction of peripheral blood mononuclear cells (PBMCs) from patients with autoimmune disease. We therefore investigated whether T cell autoimmune responses to recombinant GAD65 can be detected by the use of ELISPOT assay in the CD25-negative fraction of PMBCs from Japanese type 1 diabetes (T1D) patients. The frequency of CD4(+)CD25(+) T cells was not different among patients with newly developed T1D, established T1D, and healthy controls. The CD25 positive cell-depleted fraction was obtained by negative selection with antihuman CD25 magnetic beads, reducing the number of CD4(+)CD25(+) T cells from 4-5% to less than 1%. In whole PBMC fraction, there was a significant elevation of IFN-gamma spots in PBMCs from recently diagnosed patients with T1D (P < 0.05), whereas the number of IFN-gamma spots from patients with established T1D was not significant. In the CD25-negative fraction, unlike whole PBMCs, we observed the significant IFN-gamma spots to GAD65 in the fraction from patients with established T1D (P < 0.05), but not in those with recently diagnosed disease. The phenomena were not observed for IL-4 spots. Our data suggest a possible role of Tregs maintaining dominant peripheral tolerance in T1D and application of further improved T cell assay detecting autoimmunity even in established T1D.

    BLACKWELL PUBLISHING, 2008, Immunology of Diabetes V: From Bench to Bedside, 1150, 278 - 281, English

    [Refereed]

    Scientific journal

  • Hiroaki Moriyama, Masao Nagata, Takashi Arai, Yasuyo Okumachi, Katsumi Yamada, Reiko Kotani, Hisafumi Yasuda, Kenta Hara, Koich Yokono

    Rodents have two functional preproinsulin genes named insulin I and insulin 2 on different chromosome and have two amino acid differences in insulin B chain. We have established insulin I or insulin 2 knockout (KO) non-obese diabetic (NOD) colonies in the animal institute of Kobe University and evaluated anti-insulin autoimmunity. Similar to the previous report, insulin I-KO provides strong protection from insulitis (islet-infiltration of mononuclear cells) and diabetes, whereas the insulin 2-KO markedly accelerated insulitis and development of diabetes even at further backcross breeding with NOD/Shi/Kbe mice (P < 0.0001). Expression of serum anti-insulin autoantibodies (IAA) was enhanced in insulin 2-KO mice at a time between 10 and 15 weeks of age (P < 0.005) while the expression of insulin 1-KO NOD mice was rather reduced. Furthermore, T cell reactivity in splenocytes of insulin 2-KO, NOD mice to insulin 1 B:9-23 peptide was increased (P < 0.05), suggesting that expanding insulin-reactive T cells may contribute to the acceleration of diabetes in insulin 2-KO mice. Based on those observations, we hypothesize that insulin I is a crucial T cell antigen in murine autoinumme diabetes and modification of anti-insulin autoimmunity can be applicable to antigen-based therapy for human type I diabetic patients. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

    ELSEVIER IRELAND LTD, Sep. 2007, DIABETES RESEARCH AND CLINICAL PRACTICE, 77, S155 - S160, English

    [Refereed]

    Scientific journal

  • Masao Nagata, Hiroaki Moriyama, Reiko Kotani, Hisafumi Yasuda, Minoru Kishi, Midori Kurohara, Kenta Hara, Koichi Yokono

    'Fulminant diabetes' has been recognized as a super-acute onset and non-autoimmune type 1 diabetes. To evaluate autoimmunity against pancreatic P cell in fulminant diabetes, ELISPOT assay was applied to the peripheral blood of these patients. In our ELISPOT system, GAD65-reactive and insulin B9-23-reactive IFN-gamma spots were detected in 46.3 and 26.0% of autoantibody-positive type 1 diabetes. Also, in fulminant type 1 diabetic patients, IFN-gamma spots in response to GAD65 and insulin B9-23 peptide were detected in 69.2 and 25.0%, respectively. These results suggest that anti-beta cell autoimmunity contributes to develop fulminant type 1 diabetes. Fulminant type 1 diabetes is known to have IDDM-resistant HLA DR2 with similar frequency of non-T1D subjects. In a mouse model, when islet-reactive CD8 cells are transferred to young NOD mice, the recipients develop overt diabetes within 1 week with massive insulitis. In (NOD x Balb/c) F1 mice, which hold idd-resistant genes, transfer of islet-reactive CD8 cells induced diabetes to 60% F1 recipients within 1 week with the later disappearance of insulitis. This mouse model shows very similar feathers to fulminant type 1 diabetes; idd-resistant HLA and no insulitis. These results implicated that once anti-islet immunity is optimally activated, subjects with partially resistant alleles could become overt diabetes. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

    ELSEVIER IRELAND LTD, Sep. 2007, DIABETES RESEARCH AND CLINICAL PRACTICE, 77, S99 - S103, English

    [Refereed]

    Scientific journal

  • Katsumi Yamada, Hiroaki Moriyama, Hisafumi Yasuda, Kenta Hara, Yoshimasa Maniwa, Hirofumi Hamada, Koichi Yokono, Masao Nagata

    A replication-competent adenoviral vector deficient for expression of the early E1B55K protein has been applied in clinical studies. The vector, however, was not fully effective for the treatment of human cancer. In this study, the E1A gene (which encodes an Rb-binding domain protein) of the adenoviral vector AxE1AdB was further engineered with a point mutation designed to abolish binding to Rb protein (pRb) and arrest the cell cycle (AxdAdB-3). The difference in the cytotoxicity of these vectors in two cancer cell lines was observed in association with differences in replication, infection efficiency, and expression levels of adenovirus receptors. Relative to the parent vector (AxE1AdB), which worked in a manner similar to ONYX-015, AxdAdB-3 with the mutated pRb-binding motif demonstrated increased cytotoxicity against p53-mutant human esophageal cancer cell lines EC-GI-10 and T. Tn. AxdAdB-3 showed a greater oncolytic effect than AxE1AdB in vivo despite almost the same replication efficiency in vitro. Unexpectedly, cell cycle arrest in AxdAdB-3-infected cells was less efficient than that in cell lines infected with AxE1AdB. However, AxdAdB-3 strongly reduced NF-kappa B activity and thereby enhanced apoptosis more than AxE1AdB did. These data demonstrate that the Rb-binding domain of E1A can regulate NF-kappa B activity and that modifications to this domain may lead to advances in gene therapies for the treatment of human cancers.

    MARY ANN LIEBERT INC, May 2007, HUMAN GENE THERAPY, 18 (5), 389 - 400, English

    [Refereed]

    Scientific journal

  • N. Yamamoto, E. Sasaki, K. Goda, K. Nagata, H. Tanaka, J. Terasaki, H. Yasuda, A. Imagawa, T. Hanafusa

    The purpose of this study was to ascertain whether abdominal compression with an inflatable abdominal band, a device we developed, improved post-dialytic orthostatic hypotension (OH) in hemodialysis (HD) patients. Twenty-five chronic HD patients with intractable post-dialytic OH were recruited. Post-HD changes in systolic blood pressure (Delta SBP) in the supine and standing positions were compared in the patients, measured with or without the use of the band. The study showed Delta SBP after HD without the band was significantly greater than that measured before HD (-36.1 +/- 18.2 vs -13.1 +/- 16.8mm Hg; P < 0.0001). Delta SBP after HD with the band was reduced significantly in comparison to Delta SBP after HD without the band (-19.4 +/- 21.2 vs -36.1 +/- 18.2mm Hg; P < 0.002). Use of the band did not cause an elevation in SBP in the supine position (149.0 +/- 29.6 vs 155.4 +/- 25.7mm Hg); however, it did increase SBP upon standing (129.6 +/- 27.3 vs 117.2 +/- 22.6mm Hg; P < 0.05). Eight patients in whom an increase in SBP of 25mm Hg or more was achieved with the band were classified as responders. Ejection fraction was significantly higher (76.4 +/- 11.1 vs 61.9 +/- 13.6%; P < 0.02) and atrial natriuretic peptide concentration significantly lower (27.9 +/- 22.0 vs 68.9 +/- 47.5 pg/ml; P < 0.02) in responders than in non-responders. We conclude that the abdominal band was effective for overcoming post-dialytic OH, without elevating supine SBP in some patients.

    NATURE PUBLISHING GROUP, Nov. 2006, KIDNEY INTERNATIONAL, 70 (10), 1793 - 1800, English

    [Refereed]

    Scientific journal

  • CW Danawati, M Nagata, H Moriyama, K Hara, H Yasuda, M Nakayama, R Kotani, K Yamada, A Sakata, M Kurohara, P Wiyono, H Asdie, M Sakaue, H Taniguchi, K Yokono

    Background Peroxisome proliferators-activated receptor gamma (PPAR gamma) is a nuclear hormone receptor that serves as a master regulator of adipocytes-specific genes contributing to adipocytes differentiation, susceptibility to obesity, and insulin sensitivity. The substitution of proline to alanine at codon 12 of the PPAR gamma 2 gene (Pro12Ala polymorphism) is most frequently identified and the associations with diabetes, obesity, and other clinical parameters have been reported and discussed in several ethnic groups. Among native Javanese ethnicity, however, there is no report about this polymorphism. Aims and methods Aims of this study were to estimate the allele frequency of the Pro12Ala polymorphism of PPAR gamma 2 gene among native Javanese in Indonesia and to investigate the relationship between this polymorphism and obesity or diabetes. This study included 540 native Javanese subjects consisting of 337 diabetic patients and 203 normal glucose tolerance subjects. Both groups included totally 160 obese subjects (body mass index >= 25 kg/m(2)). PCR-restriction fragment length polymorphism was used for the genotype determination. Results The allele frequency of Pro12Ala polymorphism in PPAR gamma 2 gene among native Javanese is lower than that in other ethnic groups. No association is seen between the Pro12Ala and diabetes (0.01 vs 0.017%, p = 0.404), a trend of the higher BMI was observed in Pro12Ala carriers in nondiabetic subjects, although this association is limited by small numbers. Conclusion In this study, no association is seen between the Pro12Ala polymorphism in PPAR gamma 2 gene and diabetes; a weak association with obesity is seen. Copyright (C) 2005 John Wiley & Sons, Ltd.

    JOHN WILEY & SONS LTD, Sep. 2005, DIABETES-METABOLISM RESEARCH AND REVIEWS, 21 (5), 465 - 469, English

    [Refereed]

    Scientific journal

  • R Kotani, M Nagata, A Imagawa, H Moriyama, H Yasuda, J Miyagawa, T Hanafusa, K Yokono

    Aims/hypothesis. Fulminant Type 1 diabetes is a novel subtype of Type 1 diabetes that involves the abrupt onset of insulin-deficient hyperglycaemia. This subtype appears to be non-autoimmune because of the absence of diabetes-related autoantibodies in the serum, and of insulitis in pancreatic biopsy specimens. The pathogenesis of the disease is still unknown. In this study, we investigated whether T cell autoimmune responses are involved in fulminant Type 1 diabetes. Methods. Cellular immune responses to beta cell autoantigens were studied by enzyme-linked immunospot (ELISPOT) assay in 13 fulminant Type 1 diabetic patients and 49 autoantibody-positive autoimmune Type 1 diabetic patients. Results were compared with those of 18 Type 2 diabetic patients, six secondary diabetic patients (diabetes due to chronic pancreatitis) and 35 healthy controls. Results. Nine of 13 (69.2%) GAD-reactive Th1 cells, and three of 12 (25%) insulin-B9-23-reactive Th1 cells were identified in fulminant Type 1 diabetic patients by ELISPOT, as in autoantibody-positive Type 1 diabetic patients. Four fulminant Type 1 diabetic patients possessed the highly diabetes-resistant allele DR2, three of whom had GAD-reactive Th1 cells in the periphery. Conclusions/interpretation. Peripheral immune reaction was observed in 69.2% of fulminant Type 1 diabetic patients, indicating that autoreactive T cells might contribute, at least in part, to the development of fulminant Type 1 diabetes.

    SPRINGER, Jul. 2004, DIABETOLOGIA, 47 (7), 1285 - 1291, English

    [Refereed]

    Scientific journal

  • Critical roles of CD30/CD30L interactions in murine autoimmune diabetes

    S Chakrabarty, M Nagata, H Yasuda, L Wen, M Nakayama, SA Chowdhury, K Yamada, Z Jin, R Kotani, H Moriyama, O Shimozato, H Yagita, K Yokono

    CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. A genetic study has also suggested a possible implication of CD30 in spontaneous autoimmune diabetes in NOD mice. In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4(+) or CD8(+) T cells in the spleen and pancreatic lymph node of younger NOD mice. In addition, islet-specific CD4(+) or CD8(+) T cell lines expressed CD30 and CD30L. Administration of a neutralizing anti-CD30L monoclonal antibody (mAb) from 2 to 10 week of age completely suppressed the development of spontaneous diabetes in NOD mice. In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4(+) or CD8(+) T cell lines into NOD-SCID trice. Furthermore, anti-CD30L mAb inhibited T cell proliferation in response to islet antigens. These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice.

    BLACKWELL PUBLISHING LTD, Sep. 2003, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 133 (3), 318 - 325, English

    [Refereed]

    Scientific journal

  • Detection of GAD65-reactive T-cells in type 1 diabetes by immunoglobulin-free ELISPOT assays

    R Kotani, M Nagata, H Moriyama, M Nakayama, K Yamada, SA Chowdhury, S Chakrabarty, ZZ Jin, H Yasuda, K Yokono

    OBJECTIVE - To investigate the prevalence of beta-cell autoantigen-reactive peripheral T-cells in type I diabetes, we developed an immunoglobulin-free enzyme-linked immunospot (ELISPOT) assay and assessed its usefulness for diagnosing this disease. RESEARCH DESIGN AND METHODS - Cellular immune responses to beta-cell autoantigens were studied both by immunoglobulin-free proliferation assays and ELISPOT assays in 33 patients with type 1 diabetes and 15 patients with type 2 diabetes, compared with 23 healthy control subjects. Autoantibodies against GAD65 and IA-2 were measured by radioimmunoassay. RESULTS - Significant proliferative responses to GAD65 were observed in 10 of 31 (32.3%) type I diabetic patients (P < 0.05); whereas GAD65-reactive gamma-interferon (IFN-gamma)-secreting cells were detected in 22 of 33 patients (66.7%) by ELISPOT assay (P < 0.001). Of patients negative for both GAD65 and IA-2, five of six (83.3%) showed IFN-gamma positivity in ELISPOT and two of five (40.0%) showed significant proliferation against GAD65. CONCLUSIONS - Using a newly developed ELISPOT assay, GAD-reactive T-helper I cells in PBMC of type 1 diabetic patients could be identified at a higher frequency than by the proliferation assay. Therefore, the immunoglobulin-free ELISPOT assay is an excellent tool for detecting T-cell reactivity to autoantigens with greater specificity and, in combination with beta-cell autoantibody determination, will improve the diagnosis of type I diabetes.

    AMER DIABETES ASSOC, Aug. 2002, DIABETES CARE, 25 (8), 1390 - 1397, English

    [Refereed]

    Scientific journal

  • Fas/Fas ligand interactions play an essential role in the initiation of murine autoimmune diabetes

    M Nakayama, M Nagata, H Yasuda, K Arisawa, R Kotani, K Yamada, SA Chowdhury, S Chakrabarty, ZZ Jin, H Yagita, K Yokono, M Kasuga

    Apoptosis via Fas/Fas ligand (FasL) interactions has been proposed to be a major T-cell-mediated effector mechanism in autoimmune diabetes. To elucidate the role of Fas/FasL interactions in NOD diabetes, the effects of neutralizing anti-FasL antibody on autoimmune responses were evaluated. Islet-specific CD8(+) and CD4(+) T-cells expressed FasL upon activation and mediated FasL-dependent cytotoxicity against Fas-expressing target cells in vitro, although their cytotoxicity against islet cells was not blocked by anti-FasL antibody. Moreover, administration of anti-FasL antibody failed to inhibit diabetes in vivo in the CD8(+) T-cell adoptive transfer model. On the other hand, blockade of Fas/FasL interactions significantly inhibited CD4(+) T-cell-dependent diabetes in adoptive transfer models. These results suggest a substantial contribution of Fas/ FasL interactions to CD4(+), but not CD8(+), T-cell-mediated destruction of pancreatic beta-cells. When anti-FasL antibody was administered to NOD mice between 5 and 15 weeks of age, the onset of diabetes was slightly delayed but the incidence was not decreased. However, administration of anti-FasL antibody at 2-4 weeks of age completely prevented insulitis and diabetes. These results suggest that Fas/FasL interactions contribute to CD4(+) T-cell-mediated beta-cell destruction and play an essential role in the initiation of autoimmune NOD diabetes.

    AMER DIABETES ASSOC, May 2002, DIABETES, 51 (5), 1391 - 1397, English

    [Refereed]

    Scientific journal

  • Human insulin analog insulin aspart does not cause insulin allergy

    H Yasuda, M Nagata, H Moriyama, K Fujihira, R Kotani, K Yamada, H Ueda, K Yokono

    AMER DIABETES ASSOC, Nov. 2001, DIABETES CARE, 24 (11), 2008 - 2009, English

    [Refereed]

    Scientific journal

  • Treatment with human analog (Gly(A21), Arg(B31), Arg(B32)) insulin glargine (HOE901) resolves a generalized allergy to human insulin in type 1 diabetes

    H Moriyama, M Nagata, K Fujihira, K Yamada, SA Chowdhury, S Chakrabarty, ZZ Jin, H Yasuda, H Ueda, K Yokono

    AMER DIABETES ASSOC, Feb. 2001, DIABETES CARE, 24 (2), 411 - 412, English

    [Refereed]

    Scientific journal

  • Suppression and acceleration of autoimmune diabetes by neutralization of endogenous interleukin-12 in NOD mice

    K Fujihira, M Nagata, H Moriyama, H Yasuda, K Arisawa, M Nakayama, S Maeda, M Kasuga, K Okumura, H Yagita, K Yokono

    A corpus of evidence suggests that T-helper type 1 (Th1)-dependent cellular immunity plays a pivotal role in the pathogenesis of antoimmune diabetes, This study was intended to find ways to prevent the development of NOD diabetes using a neutralizing anti-interleukin (IL)-12 antibody (C17.8) that inhibits Th1 cell differentiation, When C17.8 was administered from 5 to 30 weeks of age, NOD mice exhibited suppression of both insulitis and diabetes. However, when C17.8 administration ceased at 15 weeks of age, 8 of 13 recipients showed diabetes at 30 weeks of age. These results suggest that IL-12 plays an important role not only in the development of effector cells but also in their activation. In contrast, when C17.8 was injected into 2-week-old female NOD mice for 6 consecutive days, all 16 recipients showed diabetes at 30 weeks of age, whereas 12 of 20 control mice became diabetic. This result suggests that depletion of endogenous IL-12 at a young age results in the enhancement of diabetes. Flow cytometric analysis indicated that activated memory T-cells were present in higher numbers after C17.8 treatment. Transfer of spleen cells from 15-meek-old C17.8-treated NOD mice to NOD-scid mice resulted in an earlier onset and a higher incidence of diabetes. Furthermore, administration of C17.8 to 2-meek-old NOD mice also resulted in a much earlier onset of diabetes. These results suggest that short-term treatment with anti-IL-12 antibody prohibits IL-2 production at a young age, which may influence the expansion and apoptosis of pathogenic T-cells, resulting in the acceleration of antoimmune diabetes.

    AMER DIABETES ASSOC, Dec. 2000, DIABETES, 49 (12), 1998 - 2006, English

    [Refereed]

    Scientific journal

  • Role of fas/fasL interaction in the NOD autoimmune diabetes

    M Nakayama, M Nagata, H Yasuda, K Arisawa, K Fujihira, H Yagita, K Okumura, K Yokono, M Kasuga

    Diabetogenic T cells in the NOD mice can destroy target cells by Fas/FasL interaction in vitro. However, diabetic transfer by diabetogenic T cells could not inhibited by anti-FasL antibody. On the other hand, administration of anti-FasL :an completely abolish spontaneous diabetes. These antibody in the young age can completely abolish spontaneous diabetes. These results suggest that Fas/FasL interaction is indespensable for the initiation of results suggest that Fas autoimmune diabetes rather than the effector phase.

    ELSEVIER SCIENCE BV, 2000, DIABETES MELLITUS: RECENT ADVANCES FOR THE 21ST CENTURY, 1209, 91 - 94, English

    [Refereed]

    International conference proceedings

  • Local expression of immunoregulatory IL-12p40 gene prolonged syngeneic islet graft survival in diabetic NOD mice

    H Yasuda, M Nagata, K Arisawa, R Yoshida, K Fujihira, N Okamoto, H Moriyama, M Miki, Saito, I, H Hamada, K Yokono, N Kasuga

    Local production of immunosuppressive cytokines will be one of the most suitable therapeutic strategies against organ-specific autoimmune diabetes. To establish such a new therapy, we constructed recombinant adenoviral vectors with inserted mIL-12p40 (Ad.IL-12p40) and mIL-10 (Ad.IL-10). Sufficient amounts of IL-12p40 and IL-10 were secreted by relevant adenovirus-transfected nonobese diabetic (NOD) islets. Shortly after transfection, 400 NOD islets transfected with Ad.IL-12p40 or Ad.IL-10 were transplanted under the renal capsule of a newly diabetic NOD mouse. NOD mice with IL-12p40-producing islet grafts kept normoglycemia in all of 14 grafted mice for over 4 wk after transplantation. In contrast, NOD mice with IL-10-producing islet grafts became diabetic in all of six grafted mice within 2 wk after transplantation. Reverse transcription-PCR analysis revealed that local production of IL-12p40 led to the decrease of interferon-gamma and the augmentation of transforming growth factor-p at the graft site. These results suggest that IL-12 plays an important role in the destruction of islet cells at the inflamed site of autoimmunity. Such a local blockade of IL-12 would be a useful gene therapy for human autoimmune diabetes.

    ROCKEFELLER UNIV PRESS, Nov. 1998, JOURNAL OF CLINICAL INVESTIGATION, 102 (10), 1807 - 1814, English

    [Refereed]

    Scientific journal

  • Administration of IL-4 prevents autoimmune diabetes but enhances pancreatic insulitis in NOD mice

    Y Tominaga, M Nagata, H Yasuda, N Okamoto, K Arisawa, H Moriyama, M Miki, K Yokono, M Kasuga

    The present study demonstrated that the administration of recombinant interleukin-4 (rIL-4) prevented overt diabetes in nonobese diabetic (NOD) mice whose T cells produced relatively low amounts of IL-4. However, massive insulitis was observed in rIL-4-treated NOD mice. The flow cytometric analysis of islet-infiltrating T cells revealed that the number of CD45RB(low)CD4(+) T cells was significantly increased by in vivo administration of rIL-4. By measuring the cytokine production of splenic T cells after stimulation, it was shown that CD45RB(low)CD4(+) T cells predominantly produced IL-4 and IL-10 but produced less IL-2 and interferon-gamma (IFN-gamma). A semiquantitative reverse-transcriptase polymerase chain reaction assay revealed a higher expression of IL-4 and IL-10 mRNA and an apparent decrease in IFN-gamma mRNA in the islets of NOD mice which were administered rIL-4. These results suggested that autoreactive CD45RB(low)CD4(+) T helper 2 (Th2)-like cells which developed following rIL-4 administration were predominant in the infiltrate of the islets, and overt diabetes was prevented. On the other hand, when splenocytes from rIL-4-treated NOD mice were transferred to irradiated NOD recipients, along with splenocytes from diabetic NOD mice, all of the recipient mice became diabetic within 8 weeks after transfer. Considered together, a supplement of rIL-4 administered to NOD mice may protect against autoimmune diabetes by facilitating the development of Th2-like autoreactive T cells in the islets. (C) 1998 Academic Press.

    ACADEMIC PRESS INC, Feb. 1998, CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 86 (2), 209 - 218, English

    [Refereed]

    Scientific journal

  • Elevated plasma nitrate in patients with crush syndrome caused by the Kobe earthquake

    J Adachi, S Morita, H Yasuda, A Miwa, Y Ueno, M Asano, Y Tatsuno

    We investigated the nitric oxide profile in the plasma of ten healthy controls and 29 patients hurt by the Kobe Earthquake. The levels of nitrite (NO2-) and nitrate (NO3-) were measured simultaneously by high-performance liquid chromatography (HPLC) with UV detection using the Griess reaction after the reduction of nitrate to nitrite. Arginine consumed in food or diet-derived nitrite had no effect on the plasma nitrite and nitrate contents of the healthy volunteers. Plasma nitrate was elevated in the crush syndrome patients; whereas neither nitrite nor nitrate was increased in patients with normal renal function. This finding suggests increased nitric oxide synthesis, decreased excretion of nitric oxide in the crush syndrome or both. (C) 1998 Elsevier Science B.V.

    ELSEVIER SCIENCE BV, Jan. 1998, CLINICA CHIMICA ACTA, 269 (2), 137 - 145, English

    [Refereed]

    Scientific journal

  • CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice

    R Yoneda, K Yokono, M Nagata, Y Tominaga, H Moriyama, K Tsukamoto, M Miki, N Okamoto, H Yasuda, K Amano, M Kasuga

    A CD8 T-cell clone (YNK1.3) generated from acutely diabetic NOD mouse islets, showed proliferation and cytotoxicity when challenged with NOD and BALB/c islet cells and NOD-derived insulinoma cells. When 1-2 x 10(7) YNK1.3 cells were administered to 7-10-day-old NOD mice, the cells transferred overt diabetes very rapidly in each of the 16 recipients within 4 days of cell transfer. However, of 14 recipients receiving YNK 1.3 cells above 14 days of age none became diabetic. Fluorescent dye-labelled YNK1.3 cells extensively accumulated in the islets by 36 h after transfer in 7-day-old NOD recipients, while no significant insulitis was seen in 21-day-old recipients. Over half of NOD-scid recipients (5/9) rapidly became diabetic within 5 days after transfer of 1-2 x 10(7) YNK1.3 cells at 7 days of age, whereas only one of 12 recipients over 14 days of age became diabetic. Furthermore, YNK1.3 cells also transferred diabetes to H-2K(d)-matched very young BALB/c-scid and CB17-scid mice, but not to C57BL/6-scid mice. Thus, optimally activated islet-specific CD8 T-cell clones are able to rapidly transfer diabetes to NOD and MHC class I compatible scid mice when a large enough number is administered at 7 days of age. Administration of monoclonal antibodies against adhesion molecules involved in the trafficking of lymphocytes from the circulation into the inflammatory tissues, could not prevent the cellular infiltration of YNK1.3 cells into the islets in 7-day-old NOD recipients. The results indicate that islet cells in the mouse around 7 days of age are generally susceptible to cytotoxic CD8 T cells, suggesting, therefore, that CD8 T cells may play an important role in the initiation of autoimmune diabetes in NOD mice.

    SPRINGER VERLAG, Sep. 1997, DIABETOLOGIA, 40 (9), 1044 - 1052, English

    [Refereed]

    Scientific journal

MISC

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第7報)

    梶尾 裕, 中條 大輔, 安田 和基, 霜田 雅之, 春日 雅人, 今川 彰久, 池上 博司, 大澤 春彦, 阿比留 教生, 島田 朗, 長澤 幹, 及川 洋一, 安田 尚史, 粟田 卓也, 川崎 英二, 高橋 和眞, 小林 哲郎, 花房 俊昭, 岩橋 博見, 香月 健志, 福井 智康, 滝澤 壮一

    (一社)日本糖尿病学会, Apr. 2019, 糖尿病, 62 (Suppl.1), S - 219, Japanese

    Summary national conference

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第7報)

    梶尾 裕, 中條 大輔, 安田 和基, 霜田 雅之, 春日 雅人, 今川 彰久, 池上 博司, 大澤 春彦, 阿比留 教生, 島田 朗, 長澤 幹, 及川 洋一, 安田 尚史, 粟田 卓也, 川崎 英二, 高橋 和眞, 小林 哲郎, 花房 俊昭, 岩橋 博見, 香月 健志, 福井 智康, 滝澤 壮一

    (一社)日本糖尿病学会, Apr. 2019, 糖尿病, 62 (Suppl.1), S - 219, Japanese

  • 1型糖尿病研究の最前線 多様化する病態と診断上の課題 GAD抗体測定結果乖離と親和性 日本人1型糖尿病の成因、診断、病態、治療に関する調査研究委員会中間報告

    川崎 英二, 及川 洋一, 福井 智康, 今川 彰久, 中條 大輔, 梶尾 裕, 阿比留 教生, 粟田 卓也, 池上 博司, 内潟 安子, 大澤 春彦, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 永淵 正法, 三浦 順之助, 安田 和基, 安田 尚史, 花房 俊昭, 小林 哲郎

    (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61 (Suppl.1), S - 22, Japanese

    Summary national conference

  • 抗ヒトPD-1抗体投与後に発症する1型糖尿病に関する疫学調査

    馬殿 恵, 今川 彰久, 阿比留 教生, 粟田 卓也, 池上 博司, 内潟 安子, 及川 洋一, 大澤 春彦, 梶尾 裕, 川崎 英二, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 中條 大輔, 永淵 正法, 福井 智康, 三浦 順之助, 安田 和基, 安田 尚史, 小林 哲郎, 花房 俊昭

    (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61 (Suppl.1), S - 399, Japanese

  • 1型糖尿病研究の最前線 多様化する病態と診断上の課題 GAD抗体測定結果乖離と親和性 日本人1型糖尿病の成因、診断、病態、治療に関する調査研究委員会中間報告

    川崎 英二, 及川 洋一, 福井 智康, 今川 彰久, 中條 大輔, 梶尾 裕, 阿比留 教生, 粟田 卓也, 池上 博司, 内潟 安子, 大澤 春彦, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 永淵 正法, 三浦 順之助, 安田 和基, 安田 尚史, 花房 俊昭, 小林 哲郎

    (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61 (Suppl.1), S - 22, Japanese

  • 抗ヒトPD-1抗体投与後に発症する1型糖尿病に関する疫学調査

    馬殿 恵, 今川 彰久, 阿比留 教生, 粟田 卓也, 池上 博司, 内潟 安子, 及川 洋一, 大澤 春彦, 梶尾 裕, 川崎 英二, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 中條 大輔, 永淵 正法, 福井 智康, 三浦 順之助, 安田 和基, 安田 尚史, 小林 哲郎, 花房 俊昭

    (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61 (Suppl.1), S - 399, Japanese

  • 1型糖尿病update2017 2型糖尿病の経過中にGAD抗体の陽転化をみた症例の臨床像 日本人1型糖尿病の成因、診断、病態、治療に関する調査研究委員会報告

    及川 洋一, 島田 朗, 粟田 卓也, 福井 智康, 池上 博司, 今川 彰久, 梶尾 裕, 川畑 由美子, 川崎 英二, 三浦 順之助, 大澤 春彦, 高橋 和眞, 田中 昌一郎, 内潟 安子, 安田 尚史, 安田 和基, 花房 俊昭, 小林 哲郎

    (一社)日本糖尿病学会, Apr. 2017, 糖尿病, 60 (Suppl.1), S - 31, Japanese

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第5報)

    梶尾 裕, 中條 大輔, 安田 和基, 霜田 雅之, 春日 雅人, 今川 彰久, 岩橋 博見, 池上 博司, 大澤 春彦, 阿比留 教生, 島田 朗, 長澤 幹, 金重 勝博, 及川 洋一, 安田 尚史, 粟田 卓也, 川崎 英二, 高橋 和眞, 福井 智康, 小林 哲郎, 花房 俊昭

    (一社)日本糖尿病学会, Apr. 2017, 糖尿病, 60 (Suppl.1), S - 152, Japanese

  • 海外文献紹介：Perinatal Tolerance to Proinsulin is Sufficient to Prevent Autoimmune Diabetes

    若藤 諒, YASUDA HISAFUMI, 木戸 良明

    Jan. 2017, Diabetes Frontier, 28 (1), 114 - 115, Japanese

    [Invited]

    Book review

  • 基礎講座・1型糖尿病の基礎研究 樹状細胞と細胞療法

    YASUDA HISAFUMI

    Jun. 2016, Diabetes Frontier, 27 (3), 363 - 370, Japanese

    [Invited]

    Introduction commerce magazine

  • 1型糖尿病の成因と治療 GAD抗体測定法の変更における問題点と対策 1型糖尿病における抗GAD抗体測定法間の相関に関する検討(TIDE-J別報)

    中條 大輔, 安田 和基, 今川 彰久, 池上 博司, 大澤 春彦, 阿比留 教生, 島田 朗, 長澤 幹, 金重 勝博, 及川 洋一, 安田 尚史, 粟田 卓也, 川崎 英二, 高橋 和眞, 小林 哲郎, 霜田 雅之, 春日 雅人, 花房 俊昭, 梶尾 裕

    (一社)日本糖尿病学会, Apr. 2016, 糖尿病, 59 (Suppl.1), S - 23, Japanese

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第4報)

    梶尾 裕, 中條 大輔, 安田 和基, 霜田 雅之, 春日 雅人, 今川 彰久, 池上 博司, 大澤 春彦, 阿比留 教生, 島田 朗, 長澤 幹, 金重 勝博, 及川 洋一, 安田 尚史, 粟田 卓也, 川崎 英二, 高橋 和眞, 小林 哲郎, 花房 俊昭

    (一社)日本糖尿病学会, Apr. 2016, 糖尿病, 59 (Suppl.1), S - 279, Japanese

  • ライフステージ別糖尿病 高齢者糖尿病の臨床的特徴

    YASUDA HISAFUMI

    日本臨床, Apr. 2016, 新時代の臨床糖尿病学（下）, 74 (増刊号2), 542 - 546, Japanese

    [Invited]

    Introduction commerce magazine

  • 【1型糖尿病の成因と病態】 1型糖尿病発症における樹状細胞、マクロファージ、NK細胞、NKT細胞、好中球の役割

    Yasuda Hisafumi, 永田正男

    May 2015, 月刊糖尿病, 7 (5号), 48 - 57, Japanese

    [Invited]

    Introduction scientific journal

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第3報)

    梶尾裕, 中條大輔, 霜田雅之, 安田和基, 春日雅人, 花房俊昭, 今川彰久, 池上博司, 大澤春彦, 川崎英二, 粟田卓也, 高橋和眞, 小林哲郎, 島田朗, Yasuda Hisafumi, 阿比留教生, 長澤幹, 田中昌一郎

    Apr. 2015, 糖尿病, 58 (Suppl.1), S - 134, Japanese

  • サイクロホスファマイド投与SR-A KO NODマウスにおける1型糖尿病発症の検討

    井上雄斗, 清水まみ, 若藤諒, 勝田敦美, Yasuda Hisafumi

    Apr. 2015, 糖尿病, 58 (Suppl.1), S - 138, Japanese

  • 汎下垂体機能低下症、橋本病および境界型耐糖能異常を呈した多腺性自己免疫症候群3型の一例

    竹内 健人, 原 賢太, 高吉 倫史, 高橋 利匡, 西山 勝人, YASUDA HISAFUMI, 横野 浩一, 安友 佳朗

    2015, 日本内分泌学会雑誌, 91 (Suppl.), 7 - 9, Japanese

    [Refereed]

    Report scientific journal

  • 【1型糖尿病の成因と病態】 1型糖尿病発症における樹状細胞、マクロファージ、NK細胞、NKT細胞、好中球の役割

    YASUDA HISAFUMI, 永田 正男

    2015, 月刊糖尿病, 7 (5), 48 - 57, Japanese

    [Invited]

    Introduction commerce magazine

  • 高齢者糖尿病の特徴とその病態 /高齢者の糖尿病 Part1-病態と治療の側面から

    YASUDA HISAFUMI

    日本糖尿病協会, Nov. 2014, 糖尿病療養指導のためのDM Ensemble, 3 (3), 7 - 10, Japanese

    [Invited]

    Introduction scientific journal

  • 【高齢者の糖尿病Part1-病態と治療の側面から】 高齢者糖尿病の特徴とその病態(解説/特集)

    Yasuda Hisafumi

    Nov. 2014, DM Ensemble, 3 (3), 7 - 10, Japanese

    [Invited]

    Introduction scientific journal

  • 高齢者に発症したレミエール症候群の1例

    Mori Hiroyuki, Nishimura Mitsushige, Hashimoto Masayoshi, Kanazawa Kenji

    May 2014, 日本老年医学会雑誌, 51 (3号), 290, Japanese

    Meeting report

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開(TIDE-J)(第2報)

    梶尾 裕, 中條 大輔, 安田 和基, 春日 雅人, 花房 俊昭, 今川 彰久, 池上 博司, 大澤 春彦, 川崎 英二, 粟田 卓也, 高橋 和眞, 小林 哲郎, 島田 朗, 安田 尚史

    (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57 (Suppl.1), S - 274, Japanese

  • 高齢者診療のディベートセッション 在宅例の管理 「発熱」は入院精査すべきか在宅管理すべきか 「入院精査すべき」の立場で

    Yasuda Hisafumi

    Oct. 2012, Geriatric Medicine, 50 (10号), 1218 - 1222, Japanese

    Introduction scientific journal

  • 【浮腫の鑑別・対処法・メカニズム】 薬剤性浮腫

    Yasuda Hisafumi

    Jul. 2012, Fluid Management Renaissance, 2 (3号), 269 - 276, Japanese

    [Invited]

  • 【最新臨床糖尿病学 下-糖尿病学の最新動向-】 ライフステージ・タイプ別糖尿病の病態と治療 高齢者糖尿病 認知機能障害を有する高齢者糖尿病の管理のあり方

    Yasuda Hisafumi

    Jul. 2012, 日本臨床, 70 (増刊5 最新臨床糖尿病学(下)), 80 - 83, Japanese

    [Invited]

    Introduction scientific journal

  • Poly(I:C)投与SR-A KO NODマウスでの1型糖尿病発症の検討

    Yasuda Hisafumi, Arai Takashi, Nagata Masao, Hara Kenta

    Apr. 2012, 糖尿病, 55 (Suppl.1), S - 217, Japanese

    [Refereed]

  • 注意を要するインスリン依存状態の治療 高齢1型糖尿病の管理

    Yasuda Hisafumi

    Mar. 2012, 別冊プラクティス ブリットル糖尿病の病態と治療・管理のコツ －進化する治療・広がる未来－, 巻, , pp. 101-107, Japanese

    Introduction scientific journal

  • 【高齢者糖尿病と認知症-糖尿病ケアにおける問題点-】 糖尿病患者における認知症の対応 現状と将来への展望

    Yasuda Hisafumi

    Jan. 2012, プラクティス, 29巻, 1号, pp. 65-71, Japanese

    Introduction scientific journal

  • 【高齢者の糖尿病管理】 高齢者糖尿病の臨床的特徴

    Yasuda Hisafumi

    Aug. 2011, 月刊糖尿病, 3巻, 8号, pp. 26-35, Japanese

    Introduction scientific journal

  • 高齢者の安全な薬物療法 (第28回) 臭化ジスチグミン（ウブレチド）によるコリン作動性クリーゼを来した高齢者の1例

    Yasuda Hisafumi

    May 2011, 老年医学, 49巻, 5, pp. 585-588, Japanese

    Introduction scientific journal

  • 高齢者糖尿病の薬物治療

    Yasuda Hisafumi

    Oct. 2009, 内分泌・糖尿病科, 29巻, 4号, pp. 367-374, Japanese

    Introduction scientific journal

  • 【1型糖尿病up-to-date】 1型糖尿病における細胞性免疫異常

    Yasuda Hisafumi

    Aug. 2009, 糖尿病, 52巻, 8号, pp. 679-682, Japanese

    Introduction scientific journal

  • 【老化の機序と周術期管理】 高齢者の周術期管理 高齢者と免疫機能

    Yasuda Hisafumi, Nagata Masao

    Dec. 2008, Surgery Frontier, 15巻, 4号, pp. 413-421, Japanese

    Introduction scientific journal

  • Upregulation of the mTOR complex 1 pathway by Rheb in pancreatic beta cells leads to increased beta-cell mass and prevention of hyperglycemia

    Kenta Hara, Suirin Hamada, Akira Nakamura, Hisafumi Yasuda, Hiroaki Moriyama, Masao Nagata, Koichi Yokono

    AMER DIABETES ASSOC, Jun. 2008, DIABETES, 57, A2 - A2, English

    Summary international conference

  • 【1型糖尿病の新展開】 1型糖尿病の成因 自己免疫(細胞性)

    Yasuda Hisafumi, Nagata Masao

    Apr. 2008, Diabetes Frontier, 19巻, 2号, pp. 185-190, Japanese

    Introduction scientific journal

  • Minoru Kishi, Hisafumi Yasuda, Mami Kameno, Takashi Arai, Yasuyo Okumachi, Midori Kurohara, Hiroaki Moriyama, Koichi Yokono, Masao Nagata

    ACADEMIC PRESS INC ELSEVIER SCIENCE, 2008, CLINICAL IMMUNOLOGY, 127, S23 - S23, English

    Summary international conference

  • Yasuyo Okumachi, Hiroaki Moriyama, Mami Kameno, Takashi Arai, Minoru Kishi, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    ACADEMIC PRESS INC ELSEVIER SCIENCE, 2008, CLINICAL IMMUNOLOGY, 127, S100 - S100, English

    Summary international conference

  • Autoreactive T cell responses in CD25 negative fraction of peripheral blood mononuclear cells from established type I diabetes

    H. Moriyama, R. Kotani, M. Kameno, T. Arai, Y. Okumachi, M. Kishi, M. Kurohara, K. Yamada, H. Yasuda, K. Yokono, M. Nagata

    SPRINGER, Nov. 2007, ACTA DIABETOLOGICA, 44, S34 - S34, English

    Summary international conference

  • One amino acid difference of insulinb : 9-23 peptides critically influence on the effect of deletional therapy for experimental autoimmune diabetes (EAD)

    Y. Okumachi, H. Moriyama, M. Kameno, T. Arai, M. Kishi, M. Kurohara, K. Yamada, H. Yasuda, K. Yokono, M. Nagata

    SPRINGER, Nov. 2007, ACTA DIABETOLOGICA, 44, S36 - S37, English

    Summary international conference

  • Preventive effect of NODLPR/LPR-derived dendritic cells to autoimmune diabetes via FAS-FASL interaction

    M. Kishi, H. Yasuda, M. Kameno, T. Arai, Y. Okumachi, M. Kurohara, K. Yamada, H. Moriyama, K. Yokono, M. Nagata

    SPRINGER, Nov. 2007, ACTA DIABETOLOGICA, 44, S27 - S27, English

    Summary international conference

  • Intravenous administration of murine proinsulin1 or 2 expressing recombinant adenovirus vector protects diabetes in NOD mice

    K. Yamada, H. Moriyama, Y. Okumachi, T. Arai, M. Kameno, M. Kishi, M. Kurohara, H. Yasuda, K. Yokono, M. Nagata

    SPRINGER, Nov. 2007, ACTA DIABETOLOGICA, 44, S56 - S56, English

    Summary international conference

  • Intravenous administration of insulin1 B9-23 peptide reduces T cell reactivity to insulin and protects autoimmune diabetes in experimental autoimmune diabetes

    Yasuyo Okumachi, Hiroaki Moriyama, Takashi Arai, Minoru Kishi, Midori Kurohara, Katsumi Yamada, Reiko Kotani, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    AMER DIABETES ASSOC, Jun. 2006, DIABETES, 55, A281 - A281, English

    Summary international conference

  • TGF-b1-modulated dendritic cells inducing high CD1d expression result in prevention of autoimmune diabetes in NOD mice

    Hisafumi Yasuda, Minoru Kishi, Midori Kurohara, Mnneaki Sakata, Kenta Hara, Hiroaki Moriyama, Koichi Yokono, Masao Nagata

    AMER DIABETES ASSOC, Jun. 2006, DIABETES, 55, A284 - A284, English

    Summary international conference

  • Subcutaneous transplantation with proinsulin2 expressing fibroblasts protects diabetes in NOD mice

    Katsumi Yamada, Hiroaki Moriyama, Yasuyo Okumachi, Takashi Arai, Minoru Kishi, Midori Kurohara, Hisafumi Yasuda, Kenta Hara, Koichi Yokono, Masao Nagata

    AMER DIABETES ASSOC, Jun. 2006, DIABETES, 55, A284 - A284, English

    Summary international conference

  • 【経口糖尿病治療薬UP-TO-DATE】 高齢者糖尿病における経口糖尿病治療薬

    Yasuda Hisafumi

    Dec. 2005, Diabetes Frontier, 16巻, 6号, pp. 733-736, Japanese

    Introduction scientific journal

  • 高齢糖尿病患者における腎症の臨床的検討

    神田水鈴, 黒原みどり, FUJIHIRA, Kazuhiro, BABA, Hisamitsu, 安田尚史, HARA, Kenta, SAKURAI, Takashi, OKANO, Hiroyuki, NAGATA, Masao, YOKONO, Kouichi

    May 2005, 日本老年医学会雑誌, 42巻, 臨増, pp.87-87, Japanese

  • Prevention of autoimune diabetes by dendritic cells treated with IL-10

    H Yasuda, L Wen

    AMER DIABETES ASSOC, Jun. 2004, DIABETES, 53, A83 - A84, English

    Summary international conference

  • 抗FasL抗体投与によるNODマウスにおけるT,B細胞免疫寛容の誘導

    中山 真紀, 永田 正男, 安田 尚史, 有澤 健司, 小谷 玲子, 山田 克己, 金 貞子, 八木田 秀雄, 横野 浩一, 春日 雅人

    Mar. 2001, 糖尿病, 44 (Suppl.1), S82 - S82, Japanese

  • 抗FasL抗体投与によるNOD糖尿病発症抑制機構の解析

    中山 真紀, 永田 正男, 安田 尚史, 森山 啓明, 有澤 健司, 藤平 和弘, 八木田 秀雄, 奥村 康, 春日 雅人, 横野 浩一

    Nov. 2000, 日本免疫学会総会・学術集会記録, 30, 302 - 302, Japanese

  • Expression of CTLA4Ig or TNF-alpha at islet grafts suppresses the autoimmune attack in NOD mice

    H Yasuda, M Nagata, K Arisawa, M Nakayama, K Yamada, T Kin, K Fujihira, H Moriyama, K Yokono

    FEDERATION AMER SOC EXP BIOL, Apr. 2000, FASEB JOURNAL, 14 (6), A1099 - A1099, English

    Summary international conference

  • Blockade of Fas/FasL interaction in the initial phase abrogates autoimmune diabetes

    M Nakavama, M Nagata, H Yasuda, K Arisawa, H Moriyama, K Fujihira, S Chakrabarty, SA Chowdhury, H Yagita, K Yokono, M Kasu

    FEDERATION AMER SOC EXP BIOL, Apr. 2000, FASEB JOURNAL, 14 (6), A1098 - A1098, English

    Summary international conference

  • 抗FasL抗体投与による1型糖尿病発症抑制機構の解析

    中山 真紀, 永田 正男, 安田 尚史, 森山 啓明, 有澤 健司, 藤平 和弘, 八木田 秀雄, 奥村 康, 横野 浩一, 春日 雅人

    Apr. 2000, 糖尿病, 43 (Suppl.1), 286 - 286, Japanese

  • 幼若期NODマウスへの抗FasL抗体投与による自己免疫性糖尿病発症抑制

    中山 真紀, 永田 正男, 安田 尚史, 有澤 健司, 藤平 和弘, 八木田 秀雄, 奥村 康, 横野 浩一, 春日 雅人

    Oct. 1999, 日本免疫学会総会・学術集会記録, 29, 296 - 296, Japanese

  • 抗Th1サイトカイン抗体投与によるNODマウス糖尿病への影響

    藤平 和弘, 永田 正男, 森山 啓明, 安田 尚史, 中山 真紀, 有澤 健司, 八木田 秀雄, 奥村 康, 横野 浩一

    Apr. 1999, 糖尿病, 42 (Suppl.1), S191 - S191, Japanese

  • 抗FasL抗体投与によるNODマウス糖尿病の抑制

    中山 真紀, 永田 正男, 安田 尚史, 有澤 健司, 藤平 和弘, 伊藤 直人, 八木田 秀雄, 奥村 康, 横野 浩一, 春日 雅人

    Apr. 1999, 糖尿病, 42 (Suppl.1), S191 - S191, Japanese

  • Suppression and acceleration of diabetes in NOD mice by administration of anti-IL-12 antibody

    M Masao, K Fujihara, H Moriyama, H Yasuda, M Nakayama, K Arisawa, K Yokono

    AMER DIABETES ASSOC, 1999, DIABETES, 48, A434 - A434, English

    Summary international conference

  • Fas-induced apoptosis is not major effector mechanism but plays an important role in the initial phase of NOD diabetes

    M Nagata, M Nakayama, H Yasuda, K Arisawa, K Fujihira, H Moriyama, K Yokono, M Kasuga

    AMER DIABETES ASSOC, 1999, DIABETES, 48, A209 - A209, English

    Summary international conference

  • 抗Th1サイトカイン抗体投与によるNODマウス糖尿病の促進

    藤平 和弘, 永田 正男, 森山 啓明, 中山 真紀, 有澤 健司, 安田 尚史, 八木田 秀雄, 奥村 康, 横野 浩一

    Oct. 1998, 日本臨床免疫学会会誌, (26回抄録集), 133 - 133, Japanese

  • NODマウスにおけるFas-FasL系を介するアポトーシスの関与

    中山 真紀, 永田 正男, 安田 尚史, 有澤 健司, 藤平 和弘, 八木田 秀雄, 奥村 康, 横野 浩一, 春日 雅人

    Oct. 1998, 日本臨床免疫学会会誌, (26回抄録集), 126 - 126, Japanese

  • IL-12p40-producing islet grafts prevent diabetes recurrence in NOD mice.

    H Yasuda, M Nagata, K Arisawa, R Yoshida, K Fujihira, N Okamoto, H Moriyama, M Miki, Y Tominaga, H Hamada, K Yokono, M Kasuga

    AMER DIABETES ASSOC, May 1997, DIABETES, 46, 245 - 245, English

    Summary international conference

  • Administration of IL-4 prevents diabetes without enhancement of suppressor T cells in NOD mice

    Y Tominaga, M Nagata, H Yasuda, K Arisawa, H Moriyama, K Amano, K Yokono

    AMER DIABETES ASSOC, May 1996, DIABETES, 45, 1126 - 1126, English

    Summary international conference

Books etc

  • 臨床検査データブック LAB DATAコンパクト版 第11版

    安田尚史

    Contributor, インスリン抗体, 医学書院, Oct. 2021

  • 月刊 糖尿病 DIABETES 1型糖尿病アップデート～その成因から治療まで～

    安田尚史

    Contributor, １型糖尿病の動物モデル（ヒトとの異同）, 医学出版, Jun. 2021

  • 臨床検査データブック LAB DATA 2021-2022 グリコサミノグリカン（酸性ムコ多糖体(AMPS)）

    安田尚史

    Contributor, グリコサミノグリカン（酸性ムコ多糖体(AMPS)）, 医学書院, Jan. 2021

  • 臨床検査データブック LAB DATA 2021-2022 インスリン抗体

    安田尚史

    Contributor, インスリン抗体, 医学書院, Jan. 2021

  • 臨床検査データブック LAB DATAコンパクト版 第10版

    安田尚史

    Contributor, インスリン抗体, 医学書院, Oct. 2019

  • 臨床検査データブック LAB DATA 2019-2020 グリコサミノグリカン（酸性ムコ多糖体(AMPS)）

    YASUDA HISAFUMI

    Others, 医学書院, Jan. 2019, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA 2019-2020 インスリン抗体

    YASUDA HISAFUMI

    Others, 医学書院, Jan. 2019, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA コンパクト版 第9版/ インスリン抗体

    YASUDA HISAFUMI

    Others, 医学書院, Oct. 2017, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA2017-2018/ グリコサミノグリカン(酸性ムコ多糖体)

    YASUDA HISAFUMI

    Others, 医学書院, Jan. 2017, Japanese

    Dictionary or encycropedia

  • 臨床検査データブック LAB DATA2017-2018/ インスリン抗体

    YASUDA HISAFUMI

    Others, 医学書院, Jan. 2017, Japanese

    Dictionary or encycropedia

  • 臨床検査データブック LAB DATAコンパクト版 第8版 / インスリン抗体

    Yasuda Hisafumi

    Others, 医学書院, Oct. 2015, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATAコンパクト版 第8版/ インスリン抗体

    YASUDA HISAFUMI

    Others, 医学書院, Oct. 2015, Japanese

    Scholarly book

  • 月刊 糖尿病 DIABETES 1型糖尿病の成因と病態

    安田尚史, 永田正男

    Contributor, １型糖尿病発症における樹状細胞、マクロファージ、NK細胞、NKT細胞、好中球の役割, 医学出版, May 2015

  • 臨床検査データブック LAB DATA2015-2016 / 酸性ムコ多糖体

    Yasuda Hisafumi

    Others, 医学書院, Feb. 2015, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA2015-2016 / グリコサミノグリカン（酸性ムコ多糖体(AMPS)

    YASUDA HISAFUMI

    Others, 医学書院, Feb. 2015, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA2015-2016 / インスリン抗体

    YASUDA HISAFUMI

    Others, 医学書院, Feb. 2015, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA2015-2016 / インスリン抗体

    Yasuda Hisafumi

    Others, 医学書院, Feb. 2015, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATAコンパクト版 第7版 / インスリン抗体

    Yasuda Hisafumi

    Others, 医学書院, Oct. 2013, Japanese

    Scholarly book

  • 症例から学ぶ 高齢者の安全な薬物療法 / 16 ジスチグミン投与中にコリン作動性クリーゼを発症した症例

    中田由香子, Yasuda Hisafumi, 岸上景子, 矢谷宏文, 原賢太, 櫻井孝, 永田正男, 横野浩一

    Others, ライフ・サイエンス, May 2013, Japanese

    Scholarly book

  • 臨床検査データブック / 酸性ムコ多糖体

    Yasuda Hisafumi

    Others, 医学書院, Feb. 2013, Japanese

    Scholarly book

  • 臨床検査データブック / インスリン抗体

    Yasuda Hisafumi

    Others, 医学書院, Feb. 2013, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATAコンパクト版 第6版 / インスリン抗体

    Yasuda Hisafumi

    Others, 医学書院, Oct. 2011, Japanese

    Scholarly book

  • 高齢者災害時医療ガイドライン -2011-（試作版）第2版

    Yasuda Hisafumi

    Joint work, 日本老年医学会, Aug. 2011, Japanese

    Others

  • 一般救護者用 災害時高齢者医療マニュアル（試作版）第2版

    Yasuda Hisafumi

    Joint work, 日本老年医学会, Apr. 2011, Japanese

    Others

  • 臨床検査データブック LAB DATA2011-2012 / グリコサミノグリカン（酸性ムコ多糖体(AMPS))

    Yasuda Hisafumi

    Others, 医学書院, Feb. 2011, Japanese

    Scholarly book

  • 臨床検査データブック LAB DATA2011-2012 / インスリン抗体

    Yasuda Hisafumi

    Others, Feb. 2011, Japanese

    Scholarly book

Presentations

  • 高齢者の無症候性末梢型DVTに対する疾患啓発の重要性

    乙井一典, 岡野光真, 森健太, 安田尚史, 坂口一彦

    第63回日本老年医学会学術集会, Jun. 2021, Japanese

    Oral presentation

  • 2-デオキシグルコース投与により細胞内代謝が抑制され、1型糖尿病発症を抑制する

    丸山菜々子, 近藤佑一, 田中沙織, 林真里奈, 勝田敦美, 安田尚史

    第64回日本糖尿病学会年次学術集会, 20 May 2021, Japanese

    Oral presentation

  • 1型糖尿病発症に対する3-ブロモピルビン酸による免疫細胞代謝調節の効果

    林真里奈, 近藤佑一, 田中紗織, 丸山菜々子, 勝田敦美, 安田尚史

    第64回日本糖尿病学会年次学術集会, 20 May 2021, Japanese

    Oral presentation

  • 2-デオキシグルコース投与による1型糖尿病発症抑制

    丸山菜々子, 田中紗織, 近藤佑一, 林真里菜, 勝田敦美, 安田尚史

    第63回日本糖尿病学会年次学術集会, Oct. 2020, Japanese

    Oral presentation

  • 3-ブロモピルビン酸投与による1型糖尿病発症抑制の検討

    林真里奈, 近藤佑一, 田中紗織, 丸山菜々子, 勝田敦美, 安田尚史

    第63回日本糖尿病学会年次学術集会, Oct. 2020, Japanese

    Oral presentation

  • 1型糖尿病発症とSemaphorin7A発現の関連

    近藤佑一, 田中紗織, 林真里奈, 丸山菜々子, 勝田敦美, 高橋和眞, 安田尚史

    第63回日本糖尿病学会年次学術集会, Oct. 2020, Japanese

    Oral presentation

  • SR-Aと LPSの1型糖尿病発症に対する影響の検討

    田中紗織, 近藤佑一, 林真里奈, 丸山菜々子, 勝田敦美, 安田尚史

    第63回日本糖尿病学会年次学術集会, Oct. 2020, Japanese

    Oral presentation

  • 地域在住高齢者における自己記入によるDASC-21の特性

    小野玲, 内田一彰、河原田里果、木戸良明、安田尚史, 古和久朋

    第62回日本老年医学会学術集会, Aug. 2020, Japanese

    Oral presentation

  • 高齢者PE/中枢型DVTに対するDOAC強化療法の有効性と安全性の検討

    乙井一典, 森健太, 安田尚史, 坂口一彦

    第62回日本老年医学会学術集会, Aug. 2020, Japanese

    Oral presentation

  • 抗PD-1抗体薬投与後に発症する１型糖尿病（第2報）

    橘恵, 今川彰久, 日本糖尿病学会, 型糖尿病の成因, 病態に関する調査研究委員会, 池上博司, 川畑由美子, 阿比留教生, 粟田卓也, 三浦順之助, 及川洋一, 島田朗, 大澤春彦, 梶尾裕, 川﨑英二, 小澤純二, 高橋和眞, 中條大輔, 福井智康, 安田和基, 安田尚史, 花房俊昭, 小林哲郎

    第17回1型糖尿病研究会, 03 Nov. 2019

  • SR-A欠損NODマウスへのLPS投与による1型糖尿病発症抑制とそのメカニズムの検討

    田中紗織, 鈴木遥, 近藤佑一, 林真里奈, 丸山菜々子, 勝田敦美, 安田尚史

    第17回1型糖尿病研究会, 03 Nov. 2019

  • Semaphorin7Aの1型糖尿病発症過程における発現の変化

    近藤佑一, 梶原菜央, 鈴木遥, 田中紗織, 林真里奈, 丸山菜々子, 勝田敦美, 高橋和眞, 安田尚史

    第17回1型糖尿病研究会, 03 Nov. 2019

  • 当院における高齢者の無症候性末梢型DVTに関する臨床的検討

    乙井一典, 森健太, 安田尚史, 坂口一彦

    第61回日本老年医学会学術集会, 06 Jun. 2019, Japanese

    Oral presentation

  • 日本人1型糖尿病患者の包括的データベースの構築と臨床研究への展開（TIDE-J）（第7報）

    梶尾裕, 中條大輔, 安田和基, 霜田雅之, 春日雅人, 今川彰久, 池上博司, 大澤春彦, 阿比留教生, 島田朗, 長澤幹, 及川洋一, 安田尚史, 栗田卓也, 川﨑英二, 高橋和, 小林哲郎, 花房俊昭, 岩橋博見, 香月健志, 福井智康, 滝澤壮一

    第62回日本糖尿病学会年次学術集会, 25 May 2019

  • SR-A欠損NODマウスでのLPS投与による1型糖尿病発症抑制

    田中紗織、鈴木遥、近藤佑一、梶原菜央、勝田敦美、安田尚史

    第62回日本糖尿病学会年次学術集会, 25 May 2019

  • 1型糖尿病発症過程におけるSemaphorin7Aの発現

    近藤佑一, 梶原菜央, 鈴木遥, 田中紗織, 勝田敦美, 高橋和眞, 安田尚史

    第62回日本糖尿病学会年次学術集会, 25 May 2019

  • The role of dendritic cells in type 1 1diabetes ~understanding the pathogenesisi from animal experiments~

    Hisafumi YASUDA

    第62回日本糖尿病学会年次学術集会, 24 May 2019

    [Invited]

  • 地域在住高齢者の認知機能に対する複合課題プログラム効果の検証

    ONO REI, 古和 久明, 村田峻輔, YASUDA HISAFUMI, TANEMURA RUMI, KIDO YOSHIAKI

    第8回日本認知症予防学会学術集会, Sep. 2018, Japanese, Domestic conference

    Oral presentation

  • 自己免疫性糖尿病における樹状細胞の役割

    YASUDA HISAFUMI

    第16回1型糖尿病研究会, Sep. 2018, Japanese, 神戸, Domestic conference

    [Invited]

    Nominated symposium

  • 1型糖尿病モデルにおけるMetforminの免疫代謝に及ぼす効果

    鈴木 遥, 田上 加奈子, 西川 みな帆, 勝田 敦美, YASUDA HISAFUMI

    第16回1型糖尿病研究会, Sep. 2018, Japanese, 神戸, Domestic conference

    Oral presentation

  • 高齢者発症急性冠症候群患者では線溶能が低下している

    乙井一典, 安田尚史, 坂口一彦

    第60回日本老年医学会学術集会, 15 Jun. 2018, Japanese

    Oral presentation

  • １型糖尿病発症における樹状細胞の役割～動物モデルより

    YASUDA HISAFUMI

    第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, Domestic conference

    [Invited]

    Nominated symposium

  • 日本人１型糖尿病の包括的データベースの構築と臨床研究への展開（TIDE-J）（第6報）

    中條 大輔, 今川 彰久, 安田 和基, 阿比留教生, 粟田 卓也, 池上 博司, 岩橋 博見, 及川 洋一, 大澤 春彦, 香月 健志, 金重 勝博, 川﨑 英二, 島田 朗, 高橋 和眞, 長澤 幹, 福井 智康, YASUDA HISAFUMI, 春日 雅人, 小林 哲郎, 花房 俊昭, 梶尾 裕

    第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, Domestic conference

    Oral presentation

  • 抗ヒトPD-1抗体投与後に発症する１型糖尿病に関する疫学調査

    馬殿恵, 今川 彰久, 阿比留教生, 粟田 卓也, 池上 博司, 内潟 安子, 及川 洋一, 大澤 春彦, 梶尾 裕, 川﨑 英二, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 中條 大輔, 永淵 正法, 福井 智康, 三浦 順之助, 安田 和基, YASUDA HISAFUMI, 小林 哲郎, 花房 俊昭

    第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, Domestic conference

    Nominated symposium

  • Metformin腹腔内投与による1型糖尿病モデルの免疫系への影響

    鈴木 遥, 田上 加奈子, 西川 みな帆, 井上 雄斗, 若藤 諒, 勝田 敦美, 清水 まみ, YASUDA HISAFUMI

    第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 盛岡, Domestic conference

    Oral presentation

  • GAD抗体測定結果乖離と親和性－日本人１型糖尿病の成因，診断，病態，治療に関する調査研究委員会中間報告－

    川﨑 英二, 及川 洋一, 福井 智康, 今川 彰久, 中條 大輔, 梶尾 裕, 阿比留教生, 粟田 卓也, 池上 博司, 内潟 安子, 大澤 春彦, 川畑 由美子, 小澤 純二, 島田 朗, 高橋 和眞, 田中 昌一郎, 永淵 正法, 三浦 順之助, 安田 和基, YASUDA HISAFUMI, 花房 俊昭, 小林 哲郎

    第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, Domestic conference

    Nominated symposium

  • １型糖尿病update

    YASUDA HISAFUMI

    第54回日本糖尿病学会近畿地方会, Nov. 2017, Japanese, 大阪, Domestic conference

    [Invited]

    Invited oral presentation

  • TLR4刺激が1型糖尿病自然発症モデルに及ぼす影響

    田上 加奈子, 西川 みな帆, 鈴木 遥, 勝田 敦美, 清水 まみ, YASUDA HISAFUMI

    第15回1型糖尿病研究会, Nov. 2017, Japanese, 盛岡, Domestic conference

    Oral presentation

  • LPSはCY投与NODマウスモデルにおいて1型糖尿病の発症を抑制する

    西川 みな帆, 田上 加奈子, 鈴木 遥, 井上 雄斗, 若藤 諒, 勝田 敦美, 清水 まみ, YASUDA HISAFUMI

    第15回1型糖尿病研究会, Nov. 2017, Japanese, 盛岡, Domestic conference

    Oral presentation

  • 1型糖尿病モデルにおけるMetforminの免疫系に及ぼす影響

    鈴木 遥, 田上 加奈子, 西川 みな帆, 井上 雄斗, 若藤 諒, 勝田 敦美, 清水 まみ, YASUDA HISAFUMI

    第15回1型糖尿病研究会, Nov. 2017, Japanese, 盛岡, Domestic conference

    Oral presentation

  • 高齢者発症急性冠症候群患者の臨床的検討

    乙井一典, 井上信孝, 安田尚史, 坂口一彦

    第59回日本老年医学会学術集会, 16 Jun. 2017, Japanese

    Oral presentation

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開（TIDE-J）（第5報）

    梶尾裕, 中條大輔, 安田和基, 霜田雅之, 春日雅人, 今川彰久, 岩橋博見, 池上博司, 大澤春彦, 阿比留教生, 島田朗, 長澤幹, 金重勝博, 及川洋一, YASUDA HISAFUMI, 粟田卓也, 川﨑英二, 高橋和眞, 福井智康, 小林哲郎, 花房俊昭

    第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

    Oral presentation

  • poly(I:C)およびCY投与によるNOD-lpr/lprマウスの免疫寛容破綻の誘導

    鈴木 遥, 若藤 諒, 清水 まみ, 井上 雄斗, 田上 加奈子, 西川 みな帆, 勝田 敦美, YASUDA HISAFUMI

    第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

    Poster presentation

  • LPS投与によるサイクロホスファミド投与NODマウスモデルでの1型糖尿病発症抑制

    西川 みな帆, 清水 まみ, 井上 雄斗, 若藤 諒, 田上 加奈子, 鈴木 遥, 勝田 敦美, YASUDA HISAFUMI

    第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

    Poster presentation

  • 2 型糖尿病の経過中にGAD 抗体の陽転化をみた症例の臨床像―日本人1 型糖尿病の成因，診断，病態，治療に関する調査研究委員会報告

    及川洋一, 島田朗, 粟田卓也, 福井智康, 池上博司, 今川彰久, 梶尾裕, 川畑由美子, 川﨑英二, 三浦順之助, 大澤春彦, 高橋和眞, 田中昌一郎, 内潟安子, YASUDA HISAFUMI, 安田和基, 花房俊昭, 小林哲郎

    第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

    [Invited]

    Nominated symposium

  • 1型糖尿病CD8モデルマウスに対するLipopolysaccharide投与による糖尿病発症への影響

    田上 加奈子, 清水 まみ, 井上 雄斗, 若藤 諒, 西川 みな帆, 鈴木 遥, 勝田 敦美, YASUDA HISAFUMI

    第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

    Poster presentation

  • SR-A KO NODマウスのサイクロホスファマイド投与モデルにおける1型糖尿病発症抑制の検討

    井上 雄斗, 清水 まみ, 若藤 諒, 田上 加奈子, 西川 みな帆, 中村 友佳, 勝田 敦美, Yasuda Hisafumi

    第13回1型糖尿病研究会, Oct. 2015, Japanese, 糖尿病学会, 東京, Domestic conference

    Oral presentation

  • NOD-lpr/lprマウスにおける高用量poly（I:C)投与による免疫寛容破綻の誘導

    若藤 諒, 清水 まみ, 井上 雄斗, 勝田 敦美, Yasuda Hisafumi

    第13回1型糖尿病研究会, Oct. 2015, Japanese, 糖尿病学会, 東京, Domestic conference

    Oral presentation

  • 咽頭痛で発症した降下性壊死性縦隔炎の1例

    宋 慎平, 南地 克洋, 世戸 博之, 三好 園子, Nishimura Mitsushige, Mori Hiroyuki, Kanazawa Kenji, Yasuda Hisafumi

    第209回日本内科学会近畿地方会, Sep. 2015, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • 摂食障害の既往があるsex workerで診断に苦慮した不明熱の1例

    南地 克洋, 世戸 博之, 三好 園子, Mori Hiroyuki, Nishimura Mitsushige, Yasuda Hisafumi, Kanazawa Kenji

    第208回日本内科学会近畿地方会, Jun. 2015, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • サイクロホスファマイド投与SR A KO NODマウスにおける1型糖尿病発症の検討

    井上 雄斗, 清水 まみ, 若藤 諒, 勝田 敦美, Yasuda Hisafumi

    第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 山口, Domestic conference

    Oral presentation

  • SR-A KO NOD マウスにおけるサイクロホスファマイド投与モデルでの１型糖尿病発症の検討

    SHIMIZU MAMI, INOUE YUTO, WAKAFUJI RYO, KATSUTA ATSUMI, NAGATA MASAO, YASUDA HISAFUMI

    第12回1型糖尿病研究会, Nov. 2014, Japanese, 姫路, Domestic conference

    Oral presentation

  • SR-A KO NOD マウスにおけるサイクロホスファマイド投与モデルでの1型糖尿病発症の検討

    井上 雄斗, 清水 まみ, 若藤 諒, 勝田 敦美, 永田 正男, Yasuda Hisafumi

    第12回1型糖尿病研究会, Nov. 2014, Japanese, 1型糖尿病研究会, 兵庫, Domestic conference

    Oral presentation

  • 1 型糖尿病に対する細胞療法と樹状細胞

    YASUDA HISAFUMI

    第12回1型糖尿病研究会, Nov. 2014, Japanese, Domestic conference

    [Invited]

    Nominated symposium

  • 1 型糖尿病に対する細胞療法と樹状細胞

    Yasuda Hisafumi

    第12回1型糖尿病研究会, Nov. 2014, Japanese, 1型糖尿病研究会, 兵庫, Domestic conference

    Oral presentation

  • 汎下垂体機能低下症を伴った膵島関連抗体陽性IGTの1例

    TAKAHASHI TOSHITADA, TAKEUCHI KENTO, HARA KENTA, HYOGO MASAHIRO, NISHIYAMA KATSUTO, YASUTOMO YOSHIROU, YOKONO KOICHI, YASUDA HISAFUMI

    第204回日本内科学会近畿地方会, Jun. 2014, Japanese, 大阪, Domestic conference

    Oral presentation

  • 汎下垂体機能低下症を伴った膵島関連抗体陽性IGTの1例

    高橋 利匡, 竹内 健人, 原 賢太, 兵庫 聖大, 西山 勝人, 安友 佳朗, 横野 浩一, Yasuda Hisafumi

    第204回日本内科学会近畿地方会, Jun. 2014, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開（TIDE-J)(第2報)

    KAJIO HIROSHI, CHUJO DAISUKE, YASUDA KAZUKI, KASUGA MASATO, HANAFUSA TOSHIAKI, IMAGAWA AKIHISA, IKEGAMI HIROSHI, OSAWA HARUHIKO, KAWASAKI EIJI, AWATA TAKUYA, TAKAHASHI KAZUMA, KOBAYASHI TETSURO, SHIMADA AKIRA, YASUDA HISAFUMI

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 大阪, Domestic conference

    Oral presentation

  • 日本人1型糖尿病の包括的データベースの構築と臨床研究への展開（TIDE-J)(第2報)

    梶尾 裕, 中條 大輔, 安田 和基, 春日 雅人, 花房 俊昭, 今川 彰久, 池上 博司, 大澤 春彦, 川崎 英二, 粟田 卓也, 高橋 和眞, 小林 哲郎, 島田 朗, Yasuda Hisafumi

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • 高齢者糖尿病の成因と病態特性

    YASUDA HISAFUMI

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 大阪, Domestic conference

    [Invited]

    Nominated symposium

  • 高齢者糖尿病の成因と病態特性

    Yasuda Hisafumi

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • Poly(I:C)投与1型糖尿病関連マウスにおける糖尿病発症の検討

    SHIMIZU MAMI, YASUDA HISAFUMI, KATSUTA ATSUMI, TAKAHASHI KAZUMA, NAGATA MASAO

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 大阪, Domestic conference

    Oral presentation

  • Poly(I:C)投与1型糖尿病関連マウスにおける糖尿病発症の検討

    清水 まみ, Yasuda Hisafumi, 勝田 敦美, 高橋 和眞, 永田 正男

    第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • 急速な経過を示した非鼻腔型NK/T細胞リンパ腫の1例

    海老沢 馨, 牟田 愛, Toyokuni Takehiro, 久保川 修, 三好園子, Mori Hiroyuki, Nishimura Mitsushige, Arai Takashi, Yasuda Hisafumi, Kanazawa Kenji

    第203回日本内科学会近畿地方会, Mar. 2014, Japanese, 日本内科学会, 大阪, 【症例】39歳、男性。【主訴】発熱、乾性咳嗽【現病歴】当院入院の約1ヶ月前から乾性咳嗽が出現し、20日前から発熱を認めるようになった。12日前の近医受診時に胸部X線にて両肺に浸潤影を認め、肺炎の診断で入院となった。抗生剤の投与が行われたが改善は見られず、浸潤影が拡大した。BAL、TBLBが行われたがBALFは正常、肺組織も壊死所見のみで診断が困難であったため当院へ転院となった。【経過】リンパ節の腫脹は認めなかったが肝脾腫を認め、肝酵素、LDHおよび可溶性IL-2Rの著明な上昇を認めたため悪性リンパ腫が疑われた。しかし、肝臓、皮膚、骨髄生検を施行するも異型細胞は認められなかった。転院7日目に開胸肺生検および再度の肝生検施行により、胸水、肝組織から異型細胞が検出され悪性リンパ腫の診断となった。肝生検後より血圧が低下し、集中治療の甲斐なく転院8日目に死亡し, Domestic conference

    Oral presentation

  • CGMによる膵腎同時移植後患者の血糖変動の検討

    中村 友昭, Hirota Yushi, 中島 進介, 西本 祐希, Yasuda Hisafumi, Matsumoto Ippei, Ku Yonson, Sakaguchi Kazuhiko, Ogawa Wataru

    第41回日本膵・膵島移植研究会, Mar. 2014, Japanese, 日本膵・膵島移植研究会, 名古屋, 膵腎同時移植では、インスリンの使用なしで平均血糖が正常耐糖能者と同程度にまで低下するだけでなく、血糖の日内変動幅も正常耐糖能者と同等にまで改善することがCGMを用いた検討で明らかとなった。, Domestic conference

    Oral presentation

  • 腎周囲膿瘍から広範囲の腸腰筋膿瘍を来たした 2型糖尿病患者の1例

    海老沢 馨, 津村 明子, 吉田 英樹, 大幡 真也, 世戸 博之, 服部 素子, Toyokuni Takehiro, Arai Takashi, Yamada Katsumi, Yasuda Hisafumi, Kanazawa Kenji, Ogawa Wataru

    第50回日本糖尿病学会近畿地方会, Nov. 2013, Japanese, 日本糖尿病学会, 京都, 【症例】77歳女性【主訴】左大腿部痛【現病歴】2型糖尿病で通院中であり、HbA1cは7.0%前後だった。2か月前、発熱と炎症反応の上昇があり気管支炎の診断で入院。抗生剤投与にて炎症反応が改善し退院となったが、同時期より左大腿部に軽度の疼痛があった。1か月前に発熱と左下肢の脱力で近医へ入院。当初、CTで左腎腫瘍が疑われ、発熱は腫瘍熱と考えられた。1週間前に家族の希望で一旦退院となるも、左大腿部痛と食欲低下が増悪し当院へ入院となった。入院時HbA1cは9.6%と悪化、CTでは左腎に接し腸腰筋内に多胞性腫瘤影が認められ、大腿筋群まで波及していた。穿刺で膿汁を確認し腎周囲及び腸腰筋膿瘍と診断。培養で大腸菌が検出された。【考察】高齢者糖尿病患者の腸腰筋膿瘍は典型的な症状を呈さないことが多く、発熱時には詳細な診察や画像検査を行う必要があると考えられた。, Domestic conference

    Oral presentation

  • 高齢者に発症したレミエール症候群の一例

    仲山舞, 阿部晶平, 牟田愛, 久保川修, 三好園子, Mori Hiroyuki, Nishimura Mitsushige, Yasuda Hisafumi, Hashimoto Masayoshi, Kanazawa Kenji

    第24回日本老年医学会近畿地方会, Nov. 2013, Japanese, 日本老年医学会, 京都, レミエール症候群は、咽頭炎後に、主に頚静脈に感染性血栓性静脈炎を生じる疾患であり、遠隔病変として肺病変が出現する場合があるため、注意を要する。【症例】66歳女性。入院5ヶ月前から関節リウマチの診断にてPSL10mg/日内服中。1ヶ月前に歯科治療を受け、その後開口障害から水分摂取困難、構音障害を認め、前医入院。胸部CTにて多発肺結節影を認めたが、発熱はなく経過観察となった。その後、発熱と左下顎部痛が出現し、扁桃周囲膿瘍が疑われた。抗生剤治療にて改善認めず、精査加療目的に当院転院となった。入院時の胸腹部CTにて咽後膿瘍、両肺に多発する空洞影及び、エコーにて右内頚静脈に血栓を認め、レミエール症候群と診断した。膿瘍の縦隔への進展が懸念されたため、入院5日目に抗生剤投与下に緊急で切開排膿を施行し、軽快した。【考察】レミエール症候群は通常若年者に多いが、近年、高, Domestic conference

    Oral presentation

  • 1型糖尿病関連マウスにおけるpoly(I:C)投与による1型糖尿病発症の検討

    清水まみ, Yasuda Hisafumi, 勝田敦美, 高橋和眞, 原 賢太, 永田正男, 横野浩一

    第11回1型糖尿病研究会, Oct. 2013, Japanese, 日本糖尿病学会後援, 軽井沢, Scavenger receptor (SR)-A KO NODマウスでは、NODマウスに比べ1型糖尿病(T1D)の自然発症は遅延したが、TLR3のリガンドとされるpoly (I:C)投与では低用量でさえNODマウスと同程度に発症を促進した。このことから、抗原提示細胞上のSR-Aの存在はdsRNAウイルス感染に伴うT1D発症に影響を及ぼす可能性を示した。, Domestic conference

    Oral presentation

  • 薬物療法による保存的治療にて改善し得た糖尿病合併気腫性腎盂腎炎の1例

    鄧 皓之, Yamada Katsumi, Toyokuni Takehiro, 服部 素子, 浅川 俊, 世戸 博之, Nishimura Mitsushige, Yasuda Hisafumi, Kanazawa Kenji, 秋田 穂束

    第200回日本内科学会近畿地方会, Jun. 2013, Japanese, 日本内科学会, 神戸, Domestic conference

    Oral presentation

  • 糖尿病患者における非閉塞性腸管虚血症（Nonocculusive mesenteric ischemia: NOMI）－自験例も含めて－

    Kido Yoshiaki, 原 賢太, Yasuda Hisafumi

    第200回日本内科学会近畿地方会, Jun. 2013, Japanese, 日本内科学会, 神戸, 血管の器質的閉塞を認めず腸管の不可逆的虚血を生ずる場合をNOMI(非閉塞性腸管虚血症）といい、早期診断がしばしば困難であり死亡率が高い。糖尿病を基礎疾患として有する場合が多いが、十分に認知されている合併症とは言いがたい。DKAやHHSに伴う報告が多いが、誘因なく発症する報告もあり、腹痛を訴える患者では本疾患の存在を想起し、適切なタイミングで画像診断を行うことが救命のためには重要である。, Domestic conference

    Oral presentation

  • FasL-Fasシグナルの1型糖尿病発症における役割の検討

    YASUDA HISAFUMI

    第８回加齢医学研究会, Jan. 2013, Japanese, 名古屋, Domestic conference

    Oral presentation

  • FasL-Fasシグナルの1型糖尿病発症における役割の検討

    Yasuda Hisafumi, 勝田敦美, 清水まみ, 佐々木弘智, 原賢太, 秋田穂束, 横野浩一

    第8回加齢医学研究会, Jan. 2013, Japanese, 興和創薬, 名古屋, 1型糖尿病発症機構においてFasL-Fasシグナルは、細胞傷害期のアポトーシスに関与するのみならず、抗原提示細胞とT細胞の抗原提示の際にも重要な役割を演じている可能性を示した。, Domestic conference

    Oral presentation

  • 髄膜炎後遷延する発熱に対しコルヒチンが著効したベーチェット病様病態を呈した1例

    田中 祐貴, 浅川 俊, 世戸 博之, 服部 素子, Toyokuni Takehiro, Nishimura Mitsushige, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第199回日本内科学会近畿地方会, Dec. 2012, Japanese, 日本内科学会, 日本, 和歌山, 【症例】25歳、女性【主訴】発熱、意識障害【現病歴】6年前にクローン病と診断され、6ヶ月前からレミケード導入。2年前から年に数回39℃超の高熱を認めていたが他院入院精査で原因不明であった。発熱のため入院し、急性咽頭炎、肺炎、クローン病増悪など疑われ、抗菌薬投与やステロイドパルス療法施行されるも解熱を認めず2週間経過し、当院転院前日には意識障害を伴い、髄液検査で髄膜炎と診断された。当院転院後、細胞性免疫低下患者の髄膜炎として、細菌に加え、結核、ヘルペスなども考慮し治療開始し、翌日に意識状態は著明に改善した。意識状態改善後も約1ヶ月間、発熱が遷延したが、感染性髄膜炎、膿瘍、悪性腫瘍、薬剤熱は経過や画像検査から否定的であった。腸管病変、口腔内アフタ、毛嚢炎、腱付着部炎、また髄液IL-6高値などから、ベーチェット病様病態の免疫疾患と考え、コルヒチン1mg/日, Domestic conference

    Oral presentation

  • 高齢者に見られた猫咬傷が原因のPasturella multocidaの一例

    Nishimura Mitsushige, 蓮池 俊和, 久保川 修, Mori Hiroyuki, 明嵜 太一, 平岡 栄治, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第23回日本老年医学会近畿地方会, Nov. 2012, Japanese, 日本老年学会, 日本, 大阪, 猫咬傷が原因で全身性化膿性筋炎に至った症例を経験した。ADLが自立していた82歳女性。糖尿病 高血圧 脳梗塞 変形性腰椎症 両変形性膝関節症の既往がある。2012年3月に数日間で増悪する右下腿痛で受診され、前医で閉塞性動脈硬化症の増悪との診断で当院心臓血管外科へ搬送となった。心臓血管外科で精査され右下肢蜂窩織炎疑いとのことで当科コンサルトとなった。 身体所見で右肘圧痛 両膝関節圧痛 右下腿圧痛 左足関節周囲痛を認めたため全身造影CTを撮影したところ皮下の濃度上昇 筋肉の不均一な造影効果 筋膜肥厚から蜂窩織炎 筋炎疑われ、抗生物質開始となった。 培養検査ではPasturella multocida検出された。加療の結果感染はコントロールされた。, Domestic conference

    Oral presentation

  • 広範囲にガス壊疽を伴う 皮膚重症感染症を来たした 血糖コントロール不良2型糖尿病の1例

    松岡 晃生, 久保川 修, 三好 園子, Mori Hiroyuki, 皆川 健太郎, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束, 横野 浩一

    第49回糖尿病学会近畿地方会, Nov. 2012, Japanese, 日本糖尿病学会, 日本, 京都, 症例は55歳、女性。2型糖尿病でインスリン加療中も、HbA1c 11.1%(NGSP)。当科入院5カ月前より右下肢から腰部に疼痛を自覚、近医にて陰部膿瘍を、3ヶ月前には左臀部膿瘍を排膿。その後も右下肢異常感覚や歩行時疼痛が持続、1カ月前に発熱、歩行困難が出現、CTにて右臀部から大腿部にガス像を認め切開するも症状持続し、当科紹介入院。CTにて右大腿部膿瘍及び筋間にガス像著明で、広域にデブリドマン施行。広域抗菌薬投与と創部の洗浄を連日施行、Streptococcus sanguinisとBacteroides fragilisが原因菌と判明し抗菌薬変更、1週間後に再度デブリドマン施行。抗菌薬投与継続にて病巣は改善傾向を示し、皮膚科にて植皮術を施行後転院となった。本症例のように血糖コントロール不良の糖尿病症例では重篤な感染症を合併しすく、血糖管理の重要性が, Domestic conference

    Oral presentation

  • グリメピリドからビルダグリプチンへの変更が非ケトン性高浸透圧性昏睡の契機となったと考えられた1例

    阿部 泰尚, 前田 ゆき, 近藤 奈央, 高井 智子, 梶川 道子, 池田 和人, Yasuda Hisafumi, 原 賢太, 横野 浩一

    第23回日本老年医学会近畿地方会, Nov. 2012, Japanese, 日本老年学会, 大阪, 症例は82歳女性、20年前に脳梗塞を発症、その際に糖尿病も指摘されていた。脳梗塞後遺症で寝たきり、経管栄養中で、入院17日前にショートステイ目的で他院に入院中され、HbA1cが徐々に上昇傾向（最終でHbA1c 7.4%）であったため、ビルダグリプチン100mgが開始、グリメピリド1mgが中止されていた。入院中に発熱、高血糖、意識障害、血圧低下を来し当院へ救急搬送、来院時意識レベルJCS3、血糖値 、血液ガス分析でpH 、尿ケトン体、血漿グルコース mg/dl、Na mEq/l、で非ケトン性高浸透圧性昏睡、急性腎不全の診断に至った。一時的なICU管理が必要となったが、補液、インスリン静注で全身状態改善し、グリメピリドを含む経口糖尿病薬の内服で退院可能であった。本患者は、HONCの原因として、感染によるストレスによるところが大きかったと考えるが、この薬剤, Domestic conference

    Oral presentation

  • TSH 受容体抗体陰性バセドウ病を契機に発症したと考えられる高齢者糖尿病の一例

    原 賢太, 明嵜 太一, Yasuda Hisafumi, 秋田 穂束, 横野 浩一

    第49回糖尿病学会近畿地方会, Nov. 2012, Japanese, 日本糖尿病学会, 日本, 京都, 65歳男性、高血圧にて近医通院中高血糖を指摘され当院紹介。身長159cm体重59kg、来院前3ヶ月で約5kgの体重減少を認めた。動悸や発汗異常、振戦などの自覚なし。甲状腺はびまん性に腫大を認めたが圧痛や発赤は認めず。空腹時血糖125mg/dL、HbA1c8.0％と上昇を認めたが、微量アルブミン尿陰性、網膜症及び神経障害は認めなかった。f-T4:2.5ng/mL、TSH<0.1uU/mLと甲状腺機能亢進を認め、TPO抗体、サイログロブリン抗体は高値を認めたが、TSH受容体抗体および甲状腺刺激抗体は陰性、炎症反応の上昇認めず、無痛性甲状腺炎が疑われた。食事療法のみにて経過観察していたが、4ヶ月後にても甲状腺機能に改善認めず、放射性ヨード検査を施行したところびまん性の取り込みを認め、バセドウ病と診断した。甲状腺機能亢進症は糖尿病の成因として重, Domestic conference

    Oral presentation

  • NODマウスにおける1型糖尿病発症に関連するSR-Aの役割の検討

    勝田 敦美, 清水 まみ, Yasuda Hisafumi, 中村 晃, 佐々木 弘智, 永田 正男, 原 賢太, 横野 浩一, 高橋和真

    第10回1方糖尿病研究会, Nov. 2012, Japanese, 1型糖尿病研究会, 日本, 佐賀県, 【目的】T細胞の活性化や抑制に関与する抗原提示細胞の細胞表面上に発現するSR-A(Scavenger Receptor class A(CD204))はマクロファージや樹状細胞の分化・機能、動脈硬化、感染免疫に関与し、polyIやpolyGなどをリガンドとするSR-Aを欠損させたSR-A-/-マウス(C57BL/6 background)では動脈硬化や易感染性を示すことが報告されている。昨年の本研究会で、われわれが作製したSR-A-/-NODマウスでは、NODマウスと比較して有意に1型糖尿病発症が遅延し、かつ、TLR3のリガンドでdsRNAアナログであるpoly(I:C)投与により糖尿病発症が促進することを報告した。そこで今回はさらに1型糖尿病発症におけるSR-Aの役割を検討した。【方法】(1)nibblingの程度をflow cytometryにて, Domestic conference

    Oral presentation

  • 視力障害、しびれ、筋力低下による歩行障害と原因不明の発熱をきたしたChordoid meningiomaの1例

    Nishimura Mitsushige, Toyokuni Takehiro, 服部 素子, 浅川 俊, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束, 千原 典夫

    第198回日本内科学会近畿地方会, Sep. 2012, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • 肺胞出血を伴い重篤化したANCA関連血管炎の1例

    秋田 朋己, 田村 純子, Toyokuni Takehiro, 三好 園子, 中村 晃, 高嶋 基嗣, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第197回日本内科学会近畿地方会, Jun. 2012, Japanese, 日本内科学会, 日本, 兵庫, 【症例】80歳、女性。【主訴】発熱、呼吸困難。【現病歴】当院転院1カ月前はCr 0.75mg/dlで明らかな腎機能障害認めず。転院1週間前より全身倦怠感が出現し前医受診。発熱、呼吸困難、貧血および尿蛋白(4+)、尿潜血(3+)、Cr 3.4mg/dlと腎機能障害を認めた。胸部CTにて両側のびまん性浸潤影を認め同日緊急入院となる。輸血および抗生剤投与が行なわれるも呼吸状態は徐々に悪化し血痰も認めたため当院転院となる。転院当日に呼吸状態が悪化したため、挿管の上で気管支鏡検査を施行し肺胞出血を認めた。その後、MPO-ANCA陽性と判明しANCA関連血管炎と診断。人工呼吸器管理下で、第1病日よりステロイドパルス療法(1g/日)を3日間、第3病日より血漿交換療法を追加するも呼吸機能、腎機能ともに改善を認めず徐々に悪化し、第9病日よりさらにエンドキサンパルス療法, Domestic conference

    Oral presentation

  • 在宅例の管理 「発熱」は入院精査すべきか在宅管理すべきか 「入院すべき」の立場で

    Yasuda Hisafumi

    第54回日本老年医学会総会, Jun. 2012, Japanese, 日本老年学会, 東京, わが国は、65歳以上の高齢者人口が急カーブを描いて増加の一途をたどり、2007年には欧米諸国がかつて経験したことのない速度で世界初の超高齢社会を迎えた。この急速な高齢化に伴い、脳血管障害や認知症などで自立困難な高齢者は今後ますます増加することが予想される。その中で、在宅医療や看護・介護の充実を推進する在宅重視の方向性が打ち出されている。高齢者は一般に、症状が非典型的で、ホメオスターシスの失調を来たしやすく、急性期からの回復が遅延しやすいなどの特徴を有している。在宅高齢者が発熱をきたす場合、感染症を含めて様々な原因が考えられ、確実に診断を行なった上で、迅速かつ適切な治療にあたることが大原則である。特に、遷延する発熱例では、高齢者の特徴を踏まえて入院精査することが、病態の重症化を未然に防ぎ迅速な改善に寄与すると考える。本セッションでは、入院精査を推奨する, Domestic conference

    Others

  • poly(I:C)投与SR-A KO NODマウスでの1型糖尿病発症の検討

    清水まみ, Yasuda Hisafumi, 中村 晃, 勝田敦美, 佐々木弘智, Arai Takashi, 永田正男, 原 賢太, 高橋和眞, 横野浩一

    第55回日本糖尿病学会総会, May 2012, Japanese, 日本糖尿病学会, 横浜, T細胞の活性に関与している樹状細胞やマクロファージの細胞表面上にはSR-A(Scavenger Receptor class A)が発現している。RNAウイルス感染を模倣することを目的として、polyIをリガンドとするSR-Aを欠損させたSR-A KO NODマウスに、TLR3のリガンドでdsRNAアナログであるpoly(I:C)を投与すると、ホモKO NODマウスでは、自然発症ではＮＯＤマウスに対し発症が遅延するのに対し、poly(I:C)投与により糖尿病発症は促進する傾向がみられた。in vitroでpoly (I:C)存在下ではSR-A KO NODマウス骨髄由来樹状細胞よりのI型IFN産生の促進を認めた。RNAウイルス感染に伴う1型糖尿病発症において、SR-AシグナルはTLR3シグナルに影響を与えている可能性が示唆された。, Domestic conference

    Oral presentation

  • Modified LDLがリガンドであるSR-Aの1型糖尿病発症への影響

    清水まみ, Yasuda Hisafumi, 中村 晃, 勝田敦美, 佐々木弘智, Arai Takashi, 永田正男, 原 賢太, 横野浩一

    第7回加齢医学研究会, Jan. 2012, Japanese, 加齢医学研究会, 名古屋, 【目的】高齢者糖尿病がますます増加している現状において、高齢者糖尿病の中には1型糖尿病も存在する。1型糖尿病は臓器特異的な自己免疫疾患で、抗原特異的T細胞を介して膵島炎が生じ膵β細胞が破壊され糖尿病が発症するが、近年、1型糖尿病発症の原因としてエンテロウイルス感染との関連も指摘されている。そのT細胞の活性化や抑制に関与し樹状細胞やマクロファージの細胞表面上に発現するSR-A(Scavenger Receptor class A)はmodified LDL、bacteria、polyI、polyGなどをリガンドとし、マクロファージや樹状細胞の分化・機能、動脈硬化、感染免疫に関与している。SR-A KOマウス(C57BL/6 background)では動脈硬化や易感染性を示すことが報告されているが、自己免疫における役割は明らかではない。今回我々が1型糖尿, Domestic conference

    Oral presentation

  • 特発性血小板減少性紫斑病の経過中に急性好酸球性肺炎を発症した1例

    倉田 啓之, Toyokuni Takehiro, 三好 園子, 北村 龍義, 高嶋 基嗣, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第196回日本内科学会近畿地方会, Dec. 2011, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • 非閉塞性腸間膜虚血症による広範囲腸管壊死をきたした高齢者1型糖尿病の一例

    藤本 冴子, 原 賢太, Arai Takashi, 三好 園子, 久保川 修, Mori Hiroyuki, 明嵜 太一, Yasuda Hisafumi, 秋田 穂束, 横野 浩一

    第22回日本老年医学会近畿地方会, Nov. 2011, Japanese, 日本老年医学会, 西宮, Domestic conference

    Oral presentation

  • 自己免疫性肝炎、Sjogren症候群、CREST症候群の経過中に発症した1型糖尿病の1例

    渡邊 周平, Yasuda Hisafumi, Toyokuni Takehiro, 三好 園子, 北村 龍義, 高嶋 基嗣, Kanazawa Kenji, 原 賢太, 横野 浩一, 秋田 穂束

    第48回日本糖尿病学会近畿地方会, Oct. 2011, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • 1型糖尿病発症におけるMSR-Aの役割の検討

    清水 まみ, Yasuda Hisafumi, 森山 啓明, 中村 晃, 勝田 敦美, 花野 智苗, 佐々木 弘智, Arai Takashi, 永田 正男, 原 賢太, 横野 浩一

    第9回1型糖尿病研究会, Oct. 2011, Japanese, 1型糖尿病研究会, 大磯, Domestic conference

    Oral presentation

  • 経過中に難治性食道潰瘍を合併し腸管ベーチェット病と考えられた一例

    Toyokuni Takehiro, 渡邉 周平, 三好 園子, Nishimura Mitsushige, 北村 龍義, 高嶋 基嗣, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第195回日本内科学会近畿地方会, Sep. 2011, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • 感染性心内膜炎に感染性動脈瘤が合併した1例

    菅原 安章, 久保川 修, 三好 園子, Mori Hiroyuki, 明嵜 太一, 平岡 栄治, Yasuda Hisafumi, Kanazawa Kenji, 原 賢太, 秋田 穂束

    第194回日本内科学会近畿地方会, Jun. 2011, Japanese, 日本内科学会, 奈良, Domestic conference

    Oral presentation

  • クレブシエラ眼内炎を契機に多発肝・脳膿瘍、全身性感染性塞栓症が判明した1例

    末松 那都, Toyokuni Takehiro, Nishimura Mitsushige, 井上 通彦, 高嶋 基嗣, Yasuda Hisafumi, Kanazawa Kenji, 秋田 穂束

    第194回日本内科学会近畿地方会, Jun. 2011, Japanese, 日本内科学会, 奈良, Domestic conference

    Oral presentation

  • Stenotrophomonas maltophiliaの保菌及び感染事例についての検討

    阿部 泰尚, Yasuda Hisafumi, 明嵜 太一, Arai Takashi, 原 賢太, 横野 浩一, Arakawa Soichi

    第53回日本老年医学会学術集会, Jun. 2011, Japanese, 日本老年医学会, 東京, Domestic conference

    Oral presentation

  • 膵β細胞特異的Rheb過剰発現NODマウスにおける1型糖尿病発症の検討.

    佐々木 弘智, Yasuda Hisafumi, 森山 啓明, 清水 まみ, 中村 晃, Arai Takashi, 永田 正男, 原 賢太, 横野 浩一

    第54回日本糖尿病学会学術集会, May 2011, Japanese, 日本糖尿病学会, 札幌, Domestic conference

    Oral presentation

  • 壊死性虚血性腸炎の術後に肺塞栓と持続する菌血症を来した1型糖尿病の一例

    Arai Takashi, Yasuda Hisafumi, 世戸 博之, 北村 龍義, 井手 茜, 明嵜 太一, 平岡 栄治, Kanazawa Kenji, 原 賢太, 秋田 穂束, 横野 浩一

    第47回 日本糖尿病学会近畿地方会, Nov. 2010, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • 膵β細胞におけるRheb過剰発現によって誘導されるmTORC1経路活性化NODマウスに及ぼす影響

    佐々木 弘智, 森山 啓明, Yasuda Hisafumi, 清水 まみ, 中村 晃, Arai Takashi, 原 賢太, 永田 正男, 横野 浩一

    第8回1型糖尿病研究会, Oct. 2010, Japanese, 日本糖尿病学会, 長崎, Domestic conference

    Oral presentation

  • 先端巨大症に合併した著明な心拡大を伴う心不全の1例

    鈴木 輝, 井上通彦, Kanazawa Kenji, Yasuda Hisafumi, 高嶋 基嗣, Toyokuni Takehiro, 小山晋太郎, 秋田穂束

    第192回日本内科学会近畿地方会, Sep. 2010, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • 無～微量アルブミン尿を呈しつつも腎機能低下を認める高齢2型糖尿病患者の特徴

    来住 稔, 奥町 恭代, Yasuda Hisafumi, 森山 啓明, 原 賢太, 櫻井 孝, 永田 正男, 横野 浩一

    第52回日本老年医学会学術集会, Jun. 2010, Japanese, 日本老年医学会, 神戸, Domestic conference

    Oral presentation

  • 特徴的な症候によりNoonan症候群が疑われ、小腸出血を来した1例

    芳野 弘, 明嵜 太一, 奥町 恭代, 河野 泰博, Yasuda Hisafumi, 森山 啓明, 原 賢太, 櫻井 孝, 横野 浩一, 秋田 穂束

    第191回日本内科学会近畿地方会, Jun. 2010, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • 小腸粘膜維持機構におけるアミノ酸‐mTORシグナルの役割

    中村 晃, 濱田 水鈴, 原 賢太, Yasuda Hisafumi, 森山 啓明, 永田 正男, 横野 浩一

    第52回日本老年医学会学術集会, Jun. 2010, Japanese, 日本老年医学会, 神戸, Domestic conference

    Oral presentation

  • 高齢者の細菌感染症におけるプロカルシトニンキットの有用性

    Arai Takashi, 黒田 祥二, 来住 稔, 奥町 恭代, Yasuda Hisafumi, 森山 啓明, 原 賢太, 永田 正男, 森田 須美春, 横野 浩一

    第52回日本老年医学会学術集会, Jun. 2010, Japanese, 日本老年医学会, 神戸, Domestic conference

    Oral presentation

  • 高齢2型糖尿病患者における腎症進展・心機能低下に影響を与える因子解析と治療介入効果の検討

    Fujihira Kazuhiro, 永田 正男, 来住 稔, 奥町 恭代, Yasuda Hisafumi, 森山 啓明, 原 賢太, 櫻井 孝, Baba Hisamitsu, 横野 浩一

    第52回日本老年医学会学術集会, Jun. 2010, Japanese, 日本老年医学会, 神戸, Domestic conference

    Oral presentation

  • 膵β細胞mTORC1経路活性化によるNODマウス糖尿病発症に対する影響

    佐々木 弘智, 森山 啓明, 清水 まみ, 中村 晃, Arai Takashi, 来住 稔, 濱田 水鈴, 奥町 恭代, Yasuda Hisafumi, 原 賢太, 永田 正男, 横野 浩一

    第53回日本糖尿病学会学術集会, May 2010, Japanese, 日本糖尿病学会, 岡山, Domestic conference

    Oral presentation

  • 免疫異常を呈し眼球運動異常を合併した高齢者AIHAの一例

    奥町恭代, 明嵜太一, 河野泰博, Yasuda Hisafumi, 森山啓明, 原 賢太, 櫻井 孝, 永田正男, 横野浩一

    第20回日本老年医学会近畿地方会, Dec. 2009, Japanese, 日本老年医学会, 大阪, Domestic conference

    Oral presentation

  • 高齢者糖尿病で進行性核上性麻痺、アルツハイマー型認知症が疑われた1例

    芳野 弘, 原 賢太, 永田正男, 森山啓明, Yasuda Hisafumi, 河野泰博, 桜井 孝, 明嵜太一, 見市義亮, 横野浩一

    第190回日本内科学会近畿地方会, Dec. 2009, Japanese, 日本内科学会, 神戸, Domestic conference

    Oral presentation

  • 急性膵炎に準じて治療した2型糖尿病の1例

    高橋利匡, 小林寛和, 河野泰博, Yasuda Hisafumi, 森山啓明, 原 賢太, 櫻井 孝, 永田正男, 横野浩一

    第20回日本老年医学会近畿地方会, Dec. 2009, Japanese, 日本老年医学会, 大阪, Domestic conference

    Oral presentation

  • 食道アカラシアを合併した多腺性自己免疫症候群の1例

    小林寛和, Yasuda Hisafumi, 河野泰博, 明嵜太一, 森山啓明, 原 賢太, 櫻井 孝, 永田正男, 横野浩一

    第46回日本糖尿病学会近畿地方会第45回日本糖尿病協会近畿地方会, Nov. 2009, Japanese, 日本糖尿病学会, 京都, Domestic conference

    Oral presentation

  • TGF-βとATRA を用いた抗原特異性CD8 陽性制御性T 細胞の誘導

    来住 稔, Yasuda Hisafumi, 阿部泰尚, 奥町恭代, Arai Takashi, 佐々木弘智, 清水まみ, 森山啓明, 永田正男, 横野浩一

    第7回1型糖尿病研究会, Nov. 2009, Japanese, 日本糖尿病学会, 栃木, Domestic conference

    Oral presentation

  • 腎症進展・心機能低下に影響を及ぼす因子の検討（高齢2型糖尿病患者における経過観察・治療介入に基づく解析）

    Fujihira Kazuhiro, Baba Hisamitsu, 永田正男, 来住 稔, 奥町恭代, Yasuda Hisafumi, 森山啓明, 原 賢太, 櫻井 孝, 横野浩一

    第26回日本老年医学会 総会第51回日本老年医学会 学術集会, Jun. 2009, Japanese, 日本老年医学会, 横浜, Domestic conference

    Oral presentation

  • 神戸大学医学部付属病院における血液培養陽性例の検討

    阿部泰尚, Yasuda Hisafumi, 森山啓明, 原 賢太, 櫻井 孝, 永田正男, 横野浩一

    第26回日本老年医学会 総会第52回日本老年医学会 学術集会, Jun. 2009, Japanese, 日本老年医学会, 横浜, Domestic conference

    Poster presentation

  • 高齢者糖尿病における推定GFRとクレアチニンクレアランス

    Arai Takashi, 森山啓明, 来住 稔, 奥町恭代, Yasuda Hisafumi, 原 賢太, 永田正男, 横野浩一

    第26回日本老年医学会 総会第52回日本老年医学会 学術集会, Jun. 2009, Japanese, 日本老年医学会, 横浜, Domestic conference

    Oral presentation

  • 興味深い経過を示し多発生筋炎を発症した間接リウマチの1例

    小林寛和, Yasuda Hisafumi, 河野泰博, 明嵜太一, 森山啓明, 原 賢太, 櫻井 孝, 永田正男, 横野浩一

    第188回日本内科学会近畿地方会, Jun. 2009, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • アミノ酸欠乏食マウスモデルを用いた小腸粘膜障害におけるmTORシグナルの関与

    中村 晃, 原 賢太, 濵田水鈴, Yasuda Hisafumi, 森山啓明, 永田正男, 横野浩一

    第26回日本老年医学会 総会第51回日本老年医学会 学術集会, Jun. 2009, Japanese, 日本老年医学会, 横浜, Domestic conference

    Oral presentation

  • ペプチド誘導1型糖尿病マウスにおける複数のエピトープペプチドを用いた発症抑制の検討

    奥町恭代, 森山啓明, 佐々木弘智, 阿部泰尚, 清水まみ, Arai Takashi, 来住 稔, Yasuda Hisafumi, 原 賢太, 永田正男, 横野浩一

    第52回糖尿病学会年次学術集会, May 2009, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • Macrophage Scavenger Receeptor classA(MSR-A) 欠失NODマウスにおける1型糖尿病発症抑制

    亀野まみ, 森山啓明, 佐々木弘智, 阿部泰尚, Arai Takashi, 中村 晃, 来住 稔, 奥町恭代, Yasuda Hisafumi, 原 賢太, 永田正男, 横野浩一, 高橋和眞

    第52回糖尿病学会年次学術集会, May 2009, Japanese, 日本糖尿病学会, 大阪, Domestic conference

    Oral presentation

  • 腎症進展・心機能低下に影響を及ぼす因子の検討（高齢2型糖尿病患者における経過観察・治療介入に基づく解析）

    Fujihira Kazuhiro, 永田 正男, 来住 稔, 奥町 恭代, Yasuda Hisafumi, 森山 啓明, 原 賢太, 櫻井 孝, Baba Hisamitsu, 横野 浩一

    第51回日本老年医学会学術集会, 2009, Japanese, 日本老年医学会, 横浜市, Domestic conference

    Oral presentation

  • インスリンの潜在的なエピトープを用いた自己免疫性糖尿病の治療

    Moriyama Hiroaki, Yasuda Hisafumi, Nagata Masao, Yokono Koichi

    第38回日本免疫学会総会, Dec. 2008, Japanese, 日本免疫学会, 京都, Domestic conference

    Poster presentation

  • NODlpr/lpr骨髄由来樹状細胞による自己免疫糖尿病の抑制

    Yasuda Hisafumi, Moriyama Hiroaki, Yokono Koichi, Nagata Masao

    第38回日本免疫学会総会, Dec. 2008, Japanese, 日本免疫学会, 京都, Domestic conference

    Poster presentation

  • 膵腎同時移植後に肺クリプトコッカス症を発症した1型糖尿病の1例

    Akisaki Taichi, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第45回日本糖尿病学会近畿地方会, Nov. 2008, Japanese, 日本糖尿病学会, 神戸, Domestic conference

    Oral presentation

  • 糖尿病の経過中に低血糖発作,低蛋白症を認めた一例

    Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第19回日本老年医学会近畿地方会, Nov. 2008, Japanese, 日本老年医学会, 京都, Domestic conference

    Oral presentation

  • 臭化ジスチグミンによるコリン作動性クリーゼをきたした高齢者の1例

    Yasuda Hisafumi, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第19回日本老年医学会近畿地方会, Nov. 2008, Japanese, 日本老年医学会, 京都, Domestic conference

    Oral presentation

  • バクタによると思われる急性膵炎と肝障害を合併した巨細胞性動脈炎の1例

    Akisaki Taichi, Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第187回日本内科学会近畿地方会, Nov. 2008, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • コントロール不良の緩徐進行型1型糖尿病(SPIDDM)に子宮留膿種を合併した1例

    Abe Yasuhisa, Yasuda Hisafumi, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第19回日本老年医学会近畿地方会, Nov. 2008, Japanese, 日本老年医学会, 京都, Domestic conference

    Oral presentation

  • インスリンの隠れたエピトープを用いた1型糖尿病の治療

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第6回1型糖尿病研究会, Oct. 2008, Japanese, 1型糖尿病研究会, 岩手, Domestic conference

    Oral presentation

  • 未分化転化により急速な憎悪を来たした甲状腺乳頭癌の1例

    Akisaki Taichi, Yasuda Hisafumi, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第186回日本内科学会近畿地方会, Sep. 2008, Japanese, 日本内科学会, 京都, Domestic conference

    Oral presentation

  • 膵β細胞におけるmTORシグナルの活性化と糖尿病発症の抑制

    Hara Kenta, Yasuda Hisafumi, Moriyama Hiroaki, Nagata Masao, Yokono Koichi

    第50回日本老年医学会学術集会・総会, Jun. 2008, Japanese, 日本老年医学会, 千葉, Domestic conference

    Oral presentation

  • 高齢者糖尿病患者の微量アルブミン尿期における腎機能低下

    Yasuda Hisafumi, Moriyama Hiroaki, Sakurai Takashi, Hara Kenta, Nagata Masao, Yokono Koichi

    第50回日本老年医学会学術集会・総会, Jun. 2008, Japanese, 日本老年医学会, 千葉, Domestic conference

    Oral presentation

  • 急速な憎悪を来すも救命し得たサリチルアミド配合総合感冒薬による間質性肺炎の1例

    Yasuda Hisafumi, Hara Kenta, Sakurai Takashi, Nagata Masao, Yokono Koichi

    第185回日本内科学会近畿地方会, Jun. 2008, Japanese, 日本内科学会, 大阪, Domestic conference

    Oral presentation

  • Fas Mutated Dendritic Cell Derived from NOD lpr/lpr Prevent Autoimmune Diabetes

    Yasuda Hisafumi, Moriyama Hiroaki, Yokono Koichi, Nagata Masao

    第８回米国臨床免疫学会議(FOCIS), Jun. 2008, English, 米国臨床免疫学会, Boston, USA, International conference

    Oral presentation

  • Experimental Autoimmune Diabetes (EAD) in Non-diabetes Prone Mice

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Yokono Koichi, Nagata Masao

    第８回米国臨床免疫学会議(FOCIS), Jun. 2008, English, 米国臨床免疫学会, Boston, USA, International conference

    Oral presentation

  • ペプチド誘導1型糖尿病マウスモデルにおける自己抗原ペプチド免疫原性の検討

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第51回日本糖尿病学会年次学術集会, May 2008, Japanese, 日本糖尿病学会, 東京, Domestic conference

    Oral presentation

  • インスリンシグナルペプチドを用いた免疫寛容の誘導による1型糖尿病治療

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第51回日本糖尿病学会年次学術集会, May 2008, Japanese, 日本糖尿病学会, 東京, Domestic conference

    Oral presentation

  • NODlpr/lprマウス由来骨髄樹状細胞によるNOD糖尿病の発症抑制におけるFasシグナルの役割

    Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Nagata Masao, Yokono Koichi

    第51回日本糖尿病学会年次学術集会, May 2008, Japanese, 日本糖尿病学会, 東京, Domestic conference

    Oral presentation

  • mTORシグナルのRhebによる活性化は膵β細胞の成長を促し高血糖を抑制する

    Hara Kenta, Yasuda Hisafumi, Moriyama Hiroaki, Nagata Masao, Yokono Koichi

    第51回日本糖尿病学会年次学術集会, May 2008, Japanese, 日本糖尿病学会, 東京, Domestic conference

    Oral presentation

  • ＲhebによるｍＴＯＲＣ１経路の活性化は膵β細胞の成長を促し高血糖を抑制する

    Hara Kenta, Yasuda Hisafumi, Moriyama Hiroaki, Nagata Masao, Yokono Koichi

    第19回分子糖尿病学シンポジウム, Dec. 2007, Japanese, 分子糖尿病学研究会, 兵庫, Domestic conference

    Oral presentation

  • Preventive effect of NODLPR/LPR_ derived dendritic cells to autoimmune diabetes via fas-fasl interaction.

    Yasuda Hisafumi, Moriyama Hiroaki, Yokono Koichi, Nagata Masao

    9thInternationalCongressoftheImmunologyofDiabetesSocietyandAmericanDiabetesAssociationReseachSymposium, Nov. 2007, English, 米国糖尿病学会, マイアミ, アメリカ, International conference

    Poster presentation

  • One amino acid difference of insulinb:9-23 peptides critically influence on the effect of deletional therapy for experimental autoimmune diabetes(ead)

    Moriyama Hiroaki, Yasuda Hisafumi, Yokono Koichi, Nagata Masao

    9thInternationalCongressoftheImmunologyofDiabetesSocietyandAmericanDiabetesAssociationReseachSymposium, Nov. 2007, English, 米国糖尿病学会, マイアミ, アメリカ, International conference

    Poster presentation

  • Intravenous administration of murine proinsulin1 or 2 expressing recombinant adenovirus vector protects diabetes in NOD mice.

    Moriyama Hiroaki, Yasuda Hisafumi, Yokono Koichi, Nagata Masao

    9thInternationalCongressoftheImmunologyofDiabetesSocietyandAmericanDiabetesAssociationReseachSymposium, Nov. 2007, English, 米国糖尿病学会, マイアミ, アメリカ, International conference

    Poster presentation

  • Autoreactive T cell responses in CD25 negative fraction of peripheral blood mononuclear cells from established type 1 diabetes

    Moriyama Hiroaki, Yasuda Hisafumi, Yokono Koichi, Nagata Masao

    9thInternationalCongressoftheImmunologyofDiabetesSocietyandAmericanDiabetesAssociationReseachSymposium, Nov. 2007, English, 米国糖尿病学会, マイアミ, アメリカ, International conference

    Poster presentation

  • 少人数の集団栄養指導の効果～栄養指導システムと高脂血症の症例～

    Shinke Toshiro, Yasuda Hisafumi, Fujihira Kazuhiro

    第27回日本肥満学会, Oct. 2007, Japanese, 日本肥満学会, 神戸, Domestic conference

    Poster presentation

  • 高齢２型糖尿病患者における腎症・心機能低下進展に影響を与える因子の解析

    Fujihira Kazuhiro, Nagata Masao, Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Sakurai Takashi, Baba Hisamitsu, Yokono Koichi

    第１８回日本老年医学会近畿地方会, Oct. 2007, Japanese, 日本老年医学会, 滋賀, Domestic conference

    Oral presentation

  • 高齢2型糖尿病患者における腎症・心機能低下の進展に影響を与える因子の解析

    Fujihira Kazuhiro, Nagata Masao, Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Sakurai Takashi, Baba Hisamitsu, Yokono Koichi

    第18回日本老年医学会近畿地方会, Oct. 2007, Japanese, 日本老年医学会, 大津, Domestic conference

    Oral presentation

  • リツキマブ・メルファラン併用療法が著効した悪性リンパ腫の一例

    Akisaki Taichi, Hara Kenta, Yasuda Hisafumi, Sakurai Takashi, Okano Hiroyuki, Nagata Masao, Yokono Koichi, Saigo Katsuyasu

    第１８回日本老年医学会近畿地方会, Oct. 2007, Japanese, 日本老年医学会, 滋賀, Domestic conference

    Oral presentation

  • オンラインHDF導入にて安定した経過を示すλ型軽鎖沈着症の１例

    Yasuda Hisafumi, Sakurai Takashi, Okano Hiroyuki, Nagata Masao, Yokono Koichi

    第183回日本内科学会近畿地方会, Sep. 2007, Japanese, 日本内科学会, 兵庫, Domestic conference

    Oral presentation

  • MRIで経過を評価しえた悪性症候群の１例

    Akisaki Taichi, Yasuda Hisafumi, Hara Kenta, Sakurai Takashi, Okano Hiroyuki, Nagata Masao, Yokono Koichi

    第183回日本内科学会近畿地方会, Sep. 2007, Japanese, 日本内科学会, 兵庫, Domestic conference

    Oral presentation

  • 低グルコースによる虚血誘導性転写因子HIF1の阻害とHIF-1amRNA翻訳経路の抑制

    Hara Kenta, Yasuda Hisafumi, Moriyama Hiroaki, Sakurai Takashi, Okano Hiroyuki, Nagata Masao, Yokono Koichi

    第49回日本老年医学会学術集会, Jun. 2007, Japanese, 日本老年医学会, 札幌, Domestic conference

    Oral presentation

  • 高齢者2型糖尿病患者における腎症および心機能低下進展に関する因子解析(5年間の経過観察に基づいて)

    Fujihira Kazuhiro, Nagata Masao, Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Baba Hisamitsu, Yokono Koichi

    第49回日本老年医学会学術集会, Jun. 2007, Japanese, 日本老年医学会, 札幌, Domestic conference

    Oral presentation

  • ＮＯＤlpr/lpr マウス由来骨髄樹状細胞を用いた自己免疫性糖尿病に対する発症制御

    Yasuda Hisafumi, Moriyama Hiroaki, Hara Kenta, Nagata Masao, Yokono Koichi

    第５０回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

    Oral presentation

  • 肥満糖尿病モデルマウスKK-AyマウスにおけるmTOR遺伝子ヘテロ欠損は肥満抵抗をもたらす

    Hara Kenta, Yasuda Hisafumi, Moriyama Hiroaki, Nagata Masao, Yokono Koichi

    第５０回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

    Oral presentation

  • インスリンペプチド誘導１型糖尿病マウスにおける同一抗原静脈内投与による糖尿病発症制御機序の検討

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第５０回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

    Oral presentation

  • インスリンノックアウトＮＯＤマウスにおける膵島細胞及び膵島浸潤細胞の解析

    Moriyama Hiroaki, Yasuda Hisafumi, Hara Kenta, Nagata Masao, Yokono Koichi

    第５０回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

    Oral presentation

  • アデノウイルスベクターを用いた１型糖尿病におけるinsulin分子の免疫原生の検討

    Moriyama Hiroaki, Yasuda Hisafumi, Nagata Masao, Yokono Koichi

    第５０回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

    Oral presentation

Association Memberships

  • 日本消化器病学会

  • 日本リウマチ学会

  • 日本免疫学会

  • 日本老年医学会

  • 日本糖尿病学会

  • 日本内科学会

Research Projects