{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=306190","label":"url"}],"paper_title":{"en":"今求められているNSTと薬剤師の役割: 臨床・研究・教育を柱とするNST活動の実践","ja":"今求められているNSTと薬剤師の役割: 臨床・研究・教育を柱とするNST活動の実践"},"authors":{"en":[{"name":"Okada Naoto"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡田 直人"},{"name":"石澤 啓介"}]},"publication_date":"2015-12","publication_name":{"en":"薬事新報","ja":"薬事新報"},"volume":"2921","starting_page":"1306","ending_page":"1310","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24882646","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=278303","label":"url"}],"paper_title":{"en":"Drug development for cardiorenal disease based on oxidative stress control","ja":"酸化ストレス制御を基盤とする新規心腎血管障害治療薬の開発"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"},{"name":"SAKURADA TAKUMI"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 啓介"},{"name":"櫻田 巧"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review.","ja":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review."},"publication_date":"2014-06","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"134","number":"6","starting_page":"715","ending_page":"719","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.13-00255-4"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/130001871942/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282681104589184/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=230718","label":"url"}],"paper_title":{"en":"Drug Discovery for Improvement of Chronic Kidney Disease and Cardiovascular Disease","ja":"腎・心血管障害における細胞内分子機構の解明とその治療法の開発"},"authors":{"en":[{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 啓介"}]},"description":{"en":"Chronic kidney disease (CKD) has been increasingly recognized as a major public health problem in the world. Recent studies have showed that CKD is an independent risk factor for the occurrence of cardiovascular disease (CVD). Reactive oxygen species (ROS), generated by reduction-oxidation actions, have been generated by reduction-oxidation actions, recognized as the important chemical mediators that regulate signal transduction in various cells including vascular smooth muscle cells (VSMC) and mesangial cells (MC). It has been showed that increase in ROS generation may relate to a risk for CVD and CKD. In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Control of the oxidative stress and ROS-mediated alterations of signaling molecules including MAP kinases may provide new therapeutic strategy against CKD and CVD. In this review, we summarize mainly our data regarding the pharmacological effects of renin-angiotensin-aldosterone system blockers, bioflavonoids and adiponectin in VSMC and MC. Also we review the data on a possible new class drug against oxidative stress to improve CKD and CVD.","ja":"Chronic kidney disease (CKD) has been increasingly recognized as a major public health problem in the world. Recent studies have showed that CKD is an independent risk factor for the occurrence of cardiovascular disease (CVD). Reactive oxygen species (ROS), generated by reduction-oxidation actions, have been generated by reduction-oxidation actions, recognized as the important chemical mediators that regulate signal transduction in various cells including vascular smooth muscle cells (VSMC) and mesangial cells (MC). It has been showed that increase in ROS generation may relate to a risk for CVD and CKD. In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Control of the oxidative stress and ROS-mediated alterations of signaling molecules including MAP kinases may provide new therapeutic strategy against CKD and CVD. In this review, we summarize mainly our data regarding the pharmacological effects of renin-angiotensin-aldosterone system blockers, bioflavonoids and adiponectin in VSMC and MC. Also we review the data on a possible new class drug against oxidative stress to improve CKD and CVD."},"publication_date":"2011-09","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"131","number":"9","starting_page":"1347","ending_page":"1352","languages":["jpn"],"invited":true,"identifiers":{"doi":["10.1248/yakushi.131.1347"],"issn":["0031-6903"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=161693","label":"url"}],"paper_title":{"en":"医療人としての薬剤師育成教育の実践 --- ∼米国の薬学教育ならび日本の医学教育から学ぶ∼","ja":"医療人としての薬剤師育成教育の実践 --- ∼米国の薬学教育ならび日本の医学教育から学ぶ∼"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"publication_date":"2007-03","publication_name":{"en":"Medicine and Drug Journal","ja":"医薬ジャーナル"},"volume":"43","number":"3","starting_page":"871","ending_page":"874","languages":["jpn"],"identifiers":{"issn":["0287-4741"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://tokushima-u.repo.nii.ac.jp/records/2003393","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=246580","label":"url"}],"paper_title":{"en":"薬理作用から見た健康食品","ja":"薬理作用から見た健康食品"},"authors":{"en":[{"name":"Tamaki Toshiaki"},{"name":"Yamaguchi Kunihisa"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"玉置 俊晃"},{"name":"山口 邦久"},{"name":"石澤 啓介"}]},"publication_date":"2007","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"63","number":"5,6","starting_page":"170","ending_page":"171","languages":["jpn"],"identifiers":{"issn":["0037-3699"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10018399832/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16971777","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001204271623040/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193074","label":"url"}],"paper_title":{"en":"Intracellular signal transduction of vascular injury in insulin resistance","ja":"インスリン抵抗性による血管障害の細胞内情報伝達機構"},"authors":{"en":[{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Izawa Yuki"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"井澤 有紀"},{"name":"玉置 俊晃"}]},"description":{"en":"近年，メタボリック症候群の疾患概念が確立され，本邦でもその診断基準が発表された．メタボリック症候群の根底にはインスリン抵抗性が存在するといわれるが，高血圧，動脈硬化などの血管病にインスリン抵抗性がどのように関っているかは未だ明らかではない．我々はこの数年，血管病の発症，進展に関わるインスリン抵抗性の細胞内情報伝達機構について研究を行なってきた．糖尿病モデル動物のOLETFラットを用いた検討では，アンジオテンシンII受容体拮抗薬の投与が末梢での糖利用臓器のインスリン抵抗性を改善させ，レニン-アンジオテンシン系のメタボリック症候群への関与が示唆された．培養血管平滑筋細胞を用いた細胞内情報伝達機構の検討では，アンジオテンシンII刺激によって活性化されるMAPキナーゼの一つ，ERK1/2がインスリン抵抗性の発現に関与していることが明らかになった．また，血管リモデリング進展過程のひとつである血管平滑筋細胞の遊走において，SrcチロシンキナーゼやCasアダプタータンパクが細胞内分子として重要な役割を果たしていることを見いだした．血管病におけるインスリン抵抗性に関わる標的分子の探求は，今後も増加することが予想されるメタボリックシンドローム治療のための創薬に有用な情報をもたらすことが期待される．<br>","ja":"近年，メタボリック症候群の疾患概念が確立され，本邦でもその診断基準が発表された．メタボリック症候群の根底にはインスリン抵抗性が存在するといわれるが，高血圧，動脈硬化などの血管病にインスリン抵抗性がどのように関っているかは未だ明らかではない．我々はこの数年，血管病の発症，進展に関わるインスリン抵抗性の細胞内情報伝達機構について研究を行なってきた．糖尿病モデル動物のOLETFラットを用いた検討では，アンジオテンシンII受容体拮抗薬の投与が末梢での糖利用臓器のインスリン抵抗性を改善させ，レニン-アンジオテンシン系のメタボリック症候群への関与が示唆された．培養血管平滑筋細胞を用いた細胞内情報伝達機構の検討では，アンジオテンシンII刺激によって活性化されるMAPキナーゼの一つ，ERK1/2がインスリン抵抗性の発現に関与していることが明らかになった．また，血管リモデリング進展過程のひとつである血管平滑筋細胞の遊走において，SrcチロシンキナーゼやCasアダプタータンパクが細胞内分子として重要な役割を果たしていることを見いだした．血管病におけるインスリン抵抗性に関わる標的分子の探求は，今後も増加することが予想されるメタボリックシンドローム治療のための創薬に有用な情報をもたらすことが期待される．<br>"},"publication_date":"2006-09-01","publication_name":{"en":"Folia Pharmacologica Japonica","ja":"日本薬理学雑誌"},"volume":"128","number":"3","starting_page":"147","ending_page":"151","languages":["jpn"],"identifiers":{"doi":["10.1254/fpj.128.147"],"issn":["0015-5691"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc","id":"30612734"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193075","label":"url"}],"paper_title":{"en":"栄養管理における薬剤師の役割 --- 大学病院における栄養サポートチーム(NST)活動","ja":"栄養管理における薬剤師の役割 --- 大学病院における栄養サポートチーム(NST)活動"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Minakuchi Kazuo"}],"ja":[{"name":"石澤 啓介"},{"name":"水口 和生"}]},"publication_date":"2005-01","publication_name":{"en":"調剤と情報","ja":"調剤と情報"},"volume":"11","number":"1","starting_page":"95","ending_page":"100","languages":["jpn"],"invited":true,"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/80016906565/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1573950401508262400/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193076","label":"url"}],"paper_title":{"en":"大学病院における栄養支援チーム(NST)と薬剤師","ja":"大学病院における栄養支援チーム(NST)と薬剤師"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Houchi Hitoshi"},{"name":"Minakuchi Kazuo"}],"ja":[{"name":"石澤 啓介"},{"name":"芳地 一"},{"name":"水口 和生"}]},"publication_date":"2004-10","publication_name":{"en":"Journal of Japnese Society of Hospital Pharmacists","ja":"日本病院薬剤師会雑誌"},"volume":"40","number":"10","starting_page":"1245","ending_page":"1248","languages":["jpn"],"invited":true,"identifiers":{"issn":["1341-8815"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc","id":"30612736"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=274833","label":"url"}],"paper_title":{"en":"米国における臨床薬剤師教育制度および卒後教育制度の研究","ja":"米国における臨床薬剤師教育制度および卒後教育制度の研究"},"authors":{"en":[{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 啓介"}]},"publication_date":"2005-03","publication_name":{"en":"厚生労働科学研究費補助金 医薬品・医療機器等レギュラトリーサイエンス総合研究推進事業","ja":"厚生労働科学研究費補助金 医薬品・医療機器等レギュラトリーサイエンス総合研究推進事業"},"starting_page":"809","ending_page":"828","languages":["jpn"],"invited":true,"misc_type":"others"},"priority":"input_data"}
{"insert":{"user_id":"6000008820","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=176514","label":"url"}],"paper_title":{"en":"インスリン抵抗性に対するロサルタンおよびロサルタンと運動の併用による効果-モデルラットを用いたin vivoでの検討-","ja":"インスリン抵抗性に対するロサルタンおよびロサルタンと運動の併用による効果-モデルラットを用いたin vivoでの検討-"},"authors":{"en":[{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2002-03-12","publication_name":{"en":"第17回 健康医科学 研究助成論文集","ja":"第17回 健康医科学 研究助成論文集"},"number":"17","starting_page":"124","ending_page":"134","languages":["jpn"],"invited":true,"misc_type":"others"},"priority":"input_data"}