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| 1.
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Takami, Akiyoshi ; Asakura, Hidesaku ; Koshida, Kiyoshi ; Namiki, Mikio ; Nakao, Shinji ; 高見, 昭良 ; 朝倉, 英策 ; 越田, 潔 ; 並木, 幹夫 ; 中尾, 眞二
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金沢大学医薬保健研究域医学系<br />We report the cases of 3 patients with advanced renal cell carcinoma who underwent reduced-intensity
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allogeneic stem cell transplantation. In 2 partial responders, histologic analyses of metastases revealed prominent accumulation of CD8+ T cells and degenerative changes of clear cell carcinoma, suggestive of induction of tumor-specific cytotoxic T lymphocytes.
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| 2.
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Terakami, Takako ; Sekiya, Akiko ; Hayashi, Kenshi ; Suzuki, Takeshi ; Furusho, Hiroshi ; Asakura, Hidesaku ; Morishita, Eriko ; Wada, Takashi ; 寺上, 貴子 ; 關谷, 暁子 ; 林, 研至 ; 鈴木, 健史 ; 古荘, 浩司 ; 朝倉, 英策 ; 森下, 英理子 ; 和田, 隆志
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[Aim] In this study, the effect of direct oral anticoagulants (DOACs) on protein C (PC) activity was examined using seve
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ral measuring reagents. [Materials and Methods] In total, 90 patients (60 male and ３0 female) with nonvalvular atrial fibrillation or venous thromboembolism (VTE) who were on anticoagulation therapy with DOACs (rivaroxaban, apixaban, or edoxaban) were studied. The plasma levels of PC activity were measured by means of a clotting assay and chromogenic substrate assay, using three reagents for each type of assay. [Result] Prothrombin time (PT) and activated partial thromboplastin time (APTT) were significantly prolonged in a dose-dependent manner in patients who were taking rivaroxaban or edoxaban. PC activity, as measured by all three reagents using the clotting assay, was influenced only by rivaroxaban, indicating an increase in PC activity in a dose-dependent manner. Apixaban did not have any influence on the measurements made using all three reagents in the clotting assay. On the other hand, none of the three FXa inhibitors had any influence on PC activity when it was measured using the three reagents in the chromogenic substrate assay. Plasma samples were collected before, as well as two and four to eight weeks after rivaroxaban administration in seven patients with AF or VTE sequentially. In all three regents using the clotting assay, plasma levels of PC activity had increased after the administration of rivaroxaban. On the other hand, all three regents using the chromogenic assay had very little influence on PC activity after the administration of rivaroxaban. [Conclusion] The inhibitory effects of the different types of DOACs on clotting activity interfere with clotting test measurement systems in patients receiving DOAC therapy. When measuring PC activity while the patient is taking rivaroxaban or edoxaban, it is necessary to use the chromogenic substrate assay to avoid false highs. Moreover, collecting specimens when blood levels of drugs are low, e.g. during the trough phase, whenever possible, would be one way to minimize interference.
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| 3.
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朝倉, 英策 ; Asakura, Hidesaku
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取得学位 : 博士（医学）, 学位授与番号 : 医博乙第1196号, 学位授与年月日：平成5年1月20日,学位授与年：1993
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Sai, Yoshimichi ; Kusaka, Akiyo ; Imanishi, Kaori ; Matsumoto, Manami ; Takahashi, Rie ; Sugimoto, Natsumi ; Sugama, Junko ; Anada, Takako ; Asakura, Hidesaku ; Miyamoto, KenIchi
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金沢大学附属病院薬剤部<br />In the initial treatment of acute myocardial infarction, it is important to administer oral low-dose ac
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etylsalicylic acid (ASA) within 10 min of arrival at the hospital. However, ASA is supplied as an enteric-coated tablet or buffered tablet to prevent gastric irritation. Although current guidelines recommended that patients should chew their initial dose of ASA, there is little evidence as to whether this is efficacious. Therefore, we aimed to make a direct comparison of the pharmacokinetics and pharmacodynamics of ASA after ingestion of intact and chewed nonenteric-coated buffered ASA tablet (NBA) and enteric-coated ASA tablet (ECA) in a quadruple crossover study in healthy volunteers. Chewing ECA accelerated tmax of ASA absorption, which became equivalent to that after ingestion of intact or chewed NBA. A significant decrease in serum thromboxane B2 was observed 20 min after ingestion of chewed ECA, or intact or chewed NBA, and inhibition of platelet aggregation was also observed within 20 min. Thus, chewing of the ECA appears to result in a similar timing of ASA action to that in the case of chewed or unchewed NBA. © 2011 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci Copyright © 2011 Wiley-Liss, Inc.<br />発行後1年より全文公開.
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Maruyama, Keiko ; Morishita, Eriko ; Yuno, Takeo ; Sekiya, Akiko ; Asakura, Hidesaku ; Ohtake, Shigeki ; Yachie, Akihiro
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Introduction: Heme oxygenase-1 (HO-1) is the rate limiting enzyme that catalyzes the conversion of heme into biliverdin,
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free iron, and carbon monoxide (CO). The first human case of HO-1 deficiency showed abnormalities in blood coagulation and the fibrinolytic system. Thus, HO-1 or HO-1 products, such as CO, might regulate coagulation and the fibrinolytic system. This study examined whether tricarbonyldichlororuthenium (II) dimer (CORM-2), which liberates CO, modulates the expression of tissue factor (TF) and plasminogen activator inhibitor type 1 (PAI-1) in human umbilical vein endothelial cells (HUVECs), and TF expression in peripheral blood mononuclear cells (PBMCs). Additionally, we examined the mechanism by which CO exerts its effects. Materials and Methods: HUVECs were pretreated with 50 μM CORM-2 for 3 hours, and stimulated with tumor necrosis factor-α (TNF-α, 10 ng/ml) for an additional 0-5 hours. PBMCs were pretreated with 50-100 μM CORM-2 for 1hour followed by stimulating with lipopolysaccharid (LPS, 10 ng/ml) for additional 0-9 hours. The mRNA and protein levels were determined by RT-PCR and western blotting, respectively. Results: Pretreatment with CORM-2 significantly inhibited TNF-α-induced TF and PAI-1 up-regulation in HUVECs, and LPS-induced TF expression in PBMCs. CORM-2 inhibited TNF-α-induced activation of p38 MAPK, ERK1/2, JNK, and NF-κB signaling pathways in HUVECs. Conclusions: CORM-2 suppresses TNF-α-induced TF and PAI-1 up-regulation, and MAPKs and NF-κB signaling pathways activation by TNF-α in HUVECs. CORM-2 suppresses LPS-induced TF up-regulation in PBMCs. Therefore, we envision that the antithrombotic activity of CORM-2 might be used as a pharmaceutical agent for the treatment of various inflammatory conditions. © 2012 Elsevier Ltd.<br />Thesis of Keiko Maruyama / 丸山 慶子 博士論文 金沢大学医薬保健学総合研究科（保健学専攻）
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| 6.
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Takami, Akiyoshi ; Hayashi, Akiyoshi ; Kita, Daisuke ; Nishimura, Ryosei ; Asakura, Hidesaku ; Nakao, Shinji
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医薬保健研究域医学系<br />We describe an immunocompetent 19-year-old man with CD20-positive primary central nervous system (CNS) l
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ymphoma refractory to chemotherapy and irradiation. After intraventricular administration of rituximab, a chimeric anti-CD20 monoclonal antibody, supplemented with autologous serum, a remarkable response developed to the CNS parenchymal lymphoma. Cytotoxicity assays showed that untreated patient's serum with rituximab, but not that of heat-inactivated patient's serum with rituximab or rituximab alone, induced potent rituximab-mediated cytotoxicity against tumor cells in the patient's cerebrospinal fluid, suggesting induction of complement-dependent cytotoxicity against CNS lymphoma. © 2006 Japanese Cancer Association.
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| 7.
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Takahashi, Ryoichi ; Ono, Kenjiro ; Ikeda, Tokuhei ; Akagi, Akio ; Noto, Daisuke ; Nozaki, Ichiro ; Sakai, Kenji ; Asakura, Hidesaku ; Iwasa, Kazuo ; Yamada, Masahito
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Objective: Familial amyloid polyneuropathy (FAP) is an autosomal dominant form of hereditary amyloidosis. Several studie
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s reported coagulation factor X deficiency and excessive fibrinolysis in immunoglobulin light chain amyloidosis. However, few have investigated coagulation and fibrinolysis in FAP. The objective of this study was to determine abnormalities in plasma biomarkers of coagulation and fibrinolysis in FAP. Methods: We prospectively recruited eight FAP patients with transthyretin mutations and ten age-matched control patients with other neuropathies in our university. We examined plasma biomarkers of coagulation and fibrinolysis including prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin/fibrinogen degradation products, D-dimer, α2-antiplasmin, antithrombin, plasminogen, thrombin-antithrombin complex, plasmin-α2-antiplasmin complex, prothrombin fragment 1+2, and coagulation factor X. The MannWhitney U test was performed for statistical comparisons between FAP and control groups. Results: FAP patients exhibited significantly decreased levels of coagulation factor X, plasminogen and α2-antiplasmin, and significantly increased levels of prothrombin fragment 1+2 compared to control patients. Conclusion: Our results indicate abnormalities of coagulation and fibrinolysis in FAP patients. © 2012 Informa UK, Ltd.
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| 8.
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朝倉, 英策 ; Asakura, Hidesaku
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金沢大学附属病院高密度無菌治療部<br />播種性血管内凝固症候群（DIC）は、基礎疾患の存在下に全身性持続性の著しい凝固活性化をきたし、微小血栓の多発する重篤な病態である。予後改善のためには、より良い診断基準の作成と、病態に応じた治療介入
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が必要である。動物DICモデルにおいては、LPSまたは組織因子（TF）のいずれで誘発するのか区別されることなく使用されてきたが、我々は両モデル間に、凝固線溶病態のみならず炎症や血管作動性物質の観点からも大きな差違が見られることを解明した。<br />Disseminated intravascular coagulation (DIC) is a serious disease that, in the presence of underlying disease, causes persistent, generalized, marked coagulation activation. Early treatment based on an appropriate diagnosis is very important for improving patients’ prognosis.The commonly used conventional animal models of DIC are induced with LPS or tissue factor (TF), and they have been considered to be essentially the same pathologically. However, our group recently showed that the pathology differs greatly depending on the DIC inducer used, at the view point of coagulofibrinolytic activation, inflammation and vasoactive substances.<br />研究課題/領域番号:25462818, 研究期間(年度):2013-04-01 – 2016-03-31
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| 9.
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朝倉, 英策 ; Asakura, Hidesaku
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LPS誘発播種性血管内凝固症候群(DIC)モデルに対して、凝固と炎症の相互作用を遮断する目的で、エリスロポイエチン、CO供給物質、HO-1阻害剤(SnPP)を投与して、血液凝固、線溶、臓器障害、血管作動性物質、病理所見(血栓)、mRNAに対
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する影響を検討した。薬物用量や臓器毎によって違った影響が観察されたが、凝固や線溶に直接影響を及ぼさないこれらの薬物であっても、DIC治療薬として展望があると考えられた。<br />We investigated the effect of erythropoietin, carbon monoxide release molecule and SnPP that may be able to interrupt interaction between coagulation and inflammation, on LPS-induced rat DIC model. The estimated markers were blood coagulation, fibrinolysis, organ injury, vasoactive substances, pathological findings and the mRNA expression of hemostatic substances. Although the effect of these drugs were different among doses or organs, such drugs without the influence on coagulation and fibrinolysis were expected as new DIC drugs.
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| 10.
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朝倉, 英策 ; Asakura, Hidesaku
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LPS または組織因子(TF)で播種性血管内凝固症候群(DIC)モデルを作成し、血管作動性物質である一酸化窒素(NO)やエンドセリン(ET)の役割を評価した。両モデル間で、血管作動性物質は全く異なった役割を果たしていることが明らかになった。
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血管作動性物質を調節する薬物やPGI2 誘導体をDIC モデルに対して投与するとDIC 病態が変化することが確認され、治療応用が可能ではないかと考えられた。<br />研究課題/領域番号:19590549, 研究期間(年度):2007-2008<br />出典：「播種性血管内凝固における炎症と凝固のクロストークと血管作動性物質の意義」研究成果報告書 課題番号19590549（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-19590549/19590549seika/)を加工して作成
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