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2. A novel haemodilution chip mounted on the total thrombus‐formation analysis system, a flow chamber system, enables stable analysis of platelet products under low platelet concentration/high shear conditions.

Author

Fuchizaki, Akihiro, Yasui, Kazuta, Hayashi, Tomoya, Tanaka, Mitsunobu, Oyamada, Chiaki, Ohnishi‐Wada, Tomoko, Hosokawa, Kazuya, Fujimura, Yoshihiro, Shimogaki, Kazushige, Hirayama, Fumiya, Kimura, Takafumi, and Takihara, Yoshihiro

Subjects
PLATELET count, ERYTHROCYTES, PLASMA products, ADENOSINE diphosphate, SHEARING force
Abstract

Background and Objectives: The total thrombus‐formation analysis system (T‐TAS) can quantitatively analyse the contribution of platelets to haemostasis using reconstituted blood samples. However, it is unsuitable in cases with low platelet counts. We introduced a haemodilution (HD) chip with a shallow chamber depth, adapted to low platelet counts and high shear conditions (1500 s−1). Materials and Methods: Blood samples were prepared by mixing red blood cell products, standard human plasma and platelet products; the final platelet count was 50 × 103/μL. Aggregation tests were performed by using the aggregation inducers collagen, adenosine diphosphate (ADP) and ristocetin. Samples with 2‐, 4‐ and 9‐day‐old platelet products (N = 10) were evaluated. Results: The HD chip enabled the stable analysis of the haemostatic function of all samples at a platelet count of 50 × 103/μL. Haemostatic function was correlated with ADP aggregation (time to 10 kPa [T10]: r = −0.53; area under the curve for 30 min: r = 0.40) and storage period (T10: r = 0.44). Conclusion: The HD chip‐mounted T‐TAS can stably analyse haemostatic function under low platelet counts and high shear conditions; this approach is expected to serve as a bridge to in vivo haemostatic tests with experimental animals. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Hereditary TTP/Upshaw–Schulman syndrome: the ductus arteriosus controls newborn survival.

Author

Fujimura, Yoshihiro

Abstract

Hereditary TTP (hTTP), termed Upshaw–Schulman syndrome, is an ultra-rare disorder caused by a severe deficiency of plasma ADAMTS13 activity that allows circulation of ultra-large von Willebrand factor (UL-VWF) multimers. The greatest risk for hTTP is in their first days after birth, when 35–50% of patients will have severe hemolysis, jaundice, and thrombocytopenia. It is often fatal without effective treatment. In utero, fetal blood flowing from the pulmonary artery through the ductus arteriosus (DA) to the aorta is under low-shear-force. At birth, blood flow through the DA reverses to a left-to-right shunt, and the diameter of the DA begins to decrease due to hyper-oxygenated blood and decreased plasma prostaglandin E2. This causes turbulent circulation that unfolds UL-VWF, allowing platelet aggregation. If the DA closes promptly, hTTP newborns survive, but if it remains patent, turbulent circulation persists, triggering microvascular thrombosis. hTTP is commonly diagnosed as hemolytic disease of the fetus and newborn (HDFN) caused by anti-red cell antibodies and treated with exchange blood transfusion, which prevents kernicterus even when the diagnosis of hTTP is missed. The diagnosis of newborn-onset hTTP should be considered because HDFN does not cause severe thrombocytopenia, which might be effectively treated with recombinant ADAMTS13. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Diagnostic and treatment guidelines for thrombotic thrombocytopenic purpura (TTP) 2017 in Japan

Author

Matsumoto, Masanori, Fujimura, Yoshihiro, Wada, Hideo, Kokame, Koichi, Miyakawa, Yoshitaka, Ueda, Yasunori, Higasa, Satoshi, Moriki, Takanori, Yagi, Hideo, Miyata, Toshiyuki, Murata, Mitsuru, and For TTP group of Blood Coagulation Abnormalities Research Team, Research on Rare and Intractable Disease supported by Health, Labour, and Welfare Sciences Research Grants

Published
2017
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14. A novel quantitative method to evaluate the contribution of platelet products to white thrombus formation in reconstituted blood under flow conditions.

Author

Fuchizaki, Akihiro, Yasui, Kazuta, Hayashi, Tomoya, Tanaka, Mitsunobu, Nagasato, Tomoka, Ohnishi‐Wada, Tomoko, Hosokawa, Kazuya, Fujimura, Yoshihiro, Shimogaki, Kazushige, Hirayama, Fumiya, Takihara, Yoshihiro, and Kimura, Takafumi

Subjects
HEMATOPOIESIS, BLOOD flow, THROMBOSIS, BLOOD platelets, ERYTHROCYTES
Abstract

Background and Objectives: Currently, the quality of platelet (PLT) products is evaluated using a series of in vitro tests, which only analyse PLTs as an inspection material. However, it would be ideal to assess the physiological functions of PLTs under conditions similar to the sequential blood haemostatic process. In this study, we attempted to establish an in vitro system where the thrombogenicity of PLT products was evaluated in the presence of red blood cells (RBCs) and plasma using a microchamber under constant shear stress (600/s). Materials and Methods: Blood samples were reconstituted by mixing PLT products, standard human plasma (SHP) and standard RBCs. Each component was serially diluted keeping the other two components fixed. The samples were applied onto a flow chamber system (Total Thrombus‐formation Analysis System [T‐TAS]), and white thrombus formation (WTF) was assessed under large arterial shear conditions. Results: We observed a good correlation between the PLT numbers in the test samples and WTF. The WTF of samples containing ≦10% SHP was significantly lower than those containing ≧40% SHP, and no difference was observed in WTF among samples containing 40%–100% SHP. WTF significantly declined in the absence of RBCs, whereas no change in WTF was observed in the presence of RBCs, over haematocrit range of 12.5%–50%. Conclusion: The WTF assessed on the T‐TAS using reconstituted blood may serve as a new physiological blood thrombus test to quantitatively determine the quality of PLT products. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Eculizumab in the treatment of atypical hemolytic uremic syndrome in an infant leads to cessation of peritoneal dialysis and improvement of severe hypertension

Author

Ohta, Toshiyuki, Urayama, Kohtaro, Tada, Yoshihiro, Furue, Takeki, Imai, Sayaka, Matsubara, Keita, Ono, Hiroaki, Sakano, Takashi, Jinno, Kazuhiko, Yoshida, Yoko, Miyata, Toshiyuki, and Fujimura, Yoshihiro

Subjects
Continuous ambulatory peritoneal dialysis -- Physiological aspects -- Research, Hemolytic-uremic syndrome -- Drug therapy -- Patient outcomes -- Research, Peritoneal dialysis -- Physiological aspects -- Research, Monoclonal antibodies -- Dosage and administration -- Complications and side effects, Hypertension -- Risk factors -- Prevention -- Research, Health
Abstract

Background Severe hypertension (HTN) and acute kidney injury frequently associated with atypical hemolytic uremic syndrome (aHUS) were refractory to various therapies in the pre-eculizumab era. Here we report the case of a 4-month-old boy who developed aHUS presenting with undetectable C3 protein, no predisposing mutations in complement factors, and no antibodies against factor H. Methods Repeated plasma infusions and nine sessions of plasmapheresis were ineffective. The patient initially required continuous hemodiafiltration and thereafter peritoneal dialysis. Despite vigorous antihypertensive treatment and improved fluid overload with dialysis, HTN persisted. His low C3 level ( Conclusions This infant with HTN and acute kidney injury associated with aHUS was treated successfully with eculizumab. Keywords Plasmapheresis-resistant * Meningococcal infection * Prophylactic antibiotics * Vaccination * Pathological findings * Atypical hemolytic uremic syndrome * Anti-C5 therapy, Introduction Hemolytic uremic syndrome (HUS) is a rare disease with manifestations of microangiopathic hemolytic anemia, thrombocytopenia, and renal impairment. There are two types of HUS: HUS which follows a diarrheal [...]

Published
2015
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20. New load transfer structure to reduce body deformation in side collisions.

Author

Hasegawa, Atsushi, Egawa, Yasuhisa, Nisida, Takuro, Kishida, Kengo, Fujimura, Yoshihiro, Takeuchi, Ryotaro, Yamada, Hitomi, Fujii, Takayuki, and Saito, Yumi

Subjects
BACKPACKS, DEFORMATIONS (Mechanics), LATERAL loads, BENDING moment, AXIAL loads, SHOULDER, BODY weight
Abstract

In this research, body technology was established for side collisions with new IIHS MDB as a representative case. In the conventional body structure, most of the load received from the barrier is absorbed by bending deformation of the door beam and B-pillar, etc. For that reason, the body is subjected to large deformation before reaching the maximum load, and the deformation increases further when subjected to a high-energy collision. Therefore, the objective of this research is to create a structure that increases the load from the initiation of impact and suppresses the deformation of the car body. An arched door beam was developed to reduce the bending moment by the axial load in the longitudinal direction generated during the deformation and to increase the load in the lateral direction. A principle equation was developed that uses the shape of the door beam as a variable. A prototype of the arched door beam was fabricated, and its performance was evaluated by an impactor test. A full-car simulation was conducted using a mass-produced sedan as a base, to which the arched door beam was added to verify the performance of the complete vehicle. The results of the impactor tests were evaluated using the load gradient, which was defined as the generated load divided by the amount of deformation. Compared to conventional straight door beams, the load gradient was 7.1 times higher. Full-car simulation results showed that for a gasoline-powered vehicle body weight, the body load gradient of the proposed structure was 4.7 times higher, and the body deformation adjacent to the dummy shoulder was reduced by 210 mm. Spine acceleration of the dummy was reduced by 56%. The body structure proposed in this research has the effect of increasing the load gradient and reducing body deformation and spine acceleration. It is expected to be applicable to EVs and FCVs, which require more energy absorption due to their increased vehicle weight. [ABSTRACT FROM AUTHOR]

Published
2023
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36. Two Mechanistic Pathways for Thienopyridine-Associated Thrombotic Thrombocytopenic Purpura: A Report From the SERF-TTP Research Group and the RADAR Project

Author

Bennett, Charles L., Kim, Benjamin, Zakarija, Anaadriana, Bandarenko, Nicholas, Pandey, Dilip K., Buffie, Charlie G., McKoy, June M., Tevar, Amul D., Cursio, John F., Yarnold, Paul R., Kwaan, Hau C., De Masi, Davide, Sarode, Ravindra, Raife, Thomas J., Kiss, Joseph E., Raisch, Dennis W., Davidson, Charles, Sadler, J. Evan, Ortel, Thomas L., Zheng, X. Long, Kato, Seiji, Matsumoto, Masanori, Uemura, Masahito, and Fujimura, Yoshihiro

Published
2007
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40. Ticlopidine-associated ADAMTS13 activity deficient thrombotic thrombocytopenic purpura in 22 persons in Japan: a report from the Southern Network on Adverse Reactions (SONAR)

Author

Bennett, Charles L., Jacob, Sony, Dunn, Brianne L., Georgantopoulos, Peter, Zheng, Long X, Kwaan, Hau C., McKoy, June M., Magwood, Jametta S., Qureshi, Zaina P., Bandarenko, Nicholas, Winters, Jeffrey L., Raife, Thomas J., Carey, Patricia M., Sarode, Ravindra, Kiss, Joseph E., Danielson, Constance, Ortel, Thomas L., Clark, William F., Ablin, Richard J., Rock, Gail, Matsumoto, Masanori, and Fujimura, Yoshihiro

Published
2013
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41. Analysis of genetic and predisposing factors in Japanese patients with atypical hemolytic uremic syndrome

Author

Fan, Xinping, Yoshida, Yoko, Honda, Shigenori, Matsumoto, Masanori, Sawada, Yugo, Hattori, Motoshi, Hisanaga, Shuichi, Hiwa, Ryosuke, Nakamura, Fumihiko, Tomomori, Maiko, Miyagawa, Shinichiro, Fujimaru, Rika, Yamada, Hiroshi, Sawai, Toshihiro, Ikeda, Yuhachi, Iwata, Naoyuki, Uemura, Osamu, Matsukuma, Eiji, Aizawa, Yoshiaki, Harada, Hiroshi, Wada, Hideo, Ishikawa, Eiji, Ashida, Akira, Nangaku, Masaomi, Miyata, Toshiyuki, and Fujimura, Yoshihiro

Published
2013
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46. Ticlopidine-, Clopidogrel-, and Prasugrel-Associated Thrombotic Thrombocytopenic Purpura: A 20-Year Review from the Southern Network on Adverse Reactions (SONAR)

Author

Jacob, Sony, Dunn, Brianne L., Qureshi, Zaina P., Bandarenko, Nicholas, Kwaan, Hau C., Pandey, Dilip K., McKoy, June M., Barnato, Sara E., Winters, Jeffrey L., Cursio, John F., Weiss, Ivy, Raife, Thomas J., Carey, Patricia M., Sarode, Ravindra, Kiss, Joseph E., Danielson, Constance, Ortel, Thomas L., Clark, William F., Rock, Gail, Matsumoto, Masanori, Fujimura, Yoshihiro, Zheng, X. Long, Chen, Hao, Chen, Fei, Armstrong, John M., Raisch, Dennis W., and Bennett, Charles L.

Published
2012

47. COVID-19 microthrombosis: unusually large VWF multimers are a platform for activation of the alternative complement pathway under cytokine storm.

Author

Fujimura, Yoshihiro and Holland, Linda Z.

Abstract

ADAMTS13, a metalloproteinase, specifically cleaves unusually large multimers of von Willebrand factor (VWF), newly released from vascular endothelial cells. The ratio of ADAMTS13 activity to VWF antigen (ADAMTS13/VWF) and indicators of the alternative complement pathway (C3a and sC5b-9) are both related to the severity of COVID-19. The ADAMTS13/VWF ratio is generally moderately decreased (0.18–0.35) in patients with severe COVID-19. When these patients experience cytokine storms, both interleukin-8 and TNFα stimulate VWF release from vascular endothelial cells, while interleukin-6 inhibits both production of ADAMTS13 and its interaction with VWF, resulting in localized severe deficiency of ADAMTS13 activity. Platelet factor 4 and thrombospondin-1, both released upon platelet activation, bind to the VWF-A2 domain and enhance the blockade of ADAMTS13 function. Thus, the released unusually-large VWF multimers remain associated with the vascular endothelial cell surface, via anchoring with syndecan-1 in the glycocalyx. Unfolding of the VWF-A2 domain, which has high sequence homology with complement factor B, allows the domain to bind to activated complement C3b, providing a platform for complement activation of the alternative pathway. The resultant C3a and C5a generate tissue factor-rich neutrophil extracellular traps (NETs), which induce the mixed immunothrombosis, fibrin clots and platelet aggregates typically seen in patients with severe COVID-19. [ABSTRACT FROM AUTHOR]

Published
2022
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48. Binding site on human von Willebrand factor of bitiscetin, a snake venom-derived platelet aggregation inducer

Author

Matsui, Taei, Hamako, Jiharu, Matsushita, Tadashi, Nakayama, Takayuki, Fujimura, Yoshihiro, and Titani, Koiti

Subjects
Poisonous snakes -- Venom, Venom -- Physiological aspects, Binding sites (Biochemistry) -- Analysis, Blood platelets -- Aggregation, Biological sciences, Chemistry
Abstract

Results indicate that the alpha-subunit of bitiscetin is closer to the platelet membrane glycoprotein 1b-binding site on human von Willebrand factor than the beta-subunit. Further, the snake venom may modulate Willebrand factor by binding to the A1 domain and inducing conformational change so as to make it accessible to glycoprotein 1b.

Published
2002

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