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Dive into the research topics where Takuma Yamamoto is active.

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Featured researches published by Takuma Yamamoto.


Molecular Genetics and Metabolism | 2011

Retrospective review of Japanese sudden unexpected death in infancy: The importance of metabolic autopsy and expanded newborn screening

Takuma Yamamoto; Hidekazu Tanaka; Hironori Kobayashi; Ko Okamura; Tatsuya Tanaka; Yuko Emoto; Kana Sugimoto; Masato Nakatome; Norio Sakai; Hisanaga Kuroki; Seiji Yamaguchi; Ryoji Matoba

Sudden unexpected death in infancy is defined as sudden unexpected death occurring before 12 months of age. The common causes of sudden unexpected death in infancy are infection, cardiovascular anomaly, child abuse, and metabolic disorders. However, the many potential inherited metabolic disorders are difficult to diagnose at autopsy and may therefore be underdiagnosed as a cause of sudden unexpected death in infancy. In the present study we retrospectively reviewed 30 Japanese sudden unexpected death in infancy cases encountered between 2006 and 2009 at our institute. With postmortem blood acylcarnitine analysis and histological examination of the liver, we found two cases of long-chain fatty acid oxidation defects. Molecular analysis revealed that the one patient had a compound heterozygote for a novel mutation (p.L644S) and a disease-causing mutation (p.F383Y) in the carnitine palmitoyltransferase 2 gene. Furthermore, retrospective acylcarnitine analysis of the newborn screening card of this patient was consistent with carnitine palmitoyltransferase II deficiency. Metabolic autopsy and expanded newborn screening would be helpful for forensic scientists and pediatricians to diagnose fatty acid oxidation disorders and prevent sudden unexpected death in infancy.


Biochemical and Biophysical Research Communications | 2009

Methamphetamine directly accelerates beating rate in cardiomyocytes by increasing Ca2+ entry via L-type Ca2+ channel

Kana Sugimoto; Ko Okamura; Hidekazu Tanaka; Seiji Takashima; Hiroshi Ochi; Takuma Yamamoto; Ryoji Matoba

Methamphetamine induces several cardiac dysfunctions, which leads to arrhythmia, cardiac failure and sudden cardiac death. Although these cardiac alterations elicited by methamphetamine were thought to be due to an indirect action of methamphetamine, namely, an excessive catecholamine release from synaptic terminals, while it seems likely that methamphetamine directly modulates the functioning of cardiomyocytes independent of neurotransmitters. However, the direct effects of methamphetamine on cardiomyocytes are still not clear. We show that methamphetamine directly accelerates the beating rate and alters Ca(2+) oscillation pattern in cultured neonatal rat cardiomyocytes. Adrenergic receptor antagonists did not block the methamphetamine-induced alterations in cardiomyocytes. Treatment with a ryanodine receptor type 2 inhibitor and a sarcoplasmic reticulum Ca(2+)-ATPase inhibitor did not affect these responses, either. In contrast, the L-type Ca(2+) channel inhibitor nifedipine eradicated these responses. Furthermore, methamphetamine elevated the internal free Ca(2+) concentration in HEK-293T cells stably transfected with the L-type Ca(2+) channel alpha1C subunit. In neonatal rat cardiomyocytes, methamphetamine accelerates beating rate and alters Ca(2+) oscillation pattern by increasing Ca(2+) entry via the L-type Ca(2+) channels independent of any neurotransmitters.


Brain & Development | 2014

Carnitine palmitoyltransferase 2 gene polymorphism is a genetic risk factor for sudden unexpected death in infancy.

Takuma Yamamoto; Hidekazu Tanaka; Yuko Emoto; Takahiro Umehara; Yuki Fukahori; Yukiko Kuriu; Ryoji Matoba; Kazuya Ikematsu

RATIONALE Carnitine palmitoyltransferase (CPT) II is one of a pivotal enzyme in mitochondrial fatty acid oxidation, which is essential for energy production during simultaneous glucose sparing and a requirement for major energy supply, such as prolonged fasting or exercise. When infants require more energy than provided by the glycolytic system, they rely on the mitochondrial fatty acid oxidation pathway. Mutations of the CPT2 gene have been reported to cause sudden unexpected death in infancy (SUDI). A thermolabile phenotype of a CPT2 polymorphism (F352C) has been recently reported to reduce CPT II enzyme activity. The F352C variant results in energy crisis at high temperature and is suspected as a risk factor for acute encephalopathy. However, a relationship between CPT2 gene polymorphism and SUDI has not been described. METHODS Single nucleotide polymorphisms of the CPT2 gene were investigated among 54 SUDI cases and 200 healthy volunteers. RESULTS The frequency of the C allele was significantly higher in the SUDI group than in the control group [25.0% vs 16.0%, odds ratio (OR)=1.75, 95% confidence interval (CI)=1.05-2.92, p=0.030). The frequency of the F352C homozygote was significantly higher in the SUDI group than in control group (11.1% vs 3.5%, OR=3.45, 95% CI=1.11-10.73, p=0.036). CONCLUSION The F352C CPT2 variant might be a genetic risk factor for SUDI.


Legal Medicine | 2013

Latent adrenal Ewing sarcoma family of tumors: A case report.

Takuma Yamamoto; Kosho Takasu; Yuko Emoto; Takahiro Umehara; Kazuya Ikematsu; Nobuaki Shikata; Morio Iino; Ryoji Matoba

Ewing sarcoma family of tumors (ESFT) is derived from the neural crest, which originates from basal embryo cells in the primitive neural tube. ESFT often arises at the bone, chest wall, and soft tissues of the thoracic region. However, ESFT that arises from the adrenal gland is much rarer and it is usually revealed by clinical symptoms. We report an autopsy case of suicidal hanging, in which adrenal ESFT was incidentally revealed. To our knowledge, this is the first case of latent ESFT arising from the adrenal gland. Autopsy can sometimes reveal latent disease. Some of these latent diseases are very rare and we would not be able to detect them without a complete autopsy. As forensic pathologists, we should attempt to perform a complete autopsy and report new discoveries for the development of medicine.


Molecular Genetics and Metabolism | 2012

Metabolic autopsy with postmortem cultured fibroblasts in sudden unexpected death in infancy: Diagnosis of mitochondrial respiratory chain disorders

Takuma Yamamoto; Yuko Emoto; Kei Murayama; Hidekazu Tanaka; Yukiko Kuriu; Akira Ohtake; Ryoji Matoba

Mitochondrial respiratory chain disorders are the most common disorders among inherited metabolic disorders. However, there are few published reports regarding the relationship between mitochondrial respiratory chain disorders and sudden unexpected death in infancy. In the present study, we performed metabolic autopsy in 13 Japanese cases of sudden unexpected death in infancy. We performed fat staining of liver and postmortem acylcarnitine analysis. In addition, we analyzed mitochondrial respiratory chain enzyme activity in frozen organs as well as in postmortem cultured fibroblasts. In heart, 11 cases of complex I activity met the major criteria and one case of complex I activity met the minor criteria. In liver, three cases of complex I activity met the major criteria and four cases of complex I activity met the minor criteria. However, these specimens are susceptible to postmortem changes and, therefore, correct enzyme analysis is hard to be performed. In cultured fibroblasts, only one case of complex I activity met the major criteria and one case of complex I activity met the minor criteria. Cultured fibroblasts are not affected by postmortem changes and, therefore, reflect premortem information more accurately. These cases might not have been identified without postmortem cultured fibroblasts. In conclusion, we detected one probable case and one possible case of mitochondrial respiratory chain disorders among 13 Japanese cases of sudden unexpected death in infancy. Mitochondrial respiratory chain disorders are one of the important inherited metabolic disorders causing sudden unexpected death in infancy. We advocate metabolic autopsy with postmortem cultured fibroblasts in sudden unexpected death in infancy cases.


Journal of Obstetrics and Gynaecology Research | 2013

Autopsy case of sudden maternal death from thrombotic thrombocytopenic purpura

Takuma Yamamoto; Yoshihiro Fujimura; Yuko Emoto; Yukiko Kuriu; Morio Iino; Ryoji Matoba

A 31‐year‐old pregnant woman was transferred to the emergency room at 27 weeks of gestation. She had one‐day history of fever and upper abdominal pain. Soon after admission, she underwent cardiopulmonary arrest. Autopsy was performed and multiple microthrombi were seen within the small‐caliber vessels of many organs, but not in the lungs. Immunohistochemical staining revealed that the thrombi were rich in von Willebrand factor. We also obtained results which showed severely deficient plasma a disintegrin‐like and metalloprotease with thrombospondin motifs (ADAMTS) 13 activity and positive ADAMTS13 inhibitor, confirming a diagnosis of thrombotic thrombocytopenic purpura. As far as we know, in Japan, this is the first autopsy report of sudden maternal death from thrombotic thrombocytopenic purpura. We expect that the routine laboratory application of ADAMTS13 assays for unknown thrombocytopenic patients during pregnancy may help in differential diagnosis at an earlier stage of the disease and facilitate tailor‐made therapeutic intervention.


International Journal of Legal Medicine | 2012

Case report of death from falling: Did heart tumor cause syncope?

Takuma Yamamoto; Kosho Takasu; Yuko Emoto; Nobuaki Shikata; Ryoji Matoba

A healthy man in his 30s was working on the balustrade of stairs on the second floor. He suddenly fell downstairs without saying anything. On emergency hospitalization, chest echogram showed left hemothorax. Cardiac echogram showed a floating mass from the mitral valve in the left ventricle and severe mitral regurgitation. Surgery for hemothorax and pulmonary contusion was immediately undertaken. However, bleeding from pulmonary contusion could not be controlled and he underwent cardiopulmonary arrest. Autopsy showed a white, elastic, pendulous mass in the left atrium and a white mass in the lower lobe of the left lung. Tumor histology showed a reticular pattern, Schiller–Duval bodies, eosinophilic hyaline globules, and positive staining for α-fetoprotein. We diagnosed primary lung yolk sac tumor with metastatic intracardiac yolk sac tumor, a rare and highly malignant germ cell tumor. It usually arises in the ovaries and testes, and intracardiac yolk sac tumor is rare. Intracavitary tumors induce obstruction of inflow into and outflow from the ventricular cavity. The most common clinical presentation is dyspnea and syncope. In the present case, metastatic cardiac yolk sac tumor might have disturbed cardiac outflow and affected hemodynamics, probably causing syncope. Unfortunately, he was in a high place at that time and fell to receive pulmonary contusion that led to death. Autopsy may sometimes reveal latent diseases which might be related to the cause of death. We should perform autopsy thoroughly to diagnose not only the cause of death but also the factors leading to death.


Legal Medicine | 2009

Diplotype analysis of the human cardiac sodium channel regulatory region in Japanese cases of sudden death by unknown causes

Masato Nakatome; Takuma Yamamoto; Ichiro Isobe; Ryoji Matoba

Inherited mutations in the human cardiac sodium channel (SCN5A) gene cause arrhythmogenic diseases such as tachyarrhythmia and bradyarrhythmia. Moreover, mutation subsets in the coding region impair SCN5A function, potentially leading to sudden cardiac death (SCD). In the present study, we performed diplotype analysis of the regulatory region of the SCN5A gene in Japanese people who died suddenly because of an unknown cause (sudden death group; n=70) and controls (n=112). There were no significant differences at six polymorphic loci between the groups. However, 38 diplotypes of 6-nucleotide polymorphism variants were identified. One of these diplotypes-Dip.D (CTG-TC/CCG-TC)-occurred significantly more frequently in the sudden death group than in the controls (p<0.01, OR=5.18, 95% CI: 1.38-19.45). Dip.D has two variants (T-1062C and T-847G), and while it is unclear whether these directly affect mRNA expression, a common polymorphism in this region modulates SCN5A expression in vitro. Our results thus suggest that the transcription of the SCN5A Dip.D variant may be associated with arrhythmogenic diseases that can induce sudden death.


The Japanese Biochemical Society/The Molecular Biology Society of Japan | 2017

Identification of specific microRNAs in diabetic-derived neutrophils: functional analysis of miR-129-2-3p and inflammation-related genes

Takahiro Umehara; Takehiko Murase; Ryoichi Mori; Yuki Abe; Takuma Yamamoto; Kazuya Ikematsu


The Molecular Biology Society of Japan | 2016

Expression dynamics of inflammation-related microRNAs in diabetic-derived neutrophils

Takahiro Umehara; Takuma Yamamoto; Takehiko Murase; Yuki Abe; Kimberly A. Mace; Kazuya Ikematsu

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