Updated on 2022/03/26

写真a

 
HORI Mika
 
Organization
Research Institute of Environmental Medicine Division of Stress Adaptation and Protection Lecturer
Graduate School
Graduate School of Medicine
Title
Lecturer
External link

Degree 1

  1. 博士(薬学) ( 2008.3   北海道大学 ) 

Research Areas 2

  1. Life Science / Pathological biochemistry

  2. Life Science / Metabolism and endocrinology

Committee Memberships 1

  1. 日本がん予防学会   評議員  

    2021.9   

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    Committee type:Academic society

Awards 1

  1. 第18回 (平成22年度) 膵臓病研究財団研究奨励賞

    2010.12  

    堀 美香

 

Papers 50

  1. Impact of LDLR and PCSK9 pathogenic variants in Japanese heterozygous familial hypercholesterolemia patients. Reviewed

    Hori M, Ohta N, Takahashi A, Masuda H, Isoda R, Yamamoto S, Son C, Ogura M, Hosoda K, Miyamoto Y, Harada-Shiba M

    Atherosclerosis   Vol. 289   page: 101-108   2019.10

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.atherosclerosis.2019.08.004

    PubMed

  2. Humoral factors secreted from adipose tissue-derived mesenchymal stem cells ameliorate atherosclerosis in Ldlr-/- mice. Reviewed

    Takafuji Y, Hori M, Mizuno T, Harada-Shiba M

    Cardiovascular research   Vol. 115 ( 6 ) page: 1041-1051   2019.5

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1093/cvr/cvy271

    PubMed

  3. Proprotein convertase subtilisin/kexin 9 V4I variant with LDLR mutations modifies the phenotype of familial hypercholesterolemia. Reviewed

    Ohta N, Hori M, Takahashi A, Ogura M, Makino H, Tamanaha T, Fujiyama H, Miyamoto Y, Harada-Shiba M

    Journal of clinical lipidology   Vol. 10 ( 3 ) page: 547 - 555.e5   2016.5

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    Authorship:Lead author, Corresponding author  

    DOI: 10.1016/j.jacl.2015.12.024

    PubMed

  4. Removal of plasma mature and furin-cleaved proprotein convertase subtilisin/kexin 9 by low-density lipoprotein-apheresis in familial hypercholesterolemia: development and application of a new assay for PCSK9. Reviewed

    Hori M, Ishihara M, Yuasa Y, Makino H, Yanagi K, Tamanaha T, Kishimoto I, Kujiraoka T, Hattori H, Harada-Shiba M

    The Journal of clinical endocrinology and metabolism   Vol. 100 ( 1 ) page: E41 - 9   2015.1

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    Authorship:Lead author  

    DOI: 10.1210/jc.2014-3066

    PubMed

  5. Worldwide experience of homozygous familial hypercholesterolaemia: retrospective cohort study Reviewed International coauthorship

    Tromp T.R., Hartgers M.L., Hovingh G.K., Vallejo-Vaz A.J., Ray K.K., Soran H., Freiberger T., Bertolini S., Harada-Shiba M., Blom D.J., Raal F.J., Cuchel M., Tromp T.R., Hovingh G.K., Ray K.K., Bertolini S.A., Pang J., Watts G.F., Greber-Platzer S., Mäser M., Stulnig T.M., Ebenbichler C.F., Bin Thani K., Cassiman D., Descamps O.S., Rymen D., Witters P., Santos R.D., Brunham L.R., Francis G.A., Genest J., Hegele R.A., Kennedy B.A., Ruel I., Sherman M.H., Jiang L., Wang L., Reiner Ž., Blaha V., Ceska R., Dvorakova J., Dlouhy L., Horak P., Soska V., Tichy L., Urbanek R., Vaverkova H., Vrablik M., Zemek S., Zlatohlavek L., Emil S., Naguib T., Reda A., Béliard S., Bruckert E., Gallo A., Elisaf M.S., Kolovou G., Cohen H., Durst R., Dann E.J., Elis A., Hussein O., Leitersdorf E., Schurr D., Setia N., Verma I.C., Alareedh M.D., Al-Khnifsawi M., Abdalsahib Al-Zamili A.F., Rhadi S.H., Shaghee F.K., Arca M., Averna M., Bartuli A., Bucci M., Buonuomo P.S., Calabrò P., Calandra S., Casula M., Catapano A.L., Cefalù A.B., Cicero A.F.G., D'Addato S., D'Erasmo L., Di Costanzo A., Fasano T., Gazzotti M., Giammanco A., Iannuzzo G., Ibba A., Negri E.A., Pasta A., Pavanello C., Pisciotta L., Rabacchi C., Ripoli C., Sampietro T.

    The Lancet   Vol. 399 ( 10326 ) page: 719 - 728   2022.2

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:The Lancet  

    Background: Homozygous familial hypercholesterolaemia (HoFH) is a rare inherited disorder resulting in extremely elevated low-density lipoprotein cholesterol levels and premature atherosclerotic cardiovascular disease (ASCVD). Current guidance about its management and prognosis stems from small studies, mostly from high-income countries. The objective of this study was to assess the clinical and genetic characteristics, as well as the impact, of current practice on health outcomes of HoFH patients globally. Methods: The HoFH International Clinical Collaborators registry collected data on patients with a clinical, or genetic, or both, diagnosis of HoFH using a retrospective cohort study design. This trial is registered with ClinicalTrials.gov, NCT04815005. Findings: Overall, 751 patients from 38 countries were included, with 565 (75%) reporting biallelic pathogenic variants. The median age of diagnosis was 12·0 years (IQR 5·5–27·0) years. Of the 751 patients, 389 (52%) were female and 362 (48%) were male. Race was reported for 527 patients; 338 (64%) patients were White, 121 (23%) were Asian, and 68 (13%) were Black or mixed race. The major manifestations of ASCVD or aortic stenosis were already present in 65 (9%) of patients at diagnosis of HoFH. Globally, pretreatment LDL cholesterol levels were 14·7 mmol/L (IQR 11·6–18·4). Among patients with detailed therapeutic information, 491 (92%) of 534 received statins, 342 (64%) of 534 received ezetimibe, and 243 (39%) of 621 received lipoprotein apheresis. On-treatment LDL cholesterol levels were lower in high-income countries (3·93 mmol/L, IQR 2·6–5·8) versus non-high-income countries (9·3 mmol/L, 6·7–12·7), with greater use of three or more lipid-lowering therapies (LLT; high-income 66% vs non-high-income 24%) and consequently more patients attaining guideline-recommended LDL cholesterol goals (high-income 21% vs non-high-income 3%). A first major adverse cardiovascular event occurred a decade earlier in non-high-income countries, at a median age of 24·5 years (IQR 17·0–34·5) versus 37·0 years (29·0–49·0) in high-income countries (adjusted hazard ratio 1·64, 95% CI 1·13–2·38). Interpretation: Worldwide, patients with HoFH are diagnosed too late, undertreated, and at high premature ASCVD risk. Greater use of multi-LLT regimens is associated with lower LDL cholesterol levels and better outcomes. Significant global disparities exist in treatment regimens, control of LDL cholesterol levels, and cardiovascular event-free survival, which demands a critical re-evaluation of global health policy to reduce inequalities and improve outcomes for all patients with HoFH. Funding: Amsterdam University Medical Centers, Location Academic Medical Center; Perelman School of Medicine at the University of Pennsylvania; and European Atherosclerosis Society

    DOI: 10.1016/S0140-6736(21)02001-8

    Scopus

  6. Association between Achilles Tendon Softness and Atherosclerotic Cardiovascular Disease in Patients with Familial Hypercholesterolemia Reviewed

    Michikura Masahito, Ogura Masatsune, Hori Mika, Matsuki Kota, Makino Hisashi, Hosoda Kiminori, Harada-Shiba Mariko

    Journal of Atherosclerosis and Thrombosis   Vol. advpub ( 0 )   2022.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Japan Atherosclerosis Society  

    <p><b>Aims: </b>Achilles tendon (AT) xanthomas are a specific physical finding of familial hypercholesterolemia (FH) and AT thickness has been used for its diagnosis and evaluation of its severity. Recently, we reported that the AT of FH patients was softer than that of non-FH patients and the combined use of a cut-off value for AT softness with that for AT thickness improved diagnostic accuracy. However, an association between AT softness and severity of atherosclerosis has not been reported. Accordingly, the present study aimed to investigate whether AT softness was associated with carotid atherosclerosis and presence of atherosclerotic cardiovascular disease (ASCVD) in FH.<b> </b></p><p><b>Methods: </b>The AT of 176 genetically diagnosed FH patients and 98 non-FH patients was examined to measure AT thickness and the elasticity index (EI) as an indicator for assessing AT softness using ultrasonography.<b> </b></p><p><b>Results: </b>Increased age was associated with AT softness, and overweight was negatively related to AT softness. There were significant inverse correlations between EI and maximum and mean intima-media thickness (IMT) within the common carotid artery only among FH patients. In multiple linear regression analysis, although the relationship between EI and mean IMT was attenuated, the association between EI and maximum IMT remained robust. In logistic regression analysis adjusted for age, sex and traditional cardiovascular risk factors (smoking history, presence of hypertension, presence of diabetes mellitus, overweight, LDL-cholesterol, HDL-cholesterol, and Log triglycerides), EI was associated with presence of ASCVD (Odds ratio per 1-SD increase, 0.37;95% CI, 0.15 – 0.86; <i>P</i>=0.0252).<b> </b></p><p><b>Conclusion: </b>The degree of lipid deposition in the AT of FH patients could be assessed by its thickness as well as its softness. AT softness is not only useful in diagnosing FH but is also associated with the severity of carotid atherosclerosis and presence of ASCVD. In addition, these findings suggest that AT softness would be helpful in risk assessment for FH patients.</p>

    DOI: 10.5551/jat.63151

    PubMed

    CiNii Research

  7. Current Diagnosis and Management of Abetalipoproteinemia. Reviewed

    Takahashi M, Okazaki H, Ohashi K, Ogura M, Ishibashi S, Okazaki S, Hirayama S, Hori M, Matsuki K, Yokoyama S, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 10 ) page: 1009 - 1019   2021.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:一般社団法人 日本動脈硬化学会  

    <p>Abetalipoproteinemia (ABL) is a rare autosomal recessive disorder caused by biallelic pathogenic mutations in the <i>MTTP</i> gene. Deficiency of microsomal triglyceride transfer protein (MTTP) abrogates the assembly of apolipoprotein (apo) B-containing lipoprotein in the intestine and liver, resulting in malabsorption of fat and fat-soluble vitamins and severe hypolipidemia. Patients with ABL typically manifest steatorrhea, vomiting, and failure to thrive in infancy. The deficiency of fat-soluble vitamins progressively develops into a variety of symptoms later in life, including hematological (acanthocytosis, anemia, bleeding tendency, etc.), neuromuscular (spinocerebellar ataxia, peripheral neuropathy, myopathy, etc.), and ophthalmological symptoms (e.g., retinitis pigmentosa). If left untreated, the disease can be debilitating and even lethal by the third decade of life due to the development of severe complications, such as blindness, neuromyopathy, and respiratory failure. High dose vitamin supplementation is the mainstay for treatment and may prevent, delay, or alleviate the complications and improve the prognosis, enabling some patients to live to the eighth decade of life. However, it cannot fully prevent or restore impaired function. Novel therapeutic modalities that improve quality of life and prognosis are awaited. The aim of this review is to 1) summarize the pathogenesis, clinical signs and symptoms, diagnosis, and management of ABL, and 2) propose diagnostic criteria that define eligibility to receive financial support from the Japanese government for patients with ABL as a rare and intractable disease. In addition, our diagnostic criteria and the entry criterion of low-density lipoprotein cholesterol (LDL-C) <15 mg/dL and apoB <15 mg/dL can be useful in universal or opportunistic screening for the disease. Registry research on ABL is currently ongoing to better understand the disease burden and unmet needs of this life-threatening disease with few therapeutic options. </p>

    DOI: 10.5551/jat.RV17056

    PubMed

  8. Current Diagnosis and Management of Primary Chylomicronemia. Reviewed

    Okazaki H, Gotoda T, Ogura M, Ishibashi S, Inagaki K, Daida H, Hayashi T, Hori M, Masuda D, Matsuki K, Yokoyama S, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 9 ) page: 883 - 904   2021.9

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Atherosclerosis and Thrombosis  

    Primary chylomicronemia (PCM) is a rare and intractable disease characterized by marked accumulation of chylomicrons in plasma. The levels of plasma triglycerides (TGs) typically range from 1,000 - 15,000 mg/dL or higher. PCM is caused by defects in the lipoprotein lipase (LPL) pathway due to genetic mutations, autoantibodies, or unidentified causes. The monogenic type is typically inherited as an autosomal recessive trait with loss-offunction mutations in LPL pathway genes (LPL, LMF1, GPIHBP1, APOC2, and APOA5). Secondary/environmental factors (diabetes, alcohol intake, pregnancy, etc.) often exacerbate hypertriglyceridemia (HTG). The signs, symptoms, and complications of chylomicronemia include eruptive xanthomas, lipemia retinalis, hepatosplenomegaly, and acute pancreatitis with onset as early as in infancy. Acute pancreatitis can be fatal and recurrent episodes of abdominal pain may lead to dietary fat intolerance and failure to thrive. The main goal of treatment is to prevent acute pancreatitis by reducing plasma TG levels to at least less than 500-1,000 mg/dL. However, current TG-lowering medications are generally ineffective for PCM. The only other treatment options are modulation of secondary/environmental factors. Most patients need strict dietary fat restriction, which is often difficult to maintain and likely affects their quality of life. Timely diagnosis is critical for the best prognosis with currently available management, but PCM is often misdiagnosed and undertreated. The aim of this review is firstly to summarize the pathogenesis, signs, symptoms, diagnosis, and management of PCM, and secondly to propose simple diagnostic criteria that can be readily translated into general clinical practice to improve the diagnostic rate of PCM. In fact, these criteria are currently used to define eligibility to receive social support from the Japanese government for PCM as a rare and intractable disease. Nevertheless, further research to unravel the molecular pathogenesis and develop effective therapeutic modalities is warranted. Nationwide registry research on PCM is currently ongoing in Japan with the aim of better understanding the disease burden as well as the unmet needs of this life-threatening disease with poor therapeutic options.

    DOI: 10.5551/jat.RV17054

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  9. Can We Clarify the Causative Gene/Variants Underlying Familial Hypercholesterolemia and Improve Genetic Diagnosis Rate? Invited Reviewed

    Hori M

    Journal of atherosclerosis and thrombosis     2021.8

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:一般社団法人 日本動脈硬化学会  

    DOI: 10.5551/jat.ED184

    PubMed

  10. Current Diagnosis and Management of Tangier Disease. Reviewed

    Koseki M, Yamashita S, Ogura M, Ishigaki Y, Ono K, Tsukamoto K, Hori M, Matsuki K, Yokoyama S, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 8 ) page: 802 - 810   2021.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Atherosclerosis and Thrombosis  

    Tangier disease is a genetic disorder characterized by an absence or extremely low level of high-density lipoprotein (HDL)-cholesterol (HDL-C). It is caused by a dysfunctional mutation of the ATP-binding cassette transporter A1 (ABCA1) gene, the mandatory gene for generation of HDL particles from cellular cholesterol and phospholipids, and it appears in an autosomal recessive hereditary profile. To date, 35 cases have been reported in Japan and 109 cases outside Japan. With dysfunctional mutations in both alleles (homozygotes or compound heterozygotes), the HDL-C level is mostly less than 5 mg/dL and there is 10 mg/dL or less of apolipoprotein A-I (apoA-I), the major protein component of HDL. In patients with Tangier disease, major physical findings are orange-colored pharyngeal tonsils, hepatosplenomegaly, corneal opacity, lymphadenopathy, and peripheral neuropathy. Although patients tend to have decreased low-density lipoprotein (LDL)-cholesterol (LDL-C) levels, premature coronary artery disease is frequently observed. No specific curative treatment is currently available, so early identification of patients and preventing atherosclerosis development are crucial. Management of risk factors other than low HDL-C is also important, such as LDL-C levels, hypertension and smoking. Additionally, treatment for glucose intolerance might be required because impaired insulin secretion from pancreatic beta cells has occasionally been reported.

    DOI: 10.5551/jat.RV17053

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  11. Diagnosis and Management of Sitosterolemia 2021. Reviewed

    Tada H, Nomura A, Ogura M, Ikewaki K, Ishigaki Y, Inagaki K, Tsukamoto K, Dobashi K, Nakamura K, Hori M, Matsuki K, Yamashita S, Yokoyama S, Kawashiri MA, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 8 ) page: 791 - 801   2021.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Atherosclerosis and Thrombosis  

    Sitosterolemia is an inherited metabolic disorder characterized by increased levels of plant sterols, such as sitosterol. This disease is caused by loss-of-function genetic mutations in ATP-binding cassette (ABC) subfamily G member 5 or member 8 (ABCG5 or ABCG8, respectively), both of which play important roles in selective excretion of plant sterols from the liver and intestine, leading to failure to prevent absorption of food plant sterols. This disorder has been considered to be extremely rare. However, accumulated clinical data as well as genetics suggest the possibility of a much higher prevalence. Its clinical manifestations resemble those observed in patients with familial hypercholesterolemia (FH), including tendon xanthomas, hyper LDL-cholesterolemia, and premature coronary atherosclerosis. We provide an overview of this recessive genetic disease, diagnostic as well as therapeutic tips, and the latest diagnostic criteria in Japan.

    DOI: 10.5551/jat.RV17052

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  12. Homozygous Familial Hypercholesterolemia. Reviewed

    Nohara A, Tada H, Ogura M, Okazaki S, Ono K, Shimano H, Daida H, Dobashi K, Hayashi T, Hori M, Matsuki K, Minamino T, Yokoyama S, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 7 ) page: 665 - 678   2021.7

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Atherosclerosis and Thrombosis  

    Familial hypercholesterolemia (FH) is an inherited disorder with retarded clearance of plasma LDL caused by mutations of the genes involved in the LDL receptor-mediated pathway and most of them exhibit autosomal dominant inheritance. Homozygotes of FH (HoFH) may have plasma LDL-C levels, which are at least twice as high as those of heterozygous FH (HeFH) and therefore four times higher than normal levels. Prevalence of HoFH had been estimated as 1 in 1,000,000 before but more recent genetic analysis surveys predict 1 in 170,000 to 300,000. Since LDL receptor activity is severely impaired, HoFH patients do not or very poorly respond to medications to enhance activity, such as statins, and have a poorer prognosis compared to HeFH. HoFH should therefore be clinically distinguished from HeFH. Thorough family studies and genetic analysis are recommended for their accurate diagnosis. Fatal cardiovascular complications could develop even in the first decade of life for HoFH, so aggressive lipid-lowering therapy should be initiated as early as possible. Direct removal of plasma LDL by lipoprotein apheresis has been the principal measure for these patients. However, this treatment alone may not achieve stable LDL-C target levels and combination with drugs should be considered. The lipid-lowering effects of statins and PCSK9 inhibitors substantially vary depending on the remaining LDL receptor activity of individual patients. On the other hand, the action an MTP inhibitor is independent of LDL receptor activity, and it is effective in most HoFH cases. This review summarizes the key clinical issues of HoFH as well as insurance coverage available under the Japanese public healthcare system.

    DOI: 10.5551/jat.RV17050

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  13. Current Status of Familial LCAT Deficiency in Japan. Reviewed

    Kuroda M, Bujo H, Yokote K, Murano T, Yamaguchi T, Ogura M, Ikewaki K, Koseki M, Takeuchi Y, Nakatsuka A, Hori M, Matsuki K, Miida T, Yokoyama S, Wada J, Harada-Shiba M

    Journal of atherosclerosis and thrombosis   Vol. 28 ( 7 ) page: 679 - 691   2021.7

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Journal of Atherosclerosis and Thrombosis  

    Lecithin cholesterol acyltransferase (LCAT) is a lipid-modification enzyme that catalyzes the transfer of the acyl chain from the second position of lecithin to the hydroxyl group of cholesterol (FC) on plasma lipoproteins to form cholesteryl acylester and lysolecithin. Familial LCAT deficiency is an intractable autosomal recessive disorder caused by inherited dysfunction of the LCAT enzyme. The disease appears in two different phenotypes depending on the position of the gene mutation: familial LCAT deficiency (FLD, OMIM 245900) that lacks esterification activity on both HDL and ApoB-containing lipoproteins, and fish-eye disease (FED, OMIM 136120) that lacks activity only on HDL. Impaired metabolism of cholesterol and phospholipids due to LCAT dysfunction results in abnormal concentrations, composition and morphology of plasma lipoproteins and further causes ectopic lipid accumulation and/or abnormal lipid composition in certain tissues/cells, and serious dysfunction and complications in certain organs. Marked reduction of plasma HDL-cholesterol (HDL-C) and corneal opacity are common clinical manifestations of FLD and FED. FLD is also accompanied by anemia, proteinuria and progressive renal failure that eventually requires hemodialysis. Replacement therapy with the LCAT enzyme should prevent progression of serious complications, particularly renal dysfunction and corneal opacity. A clinical research project aiming at gene/cell therapy is currently underway.

    DOI: 10.5551/jat.RV17051

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  14. Achilles Tendon Thickness Assessed by X-ray Predicting a Pathogenic Mutation in Familial Hypercholesterolemia Gene. Reviewed

    Tada H, Hori M, Matsuki K, Ogura M, Nohara A, Kawashiri MA, Harada-Shiba M

    Journal of atherosclerosis and thrombosis     2021.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:一般社団法人 日本動脈硬化学会  

    <p><b>Aim: </b>The 2017 Japan Atherosclerosis Society (JAS) familial hypercholesterolemia (FH) criteria adopt a cut-off value of ≥ 9 mm of Achilles tendon thickness (ATT) detected by X-ray as one of the three key items. This threshold was determined based on an old data evaluating the ATT of 36 non-FH individuals that was published in 1977. Although the specificity of these clinical criteria is extremely high due to a strict threshold, there are a significant number of patients with FH whose ATT <9 mm. We aimed to determine a cut-off value of ATT detected by X-ray to differentiate FH and non-FH based on genetic diagnosis.<b> </b></p><p><b>Methods:</b> The individuals (male/female=486/501) with full assessments of genetic analyses for FH-genes (<i>LDLR</i> and <i>PCSK9</i>), serum lipids, and ATT detected by X-ray at the Kanazawa University Hospital and National Cerebral and Cardiovascular Center Research Institute were included in this study. Receiver operating characteristic (ROC) analyses were conducted to determine a better cut-off value of ATT that predicts the pathogenic mutation of FH.<b> </b></p><p><b>Results: </b>The ROC analyses revealed that the best cut-off values of ATT are 7.6 mm for male and 7.0 mm for female, with the sensitivities/specificities of 0.83/0.83 for male and 0.86/0.85 for female, respectively. If the thresholds of ATT of 8.0/7.5 mm and 7.5/7.0 mm were applied to the diagnosis of male/female FH, the sensitivities/specificities predicting the pathogenic mutation of FH by the 2017 JAS FH clinical criteria would be 0.82/0.90 and 0.85/0.88, respectively.<b> </b></p><p><b>Conclusions: </b>These results suggest that the cut-off value of ATT detected by X-ray is obviously lower than 9.0 mm, which was adopted by the 2017 JAS FH clinical criteria.</p>

    DOI: 10.5551/jat.62869

    PubMed

  15. Achilles Tendon Softness as a New Tool for Diagnosing Familial Hypercholesterolemia. Reviewed International journal

    Masahito Michikura, Masatsune Ogura, Mika Hori, Kenji Furuta, Kiminori Hosoda, Mariko Harada-Shiba

    JACC. Cardiovascular imaging   Vol. 14 ( 7 ) page: 1483 - 1485   2021.7

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    DOI: 10.1016/j.jcmg.2021.01.033

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  16. Circulating Mature PCSK9 Level Predicts Diminished Response to Statin Therapy. Reviewed

    Kuyama N, Kataoka Y, Takegami M, Nishimura K, Harada-Shiba M, Hori M, Ogura M, Otsuka F, Asaumi Y, Noguchi T, Tsujita K, Yasuda S

    Journal of the American Heart Association   Vol. 10 ( 11 ) page: e019525   2021.6

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    BACKGROUND: Statin-mediated efficacy of lowering low-density lipoprotein (LDL) cholesterol varies in each individual, and its diminished response is associated with worse outcomes. However, there is no established approach to predict hyporesponse to statins. PCSK9 (proprotein convertase subxilisin/kexin type 9) is a serine-protease associated with LDL metabolism, which circulates as mature and furin-cleaved PCSK9. Since mature PCSK9 more potently degrades the LDL receptor, its evaluation may enable the identification of statin hyporesponders. METHODS AND RESULTS: We analyzed 101 statin-naive patients with coronary artery disease who commenced a statin. PCSK9 subtypes at baseline and 1 month after statin use were measured by ELISA. Hyporesponse to statins was defined as a percent reduction in LDL cholesterol <15%. The relationship between each PCSK9 subtype level and hyporesponse to statins was investigated. Statins significantly lowered LDL cholesterol level (percent reduction, 40%±21%), whereas 11% of study participants exhibited a hyporeseponse to statins. Multivariable logistic regression analysis demonstrated that baseline mature PCSK9 level was an independent predictor for hyporesponse to statins even after adjusting clinical characteristics (mature PCSK9 per 10-ng/mL increase: odds ratio [OR], 1.12; 95% CI, 1.01–1.24 [P=0.03]), whereas furin-cleaved level was not (per 10-ng/mL increase: OR, 1.37; 95% CI, 0.73–2.58 [P=0.33]). Receiver operating characteristic curve analysis identified mature PCSK9 level of 228 ng/mL as an optimal cutoff to predict hyporesponse to statins (area under the curve, 0.73 [sensitivity, 0.91; specificity, 0.56]). CONCLUSIONS: Baseline mature PCSK9 level >228 ng/mL is associated with hyporesponse to statins. This finding suggests that mature PCSK9 might be a potential determinant of hyporesponse to statins.

    DOI: 10.1161/JAHA.120.019525

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  17. A Resuscitated Case of Acute Myocardial Infarction with both Familial Hypercholesterolemia Phenotype Caused by Possibly Oligogenic Variants of the PCSK9 and ABCG5 Genes and Type I CD36 Deficiency. Reviewed

    Ryo Nishikawa, Masato Furuhashi, Mika Hori, Masatsune Ogura, Mariko Harada-Shiba, Takeshi Okada, Masahiro Koseki, Takeshi Kujiraoka, Hiroaki Hattori, Ryosuke Ito, Atsuko Muranaka, Nobuaki Kokubu, Tetsuji Miura

    Journal of atherosclerosis and thrombosis     2021.2

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    A 56-year-old postmenopausal woman with out-of-hospital cardiac arrest caused by acute myocardial infraction was successfully resuscitated by intensive treatments and recovered without any neurological disability. She was diagnosed as having familial hypercholesterolemia (FH) based on a markedly elevated low-density lipoprotein cholesterol (LDL-C) level and family history of premature coronary artery disease. Genetic testing in her family members showed that a variant of the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene (c.2004C>A, p.S668R), which had been previously reported as having uncertain significance, was associated with FH, indicating that the variant is a potential candidate for the FH phenotype. Next-generation sequencing analysis for the proband also showed that there was a heterozygous mutation of the ATP-binding cassette sub-family G member 5 (ABCG5) gene (c.1166G>A, R389H), which has been reported to increase LDL-C level and the risk of cardiovascular disease. She was also diagnosed as having type 1 CD36 deficiency based on a lack of myocardial uptake of 123 I-labeled 15-(p-iodophenyl)-3-R,S-methyl-pentadecanoic acid in scintigraphy and the absence of CD36 antigen in both monocytes and platelets in flow cytometry. She had a homozygous mutation of the CD36 gene (c.1126-5_1127delTTTAGAT), which occurs in a canonical splice site (acceptor) and is predicted to disrupt or distort the normal gene product. To our knowledge, this is the first report of a heterozygous FH phenotype caused by possibly oligogenic variants of the PCSK9 and ABCG5 genes complicated with type I CD36 deficiency caused by a novel homozygous mutation. Both FH phenotype and CD36 deficiency might have caused extensive atherosclerosis, leading to acute myocardial infarction in the present case.

    DOI: 10.5551/jat.58909

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  18. Patients With LDLR and PCSK9 Gene Variants Experienced Higher Incidence of Cardiovascular Outcomes in Heterozygous Familial Hypercholesterolemia. Reviewed International journal

    Takahito Doi, Mika Hori, Mariko Harada-Shiba, Yu Kataoka, Daisuke Onozuka, Kunihiro Nishimura, Ryo Nishikawa, Kosuke Tsuda, Masatsune Ogura, Cheol Son, Yoshihiro Miyamoto, Teruo Noguchi, Hiroaki Shimokawa, Satoshi Yasuda

    Journal of the American Heart Association   Vol. 10 ( 4 ) page: e018263 - 11   2021.2

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    Background Patients with familial hypercholesterolemia who harbored both low-density lipoprotein receptor (LDLR) and PCSK9 (proprotein convertase subtilisin/kexin type 9) gene variants exhibit severe phenotype associated with substantially high levels of low-density lipoprotein cholesterol. In this study, we investigated the cardiovascular outcomes in patients with both LDLR and PCSK9 gene variants. Methods and Results A total of 232 unrelated patients with LDLR and/or PCSK9 gene variants were stratified as follows: patients with LDLR and PCSK9 (LDLR/PCSK9) gene variants, patients with LDLR gene variant, and patients with PCSK9 gene variant. Clinical demographics and the occurrence of primary outcome (nonfatal myocardial infarction) were compared. The observation period of primary outcome started at the time of birth and ended at the time of the first cardiac event or the last visit. Patients with LDLR/PCSK9 gene variants were identified in 6% of study patients. They had higher levels of low-density lipoprotein cholesterol (P=0.04) than those with LDLR gene variants. On multivariate Cox regression model, they experienced a higher incidence of nonfatal myocardial infarction (hazard ratio, 4.62; 95% CI, 1.66-11.0; P=0.003 versus patients with LDLR gene variant). Of note, risk for nonfatal myocardial infarction was greatest in male patients with LDLR/PCSK9 gene variants compared with those with LDLR gene variant (86% versus 24%; P<0.001). Conclusions Patients with LDLR/PCSK9 gene variants were high-risk genotype associated with atherogenic lipid profiles and worse cardiovascular outcomes. These findings underscore the importance of genetic testing to identify patients with LDLR/PCSK9 gene variants, who require more stringent antiatherosclerotic management.

    DOI: 10.1161/JAHA.120.018263

    Scopus

    PubMed

  19. Organoid-based ex vivo reconstitution of Kras-driven pancreatic ductal carcinogenesis. Reviewed

    Matsuura T, Maru Y, Izumiya M, Hoshi D, Kato S, Ochiai M, Hori M, Yamamoto S, Tatsuno K, Imai T, Aburatani H, Nakajima A, Hippo Y

    Carcinogenesis   Vol. 41 ( 4 ) page: 490-501   2020.6

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    DOI: 10.1093/carcin/bgz122

    PubMed

  20. The first Japanese cases of familial hypercholesterolemia due to a known pathogenic APOB gene variant, c.10580 G&gt;A: p.(Arg3527Gln). Reviewed

        2020.5

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jacl.2020.05.007

    PubMed

  21. A catalog of the pathogenic mutations of LDL receptor gene in Japanese familial hypercholesterolemia. Reviewed

    Tada H, Hori M, Nomura A, Hosomichi K, Nohara A, Kawashiri MA, Harada-Shiba M

    Journal of clinical lipidology   Vol. 14 ( 3 ) page: 346-351.e9   2020.5

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jacl.2020.03.002

    PubMed

  22. The benign c.344G &gt; A: p.(Arg115His) variant in the LDLR gene interpreted from a pedigree-based genetic analysis of familial hypercholesterolemia. Reviewed

    Hori M, Takahashi A, Son C, Ogura M, Harada-Shiba M

    Lipids in health and disease   Vol. 19 ( 1 ) page: 62   2020.4

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1186/s12944-020-01252-4

    PubMed

  23. Detection of the benign c.2579C&gt;T (p.A860V) variant of the LDLR gene in a pedigree-based genetic analysis of familial hypercholesterolemia. Reviewed

    Hori M, Miyauchi E, Son C, Harada-Shiba M

    Journal of clinical lipidology   Vol. 13 ( 2 ) page: 335-339   2019.3

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jacl.2019.01.004

    PubMed

  24. Discontinuation of LDL apheresis with evolocumab in an FH patient with a duplication of exon 2-6 in the <i>LDLR</i> gene. Reviewed

    Nose D, Hori M, Miyamoto Y, Imaizumi S, Harada-Shiba M, Saku K, Miura SI

    Journal of cardiology cases   Vol. 19 ( 2 ) page: 55-58   2019.2

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jccase.2018.10.005

    PubMed

  25. Pharmaceutical Research for Inherited Metabolic Disorders of the Liver Using Human Induced Pluripotent Stem Cell and Genome Editing Technologies.

    Yamashita T, Takayama K, Hori M, Harada-Shiba M, Mizuguchi H

    Biological & pharmaceutical bulletin   Vol. 42 ( 3 ) page: 312-318   2019

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1248/bpb.b18-00544

    PubMed

  26. No enhancing effects of plasmid-specific histone acetyltransferase recruitment system on transgene expression in vivo. Reviewed

    Suzuki T, Wakao Y, Watanabe T, Hori M, Ikeda Y, Tsuchiya H, Kogure K, Harada-Shiba M, Fujimuro M, Kamiya H

    Nucleosides, nucleotides & nucleic acids   Vol. 38 ( 12 ) page: 942-949   2019

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1080/15257770.2019.1638514

    PubMed

  27. Fatty pancreas: A possible risk factor for pancreatic cancer in animals and humans. Reviewed

    Takahashi M, Hori M, Ishigamori R, Mutoh M, Imai T, Nakagama H

    Cancer science   Vol. 109 ( 10 ) page: 3013-3023   2018.10

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/cas.13766

    PubMed

  28. Activated Ductal Proliferation Induced by <i>N</i>-Nitroso<i>bis</i> (2-oxopropyl)amine in Fat-infiltrated Pancreas of KK-<i>A<sup>y</sup></i> Mice. Reviewed

    Hori M, Mutoh M, Ishigamori R, Imai T, Takahashi M

    In vivo (Athens, Greece)   Vol. 32 ( 3 ) page: 499-505   2018.5

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.21873/invivo.11267

    PubMed

  29. Glucagon-like peptide-1 receptor agonists reduced the low-density lipoprotein cholesterol in Japanese patients with type 2 diabetes mellitus treated with statins. Reviewed

    Hasegawa Y, Hori M, Nakagami T, Harada-Shiba M, Uchigata Y

    Journal of clinical lipidology   Vol. 12 ( 1 ) page: 62-69.e1   2018.1

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jacl.2017.11.006

    PubMed

  30. Coronary Artery Plaque Regression by a PCSK9 Antibody and Rosuvastatin in Double-heterozygous Familial Hypercholesterolemia with an LDL Receptor Mutation and a PCSK9 V4I Mutation. Reviewed

    Shirahama R, Ono T, Nagamatsu S, Sueta D, Takashio S, Chitose T, Fujisue K, Sakamoto K, Yamamoto E, Izumiya Y, Kaikita K, Hokimoto S, Hori M, Harada-Shiba M, Kajiwara I, Ogawa H, Tsujita K

    Internal medicine (Tokyo, Japan)   Vol. 57 ( 24 ) page: 3551-3557   2018

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.2169/internalmedicine.1060-18

    PubMed

  31. Achilles Tendon Ultrasonography for Diagnosis of Familial Hypercholesterolemia Among Japanese Subjects. Reviewed

    Michikura M, Ogura M, Yamamoto M, Sekimoto M, Fuke C, Hori M, Arai K, Kihara S, Hosoda K, Yanagi K, Harada-Shiba M

    Circulation journal : official journal of the Japanese Circulation Society   Vol. 81 ( 12 ) page: 1879-1885   2017.11

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1253/circj.CJ-17-0041

    PubMed

  32. Mature proprotein convertase subtilisin/kexin type 9, coronary atheroma burden, and vessel remodeling in heterozygous familial hypercholesterolemia. Reviewed

    Kataoka Y, Harada-Shiba M, Nakao K, Nakashima T, Kawakami S, Fujino M, Kanaya T, Nagai T, Tahara Y, Asaumi Y, Hori M, Ogura M, Goto Y, Noguchi T, Yasuda S

    Journal of clinical lipidology   Vol. 11 ( 2 ) page: 413-421.e3   2017.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jacl.2017.01.005

    PubMed

  33. Evaluation of the degree of pancreatic fatty infiltration by area-based assessment of CT images: comparison with histopathology-based and CT attenuation index-based assessments. Reviewed

    Hori M, Onaya H, Hiraoka N, Yamaji T, Kobayashi H, Takahashi M, Mutoh M, Shimada K, Nakagama H

    Japanese journal of radiology   Vol. 34 ( 10 ) page: 667 - 676   2016.10

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    Authorship:Lead author  

    DOI: 10.1007/s11604-016-0572-0

    PubMed

  34. Association Between Cholesterol Efflux Capacity and Atherosclerotic Cardiovascular Disease in Patients With Familial Hypercholesterolemia. Reviewed

    Ogura M, Hori M, Harada-Shiba M

    Arteriosclerosis, thrombosis, and vascular biology   Vol. 36 ( 1 ) page: 181 - 8   2016.1

  35. Possible involvement of pancreatic fatty infiltration in pancreatic carcinogenesis Reviewed

    Hori M, Mutoh M, Imai T, Nakagama H, Takahashi M

    Journal of Pancreas   Vol. 17   page: 166 - 175   2016

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  36. Association of pancreatic Fatty infiltration with pancreatic ductal adenocarcinoma. Reviewed

    Hori M, Takahashi M, Hiraoka N, Yamaji T, Mutoh M, Ishigamori R, Furuta K, Okusaka T, Shimada K, Kosuge T, Kanai Y, Nakagama H

    Clinical and translational gastroenterology   Vol. 5   page: e53   2014.3

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    Authorship:Lead author  

    DOI: 10.1038/ctg.2014.5

    PubMed

  37. Invasive ductal carcinoma developing in pancreas with severe Fatty infiltration. Reviewed

    Hori M, Onaya H, Takahashi M, Hiraoka N, Mutoh M, Kosuge T, Nakagama H

    Pancreas   Vol. 41 ( 7 ) page: 1137 - 9   2012.10

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    DOI: 10.1097/MPA.0b013e318252ea08

    PubMed

  38. Enhancement of carcinogenesis and fatty infiltration in the pancreas in N-nitrosobis(2-oxopropyl)amine-treated hamsters by high-fat diet. Reviewed

    Hori M, Kitahashi T, Imai T, Ishigamori R, Takasu S, Mutoh M, Sugimura T, Wakabayashi K, Takahashi M

    Pancreas   Vol. 40 ( 8 ) page: 1234 - 40   2011.11

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    DOI: 10.1097/MPA.0b013e318220e742

    PubMed

  39. Mutagenicity of secondary oxidation products of 8-oxo-7,8-dihydro-2'-deoxyguanosine 5'-triphosphate (8-hydroxy-2'- deoxyguanosine 5'-triphosphate). Reviewed

    Hori M, Suzuki T, Minakawa N, Matsuda A, Harashima H, Kamiya H

    Mutation research   Vol. 714 ( 1-2 ) page: 11 - 6   2011.9

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    DOI: 10.1016/j.mrfmmm.2011.05.015

    PubMed

  40. Experimental animal models of pancreatic carcinogenesis for prevention studies and their relevance to human disease. Reviewed

    Takahashi M, Hori M, Mutoh M, Wakabayashi K, Nakagama H

    Cancers   Vol. 3 ( 1 ) page: 582 - 602   2011.2

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  41. Suppression of mutagenesis by 8-hydroxy-2 '-deoxyguanosine 5 '-triphosphate (7,8-dihydro-8-oxo-2 '-deoxyguanosine 5 '-triphosphate) by human MTH1, MTH2, and NUDT5 Reviewed

    Hori Mika, Satou Kazuya, Harashima Hideyoshi, Kamiya Hiroyuki

    FREE RADICAL BIOLOGY AND MEDICINE   Vol. 48 ( 9 ) page: 1197 - 1201   2010.5

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  42. Early and enhanced development of N-nitrosobis(2-oxopropyl)amine-induced hamster pancreatic adenocarcinomas by high-fat diet Reviewed

    Takahashi Mami, Hori Mika, Kitahashi Tsukasa, Imai Toshio, Ishigamori Rikako, Takasu Shinji, Mutoh Michihiro, Sugimura Takashi, Wakabayashi Keiji

    CANCER RESEARCH   Vol. 70   2010.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1158/1538-7445.AM10-2478

    Web of Science

  43. NUDT5 hydrolyzes oxidized deoxyribonucleoside diphosphates with broad substrate specificity. Reviewed

    Kamiya H, Hori M, Arimori T, Sekiguchi M, Yamagata Y, Harashima H

    DNA repair   Vol. 8 ( 10 ) page: 1250 - 4   2009.10

  44. Involvement of specialized DNA polymerases in mutagenesis by 8-hydroxy-dGTP in human cells. Reviewed

    Satou K, Hori M, Kawai K, Kasai H, Harashima H, Kamiya H

    DNA repair   Vol. 8 ( 5 ) page: 637 - 42   2009.5

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    DOI: 10.1016/j.dnarep.2008.12.009

    PubMed

  45. Roles of specialized DNA polymerases in mutagenesis by oxidized guanine. Reviewed

    Kamiya H, Satou K, Hori M, Yamaguchi A, Harashima H

    Nucleic acids symposium series (2004)   ( 53 ) page: 223 - 4   2009

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  46. UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides. Reviewed

    Hori M, Ishiguro C, Suzuki T, Nakagawa N, Nunoshiba T, Kuramitsu S, Yamamoto K, Kasai H, Harashima H, Kamiya H

    DNA repair   Vol. 6 ( 12 ) page: 1786 - 93   2007.12

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    DOI: 10.1016/j.dnarep.2007.06.013

    PubMed

  47. Effects of overexpression and antisense RNA expression of Orf17, a MutT-type enzyme Reviewed

    Hori Mika, Asanuma Taketoshi, Inanami Osamu, Kuwabara Mikinori, Harashima Hideyoshi, Kamiya Hiroyuki

    BIOLOGICAL & PHARMACEUTICAL BULLETIN   Vol. 29 ( 6 ) page: 1087 - 1091   2006.6

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    Web of Science

  48. In vivo mutagenicities of damaged nucleotides produced by nitric oxide and ionizing radiation Reviewed

    Hori M, Ishiguro C, Harashima H, Kamiya H

    BIOLOGICAL & PHARMACEUTICAL BULLETIN   Vol. 28 ( 3 ) page: 520 - 522   2005.3

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    Web of Science

  49. Dual hydrolysis of diphosphate and triphosphate derivatives of oxidized deoxyadenosine by Orf17 (NtpA), a MutT-type enzyme. Reviewed

    Hori M, Fujikawa K, Kasai H, Harashima H, Kamiya H

    DNA repair   Vol. 4 ( 1 ) page: 33 - 9   2005.1

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    DOI: 10.1016/j.dnarep.2004.07.010

    PubMed

  50. Mutagenesis by damaged deoxyribonucleotides and its prevention by MutT-type hydrolyzing enzymes.

    Kamiya H, Satou K, Hori M, Iida E, Ishiguro C, Harashima H

    Nucleic acids symposium series (2004)   ( 48 ) page: 271 - 2   2004

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▼display all

MISC 80

  1. PCSK9阻害薬がLDL-C低下に有効であった小児FHホモ接合体の一例

    松木 恒太, 小倉 正恒, 山本 雅, 堀 美香, 斯波 真理子

    The Lipid   Vol. 31 ( 1 ) page: 89 - 90   2020.4

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    Language:Japanese   Publisher:(株)メディカルレビュー社  

  2. 父親の狭心症を契機に家族性高コレステロール血症と診断された1歳児

    永関 ひかる, 秋山 政晴, 堀 美香, 斯波 真理子, 井田 博幸, 宮田 市郎

    日本小児科学会雑誌   Vol. 124 ( 4 ) page: 704 - 708   2020.4

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    1歳3ヵ月、男児。父親の脂質異常症と狭心症に加え、父方祖父の病歴から、産業医が医療機関受診を勧めたため当院へ受診となった。患児は無症状であったが、血液検査や遺伝子検査の結果から、家族性高コレステロール血症と診断された。食事指導を行うもLDLコレステロール(LDL-C)値の改善は認められなかったため、コレスチラミン製剤の内服を開始したところ、治療開始10ヵ月で総コレステロール(TC)と中性脂肪(TG)は共に245mg/dL、LDL-C値は194mg/dLに低下し、コントロール良好となった。目下は25ヵ月でTC、TGは249mg/dL、LDL-Cは185mg/dLで経過している。

  3. ヒトiPS細胞技術を用いた常染色体劣性高コレステロール血症の病態再現

    冨田 純矢, 高山 和雄, 堀 美香, 斯波 真理子, 水口 裕之

    日本薬学会年会要旨集   Vol. 140年会   page: 26G - pm16S   2020.3

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  4. 家族性高コレステロール血症(Familial Hypercholesterolemia)の遺伝学的検査における大規模重複・欠損を検出目的としたMLPA法の導入

    山本 賢, 礒田 理恵子, 中西 啓美, 堀 美香, 孫 徹, 古田 賢二, 斯波 真理子, 宮本 恵宏

    国立病院総合医学会講演抄録集   Vol. 73回   page: P2 - 1689   2019.11

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  5. 遺伝性循環器疾患に対する遺伝子解析の実践 家族性高コレステロール血症の遺伝子解析とその有用性

    堀 美香, 斯波 真理子

    日本心臓病学会学術集会抄録   Vol. 67回   page: S7 - 3   2019.9

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  6. LDLRとPCSK9遺伝子変異に関する二重ヘテロ接合体における実在する心血管リスク(Substantial Cardiovascular Risks in Double-heterozygotes for LDLR and PCSK9 Gene Variants)

    土井 貴仁, 堀 美香, 斯波 真理子, 片岡 有, 西村 邦宏, 西川 諒, 津田 浩佑, 小倉 正恒, 孫 徹, 宮本 恵宏, 野口 暉夫, 下川 宏明, 安田 聡

    日本心臓病学会学術集会抄録   Vol. 67回   page: YIA - 2   2019.9

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  7. 心肺停止を伴う急性心筋梗塞を契機に診断に至った1型CD36欠損症および家族性高コレステロール血症の合併例

    西川 諒, 古橋 眞人, 伊藤 良介, 續 太郎, 小山 雅之, 村中 敦子, 國分 宣明, 堀 美香, 小倉 正恒, 斯波 真理子, 三浦 哲嗣

    日本動脈硬化学会総会プログラム・抄録集   Vol. 51回   page: 1 - 3   2019.7

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  8. 家族性高コレステロール血症(Familial Hypercholesterolemia)の遺伝学的検査におけるMLPA法導入の報告

    礒田 理恵子, 山本 賢, 増田 弘明, 堀 美香, 孫 徹, 古田 賢二, 斯波 真理子, 宮本 恵宏

    日本動脈硬化学会総会プログラム・抄録集   Vol. 51回   page: 1 - 4   2019.7

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  9. 家族性高コレステロール血症患者における遺伝子変異によるアキレス腱肥厚への影響

    道倉 雅仁, 堀 美香, 小倉 正恒, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 51回   page: 2 - 2   2019.7

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  10. 心肺停止を伴う急性心筋梗塞を契機に診断に至った1型CD36欠損症および家族性高コレステロール血症の合併例

    西川 諒, 古橋 眞人, 伊藤 良介, 續 太郎, 小山 雅之, 村中 敦子, 國分 宣明, 堀 美香, 小倉 正恒, 斯波 真理子, 三浦 哲嗣

    日本動脈硬化学会総会プログラム・抄録集   Vol. 51回   page: 1 - 3   2019.7

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  11. プラスミド特異的ヒストンアセチル化酵素リクルートシステムの効果はin vivoでは観察されない

    紙谷 浩之, 鈴木 哲矢, 若尾 祐介, 渡部 匡史, 堀 美香, 池田 義人, 土谷 博之, 小暮 健太朗, 斯波 真理子, 藤室 雅弘

    日本DDS学会学術集会プログラム予稿集   Vol. 35回   page: 182 - 182   2019.6

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  12. Prevalence, Clinical Characteristics and Cardiovascular Outcomes in Heterozygous Familial Hypercholesterolemia Patients With Double-Heterozygous Mutation of LDLR and PCSK9 Gain-Of-Function Mutation

    Takahito Doi, Mika Hori, Mariko Harada-Shiba, Yu Kataoka, Ryo Nishikawa, Kosuke Tsuda, Kunihiro Nishimura, Masatsune Ogura, Teruo Noguchi, Satoshi Yasuda

    CIRCULATION   Vol. 138   2018.11

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    Language:English   Publishing type:Research paper, summary (international conference)   Publisher:LIPPINCOTT WILLIAMS & WILKINS  

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    Web of Science

  13. FHホモ接合体におけるコレステロール引き抜き能

    小倉 正恒, 堀 美香, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 50回   page: 285 - 285   2018.6

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  14. 家族性高コレステロール血症ヘテロ接合体における遺伝子診断とLDLR/PCSK9遺伝子変異の分布

    堀 美香, 太田 直孝, 増田 弘明, 磯田 理恵子, 孫 徹, 小倉 正恒, 細田 公則, 宮本 恵宏, 斯波 真理子

    日本臨床分子医学会学術総会プログラム・抄録集   Vol. 55回   page: 65 - 65   2018.4

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  15. LDLRおよびPCSK9変異を有する二重ヘテロ接合性家族性高コレステロール血症における臨床および心血管転帰 遺伝子診断によるHeFHデータベースからの知見(Clinical and Cardiovascular Outcomes in Double Heterozygous Familial Hypercholesterolemia with LDLR and PCSK9 Mutations: Insights from Genetically-diagnosed HeFH Database)

    土井 貴仁, 堀 美香, 片岡 有, 浅海 泰栄, 西川 諒, 津田 浩佑, 小倉 正恒, 野口 暉夫, 斯波 真理子, 安田 聡

    日本循環器学会学術集会抄録集   Vol. 82回   page: OJ11 - 1   2018.3

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  16. Clinical and Cardiovascular Outcomes in Double Heterozygous Familial Hypercholesterolemia with LDLR and PCSK9 Mutations: Insights from Genetically-diagnosed HeFH Database(和訳中)

    土井 貴仁, 堀 美香, 片岡 有, 浅海 泰栄, 西川 諒, 津田 浩佑, 小倉 正恒, 野口 暉夫, 斯波 真理子, 安田 聡

    日本循環器学会学術集会抄録集   Vol. 82回   page: OJ11 - 1   2018.3

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  17. 脂質代謝異常症への多角的アプローチ PCSK9 家族性高コレステロール血症の病態および治療への関与

    太田 直孝, 堀 美香, 宮本 恵宏, 斯波 真理子

    The Lipid   Vol. 29 ( 1 ) page: 106 - 112   2018.1

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  18. 抗動脈硬化作用を有する間葉系幹細胞培養上清の血管内皮細胞,マクロファージに対する作用機序の解析

    高藤義正, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 49th   page: 290 (WEB ONLY) - 290   2017.6

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  19. GLP‐1受容体作動薬のLDL‐コレステロール低下作用とその機序に関する検討

    長谷川夕希子, 堀美香, 中神朋子, 内潟安子, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 49th   page: 225 (WEB ONLY) - 225   2017.6

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  20. GLP-1受容体作動薬のLDL-コレステロール低下作用とその機序に関する検討

    長谷川 夕希子, 堀 美香, 中神 朋子, 内潟 安子, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 49回   page: 225 - 225   2017.6

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  21. Glucagon-Like Peptide-1 Receptor Agonists Reduce Serum LDL Cholesterol Levels via LDL Receptor in Mice and Type 2 Diabetes Patient

    Yukiko Hasegawa, Mika Hori, Tomoko Nakagami, Mariko Harada-Shiba, Yasuko Uchigata

    DIABETES   Vol. 66   page: A166 - A166   2017.6

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  22. 抗動脈硬化作用を有する間葉系幹細胞培養上清の血管内皮細胞、マクロファージに対する作用機序の解析

    高藤 義正, 堀 美香, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 49回   page: 290 - 290   2017.6

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  23. GLP-1受容体作動薬の脂質代謝に及ぼす影響とその機序に関する検討

    長谷川 夕希子, 堀 美香, 中神 朋子, 斯波 真理子, 内潟 安子

    糖尿病   Vol. 60 ( Suppl.1 ) page: S - 462   2017.4

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  24. GLP-1受容体作動薬の脂質代謝に及ぼす影響とその機序に関する検討

    長谷川 夕希子, 堀 美香, 中神 朋子, 斯波 真理子, 内潟 安子

    糖尿病   Vol. 60 ( Suppl.1 ) page: S - 462   2017.4

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  25. 脂肪由来間葉系幹細胞培養上清の抗動脈硬化作用における機序の解析

    高藤義正, 堀美香, 斯波真理子

    再生医療   Vol. 16   page: 369   2017.2

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  26. 家族性高コレステロール血症診断・治療の新たな展開―PCSK9を中心として―

    堀美香, 斯波真理子

    循環器病研究の進歩   Vol. 37 ( 1 ) page: 81‐87 - 87   2016.11

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  27. LDLアフェレシスにより除去されるタンパク質の解析 FHと末梢動脈疾患

    堀 美香, 南野 直人, 斯波 真理子

    日本アフェレシス学会雑誌   Vol. 35 ( Suppl. ) page: 77 - 77   2016.11

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  28. CTを用いた病理組織像に相当する脂肪膵画像の評価

    堀 美香, 女屋 博昭, 平岡 伸介, 山地 太樹, 高橋 真美, 武藤 倫弘, 中釜 斉

    日本癌学会総会記事   Vol. 75回   page: P - 1321   2016.10

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  29. 家族性高コレステロール血症の残余リスクとしてのHDL機能

    小倉正恒, 森本めぐむ, 太田愛美, 道倉雅仁, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 48th   page: 122 (WEB ONLY)   2016.6

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  30. 家族性高コレステロール血症ホモ接合体Up to date

    小倉正恒, 堀美香, 槇野久士, 玉那覇民子, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 48th   page: 113 (WEB ONLY)   2016.6

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  31. PCSK9 V4I変異とE32K変異を有する家系について

    太田直孝, 太田直孝, 堀美香, 増田弘明, 増田弘明, 藤山啓美, 藤山啓美, 新井浩司, 宮本恵宏, 宮本恵宏, 斯波真理子, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 48回   page: 222 - 222   2016.6

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  32. 間葉系幹細胞培養上清の血中投与によるLDL受容体欠損マウスにおける抗動脈硬化作用

    高橋 義正, 堀 美香, 水野 敏秀, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 48回   page: 255 - 255   2016.6

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  33. HDLの機能評価とHDLを標的とした薬剤開発の将来展望 家族性高コレステロール血症の残余リスクとしてのHDL機能

    小倉 正恒, 森本 めぐむ, 太田 愛美, 道倉 雅仁, 堀 美香, 斯波 真理子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 48回   page: 122 - 122   2016.6

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  34. 脂肪由来間葉系幹細胞培養上清のLDL受容体欠損マウスへの血中投与による動脈硬化抑制効果

    高藤義正, 堀美香, 斯波真理子

    再生医療   Vol. 15   page: 248   2016.2

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  35. ApoE/NMU二重欠損マウスにおける脂質代謝及び動脈硬化初期病変の評価

    堀 美香, 水野 敏秀, 斯波 真理子

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   Vol. 88回・38回   page: [2P1245] - [2P1245]   2015.12

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  36. 家族性高コレステロール血症の残存リスクとしてのLDL粒子の質的評価

    小倉正恒, 道倉雅仁, 冨家千鶴, 堀美香, 森本めぐむ, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 47th   page: 171 (WEB ONLY) - 171   2015.6

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  37. 間葉系幹細胞培養上清(MSC‐CM)の動脈硬化性病変を形成する細胞に対する抗炎症作用

    高藤義正, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 47th   page: 238 (WEB ONLY) - 238   2015.6

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  38. 新規分子非ヘテロダイマー型60kDa PCSK9特異的ELISAの構築と血中動態

    岩崎忠雄, 石原光昭, 鯨岡健, 小川一行, 服部浩明, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 47th   page: 224 (WEB ONLY) - 224   2015.6

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  39. 動脈硬化性病変を形成する細胞に対する脂肪由来間葉系幹細胞培養上清の抗炎症作用

    高藤義正, 堀美香, 斯波真理子

    再生医療   Vol. 14   page: 361   2015.2

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  40. LDLアフェレーシス療法施行中の重症家族性高コレステロール血症に対する,同種脂肪組織由来多系統前駆細胞(ADMPC)を用いた細胞移植療法の確立 実施体制の確立と調整(患者会での広報)

    斯波真理子, 小倉正恒, 堀美香

    LDLアフェレーシス療法施行中の重症家族性高コレステロール血症に対する、同種脂肪組織由来多系統前駆細胞(ADMPC)を用いた細胞移植療法の確立 平成26年度 委託業務成果報告書     page: 154 - 167   2015

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  41. ヒト血中におけるPCSK9の分子形態の解析

    鯨岡健, 石原光昭, 岩崎忠雄, 小川一行, 服部浩明, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 46th   page: 1-P-104 (WEB ONLY) - 247   2014.6

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  42. Proprotein convertase subtilisin/kexin type9(PCSK9)非ヘテロダイマー型mature segment分子のLDL受容体分解活性

    石原光昭, 鯨岡健, 岩崎忠雄, 小川一行, 服部浩明, 堀美香, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 46th   page: 1-P-105 (WEB ONLY) - 248   2014.6

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  43. 超音波で測定したアキレス腱厚と頸動脈内膜中膜複合体厚の関連

    道倉雅仁, 小倉正恒, 冨家千鶴, 肥後諒, 菱田藍, 橡谷真由, 大畑洋子, 玉那覇民子, 槇野久士, 柴田映子, 堀美香, 岸本一郎, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 46th   page: 1-P-58 (WEB ONLY) - 225   2014.6

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  44. GLP‐1のコレステロール代謝に及ぼす影響

    長谷川夕希子, 堀美香, 中神朋子, 斯波真理子, 内潟安子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 46th   page: 1-P-62 (WEB ONLY)   2014.6

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  45. GLP-1のクレステロール代謝に及ぼす影響

    長谷川 夕希子, 堀 美香, 中神 朋子, 斯波 真理子, 内潟 安子

    日本動脈硬化学会総会プログラム・抄録集   Vol. 46回   page: 227 - 227   2014.6

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  46. Gadofluorine Mによるマウスの動脈硬化プラークイメージング

    圓見純一郎, 柴田映子, 柴田雅朗, 森本めぐむ, 福田肇, 橋川美子, 河嶋秀和, 堀美香, 斯波真理子, 飯田秀博

    JSMI Rep   Vol. 7 ( 2 ) page: 155 - 155   2014.5

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  47. 肝細胞におけるGLP‐1のコレステロール代謝に及ぼす影響

    長谷川夕希子, 堀美香, 中神朋子, 斯波真理子, 内潟安子

    糖尿病   Vol. 57 ( Supplement 1 ) page: S.418 - 418   2014.4

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  48. LDLアフェレシスの新たな作用機序と臨床応用 家族性高コレステロール血症に対するLDL-Aの効果

    斯波 真理子, 槇野 久士, 堀 美香, 玉那覇 民子, 小倉 正恒, 肥塚 諒, 菱田 藍, 長谷川 夕希子, 岸本 一郎, 南野 直人

    医工学治療   Vol. 26 ( Suppl. ) page: 78 - 78   2014.3

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  49. 家族性高コレステロール血症に対するLDL‐Aの効果

    斯波真理子, 槇野久士, 堀美香, 玉那覇民子, 小倉正恒, 肥塚諒, 菱田藍, 長谷川夕希子, 岸本一郎, 南野直人

    医工学治療   Vol. 26 ( Supplement ) page: 78   2014

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  50. ニューロメジンUの脂質代謝及び動脈硬化との関わり

    堀美香, 水野敏秀, 斯波真理子

    日本内分泌学会雑誌   Vol. 89 ( 2 ) page: 740 - 740   2013.9

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  51. 家族性高コレステロール血症患者における超音波によるアキレス腱計測の評価

    道倉雅仁, 冨家千鶴, 槇野久士, 橡谷真由, 玉那覇民子, 大畑洋子, 吉田晶子, 森本めぐむ, 柴田映子, 堀美香, 岸本一郎, 斯波真理子

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   Vol. 45th   page: 1-P-63 (WEB ONLY) - 226   2013.6

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  52. コレステロール代謝におけるニューロメジンUの役割と動脈硬化との関連

    堀美香, 駒井仁美, 水野敏秀, 斯波真理子

    日本分子生物学会年会プログラム・要旨集(Web)   Vol. 36th   page: 3P-0885 (WEB ONLY)   2013

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  53. 脂肪膵の膵がんにおける意義及びCTを用いた評価方法の確立(The role of fatty infiltration on pancreatic cancer and establishment of the evaluation method using CT imaging)

    堀 美香, 高橋 真美, 女屋 博昭, 平岡 伸介, 山地 太樹, 武藤 倫弘, 金井 弥栄, 中釜 斉

    日本癌学会総会記事   Vol. 71回   page: 356 - 356   2012.8

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  54. 生理活性ペプチドニューロメジンUの脂質代謝及び炎症における役割

    堀美香, 斯波真理子

    日本分子生物学会年会プログラム・要旨集(Web)   Vol. 35th   page: 4P-0548 (WEB ONLY)   2012

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  55. ヒト膵がん発生における脂肪膵の意義(The role of fatty infiltration in the pancreas on the development of pancreatic cancer in humans)

    堀 美香, 平岡 伸介, 高橋 真美, 武藤 倫弘, 山地 太樹, 金井 弥栄, 中釜 斉

    日本癌学会総会記事   Vol. 70回   page: 67 - 67   2011.9

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  56. アディポネクチンが欠損したMin及びC57BLマウスにおける腸発がん促進(Enhancement of intestinal carcinogenesis in Min and C57BL mice with adiponectin deficiency)

    武藤 倫弘, 高橋 真美, 山本 真史, 堀 美香, 若林 敬二, 中釜 斉

    日本癌学会総会記事   Vol. 70回   page: 290 - 290   2011.9

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  57. 膵臓特異的K-ras変異体発現マウスの膵臓発がんにおけるオステオポンチンの発現上昇(Increased expression of osteopontin in pancreatic carcinogenesis in pancreas-specific K-ras mutant mice)

    高橋 真美, 石ヶ守 里加子, 堀 美香, 高須 伸二, 今井 俊夫, 武藤 倫弘, 若林 敬二

    日本癌学会総会記事   Vol. 70回   page: 159 - 159   2011.9

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  58. 膵がん発生における脂肪膵の意義に関する研究

    堀美香, 平岡伸介, 高橋真美, 武藤倫弘, 金井弥栄, 中釜斉

    がん予防大会プログラム・抄録集   Vol. 2011   page: 71   2011

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  59. アゾキシメタン誘発大腸aberrant crypt fociの生成に対する肥満・糖尿病の影響の検討

    伊藤久美子, 高橋真美, 堀美香, 石ケ守里加子, 武藤倫弘, 中釜斉, 太田敏博

    がん予防大会プログラム・抄録集   Vol. 2011   page: 68   2011

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  60. Adiponectin遺伝子欠損によるマウスの腸発がん促進作用

    武藤倫弘, 寺岡直哉, 小沼邦重, 高橋真美, 堀美香, 中野勝也, 一二三佳恵, 窪田直人, 門脇孝, 若林敬二, 中釜斉

    がん予防大会プログラム・抄録集   Vol. 2011   page: 48   2011

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  61. Low density lipoprotein受容体欠損の大腸aberrant crypt foci生成に対する影響

    中野勝也, 武藤倫弘, 小沼邦重, 高橋真美, 堀美香, 一二三佳恵, 谷中昭典, 若林敬二, 中釜斉

    がん予防大会プログラム・抄録集   Vol. 2011   page: 67   2011

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  62. 8‐Hydroxy‐dGTP(8‐oxo‐7,8‐dihydro‐dGTP)二次酸化産物の変異誘発能

    紙谷浩之, 堀美香, 原島秀吉

    日本放射線影響学会大会講演要旨集   Vol. 53rd   page: 91 - 91   2010.10

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    DOI: 10.11513/jrrsabst.2010.0.113.0

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  63. ハムスター膵管発がんにおけるオステオポンチンとそのスプライシングバリアントの発現上昇(Increased expression of osteopontin and its splicing variants in hamster pancreatic ductal carcinogenesis)

    高橋 真美, 石ヶ守 里加子, 堀 美香, 小宮 雅美, 武藤 倫弘, 杉村 隆, 若林 敬二

    日本癌学会総会記事   Vol. 69回   page: 89 - 89   2010.8

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  64. 肥満KK-AyマウスにおけるアンギオテンシンII受容体拮抗薬の大腸発がんに与える影響(Effects of an angiotensin II receptor blocker on colon carcinogenesis in obese KK-Ay mouse)

    高須 伸二, 武藤 倫弘, 寺岡 直哉, 上野 俊也, 小沼 邦重, 高橋 真美, 堀 美香, 杉村 隆, 若林 敬二

    日本癌学会総会記事   Vol. 69回   page: 259 - 259   2010.8

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  65. 高脂肪食によるBOP誘発ハムスター膵管発がん促進因子の検討(Promotion factors of pancreatic carcinogenesis in BOP-treated hamsters fed a high fat diet)

    堀 美香, 北橋 宗, 高橋 真美, 今井 俊夫, 石ヶ守 里加子, 高須 伸二, 武藤 倫弘, 杉村 隆, 若林 敬二

    日本癌学会総会記事   Vol. 69回   page: 89 - 89   2010.8

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  66. ヒトNUDT5蛋白質は様々な酸化デオキシリボヌクレオシドニリン酸を分解する

    紙谷浩之, 堀美香, 有森貴夫, 関口睦夫, 山縣ゆり子, 原島秀吉

    生化学     page: ROMBUNNO.3T18P-15   2009.9

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  67. ヒトNUDT5蛋白質は様々な酸化デオキシリボヌクレオシド二リン酸を分解する

    紙谷 浩之, 堀 美香, 有森 貴夫, 関口 睦夫, 山縣 ゆり子, 原島 秀吉

    日本生化学会大会プログラム・講演要旨集   Vol. 82回   page: 3T18p - 15   2009.9

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  68. マウスでのアディポネクチンの腸発がんにおける役割(Role of adiponectin in intestinal carcinogenesis in mice)

    武藤 倫弘, 飯郷 正明, 寺岡 直哉, 上野 俊也, 高橋 真美, 高須 伸二, 堀 美香, 杉村 隆, 若林 敬二

    日本癌学会総会記事   Vol. 68回   page: 74 - 74   2009.8

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  69. ヌクレオチドプール浄化酵素は、ヒト細胞において8-ヒドロキシ-dGTPにより誘発される変異を抑制する(Nucleotide pool sanitization enzymes suppress the mutation induced by 8-hydroxy-dGTP in human cells)

    堀 美香, 原島 秀吉, 紙谷 浩之

    日本癌学会総会記事   Vol. 68回   page: 39 - 39   2009.8

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  70. NUDT5は幅広い基質特異性を有する酸化dNDP分解酵素である(NUDT5 hydrolyzes oxidized deoxyribo nucleoside diphosphates with broad substrate specificity)

    紙谷 浩之, 堀 美香, 関口 睦夫, 原島 秀吉

    日本癌学会総会記事   Vol. 68回   page: 377 - 377   2009.8

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  71. P-006 8-Hydroxyguanine and translesion synthesis DNA polymerases(Poster Session)

    Kamiya Hiroyuki, Yamaguchi Ayaka, Suzuki Tetsuya, Satou Kazuya, Hori Mika, Kawai Kazuaki, Kasai Hiroshi, Harashima Hideyoshi

    Taikai Program Yoshisyu of the Environmental Mutagen Society of Japan   ( 37 )   2008.11

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  72. 8‐ヒドロキシグアニンが誘発する変異と損傷乗り越えDNAポリメラーゼ

    紙谷浩之, 山口彩花, 鈴木哲矢, 佐藤和哉, 堀美香, 河井一明, 葛西宏, 原島秀吉

    日本環境変異原学会大会プログラム・要旨集   Vol. 37th   page: 109   2008.11

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  73. 哺乳動物細胞におけるヌクレオチドプール浄化酵素の8‐hydroxy‐dGTP誘発変異の抑制

    堀美香, 原島秀吉, 紙谷浩之

    日本放射線影響学会大会講演要旨集   Vol. 51st   page: 87 - 87   2008.11

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    DOI: 10.11513/jrrsabst.2008.0.108.0

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  74. 哺乳動物細胞におけるヌクレオチドプール浄化酵素の酸化損傷ヌクレオチド誘発変異に対する影響

    堀美香, 原島秀吉, 紙谷浩之

    生化学   Vol. 81回・31回   page: 4T4-8 - 8   2008.11

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  75. UvrAとUvrBは酸化損傷ヌクレオチドにより誘発される変異を促進する

    堀美香, 石黒智恵子, 鈴木哲矢, 中川紀子, 布柴達男, 倉光成紀, 山本和生, 葛西宏, 原島秀吉, 紙谷浩之

    日本放射線影響学会大会講演要旨集   Vol. 50th   page: 69 - 69   2007.11

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  76. 損傷ヌクレオチドによる遺伝情報不安定性誘発とその制御 酸化ヌクレオチド誘発変異とヌクレオチド除去修復酵素UvrABCとの関連

    堀 美香, 石黒 智恵子, 中川 紀子, 倉光 成紀, 山本 和生, 葛西 宏, 原島 秀吉, 紙谷 浩之

    日本放射線影響学会大会講演要旨集   Vol. 49回   page: 75 - 75   2006.9

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  77. 酸化ヌクレオチド誘発変異とヌクレオチド除去修復酵素UvrABCとの関連

    堀美香, 石黒智恵子, 中川紀子, 倉光成紀, 山本和生, 葛西宏, 原島秀吉, 紙谷浩之

    日本放射線影響学会大会講演要旨集   Vol. 49th   page: 75   2006

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  78. ヌクレオチドプール浄化酵素Orf17のアンチセンス遺伝子導入の効果

    堀美香, 原島秀吉, 紙谷浩之

    日本分子生物学会年会講演要旨集   Vol. 28th   page: 197   2005.11

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  79. γ線照射,活性窒素により生じる損傷ヌクレオチドのin vivoにおける変異誘発能の解析

    堀美香, 石黒智恵子, 原島秀吉, 紙谷浩之

    日本分子生物学会年会プログラム・講演要旨集   Vol. 27th   page: 634   2004.11

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  80. 大腸菌Orf17蛋白質の酸化損傷ヌクレオチド分解活性

    堀美香, 藤川勝義, 葛西宏, 原島秀吉, 紙谷浩之

    日本分子生物学会年会プログラム・講演要旨集   Vol. 26th   page: 946   2003.11

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KAKENHI (Grants-in-Aid for Scientific Research) 6

  1. 膵内分泌腫瘍モデルマウスを用いたアミノ酸代謝異常を介した発がん機構の解明

    Grant number:21K08705  2021.4 - 2024.3

    堀 美香

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

  2. アキレス腱の軟らかさに着目した家族性高コレステロール血症・新診断法の確立

    Grant number:19H00455  2019

    日本学術振興会  科学研究費助成事業 奨励研究  奨励研究

    道倉 雅仁, 斯波 真理子, 小倉 正恒, 堀 美香, 松木 恒太, 山本 真大

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    家族性高コレステロール血症(FH)はLDL-コレステロール(LDL-C)が高値を示す遺伝的疾患である。本国でのFH診断率は0.1%程度と報告されており、FH診断率の向上は重要未解決問題である。現在の診断基準の1つであるアキレス腱の厚さに加え軟らかさも評価することによりFH検出能が向上するか研究したところ、検出能が80%から86%と向上し、アキレス腱厚が正常で従来見逃されていた患者、特に若年者や女性を診断することができた。

  3. Elucidation of the effect of variants in the PCSK9 gene and molecular type on lifestyle-related diseases and its regulatory mechanism

    Grant number:17K08681  2017.4 - 2020.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Hori Mika

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    Authorship:Principal investigator 

    Grant amount:\4810000 ( Direct Cost: \3700000 、 Indirect Cost:\1110000 )

    The variants in the PCSK9 gene detected in Japan were annotated in familial hypercholesterolemia (FH) according to ACMG guideline. The E32K variant in the PCSK9 gene can cause FH, but the V4I variant alone does not contribute to the pathophysiology of FH. The V4I・E32K variants in the PCSK9 gene showed no difference in the levels of intracellular expression and secretion of PCSK9, intracellular and membrane expression of LDLR and LDL uptake compared to wild type of PCSK9 using cultured cells. In addition, the prevalence of diabetes mellitus was lower in patients with variants in the LDLR and PCSK9 genes than in patients without variants in the LDLR and PCSK9 genes. Patients with FH with variants in the LDLR gene and V4I/E32K variant in the PCSK9 gene had poor prognosis compared to patients with a variant in the LDLR or PCSK9 gene.

  4. Involvement of the type of PCSK9 in familial hypercholesterolemia, obesity and diabetes

    Grant number:15K19038  2015.4 - 2017.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

    Mika Hori

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    Authorship:Principal investigator 

    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

    In familial hypercholesterolemia, there were no significant differences in serum lipid levels and the prevalence of coronary artery diseases (CADs) between PCSK9 V4I carriers and non-carriers without LDLR mutations. In the patients carrying LDLR mutations and aged 30 years or more, the additional PCSK9 V4I variant is linked to a significantly increased prevalence of CADs in accord with the elevation of the LDL-C level. In vitro experiments, there were no differences in the expression of LDLR and the uptake of LDL between PCSK9 V4I-expressed cells and PCSK9 WT-expressed cells. However, in a setting, the uptake of LDL was significantly decreased in PCSK9 V4I-expressed cells as compared with PCSK9 WT- expressed cells.
    In addition, there was inverse correlation between ratio of furin-cleaved PCSK9 to total PCSK9 and serum APOB level in patients with hypercholesterolemia. Thus, it is suggested that the rate of mature PCSK9 to total PCSK9 is associated with high LDL-C levels.

  5. The effect of neuromedin U to atherosclerosis caused by chronic inflammation

    Grant number:24790793  2012.4 - 2015.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    HORI Mika

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    Serum total cholesterol level was 2-fold higher in Apoe-/-Nmu-/- mice in Apoe-/- mice by a high-fat diet (HFD) treatment. However, there were no differences between both mice in atherosclerosis progression by both en face and aortic valve section analysis. There were no differences between peritoneal macrophages in both mice in the uptake of ox-LDL or the inflammation induced by ox-LDL treatment.
    Nmu-/- mice developed hepatic steatosis induced by HFD, but Apoe-/-Nmu-/- mice did not develop it but increased the number of lipid-laden macrophages. Our findings suggest that NMU has no effect on the development of atherosclerosis, but has significant roles in cholesterol metabolism and some inflammation reaction.

  6. dGTPの酸化損傷体の生細胞における変異誘発とその防御機構の解明

    Grant number:07J03120  2007 - 2008

    日本学術振興会  科学研究費助成事業 特別研究員奨励費  特別研究員奨励費

    堀 美香

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    本研究では、酸化ストレスマーカーである8-hydroxyguanineのヌクレオチド体、8-hydroxy-dGTP(8-OH-dGTP)とその二次酸化体、spiroiminodihydantoin-2'-deoxynucleoside 5'-triphosphate(dSpTP)及びguanidinohydantoin-2'-deoxynucleoside 5'-triphosphate(dGhTP)の生細胞における変異誘発能とその除去にDNA修復機相が関与するか否かを明らかにすることを目的とする。
    1.dSpTP及びdGhTPの大腸菌における変異原性の評価とdSpTPやdGhTPを分解するヌクレオチドプール浄化酵素の探索:dSpTP及びdGhTPを大腸菌に直接導入し、変異体率を算出した。その結果、コントロールと比較して変異体率の上昇は観察されなかった。また、ヌクレオチドプール浄化酵素MTH1、MutT、Orf17蛋白質を精製し、dSpTPやdGhTPの分解活性を評価したが、分解活性は観察されなかった。
    2.哺乳動物細胞を用いたヌクレオチドプール浄化酵素の酸化損傷ヌクレオチド除去への関与:哺乳動物細胞のヌクレオチドプール浄化酵素MTH1、MTH2、NUDT5が8-OH-dGTPにより誘発される変異を抑制するか否か検討した。siRNAを用いて各蛋白質をノックダウンしたヒト293T細胞に8-OH-dGTPを直接導入し、誘発変異を調べた。その結果、MTH2及びNUDT5をノックダウンした細胞において、コントロールsiRNA導入時と比較し、8-OH-dGTP誘発変異が上昇し、さらに3種の蛋白質を同時にノックダウンすると、誘発変異が2倍に上昇した。このことから、MTH1、MTH2、NUDT5は、哺乳動物細胞において、互いに補完しあい、8-OH-dGTPにより誘発される変異を抑制していることが示唆された。

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Industrial property rights 1

  1. PCSK9関連薬剤のスクリーニング、又は、当該薬剤の投与効果の確認を行うためのPCSK9の測定方法

    石原 光昭, 鯨岡 健, 岩▲崎▼ 忠雄, 小川 一行, 服部 浩明, 星野 文則, 斯波 真理子, 堀 美香

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    Applicant:株式会社ビー・エム・エル, 独立行政法人国立循環器病研究センター

    Application no:特願2014-111680  Date applied:2014.5

    Announcement no:特開2015-007622  Date announced:2015.1

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