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Combined replacement effects of human modified β-hexosaminidase B and GM2 activator protein on GM2 gangliosidoses fibroblasts.

Biochemistry and biophysics reports

Kitakaze K, Tasaki C, Tajima Y, Hirokawa T, Tsuji D, Sakuraba H, Itoh K.
PMID: 28955902
Biochem Biophys Rep. 2016 Jun 08;7:157-163. doi: 10.1016/j.bbrep.2016.04.012. eCollection 2016 Sep.

GM2 gangliosidoses are autosomal recessive lysosomal storage diseases (LSDs) caused by mutations in the

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Kitakaze K, Tasaki C, Tajima Y, et al. Combined replacement effects of human modified β-hexosaminidase B and GM2 activator protein on GM2 gangliosidoses fibroblasts. Biochem Biophys Rep. 2016;7:157-163doi: 10.1016/j.bbrep.2016.04.012.
Kitakaze, K., Tasaki, C., Tajima, Y., Hirokawa, T., Tsuji, D., Sakuraba, H., & Itoh, K. (2016). Combined replacement effects of human modified β-hexosaminidase B and GM2 activator protein on GM2 gangliosidoses fibroblasts. Biochemistry and biophysics reports, 7157-163. https://doi.org/10.1016/j.bbrep.2016.04.012
Kitakaze, Keisuke, et al. "Combined replacement effects of human modified β-hexosaminidase B and GM2 activator protein on GM2 gangliosidoses fibroblasts." Biochemistry and biophysics reports vol. 7 (2016): 157-163. doi: https://doi.org/10.1016/j.bbrep.2016.04.012
Kitakaze K, Tasaki C, Tajima Y, Hirokawa T, Tsuji D, Sakuraba H, Itoh K. Combined replacement effects of human modified β-hexosaminidase B and GM2 activator protein on GM2 gangliosidoses fibroblasts. Biochem Biophys Rep. 2016 Jun 08;7:157-163. doi: 10.1016/j.bbrep.2016.04.012. eCollection 2016 Sep. PMID: 28955902; PMCID: PMC5613250.
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Cellular mechanisms for the treatment of chronic heart failure: the nitric oxide- and adenosine-dependent pathways.

Expert opinion on emerging drugs

Minamino T, Kitakaze M.
PMID: 15989539
Expert Opin Emerg Drugs. 2002 May;7(1):99-110. doi: 10.1517/14728214.7.1.99.

Accumulated evidence suggests that several drugs proven to improve survival in patients with chronic heart failure (CHF) enhance endogenous nitric oxide (NO)- and/or adenosine-dependent pathways. Indeed, we and others have demonstrated that: i) antagonists of either renin-angiotensin-aldosterone or beta-adrenergic...

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Minamino T, Kitakaze M. Cellular mechanisms for the treatment of chronic heart failure: the nitric oxide- and adenosine-dependent pathways. Expert Opin Emerg Drugs. 2002;7(1):99-110doi: 10.1517/14728214.7.1.99.
Minamino, T., & Kitakaze, M. (2002). Cellular mechanisms for the treatment of chronic heart failure: the nitric oxide- and adenosine-dependent pathways. Expert opinion on emerging drugs, 7(1), 99-110. https://doi.org/10.1517/14728214.7.1.99
Minamino, Tetsuo, and Kitakaze, Masafumi. "Cellular mechanisms for the treatment of chronic heart failure: the nitric oxide- and adenosine-dependent pathways." Expert opinion on emerging drugs vol. 7,1 (2002): 99-110. doi: https://doi.org/10.1517/14728214.7.1.99
Minamino T, Kitakaze M. Cellular mechanisms for the treatment of chronic heart failure: the nitric oxide- and adenosine-dependent pathways. Expert Opin Emerg Drugs. 2002 May;7(1):99-110. doi: 10.1517/14728214.7.1.99. PMID: 15989539.
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A case of caseous calcification of the mitral annulus: A potential source of embolic stroke.

Journal of cardiology cases

Higashi H, Ohara T, Nakatani S, Hashimoto S, Torii T, Miyashita K, Naritomi H, Kitakaze M.
PMID: 30532814
J Cardiol Cases. 2010 Jul 07;2(3):e141-e143. doi: 10.1016/j.jccase.2010.05.012. eCollection 2010 Dec.

Mitral annular calcification (MAC) is a common finding especially among the elderly. Caseous calcification of the mitral annulus (CCMA) is a rare variant of MAC, which may be mistaken for an intracardiac tumor or abscess. The clinical significance of...

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Higashi H, Ohara T, Nakatani S, et al. A case of caseous calcification of the mitral annulus: A potential source of embolic stroke. J Cardiol Cases. 2010;2(3):e141-e143doi: 10.1016/j.jccase.2010.05.012.
Higashi, H., Ohara, T., Nakatani, S., Hashimoto, S., Torii, T., Miyashita, K., Naritomi, H., & Kitakaze, M. (2010). A case of caseous calcification of the mitral annulus: A potential source of embolic stroke. Journal of cardiology cases, 2(3), e141-e143. https://doi.org/10.1016/j.jccase.2010.05.012
Higashi, Haruhiko, et al. "A case of caseous calcification of the mitral annulus: A potential source of embolic stroke." Journal of cardiology cases vol. 2,3 (2010): e141-e143. doi: https://doi.org/10.1016/j.jccase.2010.05.012
Higashi H, Ohara T, Nakatani S, Hashimoto S, Torii T, Miyashita K, Naritomi H, Kitakaze M. A case of caseous calcification of the mitral annulus: A potential source of embolic stroke. J Cardiol Cases. 2010 Jul 07;2(3):e141-e143. doi: 10.1016/j.jccase.2010.05.012. eCollection 2010 Dec. PMID: 30532814; PMCID: PMC6265132.
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Rationale and Design of a Prospective, Multicenter, Single-Arm Clinical Trial to Investigate the Safety and Effectiveness of Rotablator Atherectomy System as an Adjunctive Device for Endovascular Treatment of Occlusive Atherosclerotic Lesions in Below-the-Knee Arteries With Critical Limb Ischemia (RESCUE-BTK).

Circulation reports

Yagyu T, Ito S, Kawarada O, Mizuseki M, Yamamoto H, Asakura M, Funabashi S, Onda K, Ohshima K, Fukuda-Doi M, Asakura K, Kitakaze M, Noguchi T, Yasuda S.
PMID: 33693268
Circ Rep. 2020 Jun 16;2(8):449-454. doi: 10.1253/circrep.CR-20-0024.

No abstract available.

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Yagyu T, Ito S, Kawarada O, et al. Rationale and Design of a Prospective, Multicenter, Single-Arm Clinical Trial to Investigate the Safety and Effectiveness of Rotablator Atherectomy System as an Adjunctive Device for Endovascular Treatment of Occlusive Atherosclerotic Lesions in Below-the-Knee Arteries With Critical Limb Ischemia (RESCUE-BTK). Circ Rep. 2020;2(8):449-454doi: 10.1253/circrep.CR-20-0024.
Yagyu, T., Ito, S., Kawarada, O., Mizuseki, M., Yamamoto, H., Asakura, M., Funabashi, S., Onda, K., Ohshima, K., Fukuda-Doi, M., Asakura, K., Kitakaze, M., Noguchi, T., & Yasuda, S. (2020). Rationale and Design of a Prospective, Multicenter, Single-Arm Clinical Trial to Investigate the Safety and Effectiveness of Rotablator Atherectomy System as an Adjunctive Device for Endovascular Treatment of Occlusive Atherosclerotic Lesions in Below-the-Knee Arteries With Critical Limb Ischemia (RESCUE-BTK). Circulation reports, 2(8), 449-454. https://doi.org/10.1253/circrep.CR-20-0024
Yagyu, Takeshi, et al. "Rationale and Design of a Prospective, Multicenter, Single-Arm Clinical Trial to Investigate the Safety and Effectiveness of Rotablator Atherectomy System as an Adjunctive Device for Endovascular Treatment of Occlusive Atherosclerotic Lesions in Below-the-Knee Arteries With Critical Limb Ischemia (RESCUE-BTK)." Circulation reports vol. 2,8 (2020): 449-454. doi: https://doi.org/10.1253/circrep.CR-20-0024
Yagyu T, Ito S, Kawarada O, Mizuseki M, Yamamoto H, Asakura M, Funabashi S, Onda K, Ohshima K, Fukuda-Doi M, Asakura K, Kitakaze M, Noguchi T, Yasuda S. Rationale and Design of a Prospective, Multicenter, Single-Arm Clinical Trial to Investigate the Safety and Effectiveness of Rotablator Atherectomy System as an Adjunctive Device for Endovascular Treatment of Occlusive Atherosclerotic Lesions in Below-the-Knee Arteries With Critical Limb Ischemia (RESCUE-BTK). Circ Rep. 2020 Jun 16;2(8):449-454. doi: 10.1253/circrep.CR-20-0024. PMID: 33693268; PMCID: PMC7819644.
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Bisacurone suppresses hepatic lipid accumulation through inhibiting lipogenesis and promoting lipolysis.

Journal of clinical biochemistry and nutrition

Ashida H, Tian X, Kitakaze T, Yamashita Y.
PMID: 32801468
J Clin Biochem Nutr. 2020 Jul;67(1):43-52. doi: 10.3164/jcbn.20-16. Epub 2020 May 08.

Turmeric and its components have various health beneficial functions. However, little is known about function of bisacurone, which is one of the sesquiterpenes in turmeric, at the compound level. In this study, we investigated the preventive effect of bisacurone...

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Ashida H, Tian X, Kitakaze T, et al. Bisacurone suppresses hepatic lipid accumulation through inhibiting lipogenesis and promoting lipolysis. J Clin Biochem Nutr. 2020;67(1):43-52doi: 10.3164/jcbn.20-16.
Ashida, H., Tian, X., Kitakaze, T., & Yamashita, Y. (2020). Bisacurone suppresses hepatic lipid accumulation through inhibiting lipogenesis and promoting lipolysis. Journal of clinical biochemistry and nutrition, 67(1), 43-52. https://doi.org/10.3164/jcbn.20-16
Ashida, Hitoshi, et al. "Bisacurone suppresses hepatic lipid accumulation through inhibiting lipogenesis and promoting lipolysis." Journal of clinical biochemistry and nutrition vol. 67,1 (2020): 43-52. doi: https://doi.org/10.3164/jcbn.20-16
Ashida H, Tian X, Kitakaze T, Yamashita Y. Bisacurone suppresses hepatic lipid accumulation through inhibiting lipogenesis and promoting lipolysis. J Clin Biochem Nutr. 2020 Jul;67(1):43-52. doi: 10.3164/jcbn.20-16. Epub 2020 May 08. PMID: 32801468; PMCID: PMC7417797.
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Relationship between whether the planned discharge destination is decided and locomotive syndrome for admitted patients in psychiatric long-term care wards.

Physical therapy research

Kota M, Uezono S, Ishibashi Y, Kitakaze S, Arakawa H.
PMID: 33489657
Phys Ther Res. 2020 Aug 20;23(2):180-187. doi: 10.1298/ptr.E10016. eCollection 2020.

OBJECTIVE: We focused on locomotive syndrome as a low physical function factor that may prevent patients with psychiatric disease from being discharged. The purpose of this study is to clarify the factors, including locomotive syndrome, that prevent discharge from...

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Kota M, Uezono S, Ishibashi Y, et al. Relationship between whether the planned discharge destination is decided and locomotive syndrome for admitted patients in psychiatric long-term care wards. Phys Ther Res. 2020;23(2):180-187doi: 10.1298/ptr.E10016.
Kota, M., Uezono, S., Ishibashi, Y., Kitakaze, S., & Arakawa, H. (2020). Relationship between whether the planned discharge destination is decided and locomotive syndrome for admitted patients in psychiatric long-term care wards. Physical therapy research, 23(2), 180-187. https://doi.org/10.1298/ptr.E10016
Kota, Munetsugu, et al. "Relationship between whether the planned discharge destination is decided and locomotive syndrome for admitted patients in psychiatric long-term care wards." Physical therapy research vol. 23,2 (2020): 180-187. doi: https://doi.org/10.1298/ptr.E10016
Kota M, Uezono S, Ishibashi Y, Kitakaze S, Arakawa H. Relationship between whether the planned discharge destination is decided and locomotive syndrome for admitted patients in psychiatric long-term care wards. Phys Ther Res. 2020 Aug 20;23(2):180-187. doi: 10.1298/ptr.E10016. eCollection 2020. PMID: 33489657; PMCID: PMC7814226.
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Development of a selective fluorescence-based enzyme assay for glycerophosphodiesterase family members GDE4 and GDE7.

Journal of lipid research

Kitakaze K, Tsuboi K, Tsuda M, Takenouchi Y, Ishimaru H, Okamoto Y.
PMID: 34673020
J Lipid Res. 2021;62:100141. doi: 10.1016/j.jlr.2021.100141. Epub 2021 Oct 18.

Lysophosphatidic acid (LPA) is a lipid mediator that regulates various processes, including cell migration and cancer progression. Autotaxin (ATX) is a lysophospholipase D-type exoenzyme that produces extracellular LPA. In contrast, glycerophosphodiesterase (GDE) family members GDE4 and GDE7 are intracellular...

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Kitakaze K, Tsuboi K, Tsuda M, et al. Development of a selective fluorescence-based enzyme assay for glycerophosphodiesterase family members GDE4 and GDE7. J Lipid Res. 2021;62:100141doi: 10.1016/j.jlr.2021.100141.
Kitakaze, K., Tsuboi, K., Tsuda, M., Takenouchi, Y., Ishimaru, H., & Okamoto, Y. (2021). Development of a selective fluorescence-based enzyme assay for glycerophosphodiesterase family members GDE4 and GDE7. Journal of lipid research, 62100141. https://doi.org/10.1016/j.jlr.2021.100141
Kitakaze, Keisuke, et al. "Development of a selective fluorescence-based enzyme assay for glycerophosphodiesterase family members GDE4 and GDE7." Journal of lipid research vol. 62 (2021): 100141. doi: https://doi.org/10.1016/j.jlr.2021.100141
Kitakaze K, Tsuboi K, Tsuda M, Takenouchi Y, Ishimaru H, Okamoto Y. Development of a selective fluorescence-based enzyme assay for glycerophosphodiesterase family members GDE4 and GDE7. J Lipid Res. 2021;62:100141. doi: 10.1016/j.jlr.2021.100141. Epub 2021 Oct 18. PMID: 34673020; PMCID: PMC8591415.
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Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779.

Circulation

Lin H, Zhu Y, Zheng C, Hu D, Ma S, Chen L, Wang Q, Chen Z, Xie J, Yan Y, Huang X, Liao W, Kitakaze M, Bin J, Liao Y.
PMID: 33757294
Circulation. 2021 Jun 08;143(23):2277-2292. doi: 10.1161/CIRCULATIONAHA.120.047000. Epub 2021 Mar 24.

BACKGROUND: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic...

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Lin H, Zhu Y, Zheng C, et al. Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779. Circulation. 2021;143(23):2277-2292doi: 10.1161/CIRCULATIONAHA.120.047000.
Lin, H., Zhu, Y., Zheng, C., Hu, D., Ma, S., Chen, L., Wang, Q., Chen, Z., Xie, J., Yan, Y., Huang, X., Liao, W., Kitakaze, M., Bin, J., & Liao, Y. (2021). Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779. Circulation, 143(23), 2277-2292. https://doi.org/10.1161/CIRCULATIONAHA.120.047000
Lin, Hairuo, et al. "Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779." Circulation vol. 143,23 (2021): 2277-2292. doi: https://doi.org/10.1161/CIRCULATIONAHA.120.047000
Lin H, Zhu Y, Zheng C, Hu D, Ma S, Chen L, Wang Q, Chen Z, Xie J, Yan Y, Huang X, Liao W, Kitakaze M, Bin J, Liao Y. Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779. Circulation. 2021 Jun 08;143(23):2277-2292. doi: 10.1161/CIRCULATIONAHA.120.047000. Epub 2021 Mar 24. PMID: 33757294; PMCID: PMC8177494.
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ATF4-mediated transcriptional regulation protects against β-cell loss during endoplasmic reticulum stress in a mouse model.

Molecular metabolism

Kitakaze K, Oyadomari M, Zhang J, Hamada Y, Takenouchi Y, Tsuboi K, Inagaki M, Tachikawa M, Fujitani Y, Okamoto Y, Oyadomari S.
PMID: 34547510
Mol Metab. 2021 Dec;54:101338. doi: 10.1016/j.molmet.2021.101338. Epub 2021 Sep 20.

OBJECTIVE: Activating transcription factor 4 (ATF4) is a transcriptional regulator of the unfolded protein response and integrated stress response (ISR) that promote the restoration of normal endoplasmic reticulum (ER) function. Previous reports demonstrated that dysregulation of the ISR led...

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Kitakaze K, Oyadomari M, Zhang J, et al. ATF4-mediated transcriptional regulation protects against β-cell loss during endoplasmic reticulum stress in a mouse model. Mol Metab. 2021;54:101338doi: 10.1016/j.molmet.2021.101338.
Kitakaze, K., Oyadomari, M., Zhang, J., Hamada, Y., Takenouchi, Y., Tsuboi, K., Inagaki, M., Tachikawa, M., Fujitani, Y., Okamoto, Y., & Oyadomari, S. (2021). ATF4-mediated transcriptional regulation protects against β-cell loss during endoplasmic reticulum stress in a mouse model. Molecular metabolism, 54101338. https://doi.org/10.1016/j.molmet.2021.101338
Kitakaze, Keisuke, et al. "ATF4-mediated transcriptional regulation protects against β-cell loss during endoplasmic reticulum stress in a mouse model." Molecular metabolism vol. 54 (2021): 101338. doi: https://doi.org/10.1016/j.molmet.2021.101338
Kitakaze K, Oyadomari M, Zhang J, Hamada Y, Takenouchi Y, Tsuboi K, Inagaki M, Tachikawa M, Fujitani Y, Okamoto Y, Oyadomari S. ATF4-mediated transcriptional regulation protects against β-cell loss during endoplasmic reticulum stress in a mouse model. Mol Metab. 2021 Dec;54:101338. doi: 10.1016/j.molmet.2021.101338. Epub 2021 Sep 20. PMID: 34547510; PMCID: PMC8487982.
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Sphingosine 1-phosphate receptor type 2 positively regulates interleukin (IL)-4/IL-13-induced STAT6 phosphorylation.

Cellular signalling

Okamoto Y, Kitakaze K, Takenouchi Y, Yamamoto S, Ishimaru H, Tsuboi K.
PMID: 34592416
Cell Signal. 2021 Dec;88:110156. doi: 10.1016/j.cellsig.2021.110156. Epub 2021 Sep 28.

Previous reports have demonstrated that sphingosine 1-phosphate receptor type 2 (S1P

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Okamoto Y, Kitakaze K, Takenouchi Y, et al. Sphingosine 1-phosphate receptor type 2 positively regulates interleukin (IL)-4/IL-13-induced STAT6 phosphorylation. Cell Signal. 2021;88:110156doi: 10.1016/j.cellsig.2021.110156.
Okamoto, Y., Kitakaze, K., Takenouchi, Y., Yamamoto, S., Ishimaru, H., & Tsuboi, K. (2021). Sphingosine 1-phosphate receptor type 2 positively regulates interleukin (IL)-4/IL-13-induced STAT6 phosphorylation. Cellular signalling, 88110156. https://doi.org/10.1016/j.cellsig.2021.110156
Okamoto, Yasuo, et al. "Sphingosine 1-phosphate receptor type 2 positively regulates interleukin (IL)-4/IL-13-induced STAT6 phosphorylation." Cellular signalling vol. 88 (2021): 110156. doi: https://doi.org/10.1016/j.cellsig.2021.110156
Okamoto Y, Kitakaze K, Takenouchi Y, Yamamoto S, Ishimaru H, Tsuboi K. Sphingosine 1-phosphate receptor type 2 positively regulates interleukin (IL)-4/IL-13-induced STAT6 phosphorylation. Cell Signal. 2021 Dec;88:110156. doi: 10.1016/j.cellsig.2021.110156. Epub 2021 Sep 28. PMID: 34592416.
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Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner.

Biochemical and biophysical research communications

Okamoto S, Miyano K, Kitakaze K, Kato H, Yamauchi A, Kajikawa M, Itsumi M, Kawai C, Kuribayashi F.
PMID: 34872003
Biochem Biophys Res Commun. 2022 Jan 08;587:78-84. doi: 10.1016/j.bbrc.2021.11.090. Epub 2021 Nov 27.

An interaction between acute myeloid leukemia (AML) cells and endothelial cells in the bone marrow seems to play a critical role in chemosensitivity on leukemia treatment. The endothelial niche reportedly enhances the paracrine action of the soluble secretory proteins...

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Okamoto S, Miyano K, Kitakaze K, et al. Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner. Biochem Biophys Res Commun. 2021;587:78-84doi: 10.1016/j.bbrc.2021.11.090.
Okamoto, S., Miyano, K., Kitakaze, K., Kato, H., Yamauchi, A., Kajikawa, M., Itsumi, M., Kawai, C., & Kuribayashi, F. (2022). Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner. Biochemical and biophysical research communications, 58778-84. https://doi.org/10.1016/j.bbrc.2021.11.090
Okamoto, Shuichiro, et al. "Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner." Biochemical and biophysical research communications vol. 587 (2022): 78-84. doi: https://doi.org/10.1016/j.bbrc.2021.11.090
Okamoto S, Miyano K, Kitakaze K, Kato H, Yamauchi A, Kajikawa M, Itsumi M, Kawai C, Kuribayashi F. Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner. Biochem Biophys Res Commun. 2022 Jan 08;587:78-84. doi: 10.1016/j.bbrc.2021.11.090. Epub 2021 Nov 27. PMID: 34872003.
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A case of cardiac sarcoidosis masquerading as arrhythmogenic right ventricular cardiomyopathy awaiting heart transplant.

Journal of cardiology cases

Hisaoka S, Sugiyama-Kato T, Iwamura T, Okamatsu H, Kamakura T, Sato H, Nakatani T, Hashimura K, Kitakaze M, Ishibashi-Ueda H, Shishido T, Komamura K.
PMID: 30524529
J Cardiol Cases. 2010 Jan 12;1(3):e161-e165. doi: 10.1016/j.jccase.2009.12.004. eCollection 2010 Jun.

We report a case of 45-year-old man, who was diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC) and presented with right ventricular (RV) enlargement with a global decrease in RV contractility accompanied by impairment of left ventricular function. He was...

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Hisaoka S, Sugiyama-Kato T, Iwamura T, et al. A case of cardiac sarcoidosis masquerading as arrhythmogenic right ventricular cardiomyopathy awaiting heart transplant. J Cardiol Cases. 2010;1(3):e161-e165doi: 10.1016/j.jccase.2009.12.004.
Hisaoka, S., Sugiyama-Kato, T., Iwamura, T., Okamatsu, H., Kamakura, T., Sato, H., Nakatani, T., Hashimura, K., Kitakaze, M., Ishibashi-Ueda, H., Shishido, T., & Komamura, K. (2010). A case of cardiac sarcoidosis masquerading as arrhythmogenic right ventricular cardiomyopathy awaiting heart transplant. Journal of cardiology cases, 1(3), e161-e165. https://doi.org/10.1016/j.jccase.2009.12.004
Hisaoka, Sahika, et al. "A case of cardiac sarcoidosis masquerading as arrhythmogenic right ventricular cardiomyopathy awaiting heart transplant." Journal of cardiology cases vol. 1,3 (2010): e161-e165. doi: https://doi.org/10.1016/j.jccase.2009.12.004
Hisaoka S, Sugiyama-Kato T, Iwamura T, Okamatsu H, Kamakura T, Sato H, Nakatani T, Hashimura K, Kitakaze M, Ishibashi-Ueda H, Shishido T, Komamura K. A case of cardiac sarcoidosis masquerading as arrhythmogenic right ventricular cardiomyopathy awaiting heart transplant. J Cardiol Cases. 2010 Jan 12;1(3):e161-e165. doi: 10.1016/j.jccase.2009.12.004. eCollection 2010 Jun. PMID: 30524529; PMCID: PMC6264930.
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