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Cardiac failure in very long chain acyl-CoA dehydrogenase deficiency requiring extracorporeal membrane oxygenation (ECMO) treatment: A case report and review of the literature.

Molecular genetics and metabolism reports

Katz S, Landau Y, Pode-Shakked B, Pessach IM, Rubinshtein M, Anikster Y, Salem Y, Paret G.
PMID: 27995075
Mol Genet Metab Rep. 2016 Dec 08;10:5-7. doi: 10.1016/j.ymgmr.2016.11.008. eCollection 2017 Mar.

Fatty acid oxidation (FAO) defects often present with multi-system involvement, including several life-threatening cardiac manifestations, such as cardiomyopathy, pericardial effusion and arrhythmias. We report herein a fatal case of cardiac dysfunction and rapid-onset tamponade following an acute illness in...

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Katz S, Landau Y, Pode-Shakked B, et al. Cardiac failure in very long chain acyl-CoA dehydrogenase deficiency requiring extracorporeal membrane oxygenation (ECMO) treatment: A case report and review of the literature. Mol Genet Metab Rep. 2016;10:5-7doi: 10.1016/j.ymgmr.2016.11.008.
Katz, S., Landau, Y., Pode-Shakked, B., Pessach, I. M., Rubinshtein, M., Anikster, Y., Salem, Y., & Paret, G. (2017). Cardiac failure in very long chain acyl-CoA dehydrogenase deficiency requiring extracorporeal membrane oxygenation (ECMO) treatment: A case report and review of the literature. Molecular genetics and metabolism reports, 105-7. https://doi.org/10.1016/j.ymgmr.2016.11.008
Katz, Sharon, et al. "Cardiac failure in very long chain acyl-CoA dehydrogenase deficiency requiring extracorporeal membrane oxygenation (ECMO) treatment: A case report and review of the literature." Molecular genetics and metabolism reports vol. 10 (2017): 5-7. doi: https://doi.org/10.1016/j.ymgmr.2016.11.008
Katz S, Landau Y, Pode-Shakked B, Pessach IM, Rubinshtein M, Anikster Y, Salem Y, Paret G. Cardiac failure in very long chain acyl-CoA dehydrogenase deficiency requiring extracorporeal membrane oxygenation (ECMO) treatment: A case report and review of the literature. Mol Genet Metab Rep. 2016 Dec 08;10:5-7. doi: 10.1016/j.ymgmr.2016.11.008. eCollection 2017 Mar. PMID: 27995075; PMCID: PMC5154967.
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Proteomic analysis reveals metabolic and regulatory systems involved in the syntrophic and axenic lifestyle of Syntrophomonas wolfei.

Frontiers in microbiology

Sieber JR, Crable BR, Sheik CS, Hurst GB, Rohlin L, Gunsalus RP, McInerney MJ.
PMID: 25717324
Front Microbiol. 2015 Feb 11;6:115. doi: 10.3389/fmicb.2015.00115. eCollection 2015.

Microbial syntrophy is a vital metabolic interaction necessary for the complete oxidation of organic biomass to methane in all-anaerobic ecosystems. However, this process is thermodynamically constrained and represents an ecosystem-level metabolic bottleneck. To gain insight into the physiology of...

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Sieber JR, Crable BR, Sheik CS, et al. Proteomic analysis reveals metabolic and regulatory systems involved in the syntrophic and axenic lifestyle of Syntrophomonas wolfei. Front Microbiol. 2015;6:115doi: 10.3389/fmicb.2015.00115.
Sieber, J. R., Crable, B. R., Sheik, C. S., Hurst, G. B., Rohlin, L., Gunsalus, R. P., & McInerney, M. J. (2015). Proteomic analysis reveals metabolic and regulatory systems involved in the syntrophic and axenic lifestyle of Syntrophomonas wolfei. Frontiers in microbiology, 6115. https://doi.org/10.3389/fmicb.2015.00115
Sieber, Jessica R, et al. "Proteomic analysis reveals metabolic and regulatory systems involved in the syntrophic and axenic lifestyle of Syntrophomonas wolfei." Frontiers in microbiology vol. 6 (2015): 115. doi: https://doi.org/10.3389/fmicb.2015.00115
Sieber JR, Crable BR, Sheik CS, Hurst GB, Rohlin L, Gunsalus RP, McInerney MJ. Proteomic analysis reveals metabolic and regulatory systems involved in the syntrophic and axenic lifestyle of Syntrophomonas wolfei. Front Microbiol. 2015 Feb 11;6:115. doi: 10.3389/fmicb.2015.00115. eCollection 2015. PMID: 25717324; PMCID: PMC4324140.
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Ethics, genetics and public policies in Uruguay: newborn and infant screening as a paradigm.

Journal of community genetics

Larrandaburu M, Matte U, Noble A, Olivera Z, Sanseverino MT, Nacul L, Schuler-Faccini L.
PMID: 26021874
J Community Genet. 2015 Jul;6(3):241-9. doi: 10.1007/s12687-015-0236-2. Epub 2015 May 29.

Uruguay is a middle-income country and the smallest in South America. Its population is under 3.3 million. The demographic and epidemiological characteristics are similar to those of developed countries, with a high burden associated with congenital anomalies. Infant mortality...

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Larrandaburu M, Matte U, Noble A, et al. Ethics, genetics and public policies in Uruguay: newborn and infant screening as a paradigm. J Community Genet. 2015;6(3):241-9doi: 10.1007/s12687-015-0236-2.
Larrandaburu, M., Matte, U., Noble, A., Olivera, Z., Sanseverino, M. T., Nacul, L., & Schuler-Faccini, L. (2015). Ethics, genetics and public policies in Uruguay: newborn and infant screening as a paradigm. Journal of community genetics, 6(3), 241-9. https://doi.org/10.1007/s12687-015-0236-2
Larrandaburu, Mariela, et al. "Ethics, genetics and public policies in Uruguay: newborn and infant screening as a paradigm." Journal of community genetics vol. 6,3 (2015): 241-9. doi: https://doi.org/10.1007/s12687-015-0236-2
Larrandaburu M, Matte U, Noble A, Olivera Z, Sanseverino MT, Nacul L, Schuler-Faccini L. Ethics, genetics and public policies in Uruguay: newborn and infant screening as a paradigm. J Community Genet. 2015 Jul;6(3):241-9. doi: 10.1007/s12687-015-0236-2. Epub 2015 May 29. PMID: 26021874; PMCID: PMC4524831.
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Erratum to: Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency.

Metabolic brain disease

Chiplunkar S, Bindu PS, Nagappa M, Panikulam BB, Arvinda HR, Govindaraj P, Srinivas Bharath MM, Gayathri N, Jessiena Ponmalar JN, Mathuranath PS, Sinha S, Taly AB.
PMID: 28466389
Metab Brain Dis. 2017 Aug;32(4):971. doi: 10.1007/s11011-017-0018-0.

No abstract available.

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Chiplunkar S, Bindu PS, Nagappa M, et al. Erratum to: Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency. Metab Brain Dis. 2017;32(4):971doi: 10.1007/s11011-017-0018-0.
Chiplunkar, S., Bindu, P. S., Nagappa, M., Panikulam, B. B., Arvinda, H. R., Govindaraj, P., Srinivas Bharath, M. M., Gayathri, N., Jessiena Ponmalar, J. N., Mathuranath, P. S., Sinha, S., & Taly, A. B. (2017). Erratum to: Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency. Metabolic brain disease, 32(4), 971. https://doi.org/10.1007/s11011-017-0018-0
Chiplunkar, Shwetha, et al. "Erratum to: Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency." Metabolic brain disease vol. 32,4 (2017): 971. doi: https://doi.org/10.1007/s11011-017-0018-0
Chiplunkar S, Bindu PS, Nagappa M, Panikulam BB, Arvinda HR, Govindaraj P, Srinivas Bharath MM, Gayathri N, Jessiena Ponmalar JN, Mathuranath PS, Sinha S, Taly AB. Erratum to: Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency. Metab Brain Dis. 2017 Aug;32(4):971. doi: 10.1007/s11011-017-0018-0. PMID: 28466389.
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Aromatase-deficient (ArKO) mice are retrieved from severe hepatic steatosis by peroxisome proliferator administration.

Hepatology research : the official journal of the Japan Society of Hepatology

Yoshikawa T, Toda K, Nemoto Y, Ono M, Iwasaki S, Maeda T, Saibara T, Hayashi Y, Miyazaki E, Hiroi M, Enzan H, Shizuta Y, Onishi S.
PMID: 11929713
Hepatol Res. 2002 Apr;22(4):278-287. doi: 10.1016/s1386-6346(01)00145-0.

Tamoxifen is a potent antagonist of estrogen, and hepatic steatosis is a frequent complication in adjuvant tamoxifen for breast cancer. Recently, aromatase-deficient (ArKO, Ar-/-) mice lacking intrinsic estrogen was developed and the molecular mechanism involved in progression of massive...

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Yoshikawa T, Toda K, Nemoto Y, et al. Aromatase-deficient (ArKO) mice are retrieved from severe hepatic steatosis by peroxisome proliferator administration. Hepatol Res. 2002;22(4):278-287doi: 10.1016/s1386-6346(01)00145-0.
Yoshikawa, T., Toda, K., Nemoto, Y., Ono, M., Iwasaki, S., Maeda, T., Saibara, T., Hayashi, Y., Miyazaki, E., Hiroi, M., Enzan, H., Shizuta, Y., & Onishi, S. (2002). Aromatase-deficient (ArKO) mice are retrieved from severe hepatic steatosis by peroxisome proliferator administration. Hepatology research : the official journal of the Japan Society of Hepatology, 22(4), 278-287. https://doi.org/10.1016/s1386-6346(01)00145-0
Yoshikawa, Takashi, et al. "Aromatase-deficient (ArKO) mice are retrieved from severe hepatic steatosis by peroxisome proliferator administration." Hepatology research : the official journal of the Japan Society of Hepatology vol. 22,4 (2002): 278-287. doi: https://doi.org/10.1016/s1386-6346(01)00145-0
Yoshikawa T, Toda K, Nemoto Y, Ono M, Iwasaki S, Maeda T, Saibara T, Hayashi Y, Miyazaki E, Hiroi M, Enzan H, Shizuta Y, Onishi S. Aromatase-deficient (ArKO) mice are retrieved from severe hepatic steatosis by peroxisome proliferator administration. Hepatol Res. 2002 Apr;22(4):278-287. doi: 10.1016/s1386-6346(01)00145-0. PMID: 11929713.
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Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner.

PPAR research

König B, Rauer C, Rosenbaum S, Brandsch C, Eder K, Stangl GI.
PMID: 20011657
PPAR Res. 2009;2009:801609. doi: 10.1155/2009/801609.

PPARalpha is a lipid-activable transcription factor that mediates the adaptive response to fasting. Recent data indicate an important role of brain PPARalpha in physiological functions. However, it has not yet been shown whether PPARalpha in brain can be activated...

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König B, Rauer C, Rosenbaum S, et al. Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner. PPAR Res. 2009;2009:801609doi: 10.1155/2009/801609.
König, B., Rauer, C., Rosenbaum, S., Brandsch, C., Eder, K., & Stangl, G. I. (2009). Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner. PPAR research, 2009801609. https://doi.org/10.1155/2009/801609
König, Bettina, et al. "Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner." PPAR research vol. 2009 (2009): 801609. doi: https://doi.org/10.1155/2009/801609
König B, Rauer C, Rosenbaum S, Brandsch C, Eder K, Stangl GI. Fasting Upregulates PPARalpha Target Genes in Brain and Influences Pituitary Hormone Expression in a PPARalpha Dependent Manner. PPAR Res. 2009;2009:801609. doi: 10.1155/2009/801609. PMID: 20011657; PMCID: PMC2786200.
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The influence of porcine growth hormone on muscle fibre characteristics, metabolic potential and meat quality.

Meat science

Oksbjerg N, Petersen JS, Sórensen MT, Henckel P, Agergaard N, Bejerholm C, Erlandsen E.
PMID: 22059875
Meat Sci. 1995;39(3):375-85. doi: 10.1016/0309-1740(94)00012-v.

Treatment of lean female pigs with porcine growth hormone (placebo or 80 μg pGH per kg body weight per day) for 6 weeks from 50 kg to 86 kg body weight did not change the frequency and the percentage...

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Oksbjerg N, Petersen JS, Sórensen MT, et al. The influence of porcine growth hormone on muscle fibre characteristics, metabolic potential and meat quality. Meat Sci. 1995;39(3):375-85doi: 10.1016/0309-1740(94)00012-v.
Oksbjerg, N., Petersen, J. S., Sórensen, M. T., Henckel, P., Agergaard, N., Bejerholm, C., & Erlandsen, E. (1995). The influence of porcine growth hormone on muscle fibre characteristics, metabolic potential and meat quality. Meat science, 39(3), 375-85. https://doi.org/10.1016/0309-1740(94)00012-v
Oksbjerg, N, et al. "The influence of porcine growth hormone on muscle fibre characteristics, metabolic potential and meat quality." Meat science vol. 39,3 (1995): 375-85. doi: https://doi.org/10.1016/0309-1740(94)00012-v
Oksbjerg N, Petersen JS, Sórensen MT, Henckel P, Agergaard N, Bejerholm C, Erlandsen E. The influence of porcine growth hormone on muscle fibre characteristics, metabolic potential and meat quality. Meat Sci. 1995;39(3):375-85. doi: 10.1016/0309-1740(94)00012-v. PMID: 22059875.
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Splenectomy reduces fibrosis and preneoplastic lesions with increased triglycerides and essential fatty acids in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet.

Hepatology research : the official journal of the Japan Society of Hepatology

Oishi T, Terai S, Iwamoto T, Takami T, Yamamoto N, Sakaida I.
PMID: 21435125
Hepatol Res. 2011 May;41(5):463-74. doi: 10.1111/j.1872-034X.2011.00784.x. Epub 2011 Mar 21.

AIM:   This study investigated whether splenectomy is of significance in non-alcoholic steatohepatitis (NASH).METHODS:   Five-week-old Wistar rats were fed a choline-deficient diet for 8 weeks to create a NASH model. A sham-operation or splenectomy was then performed, and rats were...

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Oishi T, Terai S, Iwamoto T, et al. Splenectomy reduces fibrosis and preneoplastic lesions with increased triglycerides and essential fatty acids in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet. Hepatol Res. 2011;41(5):463-74doi: 10.1111/j.1872-034X.2011.00784.x.
Oishi, T., Terai, S., Iwamoto, T., Takami, T., Yamamoto, N., & Sakaida, I. (2011). Splenectomy reduces fibrosis and preneoplastic lesions with increased triglycerides and essential fatty acids in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet. Hepatology research : the official journal of the Japan Society of Hepatology, 41(5), 463-74. https://doi.org/10.1111/j.1872-034X.2011.00784.x
Oishi, Toshiyuki, et al. "Splenectomy reduces fibrosis and preneoplastic lesions with increased triglycerides and essential fatty acids in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet." Hepatology research : the official journal of the Japan Society of Hepatology vol. 41,5 (2011): 463-74. doi: https://doi.org/10.1111/j.1872-034X.2011.00784.x
Oishi T, Terai S, Iwamoto T, Takami T, Yamamoto N, Sakaida I. Splenectomy reduces fibrosis and preneoplastic lesions with increased triglycerides and essential fatty acids in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet. Hepatol Res. 2011 May;41(5):463-74. doi: 10.1111/j.1872-034X.2011.00784.x. Epub 2011 Mar 21. PMID: 21435125.
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Relevance of expanded neonatal screening of medium-chain acyl co-a dehydrogenase deficiency: outcome of a decade in galicia (Spain).

JIMD reports

Couce ML, Castiñeiras DE, Moure JD, Cocho JA, Sánchez-Pintos P, García-Villoria J, Quelhas D, Gregersen N, Andresen BS, Ribes A, Fraga JM.
PMID: 23430840
JIMD Rep. 2011;1:131-6. doi: 10.1007/8904_2011_28. Epub 2011 Jun 25.

Neonatal screening of medium-chain acyl-CoA dehydrogenase deficiency (MCADD) is of major importance due to the significant morbidity and mortality in undiagnosed patients. MCADD screening has been performed routinely in Galicia since July 2000, and until now 199,943 newborns have...

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Couce ML, Castiñeiras DE, Moure JD, et al. Relevance of expanded neonatal screening of medium-chain acyl co-a dehydrogenase deficiency: outcome of a decade in galicia (Spain). JIMD Rep. 2011;1:131-6doi: 10.1007/8904_2011_28.
Couce, M. L., Castiñeiras, D. E., Moure, J. D., Cocho, J. A., Sánchez-Pintos, P., García-Villoria, J., Quelhas, D., Gregersen, N., Andresen, B. S., Ribes, A., & Fraga, J. M. (2011). Relevance of expanded neonatal screening of medium-chain acyl co-a dehydrogenase deficiency: outcome of a decade in galicia (Spain). JIMD reports, 1131-6. https://doi.org/10.1007/8904_2011_28
Couce, M L, et al. "Relevance of expanded neonatal screening of medium-chain acyl co-a dehydrogenase deficiency: outcome of a decade in galicia (Spain)." JIMD reports vol. 1 (2011): 131-6. doi: https://doi.org/10.1007/8904_2011_28
Couce ML, Castiñeiras DE, Moure JD, Cocho JA, Sánchez-Pintos P, García-Villoria J, Quelhas D, Gregersen N, Andresen BS, Ribes A, Fraga JM. Relevance of expanded neonatal screening of medium-chain acyl co-a dehydrogenase deficiency: outcome of a decade in galicia (Spain). JIMD Rep. 2011;1:131-6. doi: 10.1007/8904_2011_28. Epub 2011 Jun 25. PMID: 23430840; PMCID: PMC3509827.
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Successful Treatment of Cardiomyopathy due to Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: First Case Report from Oman with Literature Review.

Oman medical journal

Sharef SW, Al-Senaidi K, Joshi SN.
PMID: 24044064
Oman Med J. 2013 Sep;28(5):354-6. doi: 10.5001/omj.2013.101.

Very long-chain acyl-CoA dehydrogenase deficiency (MIM 201475) is a severe defect of mitochondrial energy production from oxidation of very long-chain fatty acids. This inherited metabolic disorder often presents in early neonatal period with episodes of symptomatic hypoglycemia usually responding...

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Sharef SW, Al-Senaidi K, Joshi SN. Successful Treatment of Cardiomyopathy due to Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: First Case Report from Oman with Literature Review. Oman Med J. 2013;28(5):354-6doi: 10.5001/omj.2013.101.
Sharef, S. W., Al-Senaidi, K., & Joshi, S. N. (2013). Successful Treatment of Cardiomyopathy due to Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: First Case Report from Oman with Literature Review. Oman medical journal, 28(5), 354-6. https://doi.org/10.5001/omj.2013.101
Sharef, Sharef Waadallah, et al. "Successful Treatment of Cardiomyopathy due to Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: First Case Report from Oman with Literature Review." Oman medical journal vol. 28,5 (2013): 354-6. doi: https://doi.org/10.5001/omj.2013.101
Sharef SW, Al-Senaidi K, Joshi SN. Successful Treatment of Cardiomyopathy due to Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: First Case Report from Oman with Literature Review. Oman Med J. 2013 Sep;28(5):354-6. doi: 10.5001/omj.2013.101. PMID: 24044064; PMCID: PMC3769119.
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Ketone body therapy with D/L-β-hydroxybutyric acid solution in severe MADD.

Molecular genetics and metabolism reports

Fischer T, Elpers C, Och U, Fobker M, Marquardt T.
PMID: 31312603
Mol Genet Metab Rep. 2019 Jun 28;20:100491. doi: 10.1016/j.ymgmr.2019.100491. eCollection 2019 Sep.

OBJECTIVES: Multiple acyl-CoA dehydrogenase deficiency (MADD) is a severe inborn disorder of mitochondrial fatty acid oxidation. The only treatment option for MADD is the use of exogenous ketone bodies, like sodium β-hydroxybutyrate (NaβHB). However, the use of ketone body...

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Fischer T, Elpers C, Och U, et al. Ketone body therapy with D/L-β-hydroxybutyric acid solution in severe MADD. Mol Genet Metab Rep. 2019;20:100491doi: 10.1016/j.ymgmr.2019.100491.
Fischer, T., Elpers, C., Och, U., Fobker, M., & Marquardt, T. (2019). Ketone body therapy with D/L-β-hydroxybutyric acid solution in severe MADD. Molecular genetics and metabolism reports, 20100491. https://doi.org/10.1016/j.ymgmr.2019.100491
Fischer, Tobias, et al. "Ketone body therapy with D/L-β-hydroxybutyric acid solution in severe MADD." Molecular genetics and metabolism reports vol. 20 (2019): 100491. doi: https://doi.org/10.1016/j.ymgmr.2019.100491
Fischer T, Elpers C, Och U, Fobker M, Marquardt T. Ketone body therapy with D/L-β-hydroxybutyric acid solution in severe MADD. Mol Genet Metab Rep. 2019 Jun 28;20:100491. doi: 10.1016/j.ymgmr.2019.100491. eCollection 2019 Sep. PMID: 31312603; PMCID: PMC6610240.
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Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan.

Molecular genetics and metabolism reports

Yamada K, Shiraishi H, Oki E, Ishige M, Fukao T, Hamada Y, Sakai N, Ochi F, Watanabe A, Kawakami S, Kuzume K, Watanabe K, Sameshima K, Nakamagoe K, Tamaoka A, Asahina N, Yokoshiki S, Miyakoshi T, Ono K, Oba K, Isoe T, Hayashi H, Yamaguchi S, Sato N.
PMID: 29552494
Mol Genet Metab Rep. 2018 Feb 22;15:55-63. doi: 10.1016/j.ymgmr.2018.02.003. eCollection 2018 Jun.

INTRODUCTION: Fatty acid oxidation disorders (FAODs) are rare diseases caused by defects in mitochondrial fatty acid oxidation (FAO) enzymes. While the efficacy of bezafibrate, a peroxisome proliferator-activated receptor agonist, on the MATERIALS AND METHODS: This trial was an open-label,...

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Yamada K, Shiraishi H, Oki E, et al. Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan. Mol Genet Metab Rep. 2018;15:55-63doi: 10.1016/j.ymgmr.2018.02.003.
Yamada, K., Shiraishi, H., Oki, E., Ishige, M., Fukao, T., Hamada, Y., Sakai, N., Ochi, F., Watanabe, A., Kawakami, S., Kuzume, K., Watanabe, K., Sameshima, K., Nakamagoe, K., Tamaoka, A., Asahina, N., Yokoshiki, S., Miyakoshi, T., Ono, K., Oba, K., Isoe, T., Hayashi, H., Yamaguchi, S., & Sato, N. (2018). Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan. Molecular genetics and metabolism reports, 1555-63. https://doi.org/10.1016/j.ymgmr.2018.02.003
Yamada, Kenji, et al. "Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan." Molecular genetics and metabolism reports vol. 15 (2018): 55-63. doi: https://doi.org/10.1016/j.ymgmr.2018.02.003
Yamada K, Shiraishi H, Oki E, Ishige M, Fukao T, Hamada Y, Sakai N, Ochi F, Watanabe A, Kawakami S, Kuzume K, Watanabe K, Sameshima K, Nakamagoe K, Tamaoka A, Asahina N, Yokoshiki S, Miyakoshi T, Ono K, Oba K, Isoe T, Hayashi H, Yamaguchi S, Sato N. Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan. Mol Genet Metab Rep. 2018 Feb 22;15:55-63. doi: 10.1016/j.ymgmr.2018.02.003. eCollection 2018 Jun. PMID: 29552494; PMCID: PMC5852296.
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