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Artykuły w czasopismach na temat "Long-chain-acyl-CoA dehydrogenase"
Masterson, C., A. Blackburn i C. Wood. "Acyl-CoA dehydrogenase activity in pea cotyledon tissue during germination and initial growth". Biochemical Society Transactions 28, nr 6 (1.12.2000): 760–62. http://dx.doi.org/10.1042/bst0280760.
Pełny tekst źródłaTreem, William R., Jeffrey S. Hyams, Charles A. Stanley, Daniel E. Hale i Harris B. Leopold. "Hypoglycemia, Hypotonia, and Cardiomyopathy: The Evolving Clinical Picture of Long-Chain Acyl-CoA Dehydrogenase Deficiency". Pediatrics 87, nr 3 (1.03.1991): 328–33. http://dx.doi.org/10.1542/peds.87.3.328.
Pełny tekst źródłaCox, Keith B., Jian Liu, Liqun Tian, Stephen Barnes, Qinglin Yang i Philip A. Wood. "Cardiac hypertrophy in mice with long-chain acyl-CoA dehydrogenase or very long-chain acyl-CoA dehydrogenase deficiency". Laboratory Investigation 89, nr 12 (7.09.2009): 1348–54. http://dx.doi.org/10.1038/labinvest.2009.86.
Pełny tekst źródłaYu, Wenfeng, Xiquan Liang, Regina E. Ensenauer, Jerry Vockley, Lawrence Sweetman i Horst Schulz. "Leaky β-Oxidation of atrans-Fatty Acid". Journal of Biological Chemistry 279, nr 50 (4.10.2004): 52160–67. http://dx.doi.org/10.1074/jbc.m409640200.
Pełny tekst źródłaWijayabandara, Maheshi, Champika Gamakaranage i Dineshani Hettiarachchi. "Very-Long-Chain Acyl-Co-Enzyme A Dehydrogenase Deficiency Presenting as Rhabdomyolysis: First Case Report from Sri Lanka". Case Reports in Genetics 2020 (13.10.2020): 1–5. http://dx.doi.org/10.1155/2020/8894518.
Pełny tekst źródłaLiang, X., W. Le, D. Zhang i H. Schulz. "Impact of the intramitochondrial enzyme organization on fatty acid oxidation". Biochemical Society Transactions 29, nr 2 (1.05.2001): 279–82. http://dx.doi.org/10.1042/bst0290279.
Pełny tekst źródłaYamaguchi, Seiji, Yasuhiro Indo, Paul M. Coates, Takashi Hashimoto i Kay Tanaka. "Identification of Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency in Three Patients Previously Diagnosed with Long-Chain Acyl-CoA Dehydrogenase Deficiency". Pediatric Research 34, nr 1 (lipiec 1993): 111–13. http://dx.doi.org/10.1203/00006450-199307000-00025.
Pełny tekst źródłaCosta, Catarina G., Lambertus Dorland, Ulbe Holwerda, Isabel Tavares de Almeida, Bwee-Tien Poll-The, Cornelis Jakobs i Marinus Duran. "Simultaneous analysis of plasma free fatty acids and their 3-hydroxy analogs in fatty acid β-oxidation disorders". Clinical Chemistry 44, nr 3 (1.03.1998): 463–71. http://dx.doi.org/10.1093/clinchem/44.3.463.
Pełny tekst źródłaNandy, Andreas, Volker Kieweg, Franz-Georg Kräutle, Petra Vock, Burkhard Küchler, Peter Bross, Jung-Ja P. Kim, Ihab Rasched i Sandro Ghisla. "Medium-Long-Chain Chimeric Human Acyl-CoA Dehydrogenase: Medium-Chain Enzyme with the Active Center Base Arrangement of Long-Chain Acyl-CoA Dehydrogenase†". Biochemistry 35, nr 38 (styczeń 1996): 12402–11. http://dx.doi.org/10.1021/bi960785e.
Pełny tekst źródłaParsons, H. G., i V. C. Dias. "Intramitochondrial fatty acid metabolism: riboflavin deficiency and energy production". Biochemistry and Cell Biology 69, nr 7 (1.07.1991): 490–97. http://dx.doi.org/10.1139/o91-073.
Pełny tekst źródłaRozprawy doktorskie na temat "Long-chain-acyl-CoA dehydrogenase"
Keeler, Allison M. "Gene Therapy for Very Long Chain Acyl-coA Dehydrogenase Deficiency Using Adeno-Associated Virus Vectors: A Dissertation". eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/632.
Pełny tekst źródłaKrogmann, Antonia Verfasser], Ute [Gutachter] [Spiekerkötter i Anselmino Verena [Gutachter] Keitel-. "Der renale Phänotyp beim Very-Long-Chain Acyl-CoA Dehydrogenase- (VLCAD-) Mangel: Studien am VLCAD-/--Mausmodell / Antonia Krogmann ; Gutachter: Ute Spiekerkötter, Verena Keitel- Anselmino". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1217062300/34.
Pełny tekst źródłaWang, Xiao. "Investigation of Anaplerosis from Propionyl-CoA Precursors and Fatty Acid Oxidation in the Brain of VLCAD and Control Mice". Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1232676063.
Pełny tekst źródłaTawbeh, Ali. "Dysfonctionnement peroxysomal dans les cellules microgliales BV-2 : vers une meilleure compréhension du processus neurodégénératif dans l'adrénoleucodystrophie liée à l'X". Electronic Thesis or Diss., Bourgogne Franche-Comté, 2023. http://www.theses.fr/2023UBFCI010.
Pełny tekst źródłaMicroglia act as the immune sentinel of the central nervous system and play a crucial role in maintaining its homeostasis. Peroxisomes, essential organelles in cellular metabolism, mainly orchestrate the breakdown of very long-chain fatty acids (VLCFAs). The accumulation of VLCFAs is a marker of peroxisomal diseases, the most common of which is X-linked adrenoleukodystrophy (X-ALD), a rare and complex neurodegenerative disease in which microglia are thought to play an important role. The inactivation of peroxisomal genes in BV-2 microglial cells had shed light on a yet unexplored relationship between peroxisomal activity and microglial plasticity. Specifically, knocked-out genes included those encoding the very long-chain fatty acid transporters ABCD1 and ABCD2, as well as the peroxisomal β-oxidation-limiting enzyme ACOX1. Transcriptomic and functional analysis of the mutant cells revealed a disease-associated microglial signature close to that found in the most common neurodegenerative diseases. The peroxisomal defect impacts lipid metabolism in the broad sense, lysosomal and autophagic functions, as well as the response to lipopolysaccharide stimulation, including the inflammatory response and redox homeostasis. The functions of phagocytosis and antigen presentation to T lymphocytes are also altered. In addition, secretions from these mutant microglial cells induce the death of neuronal and oligodendrocyte cell lines and modify the morphology and function of neurons. Although these results need to be confirmed in primary microglia, they support the hypothesis of a major and early role for microglia in the neurodegenerative cascade observed in X-ALD and validate microglia and the molecules they secrete as a therapeutic target in peroxisomal leukodystrophies
Celorico, Ana Patrícia Monteiro. "Very long-chain Acyl-CoA dehydrogenase deficiency from gene to treatment". Master's thesis, 2015. http://hdl.handle.net/10451/26955.
Pełny tekst źródłaA ß-oxidação mitocondrial dos ácidos gordos (MFAO) é uma importante fonte de energia no músculo, especialmente quando as necessidades energéticas fisiológicas estão aumentadas. A deficiência da desidrogenase de ésteres acil-CoA de cadeia muito longa (VLCAD) é caracterizada por uma diminuição da MFAO. A VLCAD é uma das quatro desidrogenases de ésteres acil-CoA que catalisam o primeiro passo da MFAO. A VLCAD é um homodímero de 67 kDa associado à membrana interna da mitocôndria e codificado pelo gene ACADVL. O gene ACADVL, com cerca de 5,4 Kb, está localizado no cromossoma 17p13.1 e contém 2177 bases codificantes. A deficiência em VLCAD (VLCADD) é uma doença clinicamente heterogénea que apresenta três grupos clínicos principais: uma forma cardíaca grave com início na infância, uma forma hipoglicemiante mais ligeira com início na infância e uma forma miopática com início na adolescência/idade adulta. O diagnóstico é muitas vezes complicado devido às características clínicas serem comuns a todas as miopatias metabólicas. Este baseia-se no fenótipo clínico, testes bioquímicos, testes genéticos, e /ou avaliação post-mortem. O número de doentes diagnosticados com VLCADD tem aumentado, no entanto, os estudos ainda são limitados. Os tratamentos descritos consistem em: evitar jejum prolongado; perfusão com glucose no caso de crises metabólicas; terapêutica com carnitina e dieta restrita em ácidos de cadeia longa e rica em hidratos de carbono. Trabalhos recentes apontam ainda para o potencial terapêutico do resveratrol. A terapêutica génica foi já testada in vivo em modelos animais.
Oliveira, Ana Sofia Gonçalves Novo e. Rodrigues de. "Pregnancy in very long-chain acyl-CoA dehydrogenase deficiency: maternal-fetal risk (case report)". Master's thesis, 2020. https://hdl.handle.net/10216/127929.
Pełny tekst źródłaOliveira, Ana Sofia Gonçalves Novo e. Rodrigues de. "Pregnancy in very long-chain acyl-CoA dehydrogenase deficiency: maternal-fetal risk (case report)". Dissertação, 2020. https://hdl.handle.net/10216/127929.
Pełny tekst źródłaSchymik, Ina [Verfasser]. "Der Very-long-chain-Acyl-CoA-Dehydrogenase-(VLCAD)-Mangel in Deutschland / vorgelegt von Ina Schymik". 2008. http://d-nb.info/990026132/34.
Pełny tekst źródłaCzęści książek na temat "Long-chain-acyl-CoA dehydrogenase"
Schomburg, Dietmar, Margit Salzmann i Dörte Stephan. "Long-chain-acyl-CoA dehydrogenase". W Enzyme Handbook, 687–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-58051-2_145.
Pełny tekst źródłaLeung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta i in. "Long-Chain Acyl-CoA Dehydrogenase Deficiency". W Encyclopedia of Molecular Mechanisms of Disease, 1210. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7545.
Pełny tekst źródłaBalemans, Wendy, Wim Van Hul, Marian Valko, Jan Moncol, Lee A. Denson, Maria Mela, Ulrich Thalheimer i in. "Very-Long-Chain Acyl-CoA Dehydrogenase Deficiency". W Encyclopedia of Molecular Mechanisms of Disease, 2202–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3151.
Pełny tekst źródłaObaid, Abdulrahman, Marwan Nashabat, Majid Alfadhel, Ali Alasmari, Fuad Al Mutairi, Abdulrahman Alswaid, Eissa Faqeih i in. "Clinical, Biochemical, and Molecular Features in 37 Saudi Patients with Very Long Chain Acyl CoA Dehydrogenase Deficiency". W JIMD Reports, 47–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/8904_2017_58.
Pełny tekst źródłaSpiekerkoetter, U., M. Mueller, M. Sturm, M. Hofmann i D. T. Schneider. "Lethal Undiagnosed Very Long-Chain Acyl-CoA Dehydrogenase Deficiency with Mild C14-Acylcarnitine Abnormalities on Newborn Screening". W JIMD Reports, 113–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/8904_2012_129.
Pełny tekst źródłaDe Biase, Irene, Krista S. Viau, Aiping Liu, Tatiana Yuzyuk, Lorenzo D. Botto, Marzia Pasquali i Nicola Longo. "Diagnosis, Treatment, and Clinical Outcome of Patients with Mitochondrial Trifunctional Protein/Long-Chain 3-Hydroxy Acyl-CoA Dehydrogenase Deficiency". W JIMD Reports, 63–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_558.
Pełny tekst źródłaBouvier, Damien, Christine Vianey-Saban, Séverine Ruet i Cécile Acquaviva. "Development of a Tandem Mass Spectrometry Method for Rapid Measurement of Medium- and Very-Long-Chain Acyl-CoA Dehydrogenase Activity in Fibroblasts". W JIMD Reports, 71–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_22.
Pełny tekst źródłaMerinero, B., P. Alcaide, E. Martín-Hernández, A. Morais, M. T. García-Silva, P. Quijada-Fraile, C. Pedrón-Giner i in. "Four Years’ Experience in the Diagnosis of Very Long-Chain Acyl-CoA Dehydrogenase Deficiency in Infants Detected in Three Spanish Newborn Screening Centers". W JIMD Reports, 63–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/8904_2017_40.
Pełny tekst źródłaKarall, D., G. Mair, U. Albrecht, K. Niedermayr, T. Karall, W. Schobersberger i S. Scholl-Bürgi. "Sports in LCHAD Deficiency: Maximal Incremental and Endurance Exercise Tests in a 13-Year-Old Patient with Long-Chain 3-Hydroxy Acyl-CoA Dehydrogenase Deficiency (LCHADD) and Heptanoate Treatment". W JIMD Reports, 7–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/8904_2014_313.
Pełny tekst źródła"Very long chain acyl CoA dehydrogenase deficiency". W Atlas of Inherited Metabolic Diseases 3E, 289–94. CRC Press, 2011. http://dx.doi.org/10.1201/b15310-44.
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