Relevant bibliographies by topics / Beta-oxidation

Academic literature on the topic 'Beta-oxidation'

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Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Beta-oxidation"

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Treem, William R. "BETA OXIDATION DEFECTS." Clinics in Liver Disease 3, no. 1 (February 1999): 49–67. http://dx.doi.org/10.1016/s1089-3261(05)70053-2.

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Bartlett, Kim, and Simon Eaton. "Mitochondrial beta-oxidation." European Journal of Biochemistry 271, no. 3 (February 2004): 462–69. http://dx.doi.org/10.1046/j.1432-1033.2003.03947.x.

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Helser, Terry L. "β[beta]-Oxidation Wordsearch." Journal of Chemical Education 78, no. 4 (April 2001): 483. http://dx.doi.org/10.1021/ed078p483.

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Engel, Paul C. "Intramitochondrial beta-oxidation complexes." Biochemical Society Transactions 30, no. 1 (February 1, 2002): A5. http://dx.doi.org/10.1042/bst030a005c.

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SCHOLTE, H. R., I. E. M. LUYT-HOUWEN, W. BLOM, H. F. M. BUSCH, P. C. JONGE, M. VISSER, J. G. M. HUIJMANS, et al. "Defects in Mitochondrial Beta Oxidation." Annals of the New York Academy of Sciences 488, no. 1 Membrane Path (December 1986): 511–12. http://dx.doi.org/10.1111/j.1749-6632.1986.tb46585.x.

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Schulz, Horst. "Beta oxidation of fatty acids." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1081, no. 2 (January 1991): 109–20. http://dx.doi.org/10.1016/0005-2760(91)90015-a.

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Crockett, E. L., and B. D. Sidell. "Substrate selectivities differ for hepatic mitochondrial and peroxisomal β-oxidation in an Antarctic fish, Notothenia gibberifrons." Biochemical Journal 289, no. 2 (January 15, 1993): 427–33. http://dx.doi.org/10.1042/bj2890427.

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Hepatic mitochondrial and peroxisomal beta-oxidation were examined in an Antarctic marine teleost, Notothenia gibberifrons. Enzymic profiles and rates of beta-oxidation by intact organelles were determined by using a range of fatty acyl-CoA substrates to evaluate substrate preferences. Partitioning of beta-oxidation between organelles was estimated. Substrate selectivities are broader for peroxisomal beta-oxidation than for mitochondrial beta-oxidation. Mitochondria show marked preference for the oxidation of a monounsaturated substrate, palmitoleoyl-CoA (C16:1), and two polyunsaturates, eicosapentaenoyl-CoA (C20:5) and docosahexaenoyl-CoA (C22:6). Carnitine palmitoyltransferase activities with palmitoleoyl-CoA (C16:1) are 2.4-fold higher than activities with palmitoyl-CoA (C16:0). Most polyunsaturated acyl-CoA esters measured appear to inhibit by over 40% the oxidation of palmitoyl-CoA by peroxisomes. Our findings suggest that the polyunsaturates, eicosapentaenoic acid (C20:5) and docosahexaenoic acid (C22:6), found in high concentrations in Antarctic fishes [Lund and Sidell (1992) Mar. Biol. 112, 377-382], are utilized as fuels to support aerobic energy metabolism. Metabolic capacities of rate-limiting enzymes and beta-oxidation rates by intact organelles indicate that up to 30% of hepatic beta-oxidation in N. gibberifrons can be initiated by the peroxisomal pathway.
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NANRI, Hayato, Tsuyoshi ATAKA, Nobuyuki TAKEUCHI, Shingo ISHIDA, Koji WATANABE, and Mitsuru WAKAMATSU. "High Temperature Oxidation of .BETA.-SiC." Journal of the Society of Materials Science, Japan 43, no. 493 (1994): 1360–65. http://dx.doi.org/10.2472/jsms.43.1360.

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Wang, H. Y., and H. Schulz. "β-oxidation of polyunsaturated fatty acids with conjugated double bonds. Mitochondrial metabolism of octa-2,4,6-trienoic acid." Biochemical Journal 264, no. 1 (November 15, 1989): 47–52. http://dx.doi.org/10.1042/bj2640047.

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The mitochondrial beta-oxidation of octa-2,4,6-trienoic acid was studied with the aim of elucidating the degradation of unsaturated fatty acids with conjugated double bonds. Octa-2,4,6-trienoic acid was found to be a respiratory substrate of coupled rat liver mitochondria, but not of rat heart mitochondria. Octa-2,4,6-trienoyl-CoA, the product of the inner-mitochondrial activation of the acid, was chemically synthesized and its degradation by purified enzymes of beta-oxidation was studied spectrophotometrically and by use of h.p.l.c. This compound is a substrate of NADPH-dependent 2,4-dienoyl-CoA reductase or 4-enoyl-CoA reductase (EC 1.3.1.34), which facilitates its further beta-oxidation. The product obtained after the NADPH-dependent reduction of octa-2,4,6-trienoyl-CoA and one round of beta-oxidation was hex-4-enoyl-CoA, which can be completely degraded via beta-oxidation. It is concluded that polyunsaturated fatty acids with two conjugated double bonds extending from even-numbered carbon atoms can be completely degraded via beta-oxidation because their presumed 2,4,6-trienoyl-CoA intermediates are substrates of 2,4-dienoyl-CoA reductase.
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Broadway, N. M., F. M. Dickinson, and C. Ratledge. "Long-chain acyl-CoA ester intermediates of β-oxidation of mono- and di-carboxylic fatty acids by extracts of Corynebacterium sp. strain 7E1C." Biochemical Journal 285, no. 1 (July 1, 1992): 117–22. http://dx.doi.org/10.1042/bj2850117.

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beta-Oxidation of palmitate and tetradecanedioic acid was studied in cell-free extracts of the Gram-positive bacterium Corynebacterium sp. strain 7E1C, and the acyl-CoA ester intermediates formed were analysed by h.p.l.c. beta-Oxidation assays displayed a lag phase before a constant rate of NAD+ reduction was obtained. The length of the lag phase was inversely proportional to the number of units of activity added to assays. This is a characteristic feature of a system of consecutive reactions proceeding via free intermediates. During beta-oxidation of palmitate all the saturated acyl-CoAs from C16 to C8 were detected together with trace amounts of unsaturated and 3-hydroxy-intermediates. The time-course of intermediate formation again indicated a precursor-product relationship indicative of free intermediates being formed. When 3-hydroxyacyl-CoA dehydrogenase was inhibited by completely removing NAD+ from assays, the major acyl-CoAs, detected during palmitate beta-oxidation were palmitoyl-CoA, hexadeca-2-enoyl-CoA and 3-hydroxypalmitoyl-CoA. These compounds also displayed a precursor-product relationship. Under normal assay conditions the acyl-CoA dehydrogenase(s) are the probable rate-limiting enzyme(s) of the beta-oxidation spiral. These results indicate that in cell-free extracts of Corynebacterium sp. strain 7E1C, beta-oxidation proceeds via free acyl-CoA intermediates and is at variance with the concept of substrate channelling or of a ‘leaky hose pipe’ model as proposed for mitochondrial beta-oxidation in eukaryotic cells. The significant accumulation of chain-shortened acyl-CoA esters is similar to the situation observed for mammalian peroxisomal beta-oxidation.
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Dissertations / Theses on the topic "Beta-oxidation"

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Pourfarzam, Morteza. "#beta#-oxidation of dicarboxylates." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287139.

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Ogilvie, Isla Marion. "Enzymes of mitochondrial #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384937.

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Ferdinandusse, Sacha. "New insights in peroxisomal [beta]-oxidation." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/64403.

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Eaton, Simon. "Regulation of fatty acid #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311443.

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Kadlčík, Vojtěch. "Oxidation of beta-amyloid and model peptides." Paris 11, 2006. http://www.theses.fr/2006PA112008.

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Le but de mon travail de thèse était de caractériser les produits de l'oxydation du peptide beta-amyloïde (Abeta) impliqué dans le développement de la maladie d'Alzheimer. Pour étudier l'effet de la structure de peptide sur les processus redox, les propriétés du peptide Abeta (1-40) ont été comparées au peptide de séquence inverse, Abeta (40-1). Les radicaux libres choisis ont été produits en radiolyse gamma. Les produits finaux ont été caractérisés par des techniques d'analyse diverses (HPLC, GC, MALDI-TOF MS, spectrométrie de fluorescence, spectrométrie raman). Pour établir l'effet de l'environnement sur le processus d'oxydation, peptides ont été oxydés dans trois systèmes différents: solution aqueuse homogène, milieu micellaire (SDS) et système des vésicules phospholipidiques (POPC). En solution aqueuse homogène, les produits d'oxydation sont différents pour les deux peptides. Les résidus facilement oxydables sont Met35 pour Abeta(1-40) et Tyr10 pour Abeta(40-1). La présence des micelles ainsi que des vésicules phospholipidiques change profondément le cours de l'oxydation. Une étude structurale en dichroïsme circulaire nous permet d'avancer des hypothèses pour interpréter ces résultats. Nous avons montré que des produits de dégradation des peptides Abeta peuvent induire d'une manière catalytique l'altération des phospholipides. Cette propriété est attribuée à l'action des atomes d'hydrogène sur le peptide. Nos résultats sont intéressants dans le contexte du développement de la maladie d'Alzheimer, car ils peuvent aider à éclairer le rôle de l'interaction de peptide Abeta(1-40) avec des membranes phospholipidique dans les propriétés redox du peptide
The goal of my thesis work was to characterize oxidation products of beta-amyloid peptide (Abeta), which is implied in the development of Alzheimer's disease. To study the effect of peptide structure on the redox processes, oxidation properties of Abeta(1-40) were compared to the peptide with reverse sequence, Abeta(40-1). Azide and hydroxyl radicals used for oxidation were produced by gamma radiolysis. Final products were characterized by a variety of analytical techniques (HPLC, GC, MALDI-TOF MS, fluorescence and raman spectrometry). To establish the role of peptide environment on its redox properties, oxidation was carried out in three different systems: homogeneous aqueous solution, micellar system (SDS) and in the presence of phospholipids vesicles (POPC). In homogeneous aqueous solution, oxidation products are different for both peptides. The main oxidation targets are Met35 for Abeta(1-40) and Tyr10 for Abeta(40-1). The presence of micelles and phospholipid vesicles has an important impact on the oxidation pathways. These changes could be related to changes in peptide conformations studied by circular dichroism. We have also shown that Abeta degradation products may catalytically induce alternation of phospholipids. This process is initiated by reaction of hydrogen radicals with the peptide. Our results are interesting in the context of the development of Alzheimer's disease as they may bring an insight into the role of Abeta(1-40) interaction with phospholipids membrane for the redox properties of the peptide
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Lee, Wai Ming. "Oxidation reactions and antioxidant properties of #Beta#-carotene." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237679.

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Creswick, Heather Alison. "The Oxidation of beta-Cyclodextrin Via the Photolysis of 6-beta-Cyclodextrin Benzoyl Formate." W&M ScholarWorks, 1993. https://scholarworks.wm.edu/etd/1539625808.

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Watmough, N. J. "Measurement of intermediates and products of fatty acid #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234411.

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Heath, Christine Evelyn. "The Selective Oxidation of beta-Cyclodextrin on the Secondary Face." W&M ScholarWorks, 1997. https://scholarworks.wm.edu/etd/1539626108.

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Grunsven, Elisabeth Gerarda van. "Functions and dysfunctions of peroxisomal fatty acid [beta]-oxidation in man." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/82102.

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Books on the topic "Beta-oxidation"

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Oxidation characteristics of Beta-21S in the air in the temperature Range 600 to 800 ̊C. Hampton, Va: National Aeronautics and Space Administration, Langley Research Center, 1992.

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Duran, Marinus, and Isabel Tavares de Almeida. Interpretation of Acylcarnitine Analysis Results. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0085.

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The analysis of acylcarnitines in plasma or blood spot samples by tandem mass spectrometry will detect all 15 defects of mitochondrial fatty acid beta-oxidation, although false negative results may occur in well-fed, non-fasting patients. Moreover, more than 20 organic acidemias can be detected by this methodological approach. An acylcarnitine profile should be part of the work-up of patients presenting with rhabdomyolysis and/or hypoglycemia and adults with an unexplained leukoencephalopathy. Cases with abnormal acylcarnitines require an analysis of urine organic acids as well as enzyme activity evaluation and molecular investigations to confirm the inherited defect.
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van Geel, Björn M., Marc Engelen, and Stephan Kemp. X-linked Adrenoleukodystrophy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0061.

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X-linked adrenoleukodystrophy (X-ALD) is the most frequent peroxisomal disorder. Hallmarks are increased levels of plasma very long-chain fatty acids (VLCFA), mutations in the ABCD1 gene, impaired function of ALD-protein and, consequently, decreased import of VLCFA-CoA esters in peroxisomes and VLCFA beta-oxidation. Cerebral demyelination and axonal degeneration of the spinal cord are the main causes of neurological deficits. Endocrine dysfunction, particularly adrenocortical insufficiency, is very frequent. Based upon the age of onset of symptoms and the organs most severely affected, several phenotypes can be distinguished. Adrenomyeloneuropathy (AMN) and childhood cerebral adrenoleukodystrophy (CCALD) are the most frequent variants. At least 80% of female carriers will eventually develop neurological symptoms similar to men with AMN. The thin and scanty scalp hair in affected men may facilitate diagnosis of X-ALD. Identification of patients is of utmost importance, as adrenocortical insufficiency can be treated, rapidly progressive cerebral demyelination can be halted, and prenatal diagnostic testing is available. Furthermore, symptomatic therapies and multidisciplinary support may help patients coping with this disease.
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Book chapters on the topic "Beta-oxidation"

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Gooch, Jan W. "Beta Oxidation." In Encyclopedic Dictionary of Polymers, 878. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13248.

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Osmundsen, H., M. S. Thomassen, J. K. Hiltunen, and R. K. Berge. "Physiological Role of Peroxisomal Beta-Oxidation." In Proceedings in Life Sciences, 152–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71325-5_14.

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Chen, Winston W., Gerald Hoefler, and Paul A. Watkins. "Heterogeneity of Beta-Oxidation Enzyme Defects in Peroxisomal Diseases." In Lipid Storage Disorders, 389–94. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1029-7_47.

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Vamecq, Joseph, and Jean-Pierre Draye. "Beta-Oxidation of Omega-Hydroxymonocarboxylic Acids in Rat Liver Peroxisomes and Mitochondria." In Lipid Storage Disorders, 395–403. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1029-7_48.

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Reichmann, H., and D. C. DeVivo. "Enzymatic Analyses of Beta-Oxidation in Human Fibroblasts from Patients with Reye’s Syndrome." In Verhandlungen der Deutschen Gesellschaft für Neurologie, 310–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83201-7_70.

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Wanders, Ronald J. A., Carlo W. T. Van Roermund, Wouter F. Visser, Sacha Ferdinandusse, Gerbert A. Jansen, Daan M. Van den Brink, Jolein Gloerich, and Hans R. Waterham. "Peroxisomal Fatty Acid Alpha-and Beta-Oxidation in Health and Disease: New insights." In Advances in Experimental Medicine and Biology, 293–302. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9072-3_37.

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Cunnane, S. C. "New Developments in α-Linolenate Metabolism with Emphasis on the Importance of β-Oxidation and Carbon Recycling." In Fatty Acids and Lipids - New Findings, 178–83. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000059751.

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Esfandiari, Ali, and Marion Paturneau-Jouas. "Effects of Inhibitors of the Mitochondrial Electron Transport Chain on Fatty Acid Beta-Oxidation in Rat Brain Cultured Astrocytes." In Neurochemistry, 751–55. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_124.

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Brown, Robert Andrew. "Linoleic Acid and Alpha-Linolenic Acid Have Central Roles in Brain Energy Substrate Provision, Endogenous Lipid Production, Immune and Repair Function, via Peroxisomal Beta-Oxidation-Related Pathways?" In Omega-3 Fatty Acids, 413–28. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40458-5_30.

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van de Beek, Malu-Clair, Inge M. E. Dijkstra, and Stephan Kemp. "Method for Measurement of Peroxisomal Very Long-Chain Fatty Acid Beta-Oxidation and De Novo C26:0 Synthesis Activity in Living Cells Using Stable-Isotope Labeled Docosanoic Acid." In Methods in Molecular Biology, 45–54. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6937-1_5.

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Conference papers on the topic "Beta-oxidation"

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Hansen, Karyn J., and Bennett Van Houten. "Abstract POSTER-BIOL-1314: Investigating fatty acid beta-oxidation in ovarian cancer cells." In Abstracts: 10th Biennial Ovarian Cancer Research Symposium; September 8-9, 2014; Seattle, WA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.ovcasymp14-poster-biol-1314.

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Rada, Miran, Jennifer Cha, Jessica Sage, Bo Zhou, Wei Yang, Zahra Ashkavand, Kenneth Norman, Sandra Orsulic, and Dong-Joo Cheon. "Abstract 3526: Beta-oxidation inhibition as a novel therapy for cisplatin-resistant ovarian cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3526.

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Hiramatsu, Kosuke, Satoshi Serada, Minoru Fujimoto, Shinya Matsuzaki, Yutaka Ueda, Kiyoshi Yoshino, Tadashi Kimura, and Tetsuji Naka. "Abstract 1434: LSR promotes lipid metabolism via beta oxidation and contributes cell viability in epithelial ovarian cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1434.

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Aspiyanto, Agustine Susilowati, Puspa D. Lotulung, Yati Maryati, and Hani Mulyani. "The performance of microfiltration membrane of total polyphenol from fermented beetroot (Beta vulgaris L.) to prevent natural oxidation." In PROCEEDINGS OF THE 5TH INTERNATIONAL SYMPOSIUM ON APPLIED CHEMISTRY 2019. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5134581.

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Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.

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Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
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CASANI CUBEL, JULIA, and JOSE ENRIQUE DE LA RUBIA ORTI. "The role of paraoxonase 1 (PON1) as an oxidation marker, in muscle improvement after increased beta-hydroxybutyrate (BHB) in blood, in patients with multiple sclerosis." In 1st International Electronic Conference on Brain Sciences. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/iecbs-08444.

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Mannan, Sarwan, and John deBarbadillo. "Long Term Thermal Stability of INCONEL Alloy 783." In ASME 1998 International Gas Turbine and Aeroengine Congress and Exhibition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/98-gt-508.

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Recently developed INCONEL® alloy 783 (nominal composition of Ni-34Co-26Fe-5.4Al-3Nb-3Cr) is precipitation strengthened by Ni3Al-type Gamma Prime and NiAl-type Beta Phases. Due to its low co-efficient of thermal expansion (CTE), high strength, and good oxidation resistance alloy 783 has been specified for use in aircraft gas turbine components such as rings, casings, shrouds, and seals and has been considered for use in a number of other critical industrial turbine components. In this study, commercially produced alloys 783, 718, and 909 were annealed and aged following recommended heat treatments. The materials were then isothermally exposed at 1100°F (593°C) for times up to 10,000 hours. At 1000 hour intervals, specimens of these alloys were removed from the furnace and subjected to room temperature tensile (RTT) and high temperature tensile (HTT) testing at 1200°F (649°C). The microstructure of as-produced and exposed materials was characterized using optical microscopy, Scanning Electron Microscopy (SEM), and Transmission Electron Microscopy (TEM). Variation in tensile properties with isothermal exposure time was correlated with the microstructure.
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Tawancy, H. M., and Luai M. Al-Hadhrami. "Role of Platinum in Thermal Barrier Coatings Used in Gas Turbine Blade Applications." In ASME Turbo Expo 2009: Power for Land, Sea, and Air. ASMEDC, 2009. http://dx.doi.org/10.1115/gt2009-59153.

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Current technology of thermal barrier coating systems used in gas turbine blade applications relies upon the use of a metallic bond coat, which has a two-fold function: i) it develops a thin layer of aluminum oxide enhancing the adhesion of the ceramic top coat, and ii) it provides an additional resistance to oxidation. It was the objective of this study to develop an understanding of the role of platinum in bond coats of the diffusion-type deposited on a nickel-base superalloy. Two Pt-containing bond coats were included in the study: i) a platinum-aluminide and ii) a bond coat formed by interdiffusion between an electroplated layer of platinum and the superalloy substrate. In both cases, the top ceramic coat was yttria-stabilized zirconia. For reference purposes, a simple aluminide bond coat free of Pt was also included in the study. Thermal exposure tests at 1150 °C with a 24-hour cycling period to room temperature were used to compare the coating performance. Microstructural features were characterized by various electron-optical techniques. Experimental results indicated that Pt acts as a “cleanser” of the oxide-bond coat interface by decelerating the kinetics of interdiffusion between the bond coat and superalloy substrate. This was found to promote selective oxidation of Al resulting in a purer Al2O3 scale of a slower growth rate increasing its effectiveness as “glue” holding the ceramic top coat to the underlying metallic substrate. However, the exact effect of Pt was found to be a function of the state of its presence within the outermost coating layer. Of the two bond coats studied, a surface layer of Pt-rich gamma prime phase (L12 superlattice) was found to provide longer coating life in comparison with a mixture of PtAl2 and beta phase. This could be related to the effectiveness of gamma prime phase as a sink for titanium minimizing its detrimental effect on the adherence of aluminum oxide.
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Vasconcelos, Matheus Felipe de Souza, Francisco Tomaz Meneses de Oliveira, Rafael Zini Moreira da Silva, and Alex Michel Daoud. "Neurological and adrenal insufficiency symptons in adult x-linked adrenoleukodystrophy: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.347.

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Context: X-linked adrenoleukodystrophy (X-ALD) is a rare genetic demyelinating disease caused by mutations in ABC1 gen associated with an impairment of beta- oxidation of very long chain fatty acids (VLCFA) in peroxisomes. It causes accumulation of VCLFA in tissues affecting majoritary the central nervous system, testicles and the adrenal córtex resulting in symptoms which provides restricted neurological prognosis and sequels. Methods: Specific data related of a clinical case through prontuary and complementary exams in a patient attended at Santa Casa de Misericórdia de São Paulo hospital. Case report: Male patient, 39 years old, complaning about vomiting, hyperpigmented skin associated with abolish, psicoses, urinary incontinence, temporal and spacial confusion as well as were found: hyperkalaemia, hyponatremia, hypoglycemia, elevated ACTH levels, basal cortisol decresead, antibody anti-21-hidroxilase non reagente, screening for infectious agents were carried out and infection subsequently ruled out. Were observed in MRI Brain: hypersignal in cerebral white matter on T2-FLAIR sequence bilaterally in which the occipitoparietal region, frontal lobe and basal ganglia were more affected. After metabolic and hydroelectric disorders estabilization using Prednisone, Fludrocortisone per day for 5 days, he evolved with worsening of cognitive and behavioral status until nowdays. Actually, he is totally dependent on his basic activities. Conclusions: It is a rare disease, but it must be recognized by every neurologist, since it is can affect other systems and can leave serious sequelae.
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10

Foit, Jerzy Jan. "MCCI of a Metal and Oxide Melt With Reinforced Siliceous Concrete in MOCKA Experiments." In 2014 22nd International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/icone22-30200.

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Within the framework of large-scale MOCKA (KIT, Germany) experiments, a series of experiments have been performed to study the interaction of a simulant oxide (Al2O3, ZrO2, CaO) and metal melt (Fe) in a stratified configuration. To allow for a longer-term interaction, additional heating was provided by alternating additions of thermite and Zr metal to the melt. Since the heat generated by the thermite reaction and the exothermal oxidation reaction of Zr is mainly deposited in the oxide phase, prototypic heating of both melt phases is achieved. This allows the investigation of concrete erosion by metal melt as well as by the oxide which was not possible in all former experiments. Current tests in the MOCKA (KIT, Germany) program are focused on assessing the influence of concrete reinforcement (rebars) on the cavity erosion behaviour using a simulant oxide-iron melt in a stratified configuration. The experiments are performed in siliceous concrete crucibles with an inner diameter of 25 cm containing 12 wt.% reinforcement. In these experiments, the overall downward erosion by the metal melt was of the same order as the sideward one. In addition, the lateral erosion in the overlaid oxide melt region was about the same as in the metal melt region. The former experiments (BETA, COMET-L) and MOCKA tests on siliceous concrete without reinforcement have produced results with pronounced downward erosion by the metal phase. This pronounced downward erosion of the siliceous concrete without rebars seems to be inherent for melts containing a significant fraction of iron.
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Reports on the topic "Beta-oxidation"

1

Fillmore, Natasha, Osama Abo Alrob, and Gary D. Lopaschuk. Fatty Acid beta-Oxidation. AOCS, July 2011. http://dx.doi.org/10.21748/lipidlibrary.39187.

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