Spelling suggestions: "subject:"bioenergetika"" "subject:"bioenergetic""
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Visualisering av bioenergetisk modellPetter, Hidén-Rudander January 1900 (has links)
When optimizing pacing strategies for biomechanical systems such as road cycling or skiing, it is necessary to constrain the optimization to simulate the reality. It is therefore of interest to constrain the optimization according to the possibility of developing power through metabolic processes in the human body. I.e. simulating the bioenergetics of a human body.To make this possible, fluid mechanical models have been developed to approximate the metabolic combustion, since the actual metabolic processes in a body is complex. The M-M model is a bioenergetics model to approximate these processes. The model shows the energy depot as liquid filled tanks that are regulated according to known relationships of fluid mechanics, resulting in a movement of the surface level according to the varying power output of the system.The intention of this paper is to visualize the level change in the M-M model with MATLAB® and also to create an understanding of the theory behind the model and the bioenergetics processes in the human body. As visualized in the model.GUIDE is a MATLAB® tillvalsprogram used to create GUI (Graphical User Interface) to the visualization programming. A user interface was created with GUIDE for an easier understanding and to offer a possibility to run various simulation results, without restarting or altering the code.The result shows that the visualization to a high degree facilitates the understanding of the M-M model and the connection to metabolic processes. It also shows that the work done facilitated a lot with the possibility to create GUI directly in MATLAB® instead of involving external software. / Vid optimering av farthållningsstrategier av biomekaniska system som cykellopp eller skidlopp är det nödvändigt att ha bivillkor som begränsar optimeringen för att kunna efterlikna verkligheten. Det är därför av intresse att begränsa optimeringen efter möjligheten för en person att, genom metabola processer i kroppen, utveckla effekt. Det vill säga att efterlikna det bioenergetiska systemet i en människokropp.För att möjliggöra det har flödesmekaniska metoder utvecklats för att approximera den metabola förbränningen i en människokropp. Då simulering av de verkliga processerna i metabolismen är komplex. M-M modellen är en bioenergetisk modell som approximerar processerna. I modellen åskådliggörs energidepåerna som tankar och styrs enligt flödesmekaniska samband för att kunna beskriva hur bränslenivåer i en människokropp varierar vid metabol förbränning med varierande effektuttag.Syftet med arbetet är att visualisera nivåförändringarna i M-M modellen med hjälp av MATLAB®, samt att skapa en förståelse för teorin bakom modellen och en förståelse för bioenergetiska mekanismer i kroppen som visualiseras med modellen.GUIDE är ett verktyg integrerat i MATLAB® för att möjliggöra utformning av ett personligt användargränssnitt till programkod med hjälp av GUI(Graphical User Interface). Med GUIDE skapades ett användargränssnitt för en visualisering som är lätt att förstå och erbjuder möjligheten att testa olika simuleringsresultat från M-M utan att behöva starta om eller ändra koden.Resultatet visar att visualiseringen i hög grad underlättar förståelsen för M-M modellen samt dess koppling till metabolismen i kroppen. Samt att arbetet underlättades med möjligheten att skapa GUI direkt i MATLAB® som också var verktyget för optimeringen, istället för att använda externa programvaror.
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Photobiologische, energetische und genetische Aspekte des mutualistischen Zusammenlebens von Zooxanthellen (Symbiodinium sp.) und Steinkorallen im Golf von Aqaba, JordanienKampmann, Heike. Unknown Date (has links) (PDF)
Universiẗat, Diss., 2003--Köln.
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Hepatocyte Mitochondrial Dynamics and Bioenergetics in Obesity‑Related Non‑Alcoholic Fatty Liver DiseaseLegaki, Aigli-Ioanna, Moustakas, Ioannis I., Sikorska, Michalina, Papadopoulos, Grigorios, Velliou, Rallia-Iliana, Chatzigeorgiou, Antonios 30 May 2024 (has links)
Purpose of the Review
Mitochondrial dysfunction has long been proposed to play a crucial role in the pathogenesis of a considerable number of disorders, such as neurodegeneration, cancer, cardiovascular, and metabolic disorders, including obesity-related insulin resistance and non-alcoholic fatty liver disease (NAFLD). Mitochondria are highly dynamic organelles that undergo functional and structural adaptations to meet the metabolic requirements of the cell. Alterations in nutrient availability or cellular energy needs can modify their formation through biogenesis and the opposite processes of fission and fusion, the fragmentation, and connection of mitochondrial network areas respectively. Herein, we review and discuss the current literature on the significance of mitochondrial adaptations in obesity and metabolic dysregulation, emphasizing on the role of hepatocyte mitochondrial flexibility in obesity and NAFLD.
Recent Findings
Accumulating evidence suggests the involvement of mitochondrial morphology and bioenergetics dysregulations to the emergence of NAFLD and its progress to non-alcoholic steatohepatitis (NASH).
Summary
Most relevant data suggests that changes in liver mitochondrial dynamics and bioenergetics hold a key role in the pathogenesis of NAFLD. During obesity and NAFLD, oxidative stress occurs due to the excessive production of ROS, leading to mitochondrial dysfunction. As a result, mitochondria become incompetent and uncoupled from respiratory chain activities, further promoting hepatic fat accumulation, while leading to liver inflammation, insulin resistance, and disease’s deterioration. Elucidation of the mechanisms leading to dysfunctional mitochondrial activity of the hepatocytes during NAFLD is of predominant importance for the development of novel therapeutic approaches towards the treatment of this metabolic disorder.
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Insights into the ATP-dependent reductive activation of the Corrinoid/Iron-Sulfur Protein of Carboxydothermus hydrogenoformansHennig, Sandra Elisabeth 19 June 2014 (has links)
Die Verknüpfung einer exergonischen mit einer endergonischen Reaktion zur Ermöglichung der letzteren ist eine in biologischen Systemen weit verbreitete Strategie. Energetisch benachteiligte Elektronenübertragungsreaktionen im Rahmen der reduktiven Aktivierung von Nitrogenasen, Radikal-abhängigen β,α-Dehydratasen, der zu diesen verwandten Benzoyl-CoA-Reduktasen und diversen Cobalamin-abhängigen Methyltransferasen sind gekoppelt an die Hydrolyse von ATP. Der Methylgruppentransfer des reduktiven Acetyl-CoA-Weges von Carboxydothermus hydrogenoformans erfordert den Co(I)-Zustand des Corrinoid/Eisen-Schwefel Proteins (CoFeSP). Um diese superreduzierte Form nach einer oxidativen Inaktivierung zu regenerieren ist ein „Reparaturmechanismus“ erforderlich. Ein offenes Leseraster (orf7), welches möglicherweise für eine reduktive Aktivase von Corrinoid Enzymen (RACE) kodiert, wurde in dem Gencluster der am reduktiven Acetyl-CoA-Weg beteiligten Proteine entdeckt. Im Rahmen dieser Arbeit wurde dieses potenzielle RACE Protein biochemisch und strukturell charakterisiert und die ATP-abhängige reduktive Aktivierung von CoFeSP untersucht. Auf Grundlage der in dieser Arbeit gewonnenen Ergebnisse wurde ein Mechanismus für die ATP-abhängige Aktivierung entworfen. Dieser gibt Einblicke wie die durch ATP-Hydrolyse bereitgestellte Energie einen energetisch ungünstigen Elektronentransfer ermöglichen kann. Hierzu kombiniert RACo das Ausgleichen von Bindungsenergien mit Modulationen am Elektronenakzeptor. Eine vergleichbare Strategie wurde bisher in keinem anderen ATP-abhängigen Elektronenübertragungssystem wie dem von Nitrogenasen, Radikal-abhängigen β,α-Dehydratasen oder Benzoyl-CoA-Reduktasen beobachtet und könnte ein für RACE Proteine allgemein gültige Eigenschaft darstellen. / The principle of coupling an exergonic to an endergonic reaction to enable the latter is a widespread strategy in biological systems. Unfavoured electron transfer reactions in the reductive activation of nitrogenases, radical-dependent β,α-dehydratases and the related benzoyl- CoA reductases, as well as different cobalamin-dependent methyltransferases are coupled to the hydrolysis of ATP. The reductive acetyl-CoA pathway of Carboxydothermus hydrogenoformans relies on the superreduced Co(I)-state of the corrinoid/iron-sulfur protein (CoFeSP) that requires a “repair mechanism” in case of incidental oxidation. An open reading frame (orf7) coding for a putative reductive activase of corrinoid enzymes (RACE) was discovered in the gene cluster of proteins involved in the reductive acetyl-CoA pathway. In this work, this putative RACE protein was biochemically and structurally characterised and the ATP-dependent reductive activation of CoFeSP was investigated. Based on the results of this study, a mechanism for the ATP-dependent reactivation of CoFeSP was deduced providing insights into how the energy provided by ATP could trigger this unfavourable electron transfer. The reductive activator of CoFeSP combines balance of binding energies and modulations of the electron acceptor to promote the uphill electron transfer to CoFeSP. A comparable strategy has not been observed in other ATP-dependent electron transfer systems like nitrogenases, radical-dependent β,α-dehydratases and benzoyl- CoA reductases and could be a universal feature of RACE proteins.
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Die vollständige Entschlüsselung der Genomsequenz des Tetanus-Erregers <i>Clostridium tetani</i> und die Analyse seines genetischen Potentials / The complete genome sequence of the causative agent of tetanus disease, <i>Clostridium tetani</i>, and the analysis of its genesBrüggemann, Holger 30 January 2003 (has links)
No description available.
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