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Relevant bibliographies by topics / Respiratory chain

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Academic literature on the topic 'Respiratory chain'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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Journal articles on the topic "Respiratory chain"

1

Schägger, Hermann. "Respiratory Chain Supercomplexes." IUBMB Life (International Union of Biochemistry and Molecular Biology: Life) 52, no. 3-5 (September 1, 2001): 119–28. http://dx.doi.org/10.1080/15216540152845911.

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Ameyama, Minoru, Kazunobu Matsushita, Emiko Shinagawa, and Osao Adachi. "Sugar-oxidizing Respiratory Chain ofGluconobacter suboxydans. Evidence for a Branched Respiratory Chain and Characterization of Respiratory Chain-Linked Cytochromes." Agricultural and Biological Chemistry 51, no. 11 (November 1987): 2943–50. http://dx.doi.org/10.1080/00021369.1987.10868527.

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DiMauro, Salvatore, and Eric A. Schon. "Mitochondrial Respiratory-Chain Diseases." New England Journal of Medicine 348, no. 26 (June 26, 2003): 2656–68. http://dx.doi.org/10.1056/nejmra022567.

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Rich, Peter R., and Amandine Maréchal. "The mitochondrial respiratory chain." Essays in Biochemistry 47 (June 14, 2010): 1–23. http://dx.doi.org/10.1042/bse0470001.

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In the present chapter, the structures and mechanisms of the major components of mammalian mitochondrial respiratory chains are reviewed. Particular emphasis is placed on the four protein complexes and their cofactors that catalyse the electron transfer pathway between oxidation of NADH and succinate and the reduction of oxygen to water. Current ideas are reviewed of how these electron transfer reactions are coupled to formation of the proton and charge gradient across the inner mitochondrial membrane that is used to drive ATP synthesis. Additional respiratory components that are found in mammalian and plant, fungal and algal mitochondria are also reviewed.

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AMEYAMA, Minoru, Kazunobu MATSUSHITA, Emiko SHINAGAWA, and Osao ADACHI. "Sugar-oxidizing respiratory chain of Gluconobacter suboxydans. Evidence for a branched respiratory chain and characterization of respiratory chain-linked cytochromes." Agricultural and Biological Chemistry 51, no. 11 (1987): 2943–50. http://dx.doi.org/10.1271/bbb1961.51.2943.

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MBBS, Joannie Hui, Denise M. Kirby, David R. Thorburn, and A. vihu Boneh. "Decreased activities of mitochondrial respiratory chain complexes in non-mitochondrial respiratory chain diseases." Developmental Medicine & Child Neurology 48, no. 2 (February 2006): 132–36. http://dx.doi.org/10.1017/s0012162206000284.

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Meuric, Vincent, Astrid Rouillon, Fatiha Chandad, and Martine Bonnaure-Mallet. "Putative respiratory chain ofPorphyromonas gingivalis." Future Microbiology 5, no. 5 (May 2010): 717–34. http://dx.doi.org/10.2217/fmb.10.32.

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Shoubridge, Eric A. "Supersizing the Mitochondrial Respiratory Chain." Cell Metabolism 15, no. 3 (March 2012): 271–72. http://dx.doi.org/10.1016/j.cmet.2012.02.009.

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Pfeiffer, Kathy, Vishal Gohil, Rosemary A. Stuart, Carola Hunte, Ulrich Brandt, Miriam L. Greenberg, and Hermann Schägger. "Cardiolipin Stabilizes Respiratory Chain Supercomplexes." Journal of Biological Chemistry 278, no. 52 (October 15, 2003): 52873–80. http://dx.doi.org/10.1074/jbc.m308366200.

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Zhang, Mei, Eugenia Mileykovskaya, and William Dowhan. "Gluing the Respiratory Chain Together." Journal of Biological Chemistry 277, no. 46 (October 2, 2002): 43553–56. http://dx.doi.org/10.1074/jbc.c200551200.

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Dissertations / Theses on the topic "Respiratory chain"

1

Hansson, Anna. "Cellular responses to respiratory chain dysfunction /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-493-7/.

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Silva, José Pablo. "The pathophysiology of respiratory chain dysfunction /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-234-9/.

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Li, Xi. "The respiratory chain in Neisseria species." Thesis, University of York, 2013. http://etheses.whiterose.ac.uk/3989/.

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This work presents the organization of respiratory chain in Neisseria species. The localization of redox proteins was determined. Lipid-modified azurin (Laz) and nitrite reductase (AniA) are mainly associated with outer membrane. All c-type cytochrome proteins are mainly associated with inner membrane. Cytochrome c5 is the major electron donor to AniA. Reduced form cytochrome c5 is able to donate electrons to AniA at a physiologically relevant rate. In addition, the second haem domain of cytochrome c5 is the direct donor to AniA. It presents a potential problem for inter-electron transfer between c5 and AniA, which are associated with inner and outer membrane respectively. Trihaem CcoP is the alternative electron donor to AniA in N. gonorrhoeae. The 3rd haem domain of N. gonorrhoeae CcoP is able to donate electrons to AniA at a physiologically relevant rate, suggesting there is alternative route for nitrite reduction in N gonorrhoeae. N. elongata cytochrome is an electron donor to AniA. N. elongata cytochrome which has high degree of similarity with c5, is confirmed to donate electrons to AniA at a physiologically relevant rate, suggesting N. elongata has one other route for nitrite reduction. Laz is not involved in nitrite reduction. Laz is able to receive electrons from cytochrome c5 at physiological relevant rate, but cannot donate electrons to AniA. Based on laz mutagenesis study, laz mutant strain has limited affect on growth and nitrite usage compared to the wild type strain. Cytochrome cx is not involved in oxygen reduction. Cytochrome cx has presumably been found to be involved in oxygen reduction in N. meningitidis, but not in N. gonorrhoeae. N. meningitidis carrying an N. gonorrhoeae ccoP gene has a similar growth rate as the growth rate of the wild type strain and also cx mutant strains.

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Chen, Walter W. "Pathological features of mitochondrial respiratory chain dysfunction." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104099.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis. "June 2016."
Includes bibliographical references.
Mitochondria are essential organelles that carry out a multitude of important metabolic processes in mammalian organisms. These processes include ATP generation by the respiratory chain, aspartate synthesis by matrix aminotransferases, and long-chain fatty acid catabolism by the beta oxidation pathway. Given the role of mitochondria in maintaining cellular physiology, mitochondrial dysfunction often leads to disease. One major class of mitochondrial pathologies is caused by defects in the mitochondrial respiratory chain (RC). Yet while the genetic etiologies of these RC disorders are well-studied, the molecular defects that actually link RC dysfunction with impaired cellular viability are still unclear. In the work described here, we demonstrate that loss of mitochondrial membrane potential and aspartate contributes significantly to cellular pathology during RC dysfunction. In addition, we develop a novel method for rapidly isolating mitochondria and profiling their metabolite contents to study the changes in mitochondrial metabolism across various states of RC function. From this work, we find numerous alterations in matrix metabolites that had been previously unappreciated using traditional profiling of whole-cells and identify new metabolic abnormalities downstream of RC dysfunction. Collectively, this work uncovers distinct molecular events connecting RC pathology with impaired cellular viability and expands our understanding of the metabolic processes affected by RC dysfunction, thus opening up new areas for exploration.
by Walter W. Chen.
Ph. D.

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Capristo, Mariantonietta <1981&gt. "Respiratory chain complex I dysfunction in tumorigenesis." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4798/1/Capristo_Mariantonietta_Tesi.pdf.

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Diseases due to mutations in mitochondrial DNA probably represent the most common form of metabolic disorders, including cancer, as highlighted in the last years. Approximately 300 mtDNA alterations have been identified as the genetic cause of mitochondrial diseases and one-third of these alterations are located in the coding genes for OXPHOS proteins. Despite progress in identification of their molecular mechanisms, little has been done with regard to the therapy. Recently, a particular gene therapy approach, namely allotopic expression, has been proposed and optimized, although the results obtained are rather controversial. In fact, this approach consists in synthesis of a wild-type version of mutated OXPHOS protein in the cytosolic compartment and in its import into mitochondria, but the available evidence is based only on the partial phenotype rescue and not on the demonstration of effective incorporation of the functional protein into respiratory complexes. In the present study, we took advantage of a previously analyzed cell model bearing the m.3571insC mutation in MTND1 gene for the ND1 subunit of respiratory chain complex I. This frame-shift mutation induces in fact translation of a truncated ND1 protein then degraded, causing complex I disassembly, and for this reason not in competition with that allotopically expressed. We show here that allotopic ND1 protein is correctly imported into mitochondria and incorporated in complex I, promoting its proper assembly and rescue of its function. This result allowed us to further confirm what we have previously demonstrated about the role of complex I in tumorigenesis process. Injection of the allotopic clone in nude mice showed indeed that the rescue of complex I assembly and function increases tumor growth, inducing stabilization of HIF1α, the master regulator of tumoral progression, and consequently its downstream gene expression activation.

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Capristo, Mariantonietta <1981&gt. "Respiratory chain complex I dysfunction in tumorigenesis." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4798/.

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Diseases due to mutations in mitochondrial DNA probably represent the most common form of metabolic disorders, including cancer, as highlighted in the last years. Approximately 300 mtDNA alterations have been identified as the genetic cause of mitochondrial diseases and one-third of these alterations are located in the coding genes for OXPHOS proteins. Despite progress in identification of their molecular mechanisms, little has been done with regard to the therapy. Recently, a particular gene therapy approach, namely allotopic expression, has been proposed and optimized, although the results obtained are rather controversial. In fact, this approach consists in synthesis of a wild-type version of mutated OXPHOS protein in the cytosolic compartment and in its import into mitochondria, but the available evidence is based only on the partial phenotype rescue and not on the demonstration of effective incorporation of the functional protein into respiratory complexes. In the present study, we took advantage of a previously analyzed cell model bearing the m.3571insC mutation in MTND1 gene for the ND1 subunit of respiratory chain complex I. This frame-shift mutation induces in fact translation of a truncated ND1 protein then degraded, causing complex I disassembly, and for this reason not in competition with that allotopically expressed. We show here that allotopic ND1 protein is correctly imported into mitochondria and incorporated in complex I, promoting its proper assembly and rescue of its function. This result allowed us to further confirm what we have previously demonstrated about the role of complex I in tumorigenesis process. Injection of the allotopic clone in nude mice showed indeed that the rescue of complex I assembly and function increases tumor growth, inducing stabilization of HIF1α, the master regulator of tumoral progression, and consequently its downstream gene expression activation.

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7

Jackson, Margaret J. "Clinical and biochemical studies of respiratory chain disease." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294642.

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8

Heiske, Margit. "Modeling the respiratory chain and the oxidative phosphorylation." Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR21965/document.

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Mitochondria are cell organelles which play an essential role in the cell energy supply providing the universal high energetic molecule ATP which is used in numerous energy consuming processes. The core of the ATP production, oxidative phosphorylation (OXPHOS) consists of four enzyme complexes (respiratory chain) which establish, driven by redox reactions, a proton gradient over the inner mitochondrial membrane. The ATP-synthase uses this electrochemical gradient to phosphorylate ADP to ATP. Dysfunctioning of an OXPHOS complex can have severe consequences for the energy metabolism and cause rare but incurable dysfunctions in particular tissues with a high energy demand such as brain, heart, kidney and skeleton muscle. Moreover mitochondria are linked to widespread diseases like diabetes, cancer, Alzheimer and Parkinson. Further, reactive oxygen species which are a by-product of the respiratory chain, are supposed to play a crucial role in aging. The aim of this work is to provide a realistic model of OXPHOS which shall help understanding and predicting the interactions within the OXPHOS and how a local defect (enzyme deficiency or modification) is expressed globally in mitochondrial oxygen consumption and ATP synthesis. Therefore we chose a bottom-up approach. In a first step different types of rate equations were analyzed regarding their ability to describe the steady state kinetics of the isolated respiratory chain complexes in the absence of the proton gradient. Here Michaelis-Menten like rate equations were revealed to be appropriate for describing their behavior over a wide range of substrate and product concentrations. For the validation of the equations and the parameter estimation we have performed kinetic measurements on bovine heart submitochondrial particles. The next step consisted in the incorporation of the proton gradient into the rate equations, distributing its influence among the kinetic parameters such that reasonable rates were obtained in the range of physiological electrochemical potential differences. In the third step, these new individual kinetic rate expressions for the OXPHOS complexes were integrated in a global model of oxidative phosphorylation. The new model could fit interrelated data of oxygen consumption, the transmembrane potential and the redox state of electron carriers. Furthermore, flux inhibitor titration curves can be well reproduced, which validates its global responses to local effects. This model may be of great help to understand the increasingly recognized role of mitochondria in many cell processes and diseases as illustrated by some simulations proposed in this work
Les mitochondries sont l’usine à énergie de la cellule. Elles synthétisent l’ATP à partir d’une succession de réactions d’oxydo-réduction catalysées par quatre complexes respiratoires qui forment la chaîne respiratoire. Avec la machinerie de synthèse d’ATP l’ensemble constitue les oxydations phosphorylantes (OXPHOS). Le but de ce travail est de bâtir un modèle des OXPHOS basé sur des équations de vitesse simples mais thermodynamiquement correctes, représentant l’activité des complexes de la chaîne respiratoire (équations de type Michaelis- Menten). Les paramètres cinétiques de ces équations sont identifiés en utilisant les cinétiques expérimentales de ces complexes respiratoires réalisées en absence de gradient de proton. La phase la plus délicate de ce travail a résidé dans l’introduction du gradient de protons dans ces équations. Nous avons trouvé que la meilleure manière était de distribuer l’effet du gradient de proton sous forme d’une loi exponentielle sur l’ensemble des paramètres, Vmax et Km pour les substrats et les produits. De cette manière, j’ai montré qu’il était possible de représenter les variations d’oxygène, de ΔΨ et de ΔpH trouvés dans la littérature. De plus, contrairement aux autres modèles, il fut possible de simuler les courbes de seuil observées expérimentalement lors de la titration du flux de respiration par l’inhibiteur d’un complexe respiratoire donné.Ce modèle pourra présenter un très grand intérêt pour comprendre le rôle de mieux en mieux reconnu des mitochondries dans de nombreux processus cellulaires, tels que la production d’espèces réactives de l’oxygène, le vieillissement, le diabète, le cancer, les pathologies mitochondriales etc. comme l’illustrent un certain nombre de prédictions présentées dans ce travail

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Heiske, Margit. "Modeling the respiratory chain and the oxidative phosphorylation." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16720.

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Die oxidative Phosphorylierung (OXPHOS) spielt eine zentrale Rolle im Energiestoffwechsel der Zelle. Sie besteht aus der Atmungskette, deren vier Enzymkomplexe einen Protonengradienten über die innere mitochondriale Membran aufbauen, und der ATP-Synthase, die diesen Gradienten zur Phosphorylierung von ADP zu ATP, der zelluläre Energieeinheit, nutzt. In der vorliegenden Arbeit wurde ein thermodynamisch konformes OXPHOS Modell erstellt, welches auf Differentialgleichungen basiert. Dazu wurden Gleichungen entwickelt, welche die Kinetiken jedes OXPHOS-Komplexes über weite Bereiche von Substrat- und Produktkonzentrationen sowie unterschiedlichster Werte des elektrochemischen Gradientens wiedergeben. Zunächst wurden für jeden Komplex der Atmungskette kinetische Messungen in Abwesenheit des Protonengradientens durchgeführt. Für deren Beschreibung erwiesen sich Gleichungen vom Typ Michaelis-Menten als adäquat; hierbei wurden verschiedene Gleichungstypen verglichen. Anschließend wurde der Einfluss des Protonengradientens auf die kinetischen Parameter so modelliert, dass physiologisch sinnvolle Raten in dessen Abhängigkeit erzielt werden konnten. Diese neuen Ratengleichungen wurden schließlich in ein OXPHOS Modell integriert, mit dem sich experimentelle Daten von Sauerstoffverbrauch, elektrischem Potential und pH-Werten sehr gut beschreiben ließen. Weiter konnten Inhibitor-Titrationskurven reproduziert werden, welche den Sauerstoffverbrauch in Abhängigkeit der relativen Hemmung eines OXPHOS-Komplexes darstellen. Dies zeigt, dass lokale Effekte auf globaler Ebene korrekt wiedergeben werden können. Das hier erarbeitete Modell ist eine solide Basis, um die Rolle der OXPHOS und generell von Mitochondrien eingehend zu untersuchen. Diese werden mit zahlreichen zellulären Vorgängen in Verbindung gebracht: unter anderem mit Diabetes, Krebs und Mitochodriopathien, sowie der Bildung von Sauerstoffradikalen, die im Zusammenhang mit Alterungsprozessen stehen.
Oxidative phosphorylation (OXPHOS) plays a central role in the cellular energy metabolism. It comprises the respiratory chain, consisting of four enzyme complexes that establish a proton gradient over the inner mitochondrial membrane, and the ATP-synthase that uses this electrochemical gradient to phosphorylate ADP to ATP, the cellular energy unit. In this work a thermodynamically consistent OXPHOS model was built based on a set of differential equations. Therefore rate equations were developed that describe the kinetics of each OXPHOS complex over a wide concentration range of substrates and products as well for various values of the electrochemical gradient. In a first step, kinetic measurements on bovine heart submitochondrial particles have been performed in the absence of the proton gradient. An appropriate data description was achieved with Michaelis-Menten like equations; here several types of equations have been compared. The next step consisted in incorporating the proton gradient into the rate equations. This was realized by distributing its influence among the kinetic parameters such that reasonable catalytic rates were obtained under physiological conditions. Finally, these new individual kinetic rate expressions for the OXPHOS complexes were integrated in a global model of oxidative phosphorylation. This new model could fit interrelated data of oxygen consumption, the transmembrane potential and the redox state of electron carriers. Furthermore, it could well reproduce flux inhibitor titration curves, which validates its global responses to local perturbations. This model is a solid basis for analyzing the role of OXPHOS and mitochondria in detail. They have been linked to various cellular processes like diabetes, cancer, mitochondrial disorders, but also to the production of reactive oxygen species, which are supposed to be involved in aging.

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Taylor, Claire Louise. "Biochemical investigations of defects of the mitochondrial respiratory chain." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281706.

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Books on the topic "Respiratory chain"

1

Pham, Nhu-An. Generation of oxidative stress by the respiratory chain following treatment with DNA damaging agents. Ottawa: National Library of Canada, 1999.

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Wainio, Walter. Mammalian Mitochondrial Respiratory Chain. Elsevier Science & Technology Books, 2012.

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man, N. S. Gel. Bacterial Membranes and the Respiratory Chain. Springer, 2012.

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Bacterial Membranes and the Respiratory Chain. Springer, 2012.

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man, N. S. Gel. Bacterial Membranes and the Respiratory Chain. Springer, 2012.

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Hargreaves, Iain P. Mitochondrial Respiratory Chain Disorders: From Clinical Presentation to Diagnosis and Treatment. Nova Science Publishers, Incorporated, 2019.

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Merante, Frank. The molecular and biochemical characterization of human mitochondrial respiratory chain deficiencies. 1996.

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Mitochondrial Respiratory Chain Disorders: From Clinical Presentation to Diagnosis and Treatment. Nova Science Publishers, Incorporated, 2019.

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The molecular and biochemical characterization of the MLRQ subunit of NADH: Ubiquinone oxidoreductase in the human mitochondrial respiratory chain. Ottawa: National Library of Canada, 2001.

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Jou, J. Fay, Lori A. Aronson, and Jacqueline W. Morillo-Delerme. Mitochondrial Disorder for Muscle Biopsy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0049.

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Mitochondrial disease (mtD) is a genetically, biochemically, and clinically heterogeneous group of disorders that arise most commonly from defects in the oxidative phosphorylation or electron transport chain involved in energy metabolism. These patients have an increased risk for cardiac, respiratory, neurologic, and metabolic complications from anesthesia. Consequently, there are several anesthetic considerations for patients with mtD.

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Book chapters on the topic "Respiratory chain"

1

Gooch, Jan W. "Respiratory Chain." In Encyclopedic Dictionary of Polymers, 920. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14688.

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Skulachev, Vladimir P., Alexander V. Bogachev, and Felix O. Kasparinsky. "The Respiratory Chain." In Principles of Bioenergetics, 87–118. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-33430-6_4.

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Ritvo, Ariella Riva, Fred R. Volkmar, Karen M. Lionello-Denolf, Trina D. Spencer, James Todd, Nurit Yirmiya, Maya Yaari, et al. "Respiratory Chain Disorders." In Encyclopedia of Autism Spectrum Disorders, 2572. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_101177.

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Bien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko, et al. "Respiratory Chain Disorders." In Encyclopedia of Molecular Mechanisms of Disease, 1834. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6267.

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Munnich, A. "The Respiratory Chain." In Inborn Metabolic Diseases, 121–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03147-6_10.

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Azzi, Angelo, Michele Müller, and Néstor Labonia. "The Mitochondrial Respiratory Chain." In Organelles in Eukaryotic Cells, 1–8. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0545-3_1.

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Sousa, Joana S., Edoardo D’Imprima, and Janet Vonck. "Mitochondrial Respiratory Chain Complexes." In Subcellular Biochemistry, 167–227. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7757-9_7.

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Munnich, Arnold. "Defects of the Respiratory Chain." In Inborn Metabolic Diseases, 158–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-04285-4_13.

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Dudkina, Natalya V., Egbert J. Boekema, and Hans-Peter Braun. "Respiratory Chain Supercomplexes in Mitochondria." In The Structural Basis of Biological Energy Generation, 217–29. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8742-0_12.

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Munnich, Arnold, Agnès Rötig, and Marlène Rio. "Defects of the Respiratory Chain." In Inborn Metabolic Diseases, 223–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-15720-2_15.

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Conference papers on the topic "Respiratory chain"

1

Lapotko, Dmitry, Tat'yana Romanovskaya, and Elena Gordiyko. "Photothermal monitoring of respiratory chain redox state in single live cells." In International Symposium on Biomedical Optics, edited by Manfred D. Kessler and Gerhard J. Mueller. SPIE, 2002. http://dx.doi.org/10.1117/12.469461.

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PETKOVIĆ, M., O. ZSCHÖRNIG, A. VOCKS, M. MÜLLER, J. SCHILLER, K. ARNOLD, and J. ARNHOLD. "RESPIRATORY BURST RESPONSE OF HUMAN NEUTROPHILS TO EXOGENOUSLY ADDED LONG CHAIN PHOSPHATIDIC ACIDS." In Bioluminescence and Chemiluminescence - Progress and Current Applications - 12th International Symposium on Bioluminescence (BL) and Chemiluminescence (CL). WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776624_0065.

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Dusek, Pavel, Marie Rodinova, Irena Liskova, Jiri Klempir, Jiri Zeman, Jan Roth, and Hana Hansikova. "A37 Buccal respiratory chain complexes I and IV quantities in huntington’s disease patients." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.35.

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Jaeger, V. K., D. Lebrecht, A. G. Nicholson, A. U. Wells, S. George, A. Gazdhar, M. Tamm, N. Venhoff, T. Geiser, and U. A. Walker. "OP0090 Mitochondrial dna mutations and respiratory chain dysfunction in lung fibrosis of systemic sclerosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2960.

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Domingue, Scott R., Adam J. Chicco, Randy A. Bartels, and Jesse W. Wilson. "Pump-probe microscopy of respiratory chain pigments: towards non-fluorescent label-free metabolic imaging." In SPIE BiOS, edited by Ammasi Periasamy, Peter T. C. So, Karsten König, and Xiaoliang S. Xie. SPIE, 2017. http://dx.doi.org/10.1117/12.2253378.

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Sundar, Krishna M., Karl Ludwig, Jeffrey Stevenson, and David B. Nielsen. "Implications Of Cytomegalovirus Detection By Polymerase-Chain Reaction In Respiratory Secretions Of Intubated Patients." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4712.

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Baburina, Yulia, Irina Odinokova, Roman Krestinin, Linda Sotnikova, and Olga Krestinina. "INFLUENCE OF CHRONIC ALCOHOL DEPENDENCE ON CHANGES IN THE ACTIVITY OF RESPIRATORY CHAIN COMPLEXES." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2684.sudak.ns2022-18/63-64.

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Onu, Charles C., Lara J. Kanbar, Wissam Shalish, Karen A. Brown, Guilherme M. Sant'Anna, Robert E. Kearney, and Doina Precup. "A semi-Markov chain approach to modeling respiratory patterns prior to extubation in preterm infants." In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8037249.

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Konokhova, Yana, Martin Picard, Gilles Gouspillou, Sophia Kapchinsky, Jacinthe Baril, Thomas Jagoe, and Tanja Taivassalo. "Prevalence Of Mitochondrial Respiratory Chain Deficiency In Skeletal Muscle Of Chronic Obstructive Pulmonary Disease Patients." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5320.

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Feize, L., D. Minai-Tehrani, B. Behboudi, and E. Keyhani. "Identification of the respiratory chain of Armillaria mellea (A.m.) in mushroom state and cultured in vitro." In Proceedings of the II International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2007). WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789812837554_0014.

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Reports on the topic "Respiratory chain"

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Terry Ann Krulwich. The Respiratory Chain of Alkaliphilic Bacteria. Office of Scientific and Technical Information (OSTI), January 2008. http://dx.doi.org/10.2172/922628.

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Gelb, Jr., Jack, Yoram Weisman, Brian Ladman, and Rosie Meir. Identification of Avian Infectious Brochitis Virus Variant Serotypes and Subtypes by PCR Product Cycle Sequencing for the Rational Selection of Effective Vaccines. United States Department of Agriculture, December 2003. http://dx.doi.org/10.32747/2003.7586470.bard.

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Abstract:

Objectives 1. Determine the serotypic identities of 40 recent IBV isolates from commercial chickens raised in the USA and Israel. 2. Sequence all IBV field isolates using PCR product cycle sequencing and analyze their S 1 sequence to detennine their homology to other strains in the Genbank and EMBL databases. 3. Select vaccinal strains with the highest S 1 sequence homology to the field isolates and perform challenge of immunity studies in chickens in laboratory trials to detennine level of protection afforded by the vaccines. Background Infectious bronchitis (IB) is a common, economically important disease of the chicken. IB occurs as a respiratory form, associated with airsacculitis, condemnation, and mortality of meat-type broilers, a reproductive form responsible for egg production losses in layers and breeders, and a renal form causing high mortality in broilers and pullets. The causative agent is avian coronavirus infectious bronchitis virus (IBV). Replication of the virus' RNA genome is error-prone and mutations commonly result. A major target for mutation is the gene encoding the spike (S) envelope protein used by the virus to attach and infect the host cell. Mutations in the S gene result in antigenic changes that can lead to the emergence of variant serotypes. The S gene is able to tolerate numerous mutations without compromising the virus' ability to replicate and cause disease. An end result of the virus' "flexibility" is that many strains of IBV are capable of existing in nature. Once formed, new mutant strains, often referred to as variants, are soon subjected to immunological selection so that only the most antigenically novel variants survive in poultry populations. Many novel antigenic variant serotypes and genotypes have been isolated from commercial poultry flocks. Identification of the field isolates of IBV responsible for outbreaks is critical for selecting the appropriate strain(s) for vaccination. Reverse transcriptase polymerase chain reaction (RT-PCR) of the Sl subunit of the envelope spike glycoprotein gene has been a common method used to identify field strains, replacing other time-consuming or less precise tests. Two PCR approaches have been used for identification, restriction fragment length polymorphism (RFLP) and direct automated cycle sequence analysis of a diagnostically relevant hypervariab1e region were compared in our BARD research. Vaccination for IB, although practiced routinely in commercial flocks, is often not protective. Field isolates responsible for outbreaks may be unrelated to the strain(s) used in the vaccination program. However, vaccines may provide varying degrees of cross- protection vs. unrelated field strains so vaccination studies should be performed. Conclusions RFLP and S1 sequence analysis methods were successfully performed using the field isolates from the USA and Israel. Importantly, the S1 sequence analysis method enabled a direct comparison of the genotypes of the field strains by aligning them to sequences in public databases e.g. GenBank. Novel S1 gene sequences were identified in both USA and Israel IBVs but greater diversity was observed in the field isolates from the USA. One novel genotype, characterized in this project, Israel/720/99, is currently being considered for development as an inactivated vaccine. Vaccination with IBV strains in the US (Massachusetts, Arkansas, Delaware 072) or in Israel (Massachusetts, Holland strain) provided higher degrees of cross-protection vs. homologous than heterologous strain challenge. In many cases however, vaccination with two strains (only studies with US strains) produced reasonable cross-protection against heterologous field isolate challenge. Implications S1 sequence analysis provides numerical similarity values and phylogenetic information that can be useful, although by no means conclusive, in developing vaccine control strategies. Identification of many novel S1 genotypes of IBV in the USA is evidence that commercial flocks will be challenged today and in the future with strains unrelated to vaccines. In Israel, monitoring flocks for novel IBV field isolates should continue given the identification of Israel/720/99, and perhaps others in the future. Strains selected for vaccination of commercial flocks should induce cross- protection against unrelated genotypes. Using diverse genotypes for vaccination may result in immunity against unrelated field strains.

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