Literatura académica sobre el tema "Mitochondrial movement"
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Artículos de revistas sobre el tema "Mitochondrial movement":
1
Elizaveta, Bon. "Mitochondrial Movement: A Review". Clinical Research Notes 3, n.º 3 (30 de abril de 2022): 01–06. http://dx.doi.org/10.31579/2690-8816/059.
Resumen
The balance between fusion and division determines most of the functions of mitochondria, controls their bioenergetic function, mitochondrial turnover, and also protects mitochondrial DNA. The division promotes equal segregation of mitochondria into daughter cells during cell division itself and enhances the distribution of mitochondria along the cytoskeletal pathways. In addition, division can help isolate damaged mitochondrial segments and thus promote autophagy. Fusion provides protein complementation, and equal distribution of metabolites. The movement of mitochondria in the dendrites, axons and perikaryons of neurons is an important aspect of the vital activity of nerve cells. Disorders of mitochondrial fusion, division, and mobility can lead to defects in the functioning of the nervous system, which makes it important to study these processes for improvig methods of prevention, diagnosis, and correction of neurological diseases.
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Delmotte, Philippe, Vanessa A. Zavaletta, Michael A. Thompson, Y. S. Prakash y Gary C. Sieck. "TNFα decreases mitochondrial movement in human airway smooth muscle". American Journal of Physiology-Lung Cellular and Molecular Physiology 313, n.º 1 (1 de julio de 2017): L166—L176. http://dx.doi.org/10.1152/ajplung.00538.2016.
Resumen
In airway smooth muscle (ASM) cells, excitation-contraction coupling is accomplished via a cascade of events that connect an elevation of cytosolic Ca2+ concentration ([Ca2+]cyt) with cross-bridge attachment and ATP-consuming mechanical work. Excitation-energy coupling is mediated by linkage of the elevation of [Ca2+]cyt to an increase in mitochondrial Ca2+ concentration, which in turn stimulates ATP production. Proximity of mitochondria to the sarcoplasmic reticulum (SR) and plasma membrane is thought to be an important mechanism to facilitate mitochondrial Ca2+ uptake. In this regard, mitochondrial movement in ASM cells may be key in establishing proximity. Mitochondria also move where ATP or Ca2+ buffering is needed. Mitochondrial movement is mediated through interactions with the Miro-Milton molecular complex, which couples mitochondria to kinesin motors at microtubules. We examined mitochondrial movement in human ASM cells and hypothesized that, at basal [Ca2+]cyt levels, mitochondrial movement is necessary to establish proximity of mitochondria to the SR and that, during the transient increase in [Ca2+]cyt induced by agonist stimulation, mitochondrial movement is reduced, thereby promoting transient mitochondrial Ca2+ uptake. We further hypothesized that airway inflammation disrupts basal mitochondrial movement via a reduction in Miro and Milton expression, thereby disrupting the ability of mitochondria to establish proximity to the SR and, thus, reducing transient mitochondrial Ca2+ uptake during agonist activation. The reduced proximity of mitochondria to the SR may affect establishment of transient “hot spots” of higher [Ca2+]cyt at the sites of SR Ca2+ release that are necessary for mitochondrial Ca2+ uptake via the mitochondrial Ca2+ uniporter.
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Gurdon, Csanad, Zora Svab, Yaping Feng, Dibyendu Kumar y Pal Maliga. "Cell-to-cell movement of mitochondria in plants". Proceedings of the National Academy of Sciences 113, n.º 12 (7 de marzo de 2016): 3395–400. http://dx.doi.org/10.1073/pnas.1518644113.
Resumen
We report cell-to-cell movement of mitochondria through a graft junction. Mitochondrial movement was discovered in an experiment designed to select for chloroplast transfer from Nicotiana sylvestris into Nicotiana tabacum cells. The alloplasmic N. tabacum line we used carries Nicotiana undulata cytoplasmic genomes, and its flowers are male sterile due to the foreign mitochondrial genome. Thus, rare mitochondrial DNA transfer from N. sylvestris to N. tabacum could be recognized by restoration of fertile flower anatomy. Analyses of the mitochondrial genomes revealed extensive recombination, tentatively linking male sterility to orf293, a mitochondrial gene causing homeotic conversion of anthers into petals. Demonstrating cell-to-cell movement of mitochondria reconstructs the evolutionary process of horizontal mitochondrial DNA transfer and enables modification of the mitochondrial genome by DNA transmitted from a sexually incompatible species. Conversion of anthers into petals is a visual marker that can be useful for mitochondrial transformation.
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E.I,, Bon. "Mechanisms of Movement of Mitochondria in the Cell". Clinical Endocrinology and Metabolism 1, n.º 1 (26 de octubre de 2022): 01–06. http://dx.doi.org/10.31579/2834-8761/005.
Resumen
The balance between fusion and division determines most of the functions of mitochondria, controls their bioenergetic function, mitochondrial turnover, and also protects mitochondrial DNA. The division promotes equal segregation of mitochondria into daughter cells during cell division itself and enhances the distribution of mitochondria along the cytoskeletal pathways. In addition, division can help isolate damaged mitochondrial segments and thus promote autophagy. Fusion provides protein complementation, and equal distribution of metabolites. The movement of mitochondria in the dendrites, axons and perikaryons of neurons is an important aspect of the vital activity of nerve cells. Disorders of mitochondrial fusion, division, and mobility can lead to defects in the functioning of the nervous system, which makes it important to study these processes for improving methods of prevention, diagnosis, and correction of neurological diseases.
5
Yi, Muqing, David Weaver y György Hajnóczky. "Control of mitochondrial motility and distribution by the calcium signal". Journal of Cell Biology 167, n.º 4 (15 de noviembre de 2004): 661–72. http://dx.doi.org/10.1083/jcb.200406038.
Resumen
Mitochondria are dynamic organelles in cells. The control of mitochondrial motility by signaling mechanisms and the significance of rapid changes in motility remains elusive. In cardiac myoblasts, mitochondria were observed close to the microtubular array and displayed both short- and long-range movements along microtubules. By clamping cytoplasmic [Ca2+] ([Ca2+]c) at various levels, mitochondrial motility was found to be regulated by Ca2+ in the physiological range. Maximal movement was obtained at resting [Ca2+]c with complete arrest at 1–2 μM. Movement was fully recovered by returning to resting [Ca2+]c, and inhibition could be repeated with no apparent desensitization. The inositol 1,4,5-trisphosphate– or ryanodine receptor-mediated [Ca2+]c signal also induced a decrease in mitochondrial motility. This decrease followed the spatial and temporal pattern of the [Ca2+]c signal. Diminished mitochondrial motility in the region of the [Ca2+]c rise promotes recruitment of mitochondria to enhance local Ca2+ buffering and energy supply. This mechanism may provide a novel homeostatic circuit in calcium signaling.
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Kaasik, Allen, Dzhamilja Safiulina, Alexander Zharkovsky y Vladimir Veksler. "Regulation of mitochondrial matrix volume". American Journal of Physiology-Cell Physiology 292, n.º 1 (enero de 2007): C157—C163. http://dx.doi.org/10.1152/ajpcell.00272.2006.
Resumen
Mitochondrial volume homeostasis is a housekeeping cellular function essential for maintaining the structural integrity of the organelle. Changes in mitochondrial volume have been associated with a wide range of important biological functions and pathologies. Mitochondrial matrix volume is controlled by osmotic balance between cytosol and mitochondria. Any dysbalance in the fluxes of the main intracellular ion, potassium, will thus affect the osmotic balance between cytosol and the matrix and promote the water movement between these two compartments. It has been hypothesized that activity of potassium efflux pathways exceeds the potassium influx in functioning mitochondria and that potassium concentration in matrix could be actually lower than in cytoplasm. This hypothesis provides a clear-cut explanation for the mitochondrial swelling observed after mitochondrial depolarization, mitochondrial calcium overload, or opening of permeability transition pore. It should also be noted that the rate of water flux into or out of the mitochondrion is determined not only by the osmotic gradient that acts as the driving force for water transport but also by the water permeability of the inner membrane. Recent data suggest that the mitochondrial inner membrane has also specific water channels, aquaporins, which facilitate water movement between cytoplasm and matrix. This review discusses different phases of mitochondrial swelling and summarizes the potential effects of mitochondrial swelling on cell function.
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Simon, V. R., T. C. Swayne y L. A. Pon. "Actin-dependent mitochondrial motility in mitotic yeast and cell-free systems: identification of a motor activity on the mitochondrial surface." Journal of Cell Biology 130, n.º 2 (15 de julio de 1995): 345–54. http://dx.doi.org/10.1083/jcb.130.2.345.
Resumen
Using fluorescent membrane potential sensing dyes to stain budding yeast, mitochondria are resolved as tubular organelles aligned in radial arrays that converge at the bud neck. Time-lapse fluorescence microscopy reveals region-specific, directed mitochondrial movement during polarized yeast cell growth and mitotic cell division. Mitochondria in the central region of the mother cell move linearly towards the bud, traverse the bud neck, and progress towards the bud tip at an average velocity of 49 +/- 21 nm/sec. In contrast, mitochondria in the peripheral region of the mother cell and at the bud tip display significantly less movement. Yeast strains containing temperature sensitive lethal mutations in the actin gene show abnormal mitochondrial distribution. No mitochondrial movement is evident in these mutants after short-term shift to semi-permissive temperatures. Thus, the actin cytoskeleton is important for normal mitochondrial movement during inheritance. To determine the possible role of known myosin genes in yeast mitochondrial motility, we investigated mitochondrial inheritance in myo1, myo2, myo3 and myo4 single mutants and in a myo2, myo4 double mutant. Mitochondrial spatial arrangement and motility are not significantly affected by these mutations. We used a microfilament sliding assay to examine motor activity on isolated yeast mitochondria. Rhodamine-phalloidin labeled yeast actin filaments bind to immobilized yeast mitochondria, as well as unilamellar, right-side-out, sealed mitochondrial outer membrane vesicles. In the presence of low levels of ATP (0.1-100 microM), we observed F-actin sliding on immobilized yeast mitochondria. In the presence of high levels of ATP (500 microM-2 mM), bound filaments are released from mitochondria and mitochondrial outer membranes. The maximum velocity of mitochondria-driven microfilament sliding (23 +/- 11 nm/sec) is similar to that of mitochondrial movement in living cells. This motor activity requires hydrolysis of ATP, does not require cytosolic extracts, is sensitive to protease treatment, and displays an ATP concentration dependence similar to that of members of the myosin family of actin-based motors. This is the first demonstration of an actin-based motor activity in a defined organelle population.
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Förtsch, Johannes, Eric Hummel, Melanie Krist y Benedikt Westermann. "The myosin-related motor protein Myo2 is an essential mediator of bud-directed mitochondrial movement in yeast". Journal of Cell Biology 194, n.º 3 (1 de agosto de 2011): 473–88. http://dx.doi.org/10.1083/jcb.201012088.
Resumen
The inheritance of mitochondria in yeast depends on bud-directed transport along actin filaments. It is a matter of debate whether anterograde mitochondrial movement is mediated by the myosin-related motor protein Myo2 or by motor-independent mechanisms. We show that mutations in the Myo2 cargo binding domain impair entry of mitochondria into the bud and are synthetically lethal with deletion of the YPT11 gene encoding a rab-type guanosine triphosphatase. Mitochondrial distribution defects and synthetic lethality were rescued by a mitochondria-specific Myo2 variant that carries a mitochondrial outer membrane anchor. Furthermore, immunoelectron microscopy revealed Myo2 on isolated mitochondria. Thus, Myo2 is an essential and direct mediator of bud-directed mitochondrial movement in yeast. Accumulating genetic evidence suggests that maintenance of mitochondrial morphology, Ypt11, and retention of mitochondria in the bud contribute to Myo2-dependent inheritance of mitochondria.
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Finsterer, J. y S. Zarrouk-Mahjoub. "Mitochondrial movement disorders". Revue Neurologique 172, n.º 11 (noviembre de 2016): 716–17. http://dx.doi.org/10.1016/j.neurol.2016.09.002.
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Beltran-Parrazal, Luis, Héctor E. López-Valdés, K. C. Brennan, Mauricio Díaz-Muñoz, Jean de Vellis y Andrew C. Charles. "Mitochondrial transport in processes of cortical neurons is independent of intracellular calcium". American Journal of Physiology-Cell Physiology 291, n.º 6 (diciembre de 2006): C1193—C1197. http://dx.doi.org/10.1152/ajpcell.00230.2006.
Resumen
Mitochondria show extensive movement along neuronal processes, but the mechanisms and function of this movement are not clearly understood. We have used high-resolution confocal microscopy to simultaneously monitor movement of mitochondria and changes in intracellular [Ca2+] ([Ca2+]i) in rat cortical neurons. A significant percentage (27%) of the total mitochondria in cortical neuronal processes showed movement over distances of >2 μM. The average velocity was 0.52 μm/s. The velocity, direction, and pattern of mitochondrial movement were not affected by transient increases in [Ca2+]i associated with spontaneous firing of action potentials. Stimulation of Ca2+ transients with forskolin (10 μM) or bicuculline (10 μM), or sustained elevations of [Ca2+]i evoked by glutamate (10 μM) also had no effect on mitochondrial transit. Neither removal of extracellular Ca2+, depletion of intracellular Ca2+ stores with thapsigargin, or inhibition of synaptic activity with TTX (1 μM) or a cocktail of CNQX (10 μM) and MK801 (10 μM) affected mitochondrial movement. These results indicate that movement of mitochondria along processes is a fundamental activity in neurons that occurs independently of physiological changes in [Ca2+]i associated with action potential firing, synaptic activity, or release of Ca2+ from intracellular stores.
Tesis sobre el tema "Mitochondrial movement":
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Shchepinova, Maria M. "Molecular probes for monitoring mitochondrial movement and function". Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7835/.
Resumen
This thesis explores two distinct parts of mitochondrial physiology: the role of mitochondria in generation of reactive oxygen species (ROS) and mitochondrial morphology and dynamics within cells. The first area of research is covered in Chapters 1-8. Mitochondrial biofunctionality and ROS production are discussed in Chapter 1, followed by the strategy of targeting bioactive compounds to mitochondria by linking them to lipophilic triphenylphosphonium cations (TPP) (Chapter 2). ROS sensors relevant to the research are reviewed in Chapter 3. Chapter 4 presents design and synthesis of novel probes for superoxide detection in mitochondria (MitoNeo-D), cytosol (Neo-D) and extracellular environment (ExCellNeo-D). The results of biological validation of MitoNeo-D and Neo-D performed in the MRC MBU in Cambridge are presented in Chapter 5. A dicationic hydrogen peroxide sensor that utilizes in situ click chemistry is discussed in Chapter 6. Preliminary work on the synthesis of mitochondria-targeted superoxide generators, which led to the development of mitochondria-targeted analogue of paraquat, MitoPQ, is presented in Chapter 7. A set of bifunctional probes (BCN-Mal, BCN-E-BCN and Mito-iTag) for assessing the redox states of protein thiols is discussed in Chapter 8 along with their biological validation. The second part of the thesis is aimed at the study of mitochondrial morphology and dynamics and is presented in Chapters 9-11. Chapter 9 provides background on the classes of fluorophores relevant to the research, the phenomenon of fluorescence quenching and the principle of photoactivation with examples of photoactivatable fluorophores. Next, the background on mitochondrial morphology and heterogeneity is presented in Chapter 10, followed by the ways of imaging and tracking mitochondria within cells by conventional fluorophores and by photoactivatable fluorophores exploiting super-resolution microscopy. Chapter 11 presents the design and synthesis of four photoactivatable fluorophores for mitochondrial tracking, MitoPhotoRhod110, MitoPhotoNIR, Photo-E+, MitoPhoto-E+, along with results of biological validation of MitoPhotoNIR. The results and discussion concludes with Chapter 12, which is a summary and suggestions for future work, followed by the chemistry experimental procedures (Chapter 13), materials and methods for biological experiments (Chapter 14) and references.
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Vaillant-Beuchot, Loan. "Étude des mécanismes liés aux dysfonctions mitochondriales, à l'altération de la mitophagie et aux défauts du transport mitochondrial dans la maladie d'Alzheimer". Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6019.
Resumen
Les mitochondries assurent des fonctions essentielles dans les cellules via la production d'énergie sous forme d'ATP, la captation de calcium et la régulation de la mort cellulaire par apoptose. Les dysfonctions des mitochondries apparaissent à des stades précoces de la maladie d'Alzheimer (MA), et ont été particulièrement associées au peptide toxique Aβ. Ce dernier est issu du clivage séquentiel de la protéine précurseur de l'amyloïde (APP) par la β- et la γ-sécrétase. Plusieurs traitements ciblant l'Aβ se sont avérés inefficaces contre la progression de la MA, orientant les recherches sur le potentiel toxique d'autres fragments issus du clivage de l'APP. L'hypothèse de mon projet porte sur la toxicité spécifique des fragments APP C-terminaux (APP-CTFs : C83 et C99 (précurseur direct de l'Aβ)) en se focalisant sur l'étude de la structure, la fonction des mitochondries et la mitophagie. J'ai également étudié l'impact de l'APP et de ses fragments sur la machinerie de transport des mitochondries, un mécanisme clé de leur renouvellement, en particulier dans les neurones.Premier axe : Impact de l'accumulation des APP-CTFs sur la structure, la fonction des mitochondries et sur la mitophagie. Nous décrivons une accumulation des APP-CTFs dans la fraction mitochondriale de modèles mimant les formes familiales de la MA in vitro (cellules de neuroblastome humains exprimant l'APP portant la double mutation suédoise (SH-SY5Y-APPswe), ou le fragment C99 (SH-SY5Y-C99)) et in vivo (souris transgéniques 3xTgAD exprimant les mutations APPswe, TauP301L, PS1 (M146V) ou bien le fragment C99 après infection virale). Par le biais d'une approche pharmacologique bloquant l'activité de la γ-sécrétase, nous démontrons in vitro et in vivo que l'accumulation des APP-CTFs, indépendamment de l'Aβ, est associée à l'agglomération de mitochondries structurellement altérées et surproduisant des espèces oxygénées réactives toxiques, conjointement à un blocage de la mitophagie. Nous avons conclu notre étude par la démonstration de l'altération de la mitophagie dans les cerveaux de patients atteints de la MA sporadique, corrélant avec les niveaux d'APP-CTFs (1, 2).Second axe : Etude des effets de l'APP, des APP-CTFS et de l'Aβ sur les protéines de transport mitochondrial. J'ai d'abord démontré l'impact de l'APP endogène et de la surexpression de l'APPswe sur les niveaux des protéines de la machinerie de transport mitochondrial in vitro (fibroblastes de souris KO pour l'APP ainsi que dans cellules SH-SY5Y-APPswe). J'ai discriminé le rôle de l'accumulation des APP-CTFs de celui de l'Aβ sur l'expression de ces protéines en traitant les cellules APPswe avec l'inhibiteur de la γ-sécrétase. J'ai validé ces observations en utilisant des fibroblastes de souris déplétés des présénilines (composants catalytiques de la γ-sécrétase) mimant une accumulation des APP-CTFs. J'ai par ailleurs démontré une implication des APP-CTFs et de l'Aβ dans le défaut de recrutement des mitochondries à la machinerie de transport dans les cellules SHSY-5Y différentiées. En analysant des cerveaux de souris 3xTgAD et WT à différent âges et des échantillons de cerveaux de patients Alzheimer sporadiques à différents stades de la maladie, nous rapportons que le développement de la MA et l'âge en lui-même ont un impact différentiel sur l'expression de certaines protéines de transport mitochondrial (3).Ces études démontrent de nouveaux mécanismes moléculaires impactant l'homéostasie mitochondriale au cours du développement de la MA. Ces découvertes permettront la mise en place de nouvelles pistes thérapeutiques ralentissant les dysfonctions des mitochondries et, ou favorisant leur renouvellement dans le contexte de la MA.(1). Vaillant-Beuchot L.*, Mary A.* et al. Acta Neuropathologica 2020.(2). Mary A.*, Vaillant-Beuchot L.* et al. Médecine/sciences 2021.(3). Vaillant-Beuchot et al. En cours de soumissionMitochondria are essential organelles in cells, ensuring energy production with ATP synthesis, calcium buffering, apoptosis regulation. These functions are altered at early stages of Alzheimer's disease (AD) and are essentially induced by the Amyloid (Aβ), produced after the sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase. Aβ is a major actor of AD development but all the treatments targeting this peptide remain ineffective. C-terminal APP fragments (APP-CTFs: C83 and C99 (Aβ precursor) are other fragments presenting specific toxicity in AD and new potential therapeutic targets. My project is focus on the study of APP-CTFs toxicity, independently of Aβ, on the structure, function of mitochondria, their degradation by mitophagy and on mitochondrial transport proteins. They constitute the complex allowing mitochondrial transport in cells, especially in neurons, closely linked to mitochondrial renewal, particularly in neurons.First axe: APP-CTFs impact on mitochondrial structure, function and mitophagy. We described APP-CTFs accumulation in mitochondrial fraction in vitro (human neuroblastoma cells expressing APP Swedish double mutation (SH-SY5Y-APPswe) or C99 fragment (SH-SY5Y-C99)) and in vivo (3xTgAD mice expressing APPswe, TauP301L, PS1 (M146V) or C99 fragment after viral injection). We inhibit the cleavage of APP-CTFs and the production of Aβ by pharmacological approaches, to abolish γ-secretase activity. Ours results show for the first time in vitro and in vivo, that high concentration of APP-CTFs independently of Aβ, impact mitochondrial structure, function and alter mitophagy process, resulting in an accumulation of altered mitochondria producing high levels of toxic reactive oxygen species. In addition, our results in patient brains of sporadic AD (SAD) patients show altered mitophagic protein levels correlating with APP-CTFs accumulation (1-2).Second axe: study of the effects of APP, APP-CTFs and Aβ peptide on mitochondrial transport machinery. I reported the specific regulation of mitochondrial transport protein by endogenous APP (Mice fibroblasts APP WT and KO) and the overexpression of APPswe (and in SH-SY-5Y-APPswe cells). APP-CTFs and Aβ differentially regulate mitochondrial transport protein levels in treated SH-SY-5Y-APPswe cells with γ-secretase inhibitor. These results were validated in mice fibroblasts KO for presenilins (catalytic compounds of γ-secretase) avoiding APP-CTFs degradation. APP-CTFs and Aβ impair the recruitment of mitochondria to its transport machinery in differentiated SHSY-5Y. The progression of the disease deregulates the levels of mitochondrial transport protein in vivo (3xTgAD and WT mice brains, C99 injected mice brains) and in SAD patients brains. The analyses of young and old mice brains and of SAD patients samples at different stages of the disease, allowed us to demonstrate an impact of aging in the regulation of mitochondrial transport protein levels. This phenomenon occurs also in addition with AD progression (3).These studies highlight new molecular mechanisms impacting mitochondrial homeostasis during AD progression. Our findings will bring new therapeutic research to slow down mitochondrial dysfunctions and/or to stimulate their renewal in AD context.(1). Vaillant-Beuchot L.*, Mary A.* et al. Acta Neuropathologica 2020.(2). Mary A.*, Vaillant-Beuchot L.* et al. Médecine/sciences 2021.(3). Vaillant-Beuchot et al. En cours de soumission
3
Eshleman, Jason Aaron. "Mitochondrial DNA and prehistoric population movements in western North America /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.
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Murphy, Cheryl. "Influence of post-aerobic exercise nutrition on protein turnover and mitochondrial biogenesis". 2009. http://hdl.handle.net/2292/5429.
Resumen
The desire to age well is a common goal among the human population. How to do so is therefore, a popular question. One theory of ageing involves the accumulation of damage to mitochondrial protein and the subsequent loss of function the damage causes. Increasing the rate of mitochondrial protein synthesis, a variable that declines with advancing age, is one way to improve quality of life in the twilight years. A review of literature lead to a multi-level approach, with measurements of protein synthesis made at the whole body, muscle, and molecular levels. An acute bout of aerobic exercise, followed by feeding, two factors which have a positive effect on the rate of mitochondrial protein synthesis, was used. Adaptations to a period of exercise training are mediated by the accumulation of proteins due to each acute exercise bout, and so an acute intervention was postulated to be indicative of changes expected over the long term. A stable isotope infusion combined with sampling of breath, blood, and muscle was used to determine the rate of whole body protein synthesis in 12 older adults. Intracellular signalling for mitochondrial and whole body protein synthesis was examined using RT-quantitative PCR and Western blotting in eleven young adults. The rate of post-exercise whole body protein synthesis was 19% greater over the first four hours of post-exercise recovery, in subjects receiving a protein-plus-carbohydrate drink immediately after a bout of cycling than in those receiving a carbohydrate-only drink (p = 0.001). The same trend was revealed in signalling for whole body protein synthesis and the abundance of cytochrome c, a mitochondrial protein, although these results were not statistically significant (p = 0.2). In contrast there was a strong, albeit also statistically insignificant, tendency for signalling for mitochondrial protein synthesis to be higher in the skeletal muscle of subjects receiving a carbohydrate-only drink after a bout of cycling (p = 0.06). The exercise and feeding intervention described in this thesis may provide a means to enhance the rate of mitochondrial protein synthesis in older individuals and, in so doing, improve the quality of their old age.
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Granata, Cesare. "Effects of different exercise intensity and volume on markers of mitochondrial biogenesis in human skeletal muscle". Thesis, 2015. https://vuir.vu.edu.au/30176/.
Resumen
Mitochondria are key components of skeletal muscles as they provide the energy required for almost all cellular activities, and play an important role in ageing and cell pathology. Different forms of exercise training have been associated with mitochondrial adaptations, such as increased mitochondrial content and function, and enhanced mitochondrial biogenesis, as well as improved endurance performance. However, the role of training intensity and training volume, in determining these changes remains elusive. Therefore, the aim of this thesis was to investigate the role of training intensity and volume on changes in mitochondrial content and function (as measured by mitochondrial respiration in permeabilised muscle fibres), in the skeletal muscle of healthy humans, and to study the molecular mechanisms underlying these changes. It was demonstrated that training intensity is a key factor regulating changes in mitochondrial respiration, but not mitochondrial content, and that an apparent dissociation exists between changes in these two parameters. Training consisting of repeated 30-s “all-out” sprints lead to improved mitochondrial (mt)-specific respiration (indicative of improved mitochondrial quality). Conversely, training volume was shown to be a key factor regulating mitochondrial content, with the associated increase in mitochondrial respiration being likely driven by the increase in mitochondrial content (i.e., unchanged mt-specific respiration). A training volume reduction resulted in a rapid decrease in most mitochondrial parameters, underlining the importance of maintaining the training stimulus to preserve training-induced mitochondrial adaptations. The protein content of PGC-1α, p53 and PHF20 was shown to be regulated in a training intensity-dependent manner, and was more strongly associated with changes in mitochondrial respiration rather than content, whereas changes in the protein content of TFAM were primarily associated with changes in mitochondrial content. Moreover, it was demonstrated that exercise intensity induced an increase in nuclear PGC-1α protein content and nuclear p53 phosphorylation, two events that may represent the initial phase of different pathways of the exercise-induced adaptive response. Collectively, this research provides novel information regarding mitochondrial adaptations to different training stimuli, and could have important implications for the design of exercise programs in conditions of compromised mitochondrial function.
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Wang, Xiao Nan. "Skeletal muscle mitochondrial capacity and metabolism in lung transplant patients and resistance trained subjects". Thesis, 2000. https://vuir.vu.edu.au/15725/.
Resumen
Lung transplant (LTx) recipients have poor exercise tolerance, which persists in spite of the restoration of near normal lung function. This suggests that the exercise limitation is related to defects in skeletal muscle. Firstly, mitochondrial function and metabolism in resting skeletal muscle were examined for 7 LTx recipients, 3-24 months post operation. Secondly, exercise performance for patients with lung transplantation was investigated.
Resistance training is an effective exercise mode for improving muscle bulk and strength in sports and medical rehabilitation. Recently, resistance training has become a popular exercise mode to improve muscular function and enhance exercise performance in patients with cardiopulmonary diseases. In a further study sixteen male volunteers participated in a study on the effects of resistance training on mitochondrial oxidative capacity in skeletal muscle.
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Hedges, Christopher. "The effects of physiological acidosis on skeletal muscle mitochondrial function, ROS balance, and intracellular signalling". Thesis, 2017. https://vuir.vu.edu.au/35976/.
Resumen
Mitochondrial adaptation in skeletal muscle is promoted by a diverse array of stimuli, and changes in mitochondrial plasticity have been noted as a result of a many exercise modalities. High-intensity interval training is one such modality that promotes mitochondrial adaptation in response to repeated short-duration bouts of intense effort. Another result of intense muscular effort is a decrease in muscle pH, resulting in intracellular acidosis. The effect of this acidosis on oxygen consumption in muscle has received attention previously, with mixed findings. An aspect of skeletal muscle mitochondrial function that has received limited attention is the production of reactive oxygen species. To date a small number of studies have also provided evidence that attenuating the development of intracellular acidosis may have beneficial effects for mitochondrial adaptation.
This thesis aimed to further investigate the effect of acidosis on mitochondrial function, and on intracellular signalling for mitochondrial biogenesis.
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Jamnick, Nicholas. "An examination of current methods to prescribe exercise intensity: validity of different approaches and effects on cell signalling events associated with mitochondrial biogenesis". Thesis, 2019. https://vuir.vu.edu.au/40459/.
Resumen
While seemingly simple, the underlying exercise prescription to bring about the desired adaptations to exercise training is as complicated as that of any drug. Prescribing the frequency, duration, or volume of training is relatively simple as these factors can be altered by manipulating the number of exercise sessions per week, the duration of each session, or the total work performed in a given time frame (e.g., per week). However, prescribing exercise intensity is more complex and there is controversy regarding the reliability and validity of the many methods used to determine and prescribe intensity. Despite their common use, it is apparent V̇ O2 and HR based exercise prescription has no merit to elicit a homogeneous and explicit homeostatic response. Alternatively, the use of submaximal anchors has been employed and perceived to represent shifts in the metabolic state of the working muscle and represent a demarcating point to define training zones. Whereas, the domains of exercise are independent of these anchors and defined by their distinct homeostatic responses, and offer a valid concept for normalising exercise intensity (Chapter 1; Review 1). Furthermore, the relationship between graded exercise test (GXT) derived anchors and constant work load derived anchors is at this point non sequitur and we discourage using submaximal anchors interchangeably (Chapter 2; Study 1).
Mitochondria are organelles found inside skeletal muscle cells and their main role is the production of adenosine triphosphate (ATP) which is necessary for skeletal muscle contractions. The bioenergetics demands associated with aerobic exercise lead to a homeostatic perturbation, activating sensor proteins that initiates gene expression through transcriptional and translational processes leading to the development of mitochondrial proteins. The source of ATP production modulates the homeostatic perturbations that activate the sensor proteins which include: an increase in the redox state of the cell (NAD+/NADH), an increase in ATP turnover (measured via AMP/ATP), increased calcium flux and mechanical stress and these are largely influenced by the source of ATP production. These perturbations act as signals to activate sensor proteins that ultimately modulate transcriptional coactivators associated with mitochondrial biogenesis (Chapter 3; Review 2). Despite the relationship between exercise intensity and mitochondrial biogenesis, submaximal exercise intensity is almost exclusively prescribed relative to maximal oxygen uptake or maximal work rate. The well-established limitation of these methods is the inability to normalise exercise intensity; specifically, to elicit a homogenous homeostatic perturbations. Thus, employing methodology that normalises exercise intensity based on homeostatic perturbations may modulate the activation of signalling kinases and the extent of gene expression (Chapter 4; Study 2).
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Bartlett, Jonathan. "Exercise-induced cell signalling responses of human skeletal muscle: the effects of reduced carbohydrate availability". Thesis, 2012. https://vuir.vu.edu.au/29596/.
Resumen
It is well documented that regular endurance exercise induces skeletal muscle mitochondrial biogenesis. However, the optimal training stimulus and nutritional intervention for which to maximize mitochondrial adaptations to endurance exercise is not well known. Developments in molecular techniques now permit the examination of the cell signalling responses to acute exercise therefore increasing our understanding of how manipulation of the training protocol and nutrient availability may enhance the training stimulus to a given bout of exercise. The primary aim of this thesis is to therefore characterise the skeletal muscle cell signalling responses thought to regulate mitochondrial biogenesis following an acute bout of high-intensity interval exercise and moderate- intensity continuous exercise.
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Woessner, Mary. "BEET-HF: The Effects of Dietary Inorganic Nitrate Supplementation on Aerobic Exercise Performance, Vascular Function, Cardiac Performance and Mitochondrial Respiration in Patients with Heart Failure with Reduced Ejection Fraction". Thesis, 2019. https://vuir.vu.edu.au/40041/.
Resumen
Chronic heart failure (CHF) is characterised by an inability of the heart to pump enough blood to meet the body’s metabolic needs, resulting in exercise intolerance. A reduction in nitric oxide (NO) bioavailability has been implicated as an initiator and/or contributor to many of the peripheral skeletal tissue dysfunctions that contribute to the exercise intolerance in patients with CHF. Inorganic nitrate supplementation has been identified as an important mediator of exercise tolerance via increasing NO bioavailability, but the potential efficacy of this on patients with heart failure with reduced ejection fraction (HFrEF) as well as the effect on vascular function is not well understood and was the focus of Study 1. Additionally, to our knowledge, no previous study has examined the potential impact of nitrate supplementation on cardiac performance during submaximal exercise and mitochondrial respiration in individuals with HFrEF. These were the foci of Studies 2 and 3 respectively.
Study 1: The effect of dietary inorganic nitrate supplementation on exercise tolerance and vascular function in patients with HFrEF.
The primary aim of this study was to determine the effect of chronic inorganic nitrate supplementation on exercise tolerance, as measured by peak aerobic capacity (VO2peak) and time to exhaustion (TTE), during treadmill exercise in patients with HFrEF. A secondary aim was to determine the effect of chronic supplementation on vascular function (endothelial function) in these patients. Methods: Sixteen patients with HFrEF (15 men and 1 woman, 63 ± 4 y, BMI: 31.8 ±2.1 kg∙m-2) completed the primary outcome of this study (exercise tolerance), and 12 completed the vascular function component. Participants were randomly allocated, in a double-blind, crossover design, to consume either a nitrate rich beetroot juice (16mmol nitrate/day), or a nitrate-depleted placebo for five days prior to the first testing visit. Participants then continued daily dosing until they completed a cardiopulmonary exercise test (CPX) and a battery of vascular function assessments (peripheral and central blood pressure (BP) as well as aortic stiffness and brachial artery flow mediated dilation (BAFMD)). Results: There were significant increases in both plasma nitrate (p<0.001) and nitrite (p<0.05) following nitrate supplementation. No significant differences were observed in either VO2peak (nitrate 18.5 ± 5.7 ml∙kg-1∙min-1, placebo: 19.3 ± 1.4 ml∙kg-1∙min-1; p=0.13) or TTE (nitrate: 1165 ± 92 sec, placebo: 1207 ± 96 sec, p=0.16) between the two interventions. Similarly, there were no significant (p>0.05) changes in peripheral tissue oxygenation during exercise, as measured non-invasively with near-infrared spectroscopy (NIRS). There were no differences in the brachial blood pressure measurements including systolic blood pressure (SBP) (nitrate: 130 ± 4 mmHg, placebo: 132 ± 5 mmHg, p=0.58), diastolic blood pressure (DBP) (nitrate: 80 ± 3 mmHg, placebo: 81 ± 3 mmHg, p= .74) and mean arterial pressure (MAP) (nitrate: 96 ± 3 mmHg, placebo: 98 ± 4 mmHg, p=0.67). There were also no significant differences in aortic pressure or stiffness. BAFMD reactive hyperaemic percent change tended to improve (nitrate: 5.7% ± 1.1, placebo: 4.1% ± 0.7, (p=0.06), and this change had a moderate effect size (ES) (Cohen’s d 0.607). Conclusions: Results from this study indicate the nitrate appears ineffective at improving exercise tolerance and vascular function in HFrEF. Future studies should explore alternative interventions to improve peripheral muscle tissue function in HFrEF.
Study 2: The effect of dietary nitrate supplementation on cardiac output and stroke volume during submaximal exercise in men with HFrEF: a pilot study.
The primary aim of this exploratory study was to determine the effect of chronic inorganic nitrate supplementation on cardiac performance during three submaximal exercise bouts. Methods: Five male patients with HFrEF (61 ± 3y) completed this pilot study. Participants consumed either the nitrate-rich beetroot juice (16 mmol nitrate) or the placebo an average of 13 ± 2 days prior to the testing visit. They completed a three-stage (15-25 watts, 25-40 watts and 35-60 watts) discontinuous exercise protocol on an echo-compatible recumbent cycle ergometer with simultaneous Doppler echocardiography. Cardiac output (Q̇) and stroke volume (SV) were derived using the Doppler velocity time integral via the Huntsman method. Results: There were significant increases in both plasma nitrate (p=0.004, ES=3.54) and nitrite (p=0.01, ES=0.82) following nitrate supplementation. Although not statistically significant (all p>0.27), the differences in Q̇during stage two and stage three had medium to large ES (stage two: nitrate: 6.4 ± .4 L∙min-1, placebo: 5.3 ±. 2 L∙min-1, ES=1.51; stage three: nitrate: 7.5 ± 0.6 L∙min-1, placebo: 6.4 ± 0.7 L∙min-1, ES=0.50) exercise. Changes in Q̇ were accompanied by medium to large ES changes in SV (stage two: ES=0.97 and stage three: ES=0.57) and medium to large increases in heart rate (HR) at rest and all exercise stages. These differences were likely mediated by a reduction in total peripheral resistance (TPR) at stage two (ES=-1.62) and stage three (ES=-0.81). Conclusions: We report potentially clinically important improvements in measures of cardiac performance during submaximal exercise following nitrate supplementation in patients with HFrEF. The initial findings from this pilot study warrant further investigation in larger and more diverse samples in order to determine the efficacy of this intervention.
Study 3: The effect of dietary nitrate supplementation on mitochondrial respiration in men with HFrEF.
The primary aim of this exploratory study was to determine the effect of chronic inorganic nitrate supplementation on parameters of mitochondrial respiration in patients with HFrEF. Methods: Seven male participants (62 ± 2y) completed this invasive study. Participants consumed the nitrate rich beetroot juice (16mmol nitrate/day) or a placebo for an average of 15 ± 2 days prior to their muscle biopsy. Muscle samples were taken from the vastus lateralis. Mitochondrial respiration was assessed using high resolution respirometry. Western blot analysis was used to assess the protein content of mechanistic target of rapamycin complex 1 (mTORC1), p38 mitogen activated protein kinase (p38MAPK), protein kinase B (Akt), and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α). Results: Plasma nitrate increased (831%, p<0.001) following supplementation. Plasma nitrite also increased (100%) but this was not statistically significant (p=0.22). There were no differences in skeletal muscle maximal oxidative phosphorylation capacity as assessed as either mass-specific (p=0.93) or mitochondrial-specific (p=0.68) respiratory function of (CI+CII)p, nor were there any significant differences in other parameters of mitochondrial respiration (all p>0.05). Similarly, there were no differences in mitochondrial content, as assessed by citrate synthase activity (p=0.73) and no differences were noted in total and phosphorylated forms of mTORC1, p38MAPK, Akt, or PGC-1α (all p>0.10). Conclusions: Short-term nitrate supplementation, as a standalone treatment, may not be an effective way to improve mitochondrial function in patients with HFrEF and, as such, it may be clinically important to combine nitrate supplementation with other interventions known to affect mitochondrial function, such as exercise training.
General Conclusions.
Short-term inorganic nitrate supplementation had no effect on exercise tolerance (Study 1-Chapter 4), peripheral tissue oxygenation (Study 1- Chapter 4), or mitochondrial respiration (Study 3- Chapter 6) in patients with HFrEF. However, it may have a meaningful clinical effect on Q̇and SV during submaximal exercise (Study 2- Chapter 5). It may also improve vascular function (Chapter 4), reduce TPR (Chapter 5) and reduce DBP and MAP during submaximal exercise (Chapter 5) in these patients. Overall the data suggest that nitrate supplementation may be used in conjunction with other pharmacological and non-pharmacological (exercise training) interventions to improve clinical outcomes in this population. This hypothesis should be explored in the future by conducting a large-scale clinical trial.
Libros sobre el tema "Mitochondrial movement":
1
Shaibani, Aziz. Ophthalmoplegia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0004.
Resumen
Ophthalmoplegia is usually chronic, and therefore diplopia is not a feature. There is enough time for the brain to suppress one image. It is amazing how much of impairment of eye movement has to occur before the patient becomes concerned or considers it as abnormal. Neglected myasthenia gravis (MG) may be confused with mitochondrial ophthalmoplegia or oculopharyngeal muscular dystrophy (OPMD) or even congenital myasthenic syndrome (CMS). Central causes of ophthalmoplegia should be ruled out first by performing doll’s eye movement. A number of cases of different types of ophthalmoplegia are presented, along with clinical and laboratory methods to differentiate them.
2
Shaibani, Aziz. Ophthalmoplegia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0004.
Resumen
Ophthalmoplegia is usually chronic and therefore diplopia is not a feature. There is enough time for the brain to suppress one image. It is amazing how much impairment of eye movement has to occur before the patient becomes concerned or considers it as abnormal. Neglected myasthenia gravis may be confused with mitochondrial ophthalmoplegia or oculopharyngeal muscular dystrophy or even congenital myasthenic syndrome. Central cause of ophthalmoplegia should be ruled out first by performing doll’s eye movement. Detailed family history looking in particular for ptosis, ophthalmoplegia, and dysphagia is diagnostically very useful. Non neurological causes of ophthalmoplegia such as severe exophthalmus, and retroorbital pathology should be considered.
3
Jolly, Elaine, Andrew Fry y Afzal Chaudhry, eds. Neurology and neurosurgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0014.
Resumen
Chapter 14 covers the basic science and clinical topics relating to neurology and neurosurgery which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers the approach to the neurological Patient, neurological examination, neurological investigations, coma, acquired brain injury, encephalopathies, alcohol and the nervous system, brainstem disorders, common cranial nerve disorders, migraine, other primary headaches, secondary headache, neuro-ophthalmology, vertigo and hearing loss, seizures and epilepsy, intracranial pressure, stroke, central nervous system infections, neuro-oncology, multiple sclerosis, Parkinson disease, other movement disorders, spinal cord disorders (myelopathy), spinal nerve root disorders (radiculopathies), motor neurone disease, peripheral nerve disorders, mitochondrial disease and channelopathies, neuromuscular junction and muscle Disorders, sleep disorders, neurological disorders in pregnancy, the neurology of HIV infection, and functional neurology.
4
Forsyth, Rob y Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.
Resumen
This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life; non-epileptic paroxysmal phenomena; functional illness, illness behaviour; headache; hydrocephalus; spina bifida and related disorders; idiopathic intracranial hypertension; infection of the CNS; congenital infection; mitochondrial disease; movement disorders; neuromuscular disease which covers neuropathy, anterior horn cell disease, and myasthenic syndromes; neurocutaneous syndromes; neurodegenerative conditions; late presentations of metabolic disease; neurotransmitter disorders; sleep disorders; stroke and intracerebral haemorrhage; tumours of the CNS; and vitamin-responsive disorders.
5
Tick, Heather y Eric B. Schoomaker. Transforming Pain Management Through the Integration of Complementary and Conventional Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190241254.003.0021.
Resumen
This chapter discusses some of the assumptions behind the evolution of the current program of pain care and explores different strategies that could inform transformative changes to the system. It addresses the role of self-care, nutrition, mind-body strategies, and movement in improving function. The emerging scientific literature on neuroplasticity, central and peripheral sensitization, energy generation, and mitochondrial dysfunction, and the functional role of fascia is explored. Health providers in a transformed system will potentially work in more diverse settings, collaborate more broadly, and engage patients in conversations driven by patient priorities and emerging evidence-based modalities. The Veterans Health Administration and the Military Health System, acting on alarming increases in the incidence of chronic pain and associated comorbidities, have become the early adopters of transformative policies. Since pain is the most common cause for a healthcare visit, this chapter should be of interest to all healthcare providers, complementary, integrative, and conventional.
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McShane, Tony, Peter Clayton, Michael Donaghy y Robert Surtees. Neurometabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0213.
Resumen
Various disorders result from genetically determined abnormalities of enzymes, the metabolic consequences of which affect the development or functioning of the nervous system. The range of metabolic disturbances is wide, as is the resultant range of clinical syndromes. Although most occur in children, some can present in adult life, and increasing numbers of affected children survive into adult life. In some, specific treatments are possible or are being developed. The last 20 years has seen a considerable expansion in our understanding of the genetic and metabolic basis for many neurological conditions. Particular clinical presentations of neurometabolic disorders include ataxias, movement disorders, childhood epilepsies, or peripheral neuropathy. Detailed coverage of the entire range of inherited metabolic diseases of the nervous system is available in other texts (Brett 1997; Scriver et al. 2001; Menkes et al. 2005).Treatment is possible for some metabolic diseases. For instance, the devastating neurological effects of phenylketonuria have been recognized for many years. Neonatal screening for this disorder and dietary modification in the developed world has removed phenylketonuria from the list of important causes of serious neurological disability in children. This success has led to new challenges in the management of the adult with phenylketonuria and unexpected and devastating effect of the disorder on the unborn child of an untreated Phenylketonuria mother. More recently Biotinidase deficiency has been recognized as an important and easily treatable cause of serious neurological disease usually presenting with early onset drug resistant seizures. This and some other neurometabolic diseases can be identified on neonatal blood screening although a full range of screening is not yet routine in the United Kingdom. More disorders are likely to be picked up at an earlier asymptomatic stage as the sophistication of screening tests increases (Wilcken et al. 2003; Bodamer et al. 2007).Although individual metabolic disorders are rare, collectively such disorders are relatively common. In reality most clinicians will see an individual condition only rarely in a career. Furthermore, patients with certain rare conditions are often concentrated in specialist referral centres, further reducing the exposure of general and paediatric neurologists to these disorders. A recent study into progressive intellectual and neurological deterioration, PIND, gives some information about the relative frequency and distribution of some childhood neurodegenerative diseases in the United Kingdom (Verity et al. 2000; Devereux et al. 2004). Although primarily designed to identify any childhood cases of variant Creutzfeldt- Jakob disease, the study also provided much information about the distribution of neurometabolic disease in children in the United Kingdom. The commonest five causes of progressive intellectual and neurological deterioration over 5 years were Sanfilippo syndrome, 41 cases, adrenoleukodystrophy, 32 cases, late infantile neuronal ceroid lipofuschinosis, 32 cases, mitochondrial cytopathy, 30 cases, and Rett syndrome, 29 cases. Notably, geographical foci of these disorders were also found and correlate with high rate of consanguinity in some local populations.
Capítulos de libros sobre el tema "Mitochondrial movement":
1
Finsterer, Josef y Salma Majid Wakil. "Genetics of Mitochondrial Disease with Focus on Movement Disorders". En Movement Disorder Genetics, 411–30. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17223-1_18.
2
Mehta, Arpan R., Siddharthan Chandran y Bhuvaneish T. Selvaraj. "Assessment of Mitochondrial Trafficking as a Surrogate for Fast Axonal Transport in Human Induced Pluripotent Stem Cell–Derived Spinal Motor Neurons". En Methods in Molecular Biology, 311–22. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_16.
Resumen
AbstractAxonal transport is essential for the development, function, and survival of the nervous system. In an energy-demanding process, motor proteins act in concert with microtubules to deliver cargoes, such as organelles, from one end of the axon to the other. Perturbations in axonal transport are a prominent phenotype of many neurodegenerative diseases, including amyotrophic lateral sclerosis. Here, we describe a simple method to fluorescently label mitochondrial cargo, a surrogate for fast axonal transport, in human induced pluripotent stem cell–derived motor neurons. This method enables the sparse labeling of axons to track directionality of movement and can be adapted to assess not only the cell autonomous effects of a genetic mutation on axonal transport but also the cell non-autonomous effects, through the use of conditioned medium and/or co-culture systems.
3
Lehninger, Albert L., Ernesto Carafoli y Carlo S. Rossi. "Energy-Linked Ion Movements in Mitochondrial Systems". En Advances in Enzymology - and Related Areas of Molecular Biology, 259–320. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470122747.ch6.
4
Kemble, R. J., S. Gabay-Laughnan y J. R. Laughnan. "Movement of Genetic Information Between Plant Organelles: Mitochondria-Nuclei". En Genetic Flux in Plants, 79–87. Vienna: Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8765-4_5.
5
Wolkowicz, Paul. "Evidence for Hexagonal II Phase Lipid Involvement in Mitochondrial Ca2+ Movements". En Advances in Experimental Medicine and Biology, 131–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0007-7_15.
6
Somlyo, A. V., M. Bond, R. Broderick y A. P. Somlyo. "Calcium and Magnesium Movements Through Sarcoplasmic Reticulum, Endoplasmic Reticulum, and Mitochondria". En Advances in Experimental Medicine and Biology, 221–29. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0007-7_24.
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Lonsdale, David M. "Movement of Genetic Material Between the Chloroplast and Mitochondrion in Higher Plants". En Genetic Flux in Plants, 51–60. Vienna: Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8765-4_3.
8
Wong, Agnes. "Disorders Affecting the Extraocular Muscles". En Eye Movement Disorders. Oxford University Press, 2008. http://dx.doi.org/10.1093/oso/9780195324266.003.0023.
Resumen
Chronic progressive external ophthalmoplegia (CPEO) occurs in 90% of patients with mitochondrial myopathy. It is characterized by a slowly progressive ptosis and ophthalmoplegia. The ophthalmoplegia is usually preceded by ptosis for months to years, and downgaze is usually intact. Kearns-Sayre Syndrome is a subtype of chronic progressive external ophthalmoplegia. Most cases are sporadic and associated with single deletions of mitochondrial DNA. Ragged-red fibers are seen on light microscopy (using modified Gomori trichrome stain). ■ Due to accumulation of enlarged mitochondria under the sarcolemma of affected muscles ■ Found in skeletal muscles, orbicularis, and extraocular muscles ■ On electron microscopy, the mitochondria contain paracrystalline (“parking lot”) inclusions and disorganized cristae that are sometimes arranged concentrically. 1. Muscle biopsy (e.g., deltoid) 2. ERG 3. Electrocardiogram (EKG) 4. Genetic testing There is no effective treatment for CPEO. Maintaining a high-lipid, low-carbohydrate diet, taking co-enzyme Q10, biotin, or thiamine, and avoiding medications such as valproate and phenobarbital may be helpful. ■ MELAS stands for mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes. ■ Maternally inherited; caused by point mutations of mitochondrial DNA (A3243G mutation accounts for about 80% of all cases) ■ Clinical features 1. Strokelike episodes before age 40 (hallmark feature) 2. Encephalopathy characterized by developmental delay, seizures, or dementia 3. Mitochondrial dysfunction manifested as lactic acidosis or ragged-red fibers 4. Ophthalmoplegia 5. Optic atrophy and pigmentary retinopathy 6. Diabetes mellitus and hearing loss ■ MNGIE stands for mitochondrial neuro-gastrointestinal encephalomyopathy. ■ Autosomal recessive; caused by mutations in the nuclear gene ECGF1, resulting in thymidine phosphorylase deficiency, which in turn causes deletions, duplications, and depletion of mitochondrial DNA ■ Clinical features: ophthalmoplegia, peripheral neuropathy, leukoencephalopathy, and gastrointestinal symptoms (recurrent nausea, vomiting, or diarrhea) with intestinal dysmotility SANDO stands for sensory ataxic neuropathy, dysarthria, and ophthalmoplegia. It is sporadic and is caused by multiple deletions of mitochondrial DNA.
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Schapira, A. H. V. y S. Przedborski. "Mitochondrial Dysfunction". En Encyclopedia of Movement Disorders, 181–84. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00265-3.
10
Simon, D. K. "Mitochondrial Encephalopathies". En Encyclopedia of Movement Disorders, 185–87. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00351-8.
Actas de conferencias sobre el tema "Mitochondrial movement":
1
Pajic, Tanja, Miroslav Zivic, Mihailo Rabasovic, Aleksandar Krmpot y Natasa Todorovic. "THE DAMPENING OF LIPID DROPLET OSCILLATORY MOVEMENT IN NITROGEN STARVED FILAMENTOUS FUNGI BY A LOW DOSE OF MITOCHONDRIAL RESPIRATION INHIBITOR". En 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.226p.
Resumen
Lipid droplets (LDs) are small mobile organelles conserved in all eukaryotic cells. We wanted to test if the LD movement can be muffled by an incomplete inhibition of mitochondrial respiration, induced by treating hyphae of filamentous fungus Phycomyces blakesleeanus with 0.5 mM sodium azide. Nitrogen starved hyphae were used, in order to obtain LDs in larger sizes and numbers. The data obtained unequivocally showed: 1. Sodium azide treatment dramatically reduces the LD velocity and the distances LDs travel; 2. LDs in both controls and in azide-treated hyphae oscillate in a small confined space instead of travelling through the cell; 3. Azide-treated LDs oscillate less frequently and in smaller confinement than controls.
2
Perner, Petra. "The Study of the Internal Mitochondrial Movement of the Cells by Data Mining with Prototype-Based Classification". En 2014 International Conference on Intelligent Networking and Collaborative Systems (INCoS). IEEE, 2014. http://dx.doi.org/10.1109/incos.2014.30.
3
Yang, Liu, Chao Ma y Wen li Chen. "The observation of mitochondrial movement and ATG5 position in Arabidopsis during the process of infection with virulent and avirulent P. syringae strains". En SPIE BiOS, editado por Samuel Achilefu y Ramesh Raghavachari. SPIE, 2012. http://dx.doi.org/10.1117/12.907215.
4
Ferreira, Marcos Venâncio Araújo, Rafael Henrique Neves Gomes, Fabiana Carla dos Santos Correia, Mariana Beber Chamon, Sérgio Roberto Pereira da Silva Júnior, Isadora Chain Lima, Marcus Vinicius de Sousa, Murilo Justino de Almeida, Daniel Sabino de Oliveira y Thiago Cardoso Vale. "Idiopathic basal ganglia calcification and Hoarding disorder". En XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.499.
Resumen
Introduction: Basal ganglia calcifications are associated with many neurological and metabolic disorders, being present also on asymptomatic patients. It may present in its primary form, including familial and sporadic cases. Its secondary form is associated especially to hypoparathyroidism but also associated to infections, toxic exposure, rheumatologic diseases, mitochondrial disorders. It has an heterogenous clinical presentation with movement disorders and neuropsychiatric symptoms. Case presentation: A 66-year-old patient presented with a progressive hoarding disorder for the last six years. In the last 2 years started an aggressive behavior, loss of acquired skills, urinary incontinence, sleep-wake cicle disorder and one episode of focal seizure. Physical examination revealed bilateral asymmetrical tremor, bradykinesia and cogwheel rigidity. MoCA test was 23/30 for 12 years of schooling. Brain Computed Tomography showed calcifications in basal ganglia affecting predominantly pallidum e thalamus and cerebellar hemispheres. Brain Magnetic Resonance Imaging revealed hypointensites in the same regions and in nucleus caudate suggestive of calcification. Laboratory testing for endocrine and calcium metabolism was normal. No clinical signs of other disorders. Discussion: We presented a case of probable Idiopathic Basal Ganglia Calcification initially treated as a hoarding disorder. The normal laboratory results, lack of other clinical signs and familial history suggests a primary sporadic form that might be due to de novo mutations or transmitted by asymptomatic parent. The most commonly mutations in SLC20A2, PDGFB and PDGFRB but genetic testing is commonly unavailable. Parkinsonism is the most common movement disorder and the neuropsychiatric features include cognitive impairment, psychotic and obsessive compulsive disorders. Conclusion: This case demonstrates that attention is needed to the progression of psychiatric disorders suggesting some rare neurological disorders.
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Reznikov, Konstantin M. y Pavel D. Kolesnichenko. "THE EFFECT OF DRUGS ON THE THREE-DIMENSIONAL STRUCTURE OF CARDIOMYOCYTES". En International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.24.
Resumen
In experimental myocardial infarction the occurrence of contracture of the sarcomeres, while giperkeratoza
adjacent sections of the cell and movement of mitochondria. Drugs (korglikon, procainamide, potassium
orotate) have different impacts on these processes.
6
Pelloux, S., C. Ojeda y Y. Tourneur. "An original method to quantify mitochondria movement in cultured cardiomyocytes". En Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588229.
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Sardet, C., C. Rouvière, B. Flannery y J. Davoust. "Time lapse confocal microscopy of mitochondrial movements in ascidian embryos". En The living cell in four dimensions. AIP, 1991. http://dx.doi.org/10.1063/1.40578.
Informes sobre el tema "Mitochondrial movement":
1
Sadot, Einat, Christopher Staiger y Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, septiembre de 2011. http://dx.doi.org/10.32747/2011.7592652.bard.
Resumen
In the original proposal we planned to focus on two proteins related to the actin cytoskeleton: TCH2, a touch-induced calmodulin-like protein which was found by us to interact with the IQ domain of myosin VIII, ATM1; and ERD10, a dehydrin which was found to associate with actin filaments. As reported previously, no other dehydrins were found to interact with actin filaments. In addition so far we were unsuccessful in confirming the interaction of TCH2 with myosin VIII using other methods. In addition, no other myosin light chain candidates were found in a yeast two hybrid survey. Nevertheless we have made a significant progress in our studies of the role of myosins in plant cells. Plant myosins have been implicated in various cellular activities, such as cytoplasmic streaming (1, 2), plasmodesmata function (3-5), organelle movement (6-10), cytokinesis (4, 11, 12), endocytosis (4, 5, 13-15) and targeted RNA transport (16). Plant myosins belong to two main groups of unconventional myosins: myosin XI and myosin VIII, both closely related to myosin V (17-19). The Arabidopsis myosin family contains 17 members: 13 myosin XI and four myosin VIII (19, 20). The data obtained from our research of myosins was published in two papers acknowledging BARD funding. To address whether specific myosins are involved with the motility of specific organelles, we cloned the cDNAs from neck to tail of all 17 Arabidopsis myosins. These were fused to GFP and used as dominant negative mutants that interact with their cargo but are unable to walk along actin filaments. Therefore arrested organelle movement in the presence of such a construct shows that a particular myosin is involved with the movement of that particular organelle. While no mutually exclusive connections between specific myosins and organelles were found, based on overexpression of dominant negative tail constructs, a group of six myosins (XIC, XIE, XIK, XI-I, MYA1 and MYA2) were found to be more important for the motility of Golgi bodies and mitochondria in Nicotiana benthamiana and Nicotiana tabacum (8). Further deep and thorough analysis of myosin XIK revealed a potential regulation by head and tail interaction (Avisar et al., 2011). A similar regulatory mechanism has been reported for animal myosin V and VIIa (21, 22). In was shown that myosin V in the inhibited state is in a folded conformation such that the tail domain interacts with the head domain, inhibiting its ATPase and actinbinding activities. Cargo binding, high Ca2+, and/or phosphorylation may reduce the interaction between the head and tail domains, thus restoring its activity (23). Our collaborative work focuses on the characterization of the head tail interaction of myosin XIK. For this purpose the Israeli group built yeast expression vectors encoding the myosin XIK head. In addition, GST fusions of the wild-type tail as well as a tail mutated in the amino acids that mediate head to tail interaction. These were sent to the US group who is working on the isolation of recombinant proteins and performing the in vitro assays. While stress signals involve changes in Ca2+ levels in plants cells, the cytoplasmic streaming is sensitive to Ca2+. Therefore plant myosin activity is possibly regulated by stress. This finding is directly related to the goal of the original proposal.