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Widén, Jonas. "Automatisk test för myoelektroder." Thesis, Linköping University, Department of Science and Technology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-2338.
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Denna rapport avhandlar en tio veckors period på Otto Bock Scandinavia AB i Norrköping. Där analyserades en manuell testutrusning för funktionstest av myoelektroder, för att mäta muskelspänningar. Myoelektroderna används till att styra gripfunktionen hos handproteser, för patienter som förlorat en del av sin arm. Analysen ska resultera i att ge ett förslag på en automatiserad test av elektroderna. En stor del av rapporten består av studier kring hur testmetoderna fungerar och elektrodernas användning och funktion. Slutligen behandlas även ett förslag på en automatiserad test för elektroderna.
The present report concerns a ten weeks period at Otto Bock Scandinavia AB in Norrköping. An analyse of a manual test equipment for testing myoelectrodes, who is used to measure muscle potential in the arm. The myoelectrodes are used to control a grip function on hand prostheses, which is used by persons who has lost their lower arm. The analyse should result in a proposal of an automation of the manual test equipment for the electrodes.
A significant part of the report discusses the function of test methods and who the electrodes are used for and their function. Finally, discusses a proposal on an automated test for the electrodes.
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Faralli, Hervé. "Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22045/document.
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L’unité cellulaire du muscle squelettique est la myofibre, un syncytium hautement spécialisé générant la contraction musculaire. Au cours de la croissance et de la régénération musculaire, les cellules satellites quiescentes (cellules souches) du muscle squelettique adulte sont activées, prolifèrent puis fusionnent formant de nouvelles fibres. A l’aide d’un modèle murin de régénération et de cultures primaires, j’ai identifié TSHZ3 comme un nouveau marqueur des cellules satellites quiescentes et activées. Dans la lignée cellulaire C2C12, j’ai mis en évidence un effet répresseur spécifique de Tshz3 sur la différenciation myogénique. L’entrée des myoblastes dans la voie de différenciation terminale est déclenchée par le facteur Myogenin (MYOG). L’activation de la transcription du gène myogenin (Myog) est dépendante du facteur MYOD et fait intervenir le complexe de remodelage de la chromatine SWI/SNF. In vitro, TSHZ3 interagit avec BAF57 une sous unité du complexe SWI/SNF. TSHZ3 réprime l’activation dépendante de MYOD sur le promoteur proximal de Myog et cette répression dépend en partie de la présence de BAF57. L’activité répressive et la cinétique d’expression de Tshz3, indique que TSHZ3 pourrait empêcher l’activation prématurée du promoteur Myog lors de la prolifération des cellules satellites activées. TSHZ3 pourrait ainsi participer aux mécanismes de régulation permettant de contrôler l’équilibre entre prolifération, différenciation et renouvellement des progéniteurs myogéniquesSkeletal muscles are made of several units called myofibers, a syncitium into which muscular contraction is generated. During the muscle growth and repair, the quiescent Satellite Cells (SCs; adult stem cells) become activated, proliferate and differentiate to form new multinucleated myofibers. In animal model and primary culture, I found that, Tshz3 was strongly expressed in the quiescent and activated satellite cells.In C2C12 myoblast cells, I showed a specific repressive effect of TSHZ3 on the myogenic differentiation. The terminal differentiation of the myoblastes is trigger by Myogenin (Myog). The transcriptional activation of Myog promoter involves MYOD and the SWI/SNF remodelling complex. In vitro, I showed that TSHZ3 interacts with BAF57, a subunit of the SWI/SNF complex. TSHZ3 represses the MYOD-dependant activation on the Myog promoter. This specific repression involves in part BAF57.The repressive activity of and the temporal dynamic of expression of Tshz3, indicated that TSHZ3 potentially is required to impede the premature activation of the Myog promotor during the SCs proliferation. These results suggest that TSHZ3 plays important roles in the molecular mechanisms operating in activated SCs when there are poised between proliferation, differentiation and self renewal of muscular progenitors
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Brunelli, Roberta de Matos 1985. "Os efeitos do laser de baixa potência no processo de reparo muscular após criolesão em ratos = The effects of low-level laser therapy on muscle healing process after cryolesion." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308777.
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Orientadores: Daniela Cristina Carvalho de Abreu, Alberto Cliquet JuniorDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-22T07:19:52Z (GMT). No. of bitstreams: 1 Brunelli_RobertadeMatos_M.pdf: 1872583 bytes, checksum: 5ce843f202a01778398ee2807e19dd08 (MD5) Previous issue date: 2013
Resumo: O objetivo deste estudo foi verificar os efeitos da laserterapia de baixa potência no comprimento de onda ?=780nm entre diferentes períodos de tratamento 7, 14 e 21 dias e verificar a dose (10J/cm2 ou 50J/cm2) que promove melhor reparo muscular através das análises histopatológicas e imunohistoquímicas. Foram utilizados 54 ratos machos divididos em 3 grupos: GC: grupo controle (criolesão, sem tratamento); G10: criolesão do músculo tibial anterior (TA) e tratados com laser dose 10J/cm² e G50: criolesão do músculo TA e tratados com laser dose 50J/cm² que foram subdivididos em 3 subgrupos (n=6): 7, 14 e 21 dias de tratamento. Os achados histopatológicos revelaram maior organização das fibras musculares dos grupos tratados com laser 10J/cm² e 50J/cm² durante os períodos 7 e 14 dias em relação ao grupo controle; no período 21 dias os grupos apresentaram semelhanças na reparação tecidual. Em relação à área da lesão os grupos tratados com laser 10J/cm² e 50J/cm² durante 7 dias obtiveram diminuição significativa (p ? 0.05) da área da lesão em relação ao grupo controle, sendo que os grupos 14 e 21 dias não apresentaram diferenças significativas entre eles. Na contagem dos vasos o grupo tratado com laser 10J/cm² no 14° dia apresentou aumento dos vasos em relação ao grupo tratado com dose 50J/cm², mas não em relação ao grupo controle. Nos tempos de 7 e 21 dias os grupos não apresentaram diferença significativa entre si. Com relação às análises imunohistoquímicas da myoD no período de 7 dias os grupos tratados com laser 10J/cm² e 50J/cm² apresentaram maior imunomarcação comparada com o grupo controle, no período 14 e 21 dias a imunomarcação estava ausente. A imunomarcação da miogenina estava presente de forma semelhante nos períodos 7 e 14 dias para os três grupos analisados e no período 21 dias a imunomarcação da miogenina estava ausente em todos os grupos experimentais. Os resultados mostraram que o laser possui efeitos positivos no reparo muscular
Abstract: The objective of this study was to assess the effects of 780nm low-level laser therapy at different periods of 7, 14 and 21 days after cryolesion, including the dose (10 or 50J/cm2) to promote a better muscle repair evidenced by histopathological and immumohistochemical analyses. Fifty-four male rats were divided into three groups: injured control group (CG) - injured animals without any treatment; injured 780nm laser treated group, at 10 J/cm² (G10) and injured 780nm laser treated group, at 50 J/cm² (G50). Each group was divided into 3 subgroups (n=6): 7, 14 and 21 days post-injury. Histopathological findings revealed better-organized muscle fibers in the G10 and G50 during the periods of 7 and 14 days compared to CG. The G10 and G50 during 7 days showed a significant reduction (p? 0.05) of lesion area compared to CG, without differences between groups treated for 14 and 21 days. The G10 showed an increase of the amount of vessels after 14 days compared to the G50, but not in relation to controls. With regard to the immumohistochemical analyses of the MyoD factor, The G10 and G50 during 7 days showed higher concentrations of immunomarkers than controls. Myogenin immunomarkers were similarly observed at days 7 and 14 in all three groups analyzed, whereas immunomarkers were found in none of the groups after 21 days of laser therapy. The results showed that laser has positive effects on muscle repair
Mestrado
Fisiopatologia Cirúrgica
Mestra em Ciências
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Sawyer, Debbie Ann. "Analogues of myo-inositol and D-myo-inositol 1,4,5-triphosphate." Thesis, University of Leicester, 1993. http://hdl.handle.net/2381/33883.
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Oelsner, Malte. "Myon-Einfang durch den 3He-Kern." [S.l. : s.n.], 1999. http://deposit.ddb.de/cgi-bin/dokserv?idn=957152892.
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Arponen, Felicia. "Mifepristonbehandling vid myom : Effekt- och säkerhetsaspekter." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-94171.
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Bakgrund: Myom är den vanligaste gynekologiska benigna tumören hos kvinnor i fertil ålder. Det finns idag läkemedelsbehandlingar, invasiva ingrepp och icke-invasiva ingrepp vid behandling av myom. Utvecklingen av läkemedel mot myom är lågprioriterat, eftersom de främst är benigna och snarare leder till sjuklighet än dödlighet. De läkemedel som idag används vid behandling av myom är ulipristal, GnRH-agonister, NSAID, tranexamsyra, p-piller eller hormonspiral. Ulipristal och GnRH-agonister har utöver förbättring av symtom som alla de senast nämnda, en effekt på reducering av myomstorlek. Icke-invasiva ingrepp innefattar idag myolys, embolisering av arteria uterina och fokuserad ultraljudskirurgi under MRI-vägledning, framtagna för att slippa operativa ingrepp. Myomektomi och hysterektomi är två operativa ingrepp som genomförs om inga andra behandlingar fungerar, eftersom de medför en längre återhämtningstid och en större risk för komplikationer. Mifepriston är en antiprogesteron, vilket innebär att den hämmar progesterons effekt. Progesteron i sin tur spelar en stor roll i utvecklingen av ett myom. Behandling med läkemedlet har i många olika studier visat goda resultat både i avseende på myomstorlek, symtom, livskvalité och biverkningar. Syfte: Syftet med examensarbetet var att undersöka om mifepriston är ett säkert och effektivt läkemedel vid behandling av myom hos kvinnor. Metod: Examensarbetet är en litteraturstudie och baseras på 6 olika randomiserade kontrollerade vetenskapliga studier som undersökte mifepristons effekt och säkerhet vid behandling av myom. Studierna hämtades från PubMed. Resultat: Samtliga studier visade en reducering i myomvolym, en förbättring av symtom och milda biverkningar med olika doseringar av mifepriston vid behandling av myom. I 2 av studierna undersöktes livskvalitén vilket ökade hos de personer som behandlades med mifepriston. Slutsats: Det är svårt att dra generella slutsatser vilken dos och behandlingstid som är optimala på grund av de olika behandlingstiderna, doseringarna och studieuppläggen som användes i samtliga studier. Dock har mifepriston en god effekt avseende på reducering i myomstorlek, symtom, biverkningar och livskvalité. Det krävs dock fler studier för att säkerställa dosering och behandlingstid samt fler jämförelser med andra behandlingsalternativ som idag finns för behandling av myom.
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Tripet, Angèle. "The exclusive production of r0 [rho 0] mesons in polarized muon nucleon scattering within the SMC experiment at CERN." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968580343.
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ZOUBIAN, MARWAN. "La myose stromale endolymphatique (m. S. E. )." Saint-Etienne, 1988. http://www.theses.fr/1988STET6020.
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Xiao, Lei. "Transcriptional Regulation of the Xenopus MyoD Gene." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-11960.
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Styer, Jean Christine. "Regulating Inositol Biosynthesis in Plants: Myo-Inositol Phosphate Synthase and Myo-Inositol Monophosphatase." Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/9870.
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Inositol is important for normal growth and development in plants. The regulation of the inositol biosynthetic enzymes, myo-inositol phosphate synthase (MIPS) and myo-inositol monophosphatase (IMP) was investigated. The specific aims of this research were (1) to develop a tool to study MIPS protein accumulation in a model plant system, Arabidopsis thaliana (At) and potentially other plant species and (2) to determine the spatial expression patterns of Lycopersicon esculentum IMP-2 (LeIMP-2) at the cellular level.
Myo-inositol phosphate synthase (mips) genes have been identified in plants, animals, fungi and bacteria. Alignment of the predicted amino acid sequences of AtMIPS-1, -2 and Glycine max MIPS (GmMIPS) indicated that AtMIPS-1 and GmMIPS are 87% identical, and AtMIPS-2 and GmMIPS are 89% identical. Based on these data, a Gmmips cDNA was fused at the N-terminus to a 6X histidine tag (5' GAC GAC GAC GAC GAC GAC 3'), cloned into an overexpression vector and overexpressed in E. coli. The fusion protein, HISMIPS, was extracted using denaturing conditions and purified using Ni2+ affinity chromatography. Anti-GmMIPS antiserum from rabbit detected the recombinant HISMIPS protein (76 kD), and GmMIPS (64 kD). Affinity purification by subtractive chromatography yielded anti-GmMIPS antibody that detected
The tomato inositol monophosphatase (Leimp) genes are a developmentally regulated multigene family. From analysis of sequences, Leimp-2 is intron-less and has the putative start site of translation located at +108 bp downstream from the putative start site of transcription. Investigation of the 5â UTR revealed the 3' end of a partial open reading frame (338 bp) highly homologous to the gene for calmodulin. Three light responsive elements and a cold responsive element were also identified in the 5' UTR.
Transgenic Leimp-2::uidA plants were produced using the existing construct of the Leimp-2 promoter fused to the uidA gene (J. Keddie, University of California at Berkeley). Seedlings were perserved and sectioned. Using histological techniques, the analysis of the Leimp-2 promoter::uidA transgenic seedlings revealed that the Leimp-2 promoter causes expression at the base of the shoot apex and within leaflets of the first set of fully expanded leaves. Further, Leimp-2 promoter expression was localized to epidermal and cortex cells on the abaxial side of the 1st and 2nd fully expanded compound leaves.
These studies of MIPS and IMP expression lay a foundation for a better understanding of the regulation of inositol biosynthesis in Arabidopsis, tomato, and other plant species.
Master of Science
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Scionti, Isabella. "Epigenetic Regulation of Skeletal Muscle Differentiation." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN084/document.
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LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non histones en affectant leurs activités ou stabilités. Des approches fonctionnelles d’inactivation de Lsd1 ou Phf2 chez la souris ont démontré l’implication de ces enzymes dans l'engagement des cellules progénitrices au cours de la différenciation. La myogenèse est l'un des exemples les mieux caractérisés sur la façon dont les cellules progénitrices se multiplient et se différencient pour former un organe fonctionnel. Elle est initiée par une expression temporelle spécifique des gènes régulateurs cibles. Parmi ces facteurs, MYOD est un régulateur clé de l'engagement dans la différenciation des cellules progénitrices musculaires. Bien que l’action de MYOD au cours de la différenciation cellulaire ait été largement étudiée, peu de chose sont connus sur les événements de remodelage de la chromatine associés à l'activation de l'expression de MyoD. Parmi les régions régulatrices de l'expression de MyoD, la région Core Enhancer (CE) qui est transcrite en ARN activateur non codant (CEeRNA) a été démontrée pour contrôler l'initiation de l'expression de MyoD au cours de l'engagement de myoblastes dans la différenciation.Nous avons identifié LSD1 et PHF2 comme des activateurs clés du CE de MyoD. L'invalidation in vitro et in vivo de LSD1 ou l'inhibition de l'activité enzymatique de LSD1 empêche le recrutement de l'ARN PolII sur le CE, empêchant l’expression du CEeRNA. D’après nos résultats, l'expression forcée du CEeRNA restaure efficacement l'expression de MyoD et la fusion myoblastique en l'absence de LSD1. De plus, PHF2 interagit avec LSD1 en régulant sa stabilité protéique.En effet, l'ablation in vitro de PHF2 entraîne une dégradation massive de LSD1 et donc une absence d'expression du CEeRNA. Cependant, toutes les modifications d'histones qui ont lieu dans la région du CE lors de l'activation de la différenciation ne peuvent pas être directement attribuées à l'activité enzymatique de LSD1 ou PHF2. Ces résultats soulèvent la question de l'identité des partenaires de LSD1 et PHF2, qui co-participeraient à l'expression du CEeRNA et donc à l'engagement des myoblastes dans la différenciation cellulaireLSD1 and PHF2 are lysine de-methylases that can de-methylate both histone proteins, influencing gene expression and non-histone proteins, affecting their activity or stability. Functional approaches using Lsd1 or Phf2 inactivation in mouse have demonstrated the involvement of these enzymes in the engagement of progenitor cells into differentiation. One of the best-characterized examples of how progenitor cells multiply and differentiate to form functional organ is myogenesis. It is initiated by the specific timing expression of the specific regulatory genes; among these factors, MYOD is a key regulator of the engagement into differentiation of muscle progenitor cells. Although the action of MYOD during muscle differentiation has been extensively studied, still little is known about the chromatin remodeling events associated with the activation of MyoD expression. Among the regulatory regions of MyoD expression, the Core Enhancer region (CE), which transcribes for a non-coding enhancer RNA (CEeRNA), has been demonstrated to control the initiation of MyoD expression during myoblast commitment. We identified LSD1 and PHF2 as key activators of the MyoD CE. In vitro and in vivo ablation of LSD1 or inhibition of LSD1 enzymatic activity impaired the recruitment of RNA PolII on the CE, resulting in a failed expression of the CEeRNA. According to our results, forced expression of the CEeRNA efficiently rescue MyoD expression and myoblast fusion in the absence of LSD1. Moreover PHF2 interacts with LSD1 regulating its protein stability. Indeed in vitro ablation of PHF2 results in a massive LSD1 degradation and thus absence of CEeRNA expression. However, all the histone modifications occurring on the CE region upon activation cannot be directly attributed to LSD1 or PHF2 enzymatic activity. These results raise the question of the identity of LSD1 and PHF2 partners, which co-participate to CEeRNA expression and thus to the engagement of myoblast cells into differentiation
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Zhang, Hong. "Regulation of Skeletal Muscle Development And Differentiation by Ski." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1226938149.
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Armour, Christine. "Regulation of MyoD induced myogenesis in P19 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq26299.pdf.
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Maguire, Richard John. "Identifying targets of MyoD in myogenic stem cells." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516609.
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Hamed, Munerah. "Effect of p300 HAT Activity on Myogenic Differentiation." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23707.
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Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
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Sandoval, Nuñovero Jose Maria. "Desarrollo de aplicaciones con Myo." Bachelor's thesis, Universidad Peruana de Ciencias Aplicadas (UPC), 2019. http://hdl.handle.net/10757/625478.
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El accidente cerebrovascular es la principal causa de discapacidad a largo plazo en los adultos mayores en el Perú y el mundo. Una de las principales consecuencias que estas personas sufren es el debilitamiento y pérdida de la funcionalidad de manera parcial o total de las extremidades superiores; lo que puede hacer difícil la vida independiente. Sin embargo, la mayoría de pacientes podrían recuperarse ejecutando, de manera independiente, los ejercicios de repeticiones diarias de movimientos en las extremidades afectadas. Lamentablemente, los pacientes no realizan los ejercicios recomendados por el terapeuta debido a que los consideran monótonos y aburridos.
Por ello, en este trabajo se implementó un sistema de telerehabilitación basado en juegos que pretenden motivar a los pacientes para que realicen los movimientos o ejercicios necesarios para recuperarse; así como también lograr la adherencia a su régimen prescrito por el terapeuta, lo que aumenta las posibilidades de una recuperación significativa. En síntesis, el presente proyecto representa una gran oportunidad y desafío para comprobar que la propuesta logra más adherencia que la rehabilitación tradicional.
A continuación, en el primer capítulo se expondrá el proyecto y sus objetivos a mayor detalle. Luego, el segundo capítulo, documentará los Student Outcomes cumplidos en este proyecto. En el tercer capítulo se analizará la situación actual de la herramienta Myo Armband la cual permitirá desarrollar aplicaciones orientadas a la rehabilitación, debido a la presencia de electromiógrafos en su composición. Después, en el cuarto capítulo se detallarán los conceptos necesarios para el propio entendimiento del proyecto y el problema identificado. A continuación, en el quinto capítulo se presentará el desarrollo y aporte final del proyecto. En el sexto capítulo se describirá como se llevó a cabo la gestión del proyecto. Finalmente, se listarán las conclusiones propuestas para el proyecto.Strokes are the main cause of long-term disability in elderly adults in Peru and in the world. One of the major consequences these people undergo is weakening and partial or full upper limbs functionality loss, which can hinder independent living. Nonetheless, most patients could recover by doing self-consciously daily repetition movement exercises in the weakened limbs. Pitifully, patients do not do the exercises by themselves as their therapist suggested due to the fact that they consider the exercises to be monotonous and dull. Therefore, in this work, a telerehabilitation system based on games was implemented that aims to motivate patients to perform exercises or necessary movements to convalesce themselves; as well as achieving adherence to their regime prescribed by the therapist, increasing the changes of an astonishing recovery. In summary, the present project represents a great opportunity and challenge to verify that the proposal achieves more adherence than traditional rehabilitation. Chapter one explores the project and its objectives in greater detail. Chapter two documents the Student Outcomes fulfilled in this project. Chapter three analyzes the current situation of of the Myo Armband tool which will allow the development of applications oriented to rehabilitation, due to the presence of electromyographs in its composition. Chapter four details the concepts needed to identify and understand the problem space. Chapter five presents the project's development and our contributions. Chapter six describes how project management was carried out. Finally, conclusions generated from this project are listed.
Tesis
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Stuelsatz, Pascal. "Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse." Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13748/document.
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Calpaïne 3 est une cystéine protéase retrouvée principalement au niveau du tissu musculaire. Cette enzyme joue un rôle clef dans le maintient de l’intégrité des fibres musculaires. En effet, des mutations au niveau du gène de calpaïne 3 ont été identifiées comme étant responsables d’une dystrophie musculaire autosomale récessive, la LGMD2A (Limb-girdle muscular dystrophy type 2A), caractérisée par une atrophie progressive des muscles des ceintures scapulaires et pelviennes. Nos travaux montrent que calpaïne 3 inhibe l’activité transcriptionnelle de MyoD. Ce facteur de transcription myogénique (MRF) joue un rôle central dans le contrôle de la myogenèse aussi bien au cours du développement embryonnaire que chez un individu adulte au cours du processus de régénération musculaire. Cette diminution d’activité transcriptionnelle a lieu aussi bien dans des cellules myoblastiques (C2C12) que fibroblastiques (C3H10T1/2). Par contre calpaïne 3 ne modifie pas l’activité transcriptionnelle des autres MRFs (Myf5, myogénine ou MRF4). Nous avons pu montrer que calpaïne 3 affecte spécifiquement l’activité transcriptionnelle de MyoD en entraînant une diminution de son niveau protéique (Western-blot, microscopie confocale), sans affecter son niveau d’ARNm (RT-QPCR). De plus, des expériences de détermination de la demi-vie protéique ont pu montrer que calpaïne 3 intervenait sur la dégradation protéique de MyoD. Des expériences sont en cours afin de déterminer si calpaïne 3 hydrolyse directement ou non le facteur MyoD. Nos travaux montrent que l’hydrolyse de MyoD induite par calpaïne 3 représente une voie parallèle à celle du système protéolytique protéasome ubiquitine-dépendant connu pour être impliqué dans sa dégradation. Nous avons également montré qu’une modification de l’expression de calpaïne 3, soit par surexpression soit par inhibition avec des siRNA spécifiques, entraîne une perturbation du processus de différenciation myogénique. Cet effet a été plus particulièrement étudié au sein d’une sous-population de cellules qui reste indifférenciée dans les cellules C2C12 induites en différenciation. Ces cellules, appelées cellules de réserve, s’apparentent aux cellules satellites intervenant dans la régénération musculaire. Nous avons montré que calpaïne 3 participe à la régulation du nombre des cellules de réserve au cours de la différenciation des cellules C2C12. Ce rôle de calpaïne 3 pourrait être lié à son intervention dans la dégradation du facteur MyoD. L’ensemble de ces résultats suggère ainsi que calpaïne 3 pourrait jouer un rôle in vivo dans le maintien d’un stock de cellules satellites au cours de la régénération musculaireCalpain 3 (CAPN3) is a calcium-dependent cysteine protease mainly expressed in skeletal muscle. This protease plays a key role in maintaining the integrity of muscular fibers. Indeed, mutations in CAPN3 encoding gene cause limb-girdle muscular dystrophy type 2A, an autosomal recessive muscular dystrophy characterized by progressive atrophy and weakness of the proximal limb muscles. Our work reveals an inhibitory effect of CAPN3 directed against the myogenic regulatory factor (MRF), MyoD. We have shown that CAPN3 inhibits the transcriptional activity of MyoD either in myoblastic cells (C2C12 cells) or in fibroblastic ones (C3H10T1/2 cells). On the contrary, no variation in the transcriptional activity of the other members of the MRFs family (Myf5, myogenin, or MRF4) was observed. CAPN3 affects the transcriptional activity of MyoD by decreasing the quantity of the endogenous protein MyoD (Western-blots, confocal microscopy experiments), without affecting its mRNA level (RT-QPCR). Moreover, half-life determination experiments showed that CAPN3 induce MyoD degradation acts on MyoD by a proteic degradation. Experiments are in progress to determine whether CAPN3 acts directly or not on MyoD. Furthermore, the inhibitory effect of CAPN3 on MyoD is independent of the ubiquitin-proteasome proteolytic pathway that is known to play a role during MyoD degradation. Indeed, MyoD mutants resistant to proteolytic degradation by the proteasome are sensitive to CAPN3 action. Interestingly, we have shown that modifications in CAPN3 expression, induced by overexpression or downregulation (siRNA), cause perturbations in myogenic differentiation. CAPN3 appears as a regulator of myogenic differentiation by modulating the quantity of MyoD available for progressing in differentiation. In addition, we have highlighted a potential role of CAPN3 in maintaining a pool of reserve cells along C2C12 cells differentiation. These cells share numbers of similarities with satellite cells present in the adult muscles. In conclusion, we have shown that CAPN3 acts as a regulatory molecule on myogenic differentiation, and probably have implications in the area of regeneration
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Berkes, Charlotte Amelia. "Elucidating the mechanisms by which MyoD establishes muscle-specific gene expression /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5071.
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Dai, Zhijie, and 戴志洁. "The role of sodium/myo-inositol cotransporter 1 and myo-inositol in osteogenesis and bone formation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43783533.
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Dai, Zhijie. "The role of sodium/myo-inositol cotransporter 1 and myo-inositol in osteogenesis and bone formation." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43783533.
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Schwenninger, Björn. "Das Myon-Pretrigger-System für das HERA-B-Experiment." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962721522.
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Kashiwabara, Andre Yoshiaki. "MYOP: um arcabouço para predição de genes ab initio\"." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/45/45134/tde-25112009-151237/.
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A demanda por abordagens eficientes para o problema de reconhecer a estrutura de cada gene numa sequência genômica motivou a implementação de um grande número de programas preditores de genes. Fizemos uma análise dos programas de sucesso com abordagem probabilística e reconhecemos semelhanças na implementação dos mesmos. A maior parte desses programas utiliza a cadeia oculta generalizada de Markov (GHMM - generalized hiddenMarkov model) como um modelo de gene. Percebemos que muitos preditores têm a arquitetura da GHMM fixada no código-fonte, dificultando a investigação de novas abordagens. Devido a essa dificuldade e pelas semelhanças entre os programas atuais, implementamos o sistema MYOP (Make Your Own Predictor) que tem como objetivo fornecer um ambiente flexível o qual permite avaliar rapidamente cada modelo de gene. Mostramos a utilidade da ferramenta através da implementação e avaliação de 96 modelos de genes em que cada modelo é formado por um conjunto de estados e cada estado tem uma distribuição de duração e um outro modelo probabilístico. Verificamos que nem sempre um modelo probabilísticomais sofisticado fornece um preditor melhor, mostrando a relevância das experimentações e a importância de um sistema como o MYOP.The demand for efficient approaches for the gene structure prediction has motivated the implementation of different programs. In this work, we have analyzed successful programs that apply the probabilistic approach. We have observed similarities between different implementations, the same mathematical framework called generalized hidden Markov chain (GHMM) is applied. One problem with these implementations is that they maintain fixed GHMM architectures that are hard-coded. Due to this problem and similarities between the programs, we have implemented the MYOP framework (Make Your Own Predictor) with the objective of providing a flexible environment that allows the rapid evaluation of each gene model. We have demonstrated the utility of this tool through the implementation and evaluation of 96 gene models in which each model has a set of states and each state has a duration distribution and a probabilistic model. We have shown that a sophisticated probabilisticmodel is not sufficient to obtain better predictor, showing the experimentation relevance and the importance of a system as MYOP.
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Stanley, Alison Fay. "Metabolic studies of myo-inositol pentakisphosphates." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241250.
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Cole, Andrew Graham. "Mechanistic studies on myo-inositol monophosphatase." Thesis, University of St Andrews, 1994. http://hdl.handle.net/10023/14325.
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Enzymic phosphate monoester hydrolysis by inositol monophosphatase from bovine brain (EC 3.1.3.25) occurs via the direct displacement of phosphate by water rather than by a two step mechanism involving a phosphorylated enzyme intermediate. The catalytic process is believed to involve two Mg2+ ions, one of which is buried and acts as a Lewis acid and phosphate coordination site. The second metal ion appears to coordinate to the alkyl phosphate bridging oxygen, the 'catalytic' hydroxyl group (C-60H of D-Ins 1-P) and to the nucleophile, water or hydroxide. Mechanistic differences have been identified between the hydrolysis of inositol phosphate and nucleoside 2'-monophosphate substrates in that although phosphate-oxygen ligand exchange with the solvent Is facile in the presence of inositol, no such exchange occurs in the presence of adenosine. The minimum structural requirements of a substrate have been demonstrated via synthesis of ethane 1,2-diol monophosphate which shows enzyme activity (Vmax ca. 12% that of Vmax for Ins 1-P, Km = 0.7 mM and Ki = 1.0 mM). Elaboration of the free hydroxyl group to produce (S,R)-, (S)- and (R)-pentane 1,2,5-triol 2-phosphate gave inhibitors of contrasting potency ((S)-pentane 1,2,5-triol 2-phosphate Ki = 0.12 mM, (R)-pentane 1,2,5-triol 2-phosphate, Ki = 3.8 mM) as expected from the structural requirements for hydrolysis to occur. The proposed mechanism of adenosine 2'-monophosphate hydrolysis involving the N3-atom of the adenine moiety has been discounted through spectroscopic analysis of enzymic incubations of new nucleoside substrates (Uridine 2'-monophosphate; Vmax 230% that of Vmax for 2'-AMP, Km = 4.0 mM and 5,6-dihydrouridine 2'-monophosphate; Vmax 70% that of Vmax for 2'-AMP, Km = 1.4 mM), which showed no intermediate phosphates, with only the substrate and final enzymic product (uridine) detected. Ethane 1,2-diol phosphate has been further elaborated to produce 2-methoxyethanol phosphate, diethylene glycol phosphate, pentane 1,5-diolphosphate, diethylene glycol cyclic phosphate and pentane 1,5-diol cyclic phosphate (Ki values range between 3 & 8 mM). Inhibition is attributed to interaction of the substrate with the second Mg2+ ion, and displacement of the catalytic water (hydroxide) molecule. The fact that the cyclic phosphate diesters are not hydrolysed to phosphate monoesters by the enzyme demonstrates that the attacking nucleophile is not positioned on the first (buried) Mg2+ ion. The mechanistic difference of nucleoside 2'-monophosphate hydrolyses is attributed to the ribofuranosyl oxygen acting as a surrogate for the catalytic hydroxyl group of inositol 1-phosphate. Modelling studies have shown that this results in 2'-AMP adopting an unfavourable conformation which is stabilised by the second (catalytic) Mg2+ ion. The absence of the phosphate moiety in adenosine prevents this conformation being achieved at the active site, accounting for the lack of inhibitory activity of adenosine, and the absence of phosphate- oxygen ligand exchange in the presence of adenosine. The proposed mechanism is consistent with all published kinetic data, and the substrate dependency of lithium inhibition.
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GUIDOT, JEAN-PIERRE. "Syntheses d'analogues soufres du myo-inositol." Paris 11, 1992. http://www.theses.fr/1992PA112460.
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Le d-myo-inositol 1,4,5-trisphosphate est un second messager dont le role est de liberer des ions calcium intracellulaires. L'etude de son metabolisme necessite l'utilisation d'analogues chimiques du myo-inositol. Dans ce but, nous avons synthetise le d,l-deoxy-1-thio-1-myo-inositol et le deoxy-2-thio-2-myo-inositol, par des methodes originales en utilisant des reactions regioselectives. Le produit de base de ces syntheses est le 3,4,5,6-tetrabenzyl-myo-inositol dont nous avons obtenu l'enantiomere pur d, a partir d'un dialdehyde, par couplage pinacolique stereoselectif. Les premieres etudes biologiques montrent que ces analogues sont vraisemblablement incorpores dans les cellules
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Feldmann, Jamie Marie. "Analysis of Myogenin Function in Rhabdomyosarcoma Cells." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/7.
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Rhabdomyosarcomas (RMS) are the most common soft tissue cancer among children and are characterized by their expression of the myogenic regulatory factors MyoD and myogenin. Yet RMS cells cannot undergo normal myogenesis and are caught between the proliferation program and the terminal differentiation program. Many questions still remain about the defects present in rhabdomyosarcoma cells. In this work, we set out to understand the role of myogenin in these cells. To begin, we found that myogenin and its co-factors were present in rhabdomyosarcoma cells at levels that should support terminal differentiation. We examined the expression profile of several myogenin target genes in rhabdomyosarcoma cells and then assayed for myogenin activity using luciferase reporter constructs that contain myogenin dependent promoters to test for myogenin function. Many myogenin target genes were down regulated in RMS cells but that the target promoters on the luciferase constructs were activated. Terminal differentiation is a complicated process that involves many proteins. In cancer cells, it is important to compare the levels proteins with known functions to those levels in wild-type cells at the protein and RNA levels. Establishing the defect of rhabdomyosarcoma cells can lead to further insights into normal myogenesis, and may also lead to new therapeutic approaches in the treatment of this childhood cancer.
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Wang, Jianyu. "Effects of mechanical overload and aging on MyoD and effects of oxandrolone treatment and overload on IGF-1 and MyoD in old rats /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488186329501203.
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Bruggeman, Quentin. "Caractérisation de suppresseurs de la mort cellulaire programmée chez Arabidopsis thaliana." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112317/document.
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La Mort Cellulaire Programmée (MCP) est un processus essentiel pour plusieurs aspects de la vie des plantes, incluant le développement et les réponses aux stress. Des analyses génétiques ont permis d’identifier plusieurs acteurs clés de la MCP chez Arabidopsis thaliana,, dont l’enzyme MIPS1, qui catalyse une étape limitante de la biosynthèse du myo-inositol (MI), composé cellulaire majeur à l’origine de nombreux dérivés. Une des caractéristiques les plus importantes du mutant mips1, désactivé pour cette protéine, est l’apparition de lésions sur les feuilles de rosette, dépendante des conditions lumineuses et due à de la MCP impliquant la voie de l’acide salicylique. Ces données avaient permis de révéler un rôle du MI, ou de ses dérivés, dans le contrôle de la MCP. Mon travail de thèse a consisté à rechercher et à caractériser des suppresseurs du mutant mips1 par deux approches complémentaires : une approche gène candidat par comparaison de transcriptome et une stratégie de génétique directe suite au crible de mutations secondaires extra-géniques abolissant le phénotype de mort cellulaire de mips1. Les analyses effectuées sur différents suppresseurs ont mis en évidence l’implication de plusieurs facteurs dans la MCP, tels que le facteur de polyadénylation CPSF30, d’une héxokinase ou encore de la protéine PCB2 intervenant dans la biosynthèse de la chlorophylle. La caractérisation de ces suppresseurs a permis de démontrer l’importance de différentes voies comme la maturation des ARNm, le métabolisme carboné primaire ou l’activité chloroplastique dans le contrôle de la MCP dépendante de l’accumulation de MI. Ce travail apporte de nombreuses perspectives, visant à mieux appréhender les différentes voies de régulation de la MCP indispensables pour un développement correct et pour faire face à des stress biotiques et abiotiques chez les plantesProgrammed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. Mutational analyses have identified several key PCD components in Arabidopsis thaliana, as the enzyme MIPS1 catalysing the limiting step of myo-inositol (MI) synthesis, crucial cellular compound at the root of many derivatives. One of the most striking features of mips1, disrupted for this protein, is the light-dependent formation of lesions on leaves due to Salicylic Acid (SA)-dependent PCD, revealing roles for MI or inositol derivatives in the regulation of PCD. My thesis work was to find and characterize suppressor of mips1 mutant using two complementary approaches: a gene candidate approach by transcriptomic comparisons and a strategy of direct genetic by screening for extra genic secondary mutations that abolish mips1 cell death phenotype. Analysis of different suppressors revealed the involvement of several factors in MCP, such as the polyadenylation factor CPSF30, a hexokinase or the protein PCB2 operating in chlorophyll biosynthesis. Characterization of these suppressors allowed us to demonstrate crucial role of functions as mRNA maturation, primary carbohydrate metabolism or chloroplastic activity in the regulation of MCP depending on MI accumulation. This work brings many opportunities, to better understand the different regulatory pathways of PCD essential for proper development and to cope with biotic and abiotic stress in plants
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Gerber, Anthony Nicholas. "MyoD induces chromatin remodeling : implications for lineage determination and tumorigenesis /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6342.
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Harford, Terri J. "Regulation of Apoptosis by the Muscle Regulatory Transcription Factor MyoD." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933.
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Egarter, Saskia M. "Characterisation of the Acto-MyoA motor complex in Toxoplasma gondii." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5351/.
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In apicomplexan parasites, the machinery required for gliding motility is located between the plasma membrane and the Inner Membrane Complex (IMC). This type of motility depends on the regulated polymerisation and depolymerisation of actin and a multi-subunit complex, known as the Myosin A motor complex. This complex consists of the myosin heavy chain A (MyoA), the myosin light chain 1 (MLC1), the essential light chain 1 (ELC1) and three gliding-associated proteins (GAP40, GAP45 and GAP50). Gliding motility is thought to be essential for host cell egress and linked to active, parasite driven penetration of the host cell. Many components of this complex are extensively studied using either the ddFKBP system or the tetracycline-inducible knockdown system (Tet-system). Strikingly, while depletion of myoA has no impact on IMC formation, overexpression of the tail domain of MyoA results in a severe IMC biogenesis phenotype. In order to investigate this issue, conditional knockout (KO) mutants of the interacting partners of MyoA-tail were generated using the conditional site-specific DiCre recombination system. Indeed, GAP40 and GAP50 were identified as being essential for parasite replication and having a crucial role during IMC biogenesis. This is the first evidence showing that components of the MyoA motor complex fulfil essential functions during IMC formation and thus are not exclusively important for gliding motility dependant processes. Several components of the MyoA motor complex were characterised using the Tet-system and showed a complete block in gliding motility, but not in host cell invasion. While it is possible that leaky expression of the gene in the knockdown mutants is responsible for this uncoupling of gliding motility and invasion, it remains feasible that different mechanisms are involved in these two processes. In order to shed light on this issue, conditional KOs for the Acto-MyoA motor complex were generated in this study and their functions during gliding dependent processes thoroughly analysed. Intriguingly, while depletion of individual components of this complex caused a severe block in host cell egress, gliding motility and host cell penetration were decreased, but not blocked, demonstrating an important, but not essential role of the Acto-MyoA motor complex during these processes. Altogether, this study raises questions of our current view of what drives gliding motility and invasion and supports the argument for critical revision of the linear motor model.
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Münch, Friederike [Verfasser]. "Subjektive Krankheitstheorien von Myom- und Endometriosepatientinnen im Vergleich / Friederike Münch." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/124154137X/34.
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Giles, M. "Novel polymers based on myo-inositol orthoformate." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599410.
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The work in this dissertation is directed towards the synthesis of novel polymers based on myo-inositol orthoformate 23. (Fig. 1068A). Chapter 1 provides an introduction to the biological significance, synthesis, and metal ion chelating abilities of inositol derivatives. The proposed synthesis of inositol-based polymers and their proposed metal ion chelating abilities are then discussed with reference to existing metal chelating polymers and vinyl sugars. The utilisation of the rigid inositol scaffold to give orientation of monomer units is then considered with reference to current cyclopolymerisation techniques. Chapter 2 explores routes to the synthesis of linear inositol polymers and inositol-based resins which do not utilise the orientation effect of the inositol framework. (Fig. 1668B). Chapter 3 explores the orientation effect of the rigid inositol framework on the formation of novel cyclopolymers 161a and 161b from di(vinylbenzyl) inositol monomers 142 and 157. The synthesis of the monomers and polymers and the methods used to characterise the cyclopolymers are discussed. At the end of the chapter the copolymerisation of these monomers with styrene, methyl methacrylate, butyl methacrylate and maleic anhydride are discussed. In Chapter 4 the properties of the inositol polymers are considered. The first section discusses the thermal properties and the second section summarises the formation and properties of thin coatings of inositol-based polymers on polyethylene terephthalate (PET) films. Chapter 5 summarises the work that has been carried out and looks toward the future.
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Poirot, Emmanuel. "Synthèses d'analogues du myo-inositol-1,4,5-trisphosphate." Nancy 1, 1997. http://www.theses.fr/1997NAN10025.
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Une étude bibliographique préliminaire permet, dans un premier temps, de développer brièvement le rôle de second messager naturel joué au sein de la cellule par le D-myo-inositol-1,4,5-trisphosphate, puis, dans un second temps de situer ce travail dans le contexte général des synthèses d'inositols phosphate et d'analogues. Nous détaillons ensuite, dans la première partie, les résultats obtenus dans une synthèse énantiospécifique, présentant un caractère biomimétique, de deux analogues du produit naturel, désoxy en position 3. Cet objectif a été atteint en utilisant la réaction de carbocyclisation de Ferrier sur un dérivé de D-glucose. Les tests préliminaires d'activité biologique de ces composés nous ont amenés à envisager la synthèse de molécules dérivées perméantes, portant des groupements phosphates lipophiles. Cette partie s'achève par l'exposé des résultats obtenus dans ce domaine. La seconde partie est consacrée à la synthèse sous forme racémique, d'une série d'analogues conformationnellement bloqués. Puis, dans le but de confirmer des résultats obtenus en série 3-désoxy, nous avons préparé le myo-inositol-1,2,4-trisphosphate. Enfin, nous avons adapté la synthèse développée pour atteindre ces objectifs, à la préparation du fragment aminocyclitol d'un antibiotique : l'Hygromycin A.
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Lima, Amanda de Paula. "EFEITOS DA SUPLEMENTAÇÃO COMBINADA DE LISINA E METIONINA NO DESEMPENHO E EXPRESSÃO DE GENES RELACIONADOS AO CRESCIMENTO MUSCULAR DE ALEVINOS DE TILÁPIA DO NILO, Oreochromis niloticus." Universidade Estadual de Ponta Grossa, 2018. http://tede2.uepg.br/jspui/handle/prefix/2677.
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Fundação Araucária de Apoio ao Desenvolvimento Científico e Tecnológico do Paraná
A presente pesquisa foi realizada com o objetivo avaliar os efeitos da suplementação combinada de lisina e metionina sobre o desempenho produtivo e expressão de genes relacionados com o crescimento muscular em alevinos de tilápia do Nilo revertidos sexualmente. Trezentos e trinta e seis alevinos de tilápia do Nilo (peso inicial 0,90 ± 0,01 g) foram distribuídos em 24 aquários de 70L com sistema contínuo de fluxo de água (2,0 L/min), em um delineamento inteiramente casualizado com quatro tratamentos e seis repetições. Foram elaboradas quatro dietas isoproteicas (~330,50 g/kg de proteína bruta) e isocalóricas (~18,59 MJ/kg) sem suplementação de lisina e metionina (Controle), suplementada com lisina (Lys), suplementada com metionina (Met) e suplementada com lisina e metionina (Lys+Met) durante oito semanas. Os peixes foram alimentados manualmente, quatro vezes por dia até saciedade aparente. Peixes tratados com as dietas Lys e Met apresentaram maior peso corporal e taxa de crescimento específico em relação aos peixes mantidos com as demais dietas. Peixes tratados com dieta Lys apresentaram maior taxa de eficiência proteica em comparação aos peixes mantidos com as outras dietas. O índice hepatostomático e a gordura corporal foram menores nos peixes alimentados com as dietas Met e Lys+Met em comparação aos peixes tratados com a dieta controle. O consumo, sobrevivência, umidade, proteína bruta, cinzas corporais e a expressão do mRNA da miostatina não foram influenciados pelas dietas. Peixes que receberam dieta Lys+Met apresentaram maior nível de expressão de mRNA da MyoD em comparação aos peixes que receberam a dieta controle, mas nenhum efeito da suplementação isolada de lisina e metionina foi observada. Em conclusão, a suplementação combinada de lisina e metionina melhora o desempenho produtivo e aumenta a expressão de mRNA de MyoD e miogenina e reduz conteúdo de gordura corporal de alevinos de tilápias do Nilo.
This work was carried out with the objective of evaluating the effects of the combination of lysine and methionine on the performance of growth and expression of genes related to muscle growth in sexually reversed Nile tilapia fingerlings. Fish (n = 336, initial weight 0.90 ± 0.01 g) were randomly distributed into 24 70 L aquaria with a continuous water flow system in an entirely randomized design with four treatments and six replicates. Four isoproteic (~330.50 g/kg crude protein) and isocaloric (~ 18.59 MJ / kg) diets without lysine or methionine supplementation (Control), or supplemented with lysine (Lys), methionine (Met) and lysine and methionine (Lys + Met) were elaborated. Fish were hand fed until apparent satiety. Fish fed diets Lys+Met and Met showed higher final body weight and specific growth ratio compared to fish fed other diets. The protein efficiency ratio was higher in fish diet Lys compared to fish fed other diets. Fish fed Met and Lys+Met diets showed lower hepatosomatic index and whole-body fat compared to fish fed the control diet. Feed intake, survival and whole-body moisture, crude protein, ash and mRNA expression of myostatin of fish were not affected by diets. Fish fed diet Lys+Met demonstrated higher mRNA expression level of MyoD compared to those fed the control diet. In conclusion, Nile tilapia fingerlings fed combined lysine and methionine demonstrates improved growth performance in line to higher mRNA expression of MyoD and myogenin, and also reduced body fat contents
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Martyniak-Stronczek, Aleksandra. "Using spin polarised positive muons for studying guest molecule partitioning in soft matter structures." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-29731.
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Vujosevic, Danilo. "Solvent ordering near cyclohexadienyl type radicals, and ferroelectric ordering of pyridinium perchlorate." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-31836.
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Odeh, Rula S. "Thymopoietin and MyoD : their effects on the muscle nicotinic acetylcholine receptor." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68233.
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The present study was done to determine whether the muscle nicotinic acetylcholine receptor (nAChR) function and expression could be regulated by two different factors: (a) thymopoietin (TPO)$ sp *$, a nicotinic antagonist and (b) MyoD, a myogenic transcription factor.Exposure of rat neonatal muscle cells in culture to TPO on a long-term (days) and short-term (minutes) basis resulted in the inhibition of $ sp{125}$I-$ alpha$-bungarotoxin (BGT) binding. Short-term pretreatment with TPO also led to a decrease in carbachol-stimulated $ sp{22}$Na uptake; however, long-term exposure resulted in an enhanced carbachol-stimulated uptake. Chronic treatment also resulted in greater muscle cell morphological development. These results suggest that TPO regulates the nAChR and exerts trophic effects on myotube morphology.
As another approach to study factors that affect nAChR expression, non-muscle cells were transfected with MyoD cDNA. After transfection, saturable, high affinity $ sp{125}$I-$ alpha$-BGT binding was readily detectable, as was carbachol-stimulated $ sp{22}$Na uptake. Both these parameters developed in parallel over time and were inhibited by nicotinic antagonists. These results suggest that the transfection of a non-muscle cell line with MyoD cDNA results in the expression, at the cell surface, of a functional muscle-type nAChR.
This work shows that the nAChR function and expression can be regulated through (a) the chronic interaction of TPO at the nAChR at the cell surface and (b) the action of MyoD at the gene level. ftn$ sp *$ As stated in the addendum to this thesis, recent work by Quik et al. 1993a has shown that the preparation presumed to be TPO, contained $ alpha$-cobratoxin; the effects observed in the present thesis must therefore now be attributed to the presence of $ alpha$-cobratoxin contaminant.
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Siedel, Torsten. "Hybride Steuerung parallel gekoppelter Aktoren am Beispiel des humanoiden Roboters Myon." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17368.
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Die motorischen Fähigkeiten humanoider Roboter werden häufig von antriebsbedingten Nichtlinearitäten und Reibungseffekten negativ beeinflusst. Zur deren Kompensation werden üblicherweise modellbasierte Regelkreise genutzt, die i.d.R. von einer hochfrequenten Signalverarbeitung und mehreren Sensorqualitäten abhängen. Entgegen solch modellbasierten Techniken werden in der vorliegenden Arbeit modellfreie Steuerungsmethoden auf Basis parallel gekoppelter Antriebe entwickelt. Zur Entwicklung und Untersuchung dieser Steuerungsmethoden wird nach der von Pfeifer in seinem Werk “How the body shapes the way we think” beschriebenen synthetischen Methodik vorgegangen. Entgegen modellbasierten Untersuchungen auf Basis von Simulationen stehen bei der synthetischen Methodik empirische Untersuchungen am realen System im Vordergrund. Als Ausgangspunkt dienen konventionelle elektromechanische Antriebe mit deren bekannten leistungseinschränkenden Nichtlinearitäten und Reibungseffekten. Durch die parallele Kopplung mehrerer Antriebe an einem einzelnen Gelenk wird das Spektrum der Steuerungsmöglichkeiten deutlich erweitert. Es zeigt sich, dass (1) durch eine konstante antagonistische Vorspannung das Arbeitsverhalten von konventionellen Proportionalreglern optimiert werden kann, (2) durch dynamische asymmetrische Änderung der Vorspannung Nichtlinearitäten bei niedrigen Geschwindigkeiten ausgeglichen werden können und (3) getriebebedingte Reibungseffekte mit einer phasenverschobenen Pulsmodulation der Steuersignale kompensiert werden können. Weiterhin wird gezeigt, wie die erarbeiteten Steuerungsmethoden auf beliebig viele parallel gekoppelte Antriebe übertragen werden können. Für den praktischen Einsatz der Steuerungsmethoden werden diese in einer hybriden Steuerung zusammengeführt. Diese wird durch eine weitere Funktion, den Energiesparmodus beim Halten statischer Positionen, ergänzt und am humanoiden Roboter Myon implementiert und experimentell evaluiert.Motor functions of humanoid robots are often negatively influenced by nonlinearities and friction effects of the actuators. The popular means of compensation are control circuits based on modelling, which rely on powerful HF Signal processing and various sensor qualities. In contrast, this thesis develops non-modelling control methods based on parallel coupled actuators. Development and exploration of these control methods follow Pfeifer’s synthetic methodology as described in his work “How the body shapes the way we think”. In contrast to the analysis based on emulation as used in modelling, the synthetic methodology focuses rather on empirical tests within the real system. The present work explores control methods for parallel coupled actuators for use in robot points. It starts from conventional electromechanical actuators with their known power limiting nonlinearities and frictional effects. Linking several parallel coupled actuators to a single joint significantly expands the spectrum of control capabilities. Using two parallel coupled actuators as an example, it is examined to which extent undesirable properties of single actuators can be compensated. The results show that (1) the Performance of conventional proportional controllers can be optimized by a constant antagonistic bias voltage, (2) nonlinearities at low velocities can be balanced out by a dynamic asymmetrical adjustment of the bias, and that (3) gear related frictional effects can be compensated by a phase shifted pulse modulation of the control signals. In addition, it is shown how the developed control methods can be applied to a random number of parallel coupled actuators. For practical use, the various control methods are combined in a hybrid control, which is supplemented by an energy saving mode when maintaining static positions. The hybrid control is being implemented into the humanoid robot Myon and evaluated by experiment.
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Ma, Philip Chun-Ming. "Structural studies on the basic-helix-loop-helix region from MyoD." Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/28070.
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Borensztein, Maud. "Rôle des gènes Myod et Igf2 dans le développement embryonnaire murin." Paris 6, 2010. http://www.theses.fr/2010PA066374.
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Le développement du muscle squelettique murin s’effectue sous le contrôle de plusieurs facteurs de transcription tels que Myod et Myf5. Les facteurs de croissance IGF (Igf1 et Igf2) sont également impliqués. Pour étudier les interactions entre Myod et Igf2, un modèle murin d’invalidation de ces gènes a été obtenu. Bien que les animaux simples mutants soient viables, les souris Myod-/- Igf2-/- présentent une létalité périnatale, due à une insuffisance respiratoire. Des analyses histologiques, à 18,5 dpc, ont montré une atrophie importante du diaphragme ainsi qu’une hypertrophie du tissu adipeux brun des doubles mutants en comparaison aux contrôles. Etonnamment, l’atrophie musculaire est spécifique du diaphragme et s’explique par un nombre réduit de fibres. De plus, une désorganisation importante des sarcomères a été mise en évidence et la capacité contractile du diaphragme est sévèrement réduite en comparaison aux diaphragmes contrôles. Enfin, les interactions moléculaires ont été étudiées dans le diaphragme et les muscles des cuisses à 18,5 dpc. Nous avons pu montrer l’existence d’une boucle de rétrocontrôle négative entre Myod et Igf2, au niveau transcriptionnel, ainsi qu’un contrôle de l’expression de Myod et Myf5 par Igf2, de façon spécifique au diaphragme. Des expériences de ChIP ont mis en évidence une fixation du facteur de transcription Myod au niveau d’une séquence activatrice contrôlant l’expression du locus Igf2/H19, spécifiquement dans les tissus mésodermiques. Enfin, une expérience de 3C a permis de corroborer l’interaction de cette séquence activatrice du mésoderme avec le promoteur H19, permettant l’introduction d’un nouvel acteur dans la myogenèse.
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AURADE, FREDERIC. "Fonctions et regulations de l'expression de genes de la famille myod." Paris 7, 1997. http://www.theses.fr/1997PA077166.
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Les genes de la famille myod (myf-5, myod, myogenine et mrf4) sont des facteurs de transcription specifiques du muscle squelettique. Ils controlent le processus de myogenese dans ce tissu, depuis le recrutement des cellules precurseurs jusqu'a la differenciation de ces cellules et l'etablissement du phenotype mature. De plus, ces genes semblent intervenir dans la regeneration du muscle blesse. Nous avons etudie, au moyen de modeles cellulaires, plusieurs aspects du fonctionnement de ces 4 genes : - le role des membres de la famille myod dans la mise en place du programme myogenique, ainsi que l'implication de mrf4 dans le controle de la maturation. Cette etude, basee sur la conversion des fibroblastes de la lignee c3h10t1/2, a permis de conclure que, si chaque gene permet la convertion myogenique, sa capacite a accomplir un programme myogenique complet varie. De plus, les proprietes d'auto-activation et d'activation croisee de ces genes evoquees dans la litterature ne semblent pas une regle generale. Enfin, la surexpression de mrf4 n'a pu etre correlee avec l'apparition de l'expression de genes specifiques du muscle mature. - le lien entre les somatomedines et les facteurs myogeniques. L'insuline et les facteurs insulino-mimetiques (igfs) sont des activateurs puissants de la differenciation musculaire. Par une approche de molecules d'arn anti-sens, nous avons mis en evidence l'existence d'une boucle de regulation positive entre igfs et myod qui prepare les myoblastes a la differenciation. Cette etude a permis une avancee dans la comprehension des mecanismes reliant des facteurs a specificite tissulaire, comme les genes de la famille myod, et des facteurs ubiquitairement exprimes comme les igfs. - la regulation de l'expression de myf5. Nous avons montre que des evenements transductionnels mobilises par l'usage simultane de la dexamethasone, un glucocorticoide, et de l'anisomycine, un agoniste de voies de transduction du stress, permettent une forte stimulation de l'expression de myf5. Le role de ce mecanisme reste indetermine, mais pourrait intervenir dans le processus de regeneration.
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Bello, Davide. "Synthesis of D-myo-inositol 1,4,5-triphosphate analogues." Thesis, St Andrews, 2007. http://hdl.handle.net/10023/156.
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Fry, Judith. "myo-Inositol utilisation by Rhizobium leguminosarum biovar viciae." Thesis, University of Reading, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326187.
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Kim, Tae-Hyun. "Functional polymers based on myo- and scyllo-inositol." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621099.
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髙田, 尚寛. "ヒト疾患型VCPの出芽酵母を用いた機能解析." 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/180534.
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Zhang, Meiling. "MOLECULAR DEFECTS OF MEF2 FAMILY PROTEINS AND NAC PROTEINS THAT BLOCK MYOGENESIS AND PROMOTE TUMORIGENESIS IN RHABDOMYOSARCOMA." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1079.
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Rhabdomyosarcoma (RMS) is a highly malignant pediatric cancer that is the most common form of soft tissue tumors in children. RMS cells have many features of skeletal muscle cells, yet do not differentiate. Thus, our studies have focused on the molecular defects present in these cells that block myogenesis. We have found MEF2D is absent in RMS cell lines representing both major subtypes of RMS and primary cells derived from an embryonal RMS mice model. We have shown that the down regulation of MEF2D is a major cause for the failure of RMS cells to differentiate. We find MEF2D cannot bind to muscle specific gene promoters. Exogenous expression of MEF2D activates muscle specific luciferase constructs, upregulates p21 expression and increases muscle specific gene expression including the expression of myosin heavy chain, a marker for skeletal muscle differentiation. Restoring expression of MEF2D also inhibits proliferation, cell motility, anchorage independent growth in vitro, and tumor growth in vivo by xenograft assay. We also have found MEF2C is deregulated in rhabdomyosarcoma with the aberrant alternative splicing. We have shown that exon α in MEF2C is aberrantly alternatively spliced in RMS cells, with the ratio of α2/α1 being highly downregulated in RMS cells compared with normal myoblasts. We find that MEF2Cα1 is the ubiquitously expressed isoform which exhibits no myogenic activity and that MEF2Cα2, the muscle specific MEF2C isoform, is required for efficient differentiation. Compared with MEF2Cα2, MEF2Cα1 more strongly interacts with and recruits HDAC5 to myogenic gene promoters to repress muscle specific genes. Overexpression of the MEF2Cα2 isoform in RMS cells increases myogenic activity and promotes differentiation in RMS cells. We have also identified a serine protein kinase, SRPK3, which is downregulated in RMS cells and found that expression of SRPK3 promoted the splicing of the MEF2Cα2 isoform and induced differentiation. Restoration of either MEF2Cα2 or SPRK3 inhibited both proliferation and anchorage independent growth of RMS cells. The NAC complex performs many diverse biological functions, and the deregulation of its subunits has been correlated with many cancers. We sought to understand the function of the NAC complex in normal myogenesis and tumor progression in rhabdomyosarcoma cells. We found that the muscle specific subunit of the NAC complex, skNAC, which is the alternatively spliced isoform of NACα, was induced in normal cells and downregulated in RMS cells, while BTF3, also known as NACβ, was induced in normal cells and severely downregulated in RMS cells. We also showed that skNAC associated with muscle specific promoters together with BTF3 in differentiated normal cells, and this association was dependent on the expression of BTF3. We further investigated the involvement of skNAC in RMS progression. We found that the muscle specific expressed methyltransferase Smyd1 was nuclear localized in RMS cells and its interaction partner skNAC was switched with corepressors (HDAC1 and TBX2). We also confirmed the expression of skNAC was regulated by the splicing factor kinase SRPK3 and overexpression of SPRK3 induced skNAC expression and muscle differentiation in RMS cells. We also confirmed the overexpression of BTF3 in patient RMS tumors and depletion of BTF3 induced apoptosis in RMS cells and decrease RMS cell survival. BTF3 depletion also sensitized TRAIL induced cell apoptosis in RMS cells. However, BTF3 played a different role in normal cells. Deletion of BTF3 in C2C12 cells does not induce cell apoptosis, which suggests BTF3 functions as an anti-apoptosis factor in RMS cells and could be used as a cancer specific therapeutic target in RMS cells.
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Croze, Marine. "Study of the insulin-sensitizing effect of myo-inositol in mouse : Evaluation of the nutritional interest of a myo-inositol supplementation." Thesis, Lyon, INSA, 2013. http://www.theses.fr/2013ISAL0139/document.
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Le diabète de type 2 constitue un enjeu majeur de santé publique et la mise au point de stratégies insulino-sensibilisantes est un défi permanent pour les scientifiques. Cette étude montre qu’un traitement chronique au myo-inositol améliore la sensibilité à l’insuline, réduit l’accrétion adipeuse et augmente la capacité de survie des souris au paraquat. L’effet insulino-sensibilisant semble passer, au moins en partie, par un effet direct sur la voie de signalisation insuline (éventuelle implication de médiateurs de type inositol glycanes). La diminution de l’accrétion adipeuse semble, quant à elle, liée à une réduction de l’activité de lipogenèse de novo et doit probablement aussi contribuer à l’effet insulino-sensibilisant sur le long terme. Une supplémentation en myo-inositol a également amélioré la sensibilité à l’insuline et réduit l’accrétion adipeuse chez la souris sous régime riche en graisses, mais n’a pu prévenir le dévelopement d’une obésité et d’une insulino-résistance associée à une lipotoxicité. Par ailleurs, chez des souris âgées obèses et au contrôle glycémique altéré, la supplémentation en myo-inositol fut inefficace. Cette réduction ou perte d’effet insulino-sensibilisant dans ces deux modèles murins pourrait être liée à la perte d’efficacité du myo-inositol sur la réduction de la masse adipeuse dans un contexte d’obésité déjà installée (souris âgées) et d’activité de lipogenèse de novo réduite (régime gras). De plus, la génération de messagers secondaires putatifs de l’insuline de type inositol glycanes est probablement réduite en cas d’insulino-résistance et pourrait aussi expliquer la perte d’efficacité du myo-inositol dans ces deux cas. Finalement, le myo-inositol seul et/ou utilisé dans le contexte d’une suralimentation chronique n’est pas une stratégie viable de prévention ou de traitement de la résistance à l’insuline. Par contre, son association avec d’autres stratégies insulino-sensibilisantes pourrait potentialiser son/leurs action(s) et éventuellement aider à réduire l’utilisation de stratégies médicamenteusesInsulin resistance is the first step in the development of type 2 diabetes so finding insulin-sensitizing strategies is challenging for scientists. Some inositol isomers or derivatives have been reported to exert insulin-mimetic activity. myo-Inositol being the most abundant stereoisomeric form of inositol in foodstuffs, we tested its insulin-mimetic potential in the long term and as a nutritional strategy for insulin resistance prevention and/or treatment. This study demonstrates that chronic myo-inositol treatment improves insulin sensitivity, reduces white adipose tissue accretion and improves mice survival mice to paraquat challenge. The insulin-sensitizing effect seems to be related to a direct effect on insulin signaling pathway. Reduction in adipose tissue mass also probably contribute to the long term effect of myo-inositol on insulin sensitivity. Myo-Inositol supplementation also improved insulin sensitivity and reduced white adipose tissue deposition in mice fed a high fat diet, but did not prevent insulin-resistance or obesity development. On one year-old mice with established obesity and altered glycemic control, myo-inositol supplementation showed no beneficial effect. myo-Inositol apparently acts on adipose tissue through reduction of de novo lipogenesis rather than stimulation of lipolysis. This may explain the lack or loss of myo-inositol efficiency in reducing adipose tissue mass in contexts of already well-established obesity (old mice) or reduced de novo lipogenesis (high fat diet feeding). Generation of inositol glycan putative insulin second messengers is probably reduced in context of insulin resistance which may explain the reduced effect of myo-inositol in both obese mice models. Moreover, myo-Inositol did not prevent lipotoxicity and so the associated insulin-resistance in high fat diet fed mice. In conclusion, myo-inositol alone and/or in a context of overnutrition is not a suitable strategy for the prevention or treatment of insulin resistance. Combining it with other insulin sentitizing strategies may however potentiate their action and help reducing insulin-sensitizing drugs use
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Crutzen, Helene Sabine Giovanna. "Cis-regulation of MyoD : a systems analysis of a fate master regulator." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17977/.
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Myogenesis is highly regulated and its activation in the embryo is controlled by a series of complex transcriptional regulatory networks that ultimately result in the expression of myogenic regulatory factors (MRFs). The MRFS, particularly MyoD and Myf5, are responsible, in concert with a vast range of cofactors, for directing the expression of genes responsible for muscle formation and activity. Several candidate proteins have emerged as being responsible for MRF expression, as well as numerous downstream effectors involved in muscle formation in vivo. Several cis-regulatory elements have been identified for MyoD, but only a handful of factors have been identified that bind these elements. In addition, knockout experiments of these regions do not result in a complete loss of MyoD expression, suggesting a certain level of redundancy and the existence of other yet unidentified cis-regulatory modules. In this study, novel potential regulatory regions within the MyoD upstream genomic locus were identified by comparative genomics. These regions, named ReMos 9, 10 and 11, were conserved in mammals, chick and fish. Reporter assays in C2C12 cells using these regions cloned upstream of the MyoD promoter revealed that they positively enhanced the promoter activity. A synergy was uncovered between ReMo 9 and 10, which have a strong positive effect on promoter activity, but none individually; ReMo 11 seemed to disrupt this synergy. In addition, ReMos 9+10 and the CER enhancer were shown, by double fluorescent RNA in situ hybridisations, to be transcribed and possess cryptic promoter activity. This suggested that these elements acted as alternative promoters and encoded RNAs that regulated MyoD gene expression. Furthermore, the use of a newly engineered database generated predictions of DNA-binding factors interacting with the cis-regulatory regions, as well as protein interaction networks involved in MyoD regulation. These predictions were refined and constrained with biological input data derived by microarrays of single-cells transiently expressing relevant constructs. A list of candidate muscle-specific binding factors was then tested in vitro by siRNA knockdown experiments, and showed that MyoD disrupts the positive synergistic effect of ReMos 9 and 10 on the PRR. In conclusion, this study identified a number of regions that seem to be involved in MyoD regulation, and candidate factors binding to the MyoD cis-regulatory regions. Further in vivo validation will identify their function in MyoD spatio-temporal gene expression.
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B, Huot Nicolas. "Un adenovirus exprimant MyoD induit la myogenèse des cellules souches embryonnaires humaines." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26054/26054.pdf.
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