Dissertations / Theses on the topic 'Skeletal change'
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McKnight, David. "Fatigue-induced change in the rates of human skeletal muscle contraction and activation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22865.pdf.
Full textFitzpatrick, Tony A. "Analysis of Secular Change and a Novel Method of Stature Estimation Utilizing Modern Skeletal Collections." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/anthro_theses/63.
Full textAtkinson, Sarah Jane. "Variation in rates of age-related change in skeletal tissue in a Romano-British population." Thesis, Durham University, 1985. http://etheses.dur.ac.uk/7594/.
Full textThacker, Bryan Edward. "The passive mechanical properties and protein composition of skeletal muscle change with Botulinum neurotoxin A treatment." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453650.
Full textTitle from first page of PDF file (viewed July 30, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 41-44).
Spires, Jessica Rose. "Model analysis of oxygen transport and metabolism in skeletal muscle: responses to a change in energy demand." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1365177364.
Full textJanssen, Ian Michael. "Effects of sex on the change in visceral, subcutaneous adipose tissue and skeletal muscle in response to weight loss." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq28207.pdf.
Full textMays, S. "Social organisation and social change in the early and middle Bronze Age of central Europe : A study using £Thuman skeletal remains£T." Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377647.
Full textCANTARELLA, DANIELE. "MINIMALLY INVASIVE SURGERY TO FACILITATE MICRO-IMPLANT SUPPORTED MAXILLARY SKELETAL EXPANSION IN ADULT PATIENTS." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/914517.
Full textDiana, Annamaria. "Medieval populations, society and climate : an interdisciplinary approach to the study of two skeletal assemblages from Bucharest and Braşov (Romania), 14th-18th cent. AD." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25795.
Full textCarvalho, Wendy Irene. "Structural changes of unipennate skeletal muscle during isometric contractions." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/MQ49602.pdf.
Full textBosman, Jacqueline. "Flow cessation and capillary diameter changes in skeletal muscle." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=6322.
Full textMaden-Wilkinson, Thomas M. "Age related changes in skeletal muscle mass and function." Thesis, Manchester Metropolitan University, 2013. http://hdl.handle.net/2173/314011.
Full textSommer, Barbara. "Changes of skeletal muscle in adult dystrophin-deficient cats /." [S.l.] : [s.n.], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Full textChristensen, Samuel James. "Adolescent skeletal and dental changes with rapid maxillary expansion." Thesis, University of Iowa, 2018. https://ir.uiowa.edu/etd/6075.
Full textBell, Lynne Sevon. "Post mortem microstructural change to the skeleton." Thesis, University College London (University of London), 1995. http://discovery.ucl.ac.uk/1317796/.
Full textCasellas, Clemente. "Skeletal and dental changes with the acrylic splint Herbst appliance." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=1868.
Full textTitle from document title page. Document formatted into pages; contains vii, 73 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 64-69).
Chan, Wing Nam Joyce. "Craniofacial Differences Between Modern and Archaeological Asian Skeletal Populations." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306430849.
Full textWeston, Eleanor Mary. "A biometrical analysis of evolutionary change within the Hippopotamidae." Thesis, University of Cambridge, 1998. https://www.repository.cam.ac.uk/handle/1810/283727.
Full textJanssen, Ian. "Linking age-related changes in skeletal muscle morphology with metabolism and disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ65676.pdf.
Full textFisher, Ivan Brian. "Glucocorticoid-induced changes in the skeletal muscle of the dystrophic MDX mouse." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407223.
Full textFisher, Lauren Marie. "Time- and activity-dependence of transcriptional changes in stimulated rat skeletal muscle." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540051.
Full textDay, Samantha E., Richard L. Coletta, Joon Young Kim, Latoya E. Campbell, Tonya R. Benjamin, Lori R. Roust, Filippis Elena A. De, et al. "Next-generation sequencing methylation profiling of subjects with obesity identifies novel gene changes." BioMed Central, 2016. http://hdl.handle.net/10150/618693.
Full textDobson, Brent S. "Skeletal and dental changes associated with the treatment of anterior open bite malocclusion." Oklahoma City : [s.n.], 2006.
Find full textMalm, Christer. "Immunological changes in human blood and skeletal muscle in response to physical exercise /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-035-0/.
Full textHawke, Thomas James. "Intracellular calcium's role in methylxanthine-induced changes in potassium uptake in mammalian skeletal muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/NQ51039.pdf.
Full textPickering, James David. "Mechanisms underlying changes in cellular calcium regulation during osmotic stress in mammalian skeletal muscle." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511173.
Full textMcDonald, Joanne Hazel Christina. "Conditioning fast-twitch skeletal muscles for fatigue resistance : early changes with low frequency stimulation." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250427.
Full textUllinger, Jaime. "Skeletal Health Changes and Increasing Sedentism at Early Bronze Age Bab edh-Dhra’, Jordan." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275258919.
Full textBelli, Stephen J. "Long term anteroposterior, transverse, and vertical skeletal changes following rapid maxillary expansion in adults." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1412936018.
Full textKeough, Natalie. "Skeletal changes after post-mortem exposure to fire as an indicator of decomposition stage." Thesis, University of Pretoria, 2013. http://hdl.handle.net/2263/40277.
Full textThesis (PhD)--University of Pretoria, 2013.
gm2014
Anatomy
unrestricted
Bopp, Christopher Michael. "Changes in microvascular hematocrit during post-occlusive reactive hyperemia: descriptions and mechanisms." Diss., Kansas State University, 2015. http://hdl.handle.net/2097/20543.
Full textDepartment of Anatomy and Physiology
Thomas J. Barstow
The primary aim of this dissertation was to describe the changes in microvascular hematocrit, as total[hemoglobin+myoglobin] (T[Hb+Mb] measured with near-infrared spectroscopy (NIRS), during post-occlusive reactive hyperemia (PORH). Mechanisms of reactive hyperemia within skeletal muscle were also explored. The investigation detailed in Chapter 2 of this dissertation found that the differing time courses of the kinetic responses of both oxy- and deoxy[Hb+Mb], are related to changes in T[Hb+Mb]. We also determined that adipose tissue thickness had no effect on a purely temporal analysis of NIRS data. In Chapter 3 we observed that brachial artery reactive hyperemia preceded changes in T[Hb+Mb] during reactive hyperemia. Assuming that myoglobin remained constant, we posited that changes in T[Hb+Mb] must reflect alterations in red blood cell concentration in the microvasculature, i.e., microvascular hematocrit. In Chapter 4 comparisons were made between brachial artery blood flow, cutaneous and skeletal muscle flux and T[Hb+Mb]. The conduit artery response was faster than the microvascular responses in all tissues. Within skeletal muscle, time to peak and the time constant for the on-kinetics were faster in T[Hb+Mb] compoared with intramuscular flux as measured with intramuscular laser-Doppler. We observed no differences in temporal responses between cutaneous and intramuscular measures and suggested that in a purely temporal analysis the cutaneous microvasculature could serve as an analog for the skeletal muscle microvasculature. Finally, in Chapter 5 we found that prostaglandin inhibition with ibuprofen altered the initial T[Hb+Mb] response during PORH without impacting cutaneous flux or brachial artery blood flow. Chapter 5 also discussed that the addition of a wrist cuff to our standard instrumentation prevented the accumulation of T[Hb+Mb] during the occlusion period.
Shimizu, Kevin. "Facial Tissue Changes with Microimplant Assisted Rapid Palatal Expanders." Scholarly Commons, 2019. https://scholarlycommons.pacific.edu/dugoni_etd/1.
Full textWretman, Charlott. "Changes in mitogen-activated protein kinase phosphorylation and inorganic phosphate induced by skeletal muscle contraction /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-320-1/.
Full textLin, Sally. "Characterization of histological changes in the microvasculature of rat skeletal muscle after spinal cord injury." Thesis, Marquette University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10243099.
Full textThe purpose of this study was to determine whether there are histological changes in the microvasculature of rat skeletal muscle following chronic spinal cord injury both above and below the level of injury. This study is important because microvascular structure likely impacts muscle performance and cardiovascular health. To the best of our knowledge, this is the only study to investigate microvascular structure within rat skeletal muscle after spinal cord injury. We hypothesized structural remodeling would occur in both the myofibers and microvasculature, which would then manifest in differences in myofiber cross sectional area and microvascular diameter, wall thickness, wall to lumen ratio, and wall cross sectional area.
Changes in sympathetic tone and reduced muscular activity following spinal cord injury may induce microvascular structural remodeling. Initially after injury, sympathetic activity below the level of injury is diminished. Over time, neuroplasticity results in recovery of sympathetic tone, which increases vascular smooth muscle contraction and may lead to alterations in vasculature structure. In addition, the spinal lesion leads to loss of descending drive, which causes physical deconditioning below the level of injury. Physical deconditioning is known to induce vascular remodeling, and effects may be opposite of those associated with increased sympathetic tone.
We conducted a test of vascular remodeling in a rat contusion model of spinal cord injury. Ten adult female rats were evenly divided into control and spinal cord injury groups. Severe spinal cord injury was induced using a controlled weight drop onto the spinal cord, resulting in a contusion injury. After a 90 day survival period, the biceps brachii, triceps brachii, tibialis cranialis, and soleus muscles were removed, processed, and stained with Verhoeff van Gieson elastin and hematoxylin and eosin stains for histological analysis. Ultrastructural features of the myofibers and non-capillary microvessels were quantified. There was no significant difference between spinal cord injury and control skeletal muscles with regards to muscle cross sectional area, myofiber cross sectional area, microvascular diameter, wall thickness, wall to lumen ratio, or wall cross sectional area. Results indicated similar myofiber integrity and microvascular structure between control and spinal cord injury groups above and below level of injury.
While results did not support our original hypothesis, the findings also did not contradict previous studies. Following chronic spinal cord injury, recovery of spontaneous muscle activation and sympathetic activity may maintain integrity of skeletal muscle and associated microvasculature. Future research could assess microvascular function post spinal cord injury and identify an alternate animal model to study effects of spinal cord injury on muscle atrophy and associated microvasculature changes.
Beeler, Matthew K. "The Validity of Estimating Morphological Changes in Skeletal Muscle Using MRI in Resistance Trained Men." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1594736695258459.
Full textLima, Tãnia Marisa da Costa. "Molecular and functional changes in cardiac and skeletal muscle in HFpEF remodelling and reverse remodelling." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22238.
Full textA insuficiência cardíaca (IC) com fração de ejeção preservada (ICFEp) é uma síndrome com uma etiologia muito diversificada, cuja disfunção metabólica tem sido apontada como um importante mecanismo associado à sua severidade. A remodelagem do miocárdio, resulta de uma agressão ao coração que pode ser direta (isquemia, estenose aórtica, etc) ou indireta (diabetes, disfunção renal, etc). Quando esta agressão é atenuada, por tratamento farmacológico ou cirúrgico, o coração sofre uma remodelagem reversa (RR) e o miocárdio retoma à sua estrutura e função normais. Conhecer os mecanismos subjacentes ao padrão de remodelagem e RR do miocárdio irá certamente potenciar novas oportunidades de tratamento da ICFEp. Por ser uma síndrome multisistémica, os doentes com ICFEp apresentam frequentemente sinais e sintomas extra-cardíacos característicos do diagnóstico desta patologia, como é o caso da intolerância ao esforço. Assim este trabalho teve como objetivos implementar e caracterizar um modelo animal de ICFEp, bem como avaliar as alterações estruturais, funcionais e moleculares que ocorrem ao nível do músculo cardíaco e esquelético na remodelagem e RR. Os nossos resultados mostram que a implementação de um modelo animal que mimetiza o fenótipo de ICFEp foi bem-sucedida. De facto, os animais banding apresentaram uma marcada hipertrofia do ventrículo esquerdo (VE), disfunção diastólica com rigidez do miocárdio, alterações na regulação do cálcio e aumento do stress oxidativo. Observaram-se ainda alterações que sugerem um aumento da biogénese e da fissão mitocondrial bem como um aumento dos transportadores de glucose. Apesar do aumento da expressão da proteína desacopladora 1 (UCP-1), funcionalmente, as mitocôndrias apresentaram uma melhoria da sua função. A redução da performance física dos animais banding foi acompanhada de alterações estruturais ao nível do músculo-esquelético, assim como de uma alteração dos transportadores dos substratos metabólicos. Curiosamente, nos animais debanding, apesar da recuperação funcional, morfologicamente o miocárdio não normalizou totalmente. Adicionalmente, observou-se um aumento dos transportadores de ácidos gordos, acompanhado por uma diminuição do stress oxidativo e da apoptose no VE. Além disso, apesar da melhoria metabólica, as mitocôndrias do VE dos animais debanding mantém-se menores. Relativamente à capacidade aeróbica dos animais, observou-se uma melhoria após o debanding acompanhada por uma reversão da atrofia e a fibrose das fibras musculares, assim como da oxidação dos ácidos gordos. Este trabalho mostra evidências do envolvimento mitocondrial e metabólico na progressão da ICFEp, ao nível dos músculo-esquelético e cardíaco.
Heart failure (HF) with preserved ejection fraction (HFpEF) is a complex syndrome with a diverse aetiology in which the metabolic dysfunction has been pointed out as an important mechanism that underlies the disease severity. Myocardial remodelling results from cardiac injury that can be direct (ischemia, aortic stenosis, etc) or indirect (diabetes, renal dysfunction, etc). When the deleterious stimulus is attenuated by pharmacological or surgical treatment, the heart enrols in a process called reverse remodelling (RR), and myocardial structure and function returns to normal. The knowledge of the molecular mechanism that underlie the RR process could represent an opportunity to develop novel therapeutic approaches and thus improve the treatment of HFpEF patients. As being a multi-systemic syndrome, HFpEF presents several extra-cardiac signals and symptoms typical of its diagnosis, such as effort intolerance. Thus, the aims of this work was to implement and characterize an animal model of cardiac remodelling and reverse remodelling of HFpEF and thus characterize structurally, functionally and molecularly the changes that occurs at the myocardium and at the skeletal muscle. Our results showed that we successfully implemented an animal model of HFpEF that presents an LV hypertrophic and increased stiffness. Additionally to LV diastolic dysfunction (DD) we also observed abnormalities on calcium and oxidative stress. In banding rats we denoted an increase of peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1α) and downregulation of mitofusin (MNF1,2) as well as an augment of glucose transporters. Despite de increase of uncoupled protein 1 (UCP-1) expression, functionally we denoted an improvement of mitochondria respiration and membrane potential. The physical performance of banding animals was impaired and accomplished by structural changes at skeletal muscle level as well as at metabolic substrate transporters. Curiously, after afterload relief despite the functionally recovery, morphologically the myocardial reverse remodelling was incomplete. Moreover, regardless the metabolic transporters reversion the mitochondria continue smaller. After overload relief the rats showed an improvement on aerobic capacity as well as a reversion on skeletal muscle atrophy, fibrosis and an upregulation of FA oxidation. The present study shows clearly the involvement of mitochondria and metabolism on myocardial and skeletal muscle remodelling and RR.
Isaacs, Ashwin Wayne. "Muscle damage and adaptation in response to plyometric jumping." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20384.
Full textENGLISH ABSTRACT: The aim of the study was to investigate skeletal muscle changes induced by an acute bout of plyometric exercise before and after plyometric training. The study consisted of an acute study and training intervention study. The acute study, investigated whether direct evidence of ultrastructural damage and identification of indirect factors were more evident in subjects presenting with rhabdomyolysis. Moreover the training intervention study investigated whether plyometric training would protect the muscle from ultrastructural damage and rhabdomyolysis. During the acute intervention, twenty six healthy untrained individuals completed an acute bout of plyometric exercise (10 x 10 squat-jumps, 1 min rest). After, thirteen subjects continued with the training intervention. Eight of these subjects completed 8 weeks of plyometric jump training, while five subjects were instructed to rest from physical activity for 8 weeks. Seven days after the final training session the training and rest group repeated a second acute bout of plyometric exercise. Acute Study: Creatine kinase (CK) activity increased significantly following the single bout of plyometric exercise in all subjects (baseline: 129 to day 4: 5348 U/l). This was accompanied by an increase in perceived pain, C-reactive protein (CRP) a marker of inflammation as well as white blood cells (WBCs). Electron micrographs of muscle biopsies taken 3 days post exercise showed evidence of ultrasructural damage and membrane damage was apparent by immunofluorescence by the loss of dystrophin staining. A stretch of the c-terminus of titin was observed by immunogold, and western blot analysis indicated an increase in calpain-3 autolysis. Based on individual CK responses (CK range: 153-71,024 U/L at 4days after exercise) the twenty six subjects were divided into two groups, namely the high (n=10) and low responders (n=16). Training intervention: Following training the trained group did not experience: a rise of CK activity (110.0 U/l), perceived pain, CRP, WBCs, Z-line streaming, a stretch of titin or calpain-3 activation; while in the control group only two subjects presented with Z-line streaming. The results indicate that high responders have a more pronounced inflammatory response compared to low responders after eccentric exercise, therefore more WBCs and more specifically neutrophils are recruited to damaged areas resulting in greater membrane damage by respiratory burst in high responders. This damage can be limited with training by remodelling sarcomeric proteins via calpain activation resulting in the stable assembly of proteins in the sarcomere preventing the release of proteins.
AFRIKAANSE OPSOMMING: Die doel van die studie was om skeletspier veranderinge wat teweeggebring is deur voor en na afloop van akute pleometriese oefening, te ondersoek. Die studie bestaan uit ‘n akute intervensie en ‘n oefeningsintervensie gedeelte. Die akute intervensie het ondersoek ingestel na die direkte bewyse van ultrastrukturele skade en identifikasie van indirekte faktore meer sigbaar is in proefpersone wat met rhabdomiolose presenteer. Meerso het die oefningsintervensie die moontlikheid dat pleometriese oefening die spier van ultrastrukturele skade en rhabdomiolose beskerm, ondersoek. Tydens die akute intervensie is 26 gesonde ongeoefende individue die akute pleometriese oefeningsessie (10 x 10 hurkspronge, 1 min rus) voltooi. Hierna het 13 proefpersone voortgegaan met die oefeningsintervensie. Agt van hierdie proefpersone het agt weke pleometriese sprongsessie oefeninge voltooi, terwyl vyf proefpersone gevra is om vir 8 weke geen oefeninge te doen nie. Sewe dae na afloop van die finale oefeningssessie het die oefening en kontrole groep in ‘n tweede herhaalde akute pleometriese oefeningsessie deelgeneem. Akute intervensie: kreatienkinase (KK) aktiwiteit het betekenisvol verhoog na die enkel pleometriese oefeningsessie in all proefpersone (basislyn: 129 tot op dag vier: 5348 U/l). Hierdie is vergesel met ‘n toename in die persepsie van pyn, c-reaktiewe proteïen (CRP) ‘n merker van inflammasie sowel as witbloedselle (WBS). Elektronmikrograwe van spierbiopsies wat geneem is drie dae na afloop van die oefeninge, het tekens van ultrastrukturele skade en membraanskade getoon wat ook deur immunofluoresensie duidelik warneembaar was deur die verlies van distrofienverkleuring. ‘n Verrekking van die c-terminus van titin is ook waargeneem deur middel van immunogold. Westernblot analyse het ‘n toename in calpain-3 outolise getoon. Gegrond op individuele KK response (KK grense: 153-71,024 U/L na vier dae post oefening) is 26 proefpersone verdeel in twee groepe naamlik ‘n hoë (n=10) en lae responders (n=16). Oefeningintervensie:: Na oefening het die geoefende groep nie ‘n toename in KK aktiwiteit getoon nie (KK aktiwiteit (110.0 U/l)), pynervaring, CRP, WBS, Z-lynstroming, ‘n strekking van titin of calpain-3 aktivering; terwyl in die kontrole groep daar slegs twee proefpersone met Z-lynstroming geïdentifiseer is. Die resultate wyse daarop dat hoë responders ‘n meer uitgesproke inflammatoriese reaksie toon vergeleke met die lae responders na afloop van essentriese oefening. Daar word dus meer WBS en spesifiek meer neutrofiele na beskadigde areas gelokaliseer wat in grootter membraanskade deur respiratoriese inspanning in die hoë responders. Hierdie skade kan beperk word deur oefening waardeur hermodulering van sarkomeriese proteïene via calpain aktivering tot stabiele rangskiking van proteïene in die sarcomere lei en daardeur proteïen vrystelling verhinder.
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Stirland, Ann Jane. "Asymmetry and activity-related change in selected bones of the human male skeleton." Thesis, University College London (University of London), 1993. http://discovery.ucl.ac.uk/1317543/.
Full textStirland, Ann Jane. "Asymmetry and activity-related change in selected bones of the human male skeleton." Online version, 1992. http://ethos.bl.uk/OrderDetails.do?did=1&uin=uk.bl.ethos.246214.
Full textBooth, C. M. "A study of the changes of the surface of skeletal muscle fibres on denervation and paralysis." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379876.
Full textAllen, Emily E. "Changes in Skeletal Muscle Sarcoplasmic Reticulum Calcium Handling and Regulatory Protein Content in Congestive Heart Failure." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31865.
Full textMaster of Science
Ciambotti, Christopher. "A comparison of dental and skeletal changes between rapid palatal expansion and nickel titanium palatal expansion." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=515.
Full textTitle from document title page. Document formatted into pages; contains x, 135 p. : ill. Includes abstract. Includes bibliographical references (p. 88-91).
Tezze, Caterina. "OPA1 orchestrates precocious senescence, degeneration of multiple organs and premature death thought inflammation and metabolic changes." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3425910.
Full textUn network funzionale di mitocondri e essenziale per un tessuto post-mitotico come il muscolo. Il macchinario delle dinamiche mitocondriali e downregolato nella sarcopenia e preservato nei soggetti che fanno attvita fisica costante. La proteina OPA1, coinvolta nel processo di fusione mitocondriale, gioca un ruolo essenziale nelle dinamiche mitocondriali. I livelli di espressione di questa proteina correlano significativamente con la disfunzione muscolare associata all’invecchiamento, in umani e topi. Per caratterizzare il ruolo della proteina OPA1 nel muscolo scheletrico, e soprattutto il suo coinvolgimento nell’invecchiamento, abbiamo generato 2 modelli di delezione del gene nel tessuto muscolare. Il primo modello (costitutivo) presenta la delezione del gene a partire dallo stadio embrionale e il secondo (condizionale) permette di effettuare la delezione in seguito a somministrazione farmacologica, in eta adulta. Il modello costitutivo ha un fenotipo molto grave che porta alla morte dopo otto giorni post-nascita. Per questa ragione ci siamo concentati su quello condizionale. I topi adulti con delezione di OPA1 mostrano un fenotipo di invecchiamento precoce. Il blocco della fusione e sufficiente a indurre cambiamenti metabolici e infiammazione sistemica. Il fattore chiave in questo processo e la miochina FGF21. La delezione simultanea di OPA1 e FGF21 non presenta le principali caratteristiche patologiche del fenotipo, ma pensiamo che altri fattori siano coinvolti nel processo di invecchiamento precoce. Dal confronto tra i diversi modelli a nostra disposizione (Opa1 ko, Opa1/fgf21 ko, Drp1 ko e Opa1/Drp1 ko), che a differenza degli OPA1 ko non muoiono ma hanno livello di FGF21 elevati, abbiamo capito che la differenza principale e l’infiammazione sistemica, presente solo negli Opa1 ko. In particolare, l’unica citochina di origine muscolare espressa per un periodo prolungato e secreta e l’interleuchina 6 (IL6). Vista la mancanza di dati in letteratura sui segnali molecolari che portano all’induzione di IL6, nel muscolo scheletrico, ci siamo concentrati su questo aspetto.
Rabon, Karma Melisa. "Changes in Skeletal Muscle Sarcoplasmic Reticulum Function in Adult and Aged Fisher 344 Brown x Norway Rats." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/36800.
Full textMaster of Science
Sakellariou, Yorgos. "Superoxide in skeletal muscle : sites that regulate intracellular changes during contractions and role in age related degeneration." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/13793/.
Full textJawaid, S. "Differential changes in neuromuscular junction morphology after divergence of activity pattern in rat slow and fast skeletal muscles." Thesis, University of Aberdeen, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.592627.
Full textNordlund, Maria M. "On spinal mechanisms for reflex control in man : modulation of Ia-afferent excitation with changes in muscle length, activation level and fatigue /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-821-1/.
Full textPasniciuc, Silviu Valeriu. "Complex mechanisms of metabolic regulation in nonperfused muscle." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1049304386.
Full textLuk, Hui Ying. "Effect of the Resistance Exercise-Induced Hormonal Changes on Satellite Cell Myogenic State." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1157528/.
Full textPuhke, Raivo. "Adaptive changes of myosin isoforms in response to long-term strength training in skeletal muscle of middle-aged persons /." Online version, 2006. http://dspace.utlib.ee/dspace/bitstream/10062/1129/5/puhkeraivo.pdf.
Full text