Thèses : « Skeletal change »

1

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.

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Fitzpatrick, 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.

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Reconstructing stature is at the core of providing information on unidentified human remains. This research shows that there are significant differences between modern populations and those used to create the most common stature estimation formulae. New formulae for the femur and fibula in males and females were created to provide accurate estimates for modern forensic cases. Additionally, a novel measurement of the femur is shown to be moderately correlated with stature and stature estimation formulae for this measurement are included.

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Atkinson, 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/.

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1228 skeletons from the Romano-British cemetery at Poundbury have been used to compare methods of assessment of age at death on archaeological material. The main aim was to evaluate the potential use of methods based on cortical bone structure and of the occurrence of degenerative joint disease in the spine. Changes in cortical bone do not proceed linearly with age, so methods currently available, which are based of single regression equations, are inadequate. The measures of bone structure are found to be useful in conjunction with other methods in terms of calibration. The expectations of greater variation in bone structure measurements amongst males was not observed. In the case of cortical thickness exactly the reverse is found. Possible explanations are discussed. Degenerative joint disease of the spine offers a promising means of age assessment as it is found to increase in incidence, severity and extent with age. Males show a faster rate of deg,3neration than females particularly in extent. The best measure indicated is the combined number of facet and disc joints affected in the lumbar region.

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Thacker, 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.

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Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed July 30, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 41-44).

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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.

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Janssen, 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.

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Mays, S. « Social organisation and social change in the early and middle Bronze Age of central Europe : A study using Â£Thuman skeletal remainsÂ£T ». Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377647.

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CANTARELLA, 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.

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Introduction The aim of the present study is to evaluate the skeletal modifications induced by maxillary expansion supported by palatal micro-implants and localized osteotomies produced with minimally invasive surgical technique in young-adult and adult patients. In the present investigation, osteotomies had a lower extension than the ones used in conventional surgically assisted rapid palatal expansion (SARPE), to adopt a minimally invasive surgical technique that can be performed with greater comfort for the patient and less post-operative sequelae. More in detail, the localized osteotomies were executed only in the anterior part of the midpalatal suture and bilaterally at the basis of the zygomatic process of the maxilla without involvement of the piriform rim. These areas represent a great resistance to the lateral maxillary movement. Furthermore, they are of simple surgical access and don’t present important arterial plexuses. Patients requiring micro-implant supported maxillary expansion and/or SARPE routinely undergo a pre-treatment cone-beam computed tomography (CBCT) of the skull, to plan the surgical operation and, one month after treatment a secondary CBCT for a surgical and orthodontic control. CBCT is a low radiation tomography, extensively used in maxillofacial surgery and in dentistry. For the implementation of this study, that aims at evaluating the efficacy of micro-implant-supported maxillary expansion in combination with localized osteotomies, only radiologic exams that are anyway needed for the planning and post-treatment evaluation were used. Aim The aim of the present study is to evaluate the advantages introduced in the treatment of maxillary constriction by the therapy with micro-implant supported Maxillary Skeletal Expander (MSE) and localized osteotomies in young-adult and adult patients. The main objective is to evaluate the efficacy of the technique, by measuring the movement of skeletal landmarks in the midface, particularly on the maxillary and zygomatic bones, and on the lateral wall of the nose, by comparing the pre-treatment and post-treatment CBCT. For this particular technique, a new methodology for digital planning of position of MSE and miniscrews on patient CBCT was developed. Furthermore, incorporation of 2 additional miniscrews to the original MSE design, which conventionally features only 4 miniscrews, was developed with the aid of computer aided design – computer aided manufactured (CAD-CAM) technology. Methods The study presented the following steps: ▪ Development of a digital planning methodology for positioning the miniscrews and MSE appliance on pre-treatment CBCT ▪ Development of a CAD-CAM methodology for incorporating 2 additional miniscrews to the original MSE design with 4 miniscrews ▪ Selection of patients with age above 17 years, without congenital craniofacial syndromes, who require intervention of maxillary skeletal expansion ▪ Acquisition of initial CBCT with 17 x 13.5 cm field of view (FOV) ▪ Intervention of maxillary expansion supported by palatal micro-implants and localized osteotomies executed with minimally invasive surgical technique ▪ One month after treatment, acquisition of post-treatment CBCT with 17 x 13.5 cm FOV ▪ Analysis of skeletal modifications in the midface (maxillary bone, sphenoid bone, zygomatic arch, nasal cavity, etc.), by comparing the pre- and post- treatment CBCT with a 3D software (OnDemand software by Cybermed) Results The new methodology allowed the digital planning of MSE and miniscrews positioning on patients’ CBCTs, and the incorporation of two additional miniscrews to the original MSE design through CAD-CAM technology. In the clinical trial, a total of four patients had an average age of 27.6 years (range 22.1 – 39.9 years). MSE appliance was activated by an average of 6.0 mm and generated a parallel split of the midpalatal suture of 3.4 mm, 3.0 mm and 3.6 mm at anterior nasal spine (ANS), nasopalatine foramen (NPF) and posterior nasal spine (PNS), respectively. Skeletal modifications were found in all CBCT sections evaluated in the study (axial palatal, upper nasal, coronal zygomatic, axial zygomatic), indicating that all midfacial bones are affected by maxillary expansion with MSE and localized osteotomies. Particularly, skeletal changes were noticed also in CBCT sections above the lateral maxillary osteotomies (LMOs), in the maxilla, zygomatic bone, zygomatic arches, and nasal cavity. In the upper nasal section (UNS) the maxilla was laterally displaced by 2.4 mm and 0.9 mm, at its anterior and posterior extremities, respectively. The frontozygomatic angle (FZA) increased by 1.9° (average of right and left side), while the lower interzygomatic distance increased by 2.9 mm, indicating a rotation of the zygomatic bone in a lateral direction. The zygomatic arch was affected by bone bending phenomena and was deflected in an outward direction, with increase in the anterior intermaxillary distance by 1.7 mm and in the posterior inter-zygomatic distance by 1.6 mm. The nasal width (NW) parameter increased by 2.9 mm with treatment: this anatomical finding is the basis for a potential improvement in nasal breathing for patients suffering from increased nasal airway resistance. The cited modifications in skeletal structures above lateral maxillary osteotomies (LMOs) are most likely due to the fact that LMOs didn’t involve the piriform rim of the maxilla, and this point needs further investigations. Regarding dentoalveolar modifications, the inter-molar distance increased by 7.4 mm, and molars underwent a small dentoalveolar tipping in a buccal direction by 1.1° (average of right and left side), as evidenced by the change in molar basal bone angle (MBBA). No intra-operatory hemorrhage nor post-operatory bleeding was reported in treated patients, probably due to the lack of pterygopalatine suture surgical disjunction. A limitation of the study is its small sample size, represented by 4 patients. A larger number of patients is required to confirm the above results.

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Diana, 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.

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The complex relationship between human societies and the environment has become a thriving field of research over the past three decades. The contribution of human osteoarchaeology to exploring this relationship, however, has been rather limited. Two unpublished late medieval skeletal assemblages unearthed in the historical centres of Bucharest and Braşov (located in southern and north-central Romania respectively) seemed ideal choices for investigating the impact of substantial climatic and environmental changes that took place worldwide between the 14th and the 18th century AD. As witnessed by medieval artistic and documentary sources, this unsettled climate was mirrored by human populations with social and political instability, epidemics, famine, but also through the rise of new cultural movements. The analysis of over 600 individuals (a minimum number of 421 individuals from Bucharest and 206 from Braşov) was carried out to: 1) Provide a thorough osteological analysis, and compare and test statistically the collected data to reconstruct demographic and pathological patterning; 2) Identify ‘skeletal environmental markers’, i.e. possible indicators of the effect of climatic shifts on the human body; 3) Cross-reference osteological, archaeological, historical and climatological data in order to present a robust biocultural assessment of the impact of environmental and historical events on the Romanian population during the Middle Ages. The identification of low life-expectancy, higher mortality rates for children and young adults and general high morbidity levels were in line with other studies on medieval populations. However, evidence for a high prevalence of specific physiological and psychological stress markers was observed in these two geographically, culturally and economically different urban communities. As a strong mortality- and morbidity-shaping factor, the detrimental effect of climate anomalies is one of the main explanations for such findings, and is supported by medieval historical sources and recent advances in Romanian climatological studies. Despite some limitations (i.e. incomplete chronological information for most of the burial contexts, minimal local historical sources, lack of funding for isotopic analyses, and time constraints), the results of the present study have offered a new perspective on the relationship between Romanian medieval populations and their living environment, and have shown the enormous potential of interdisciplinary bioarchaeological research in Romania.

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Carvalho, 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.

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Bosman, 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.

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Maden-Wilkinson, Thomas M. « Age related changes in skeletal muscle mass and function ». Thesis, Manchester Metropolitan University, 2013. http://hdl.handle.net/2173/314011.

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The loss of muscle mass with age (Sarcopenia) has received growing attention over the past decade. Despite efforts to provide a universal definition with clinically meaningful cut-off points for diagnosis, there is no clear consensus on how to best quantify and assess the impact of loss of muscle mass and function on functional limitations. Whilst most previous studies have used dual energy x-ray absorptiometry (DXA) to quantify this loss, chapter 2 of this thesis shows that DXA underestimates the loss of muscle mass with age in comparison to the gold standard MRI. Muscle mass per se is not enough to determine whether a person has an exceptionally low muscle mass, as it can be readily seen that a healthy tall person will have a larger muscle mass than a small person. Clinicians and researchers thus need an index of muscle mass that takes differences in stature into account and also gives an objective cut off point to define low muscle mass. In Chapter3, we show that femur volume does not significantly differ between young and old. We used this observation to introduce a new index: thigh muscle mass normalised to femur volume, or the muscle to bone ratio. This index allows the examination of the true extent of muscle atrophy within an individual. In previous studies the appendicular lean mass (determined with DXA) divided by height squared appeared to be a relatively poor predictor of functional performance. In Chapter 4, the index introduced in Chapter 3, the muscle to bone ratio, proved to be a somewhat better predictor of functional performance in the overall cohort. This was, however, not true when examining the intra-group relationships. A similar situation applied to the maximal muscle strength. In older adults, the parameter which predicted functional performance best was muscle power per body mass, measured during a counter-movement jump. Chapter 5 shows that part of the larger loss power and force than muscle mass is attributable to a left-ward shift of the torque-frequency relationship, indicative of a slowing of the muscle, and reduction in maximal voluntary activation, as assessed using the interpolated twitch technique in older adults. Chapter 5 also shows that the fatigue resistance during a series of intermittent contractions was similar in young and older adults. However, older adults could sustain a 50% maximal voluntary contraction force longer than young people. Part of this discrepancy maybe due to an age-related slowing of the muscle.

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Sommer, 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.

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Christensen, Samuel James. « Adolescent skeletal and dental changes with rapid maxillary expansion ». Thesis, University of Iowa, 2018. https://ir.uiowa.edu/etd/6075.

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Introduction A constricted maxilla can be associated with a unilateral or bilateral posterior cross bite, CR-CO shift, maxillary or mandibular growth asymmetry, and dental crowding. Correction of adolescent maxillary constriction typically includes rapid maxillary expansion (RME). However, maxillary skeletal expansion becomes more difficult with age due to increasing facial, and mid-palatal, skeletal resistance. The purpose of this study is to evaluate the age and maturation at which a successful split of the maxillary midpalatal suture (MPS) can be achieved. A secondary aim is to assess the dental arch changes that are associated with a MPS split or no split. Material and Methods In this retrospective study, 39 (13 M, 26 F) consecutively treated subjects exhibiting maxillary skeletal constriction underwent orthodontic treatment with RME to alleviate unilateral or bilateral posterior cross bites. Subjects were divided into pre-pubertal and post-pubertal groups based on maturation. Evidence of a MPS split was confirmed by development of a diastema between upper central incisors and using a maxillary occlusal radiograph. Measurements were made on initial and post-expansion maxillary models to assess dental changes. Results Average age of pre-pubertal and post-pubertal subjects was 11.9± 1.1 years (n=13) and 14.6 ± 1.4 years (n=26) respectively. A MPS split occurred for 100% of pre-pubertal group compared with 65% of the post-pubertal group (p < 0.05). No significant differences were seen in dental movements between the pre-pubertal and post-pubertal groups while significant differences were seen for arch perimeter, crowding, intercanine width, and intermolar width in the split and no-split groups. There was a significantly strong negative correlation between age and percent ability to get a MPS split. Conclusions These results demonstrate that MPS separation is more likely to occur pre-pubertally than post-pubertally but that MPS separation after puberty is still possible. This finding supports the importance of appropriate timing in the use of rapid maxillary expanders.

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Bell, Lynne Sevon. « Post mortem microstructural change to the skeleton ». Thesis, University College London (University of London), 1995. http://discovery.ucl.ac.uk/1317796/.

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The microstructural impact of diagenetic or post mortem alteration has been assessed in predominately human skeletal tissues. The method of assessment selected was microscopical analysis, mainly using backscattered electron imaging in a scanning electron microscope and, to a lesser extent, confocal reflection microscopy. The microstructural morphologies of post mortem alteration were investigated in archaeological material, both normal and pathological, from terrestrial and marine contexts. Further studies were undertaken on a case-by-case basis on skeletal material which offered some unique pathology, environmental context, spatial relationship, time variable, or mortuary practice. Additionally, the effect of diagenetic change on mitochondrial DNA (mtDNA) recovery and the potential location of DNA within the skeletal tissues were investigated. Two quantitative studies were undertaken to validate and measure the observed mineral density changes. The investigations showed that post mortem alteration or diagenetic change to skeletal material can be extensive, and can occur shortly after death. Diagenesis did not represent a post burial phenomenon as the term diagenesis suggests, but was found to have begun above ground in a range of exposural contexts. The implication of gut bacteria in the promotion of early bacterially-related microstructural change was strong, and it is proposed that body status at the point of, or soon after, death is important. Post mortem alteration to skeletal microstucture can provide environmental information, since terrestrial and marine contexts exhibited distinct morphologies. It may also provide localized environmental information within a stratigraphic matrix. Characterizing the post mortem microstructural and density changes to bone has helped to elucidate the preservational status of mtDNA in terms of its relative retrieval in archaeological specimens, and the potential location of mtDNA in bone. It is proposed that the shift in mineral density that was found in bacterially-remodelled specimens from terrestrial contexts, relative to the excellent preservation of marine specimens, may help to explain why marine vertebrates far outnumber terrestrial ones in the fossil record, since bacterially driven microstructural change is here considered to be a destructive form of fossilisation.

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Casellas, 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.

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Thesis (M.S.)--West Virginia University, 2001.
Title from document title page. Document formatted into pages; contains vii, 73 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 64-69).

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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.

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Weston, 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.

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Janssen, 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.

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Fisher, 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.

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Fisher, 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.

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Day, 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.

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Background: Obesity is a metabolic disease caused by environmental and genetic factors. However, the epigenetic mechanisms of obesity are incompletely understood. The aim of our study was to investigate the role of skeletal muscle DNA methylation in combination with transcriptomic changes in obesity. Results: Muscle biopsies were obtained basally from lean (n = 12; BMI = 23.4 +/- 0.7 kg/m(2)) and obese (n = 10; BMI = 32.9 +/- 0.7 kg/m(2)) participants in combination with euglycemic-hyperinsulinemic clamps to assess insulin sensitivity. We performed reduced representation bisulfite sequencing (RRBS) next-generation methylation and microarray analyses on DNA and RNA isolated from vastus lateralis muscle biopsies. There were 13,130 differentially methylated cytosines (DMC; uncorrected P < 0.05) that were altered in the promoter and untranslated (5' and 3'UTR) regions in the obese versus lean analysis. Microarray analysis revealed 99 probes that were significantly (corrected P < 0.05) altered. Of these, 12 genes (encompassing 22 methylation sites) demonstrated a negative relationship between gene expression and DNA methylation. Specifically, sorbin and SH3 domain containing 3 (SORBS3) which codes for the adapter protein vinexin was significantly decreased in gene expression (fold change -1.9) and had nine DMCs that were significantly increased in methylation in obesity (methylation differences ranged from 5.0 to 24.4 %). Moreover, differentially methylated region (DMR) analysis identified a region in the 5' UTR (Chr. 8: 22,423,530-22,423,569) of SORBS3 that was increased in methylation by 11.2 % in the obese group. The negative relationship observed between DNA methylation and gene expression for SORBS3 was validated by a site-specific sequencing approach, pyrosequencing, and qRT-PCR. Additionally, we performed transcription factor binding analysis and identified a number of transcription factors whose binding to the differentially methylated sites or region may contribute to obesity. Conclusions: These results demonstrate that obesity alters the epigenome through DNA methylation and highlights novel transcriptomic changes in SORBS3 in skeletal muscle.

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Dobson, Brent S. « Skeletal and dental changes associated with the treatment of anterior open bite malocclusion ». Oklahoma City : [s.n.], 2006.

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Malm, 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/.

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Hawke, 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.

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Pickering, 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.

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McDonald, 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.

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Ullinger, 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.

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Belli, 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.

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Keough, 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.

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Forensic anthropologists and taphonomists are often tasked with interpreting the sequence of events from death through decomposition to skeletonisation. Discovery of burnt bone often evokes questions as to the condition of the body prior to the burn event. The purpose of this study was to evaluate features of thermal damage on bones in relationship to the condition of the bone (dry/wet) and progression of decomposition. Twenty-five pigs in various stages of decomposition (fresh, early, advanced, early & late skeletonisation) were exposed to fire for 30 minutes. The skeletal elements were scored and features included: colour change (unaltered, charred, calcined), brown and heat borders, heat lines, delineation, greasy bone, joint shielding, predictable and minimal cracking, delamination and heatinduced fractures. Colour changes were scored according to a ranked percentage scale (0 – 3) and the remaining traits as absent or present (0/1). Cohen’s Kappa statistics evaluated intraand interobserver error. Density plots and frequency distributions were constructed and multiple regression (categorical variables) and transition analysis were employed. The majority (8) of the 13 traits displayed potential to predict decomposition stage from burned remains. An increase in calcined and charred bone occurred synchronously with an advancement in decomposition. The organic composition of bone and presence of flesh affect the characteristics features of burned bone. Greasy bone occurred most often in the early/fresh stages (fleshed bone). Heat borders, heat lines, delineation, joint shielding, predictable and minimal cracking were associated with wet tissue/bone; whereas brown burn/borders, delamination and other heat-induced fractures were associated with early and late skeletonisation. No statistically significant differences were noted among observers for the majority of the traits except for predictable and minimal cracking and heat-induced fractures in the cranium. Heat-induced changes may assist in estimating decomposition stage from unknown, burnt remains and thereby aid in a providing an indication as to the condition of the bone prior to the burn event.
Thesis (PhD)--University of Pretoria, 2013.
gm2014
Anatomy
unrestricted

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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.

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Doctor of Philosophy
Department 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.

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Shimizu, Kevin. « Facial Tissue Changes with Microimplant Assisted Rapid Palatal Expanders ». Scholarly Commons, 2019. https://scholarlycommons.pacific.edu/dugoni_etd/1.

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Introduction: Skeletal expansion has been a treatment modality in orthodontics and orthopedics to correct skeletal transverse discrepancies with maxillary constriction. The utilization of microimplants in conjunction with these palatal expanders offers a higher degree of pure skeletal expansion and minimizes the dental side effects. The purpose of this study is to evaluate the changes of the hard and soft tissues of the face after skeletal expansion for orthodontics. Methods: 36 patients who had received successful expansion with a microimplant assisted rapid palatal expander were compared to their pre-expansion records. All patients received CBCTs from which a 3-D analysis configuration was created to trace hard and soft tissue landmarks of the midface and nasal cavity regions. 3 judges analyzed each set of records and the average was used to calculate the amount of expansion experienced at each anatomical region. A paired T-test and Wilcoxon signed-rank test were used for statistical comparison between time points. Results: Expansion can affect all of the midfacial hard tissues that support the overlying soft tissues. Increases in skeletal width from the Frontozygomatic suture down to the maxillary alveolar bone were all significant. The nasal cavity increased in width in all locations measured. Soft tissue changes were significant at the base of the ala suggesting a widening of the nose with expansion therapy. Conclusion: Maxillary expansion with microimplant assisted expanders can have skeletal changes throughout the entire midface and may affect the width of the nasal cavity. Soft tissue changes were less pronounced, and though a widening of the base of the nose may be expected this may not be noticed by the patient.

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Wretman, 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/.

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Lin, 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.

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The 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.

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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.

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Lima, 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.

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Mestrado em Bioquímica
A 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.

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Isaacs, Ashwin Wayne. « Muscle damage and adaptation in response to plyometric jumping ». Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20384.

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Thesis (MSc)--Stellenbosch University, 2012.
ENGLISH 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.
The NRF for financial assistance

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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/.

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Statistical analyses of measurements were used to evaluate congenital asymmetry and activity-related change in 100 pairs of humeri and 112 pairs of femora. Bone pairs in samples from the Nary Rose and an earlier medieval site in Norwich were subdivided into age categories and their archaeological groups for analysis. Internal bone dimensions were determined from radiographs and compared with those of a modern group of divers. Muscle insertions were ranked and femoral morphological traits were recorded. Differences were tested at the p<0.05 level of confidence. Congenital asymmetry was accepted from earlier work for maximum length of the humerus. Asymmetries decreased with age in the humerus and to a lesser extent in the femur. The humerus was shown to have significant right-sided dominance while the femur was more symmetric. Accepted methods of measuring femoral torsion were demonstrated to be inadequate. Femoral morphological traits were shown to be affected by environment. Significant results obtained from new measurements may be attributable to patterns of activity In the Nary Rose sample. These individuals were significantly taller and larger than those of the Norwich sample. Selection, diet and activity are discussed as possible explanations for these increases. Statistical comparison of compatible groups may reveal patterns of activity, if the occupations in the groups are known.

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Stirland, 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.

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Booth, 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.

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Allen, 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.

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Fatigue and skeletal muscle weakness are problems associated with congestive heart failure. Research does not support the theory that the affected cardiac function is responsible for the fatigue. During skeletal muscle fatigue, calcium handling is altered. Thus, the fatigue associated with congestive heart failure could be attributed to altered calcium handling. The main proteins involved in calcium release are the ryanodine receptor (RyR) and the dihydropyridine receptor (DHPR). The main proteins involved in calcium uptake are the fast and slow isoforms of sarco(endo)plasmic reticulum calcium ATPase (SERCA 1 and SERCA 2 respectively). Calsequestrin (Csq) and calmodulin (CaM) play regulatory roles in calcium handling. Changes in the levels of these proteins could explain alterations in calcium handling and subsequent muscle function. The purpose of this study was to use a genetic model of heart failure, the SHHF rat, to examine the levels of regulatory calcium handling proteins to determine if changes in the amounts of RyR, DHPR, SERCA1, SERCA2, Csq and CaM are altered in congestive heart failure. A significant decrease was found in the amounts of RyR, DHPR, and SERCA 1 of the SHHF gastrocnemius and diaphragm samples in comparison to the control. There was no significant difference found in the amounts of CaM or SERCA 2 between the two groups. Csq was not found to be statistically different between the two groups of the gastrocnemius samples. However, there was an increase in Csq in the SHHF diaphragm samples in comparison to the control. In conclusion, the calcium handling proteins are affected in the genetic model of heart failure. These changes could explain previous reports of altered calcium handling within the skeletal muscles of congestive heart failure animals.
Master of Science

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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.

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Thesis (M.S.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains x, 135 p. : ill. Includes abstract. Includes bibliographical references (p. 88-91).

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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.

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A healthy mitochondrial network is essential for post-mitotic tissues like muscles. During aging sarcopenia, mitochondria-shaping machinery declines. On the contrary, lifelong exercise preserves it. OPA1 is a profusion protein that plays an essential role in mitochondrial dynamics. Interesting, OPA1 protein decreases in sedentary seniors and in 18 months-old mice. Exercise in aged mice is sufficient to increase OPA1 levels in old muscles. To address the OPA1 role in skeletal muscle and further investigate its involvement in aging, we generated muscle-specific ko mice. Indeed, Opa1 mice show severe precocious senescence, degeneration of multiple organs, and premature death. Surprisingly, mitochondrial dysfunction in muscle tissue is sufficient to directly drive metabolic changes and systemic inflammation by increasing the expression and secretion of the mitokine FGF21. Although the simultaneous deletion of OPA1 and FGF21 almost reverted the phenotype, we have new evidence that connects aging with mitochondrial dysfunction, autophagy alteration, and inflammation. Our findings underscore the central role of muscle mitochondria in the regulation of signaling pathways and the maintenance of total body metabolism, underlying the importance of a functional mitochondrial population for healthy aging.
Un 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.

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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.

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The decline of physical ability that occurs with aging has been linked to reduced skeletal muscle function. It has been theorized that Ca2+ uptake and release by the sarcoplasmic reticulum (SR) is altered with aging. Data pertaining to the actual structural and functional changes of SR due to aging are limited; thus, this theory has not yet been fully proven. The purpose of this research was to determine if SR function is altered as a result of aging in the following muscles: soleus, plantaris, and diaphragm. The soleus is composed of slow twitch muscle fibers. The plantaris is composed of fast twitch muscle fibers, and the diaphragm is composed of both slow and fast twitch muscle fibers. Fisher 344 Brown x Norway Cross Rats were used as subjects for this project. A total of 12 animals were used: six in group 12 months and six in group 27 months. A Jasco CAF-110 Fluorometer and fura-2 were used to determine the rate of Ca2+ uptake and release by isolated SR vesicles. In the aged animals, mass of the soleus was reduced by 22%, while the plantaris was reduced by 23%, and the diaphragm by 15%. However, these differences were eliminated when masses were normalized by body mass. In all three muscles examined, the rates of Ca2+ uptake were not significantly different between the young and aged animals. Rates of Ca2+ release, however, were reduced by 30% in both the plantaris and diaphragm of the aged animals. These results suggest that SR function is altered in "fast" muscles of the rat. It is possible that changes in SR Ca release may contribute to diminished muscle function and also lead to the decline in physical ability of older adults.
Master of Science

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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/.

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Ageing is defined as an age-related increase in susceptibility to diseases and death and is a complex process that affects every major system at the molecular, cellular and organ level. Although the exact cause of ageing is unknown, there is significant evidence that oxidative stress plays a major role in the ageing process. Skeletal muscle produces oxidants from a variety of different sources with nitric oxide and superoxide being the primary radical species. Nitric oxide is regulated by the activity of nitric oxide synthases, however the sites that modulate changes in superoxide remain unclear. Skeletal muscle ageing is associated with a reduction in muscle mass and strength and leads to a significant vulnerability that opposes healthy ageing. Reports have indicated a positive correlation between tissue concentrations of oxidised macromolecules in skeletal muscle of old individuals, which implies the possible involvement of reactive species in the processes of skeletal muscle ageing. The role of oxidants in skeletal muscle ageing has also been extensively examined in different model organisms, which have undergone genetic manipulations and reports have shown that absence of Cu, Zn superoxide dismutase (SOD1) in homozygotic SOD1 knockout mice, induces an acceleration of skeletal muscle ageing phenotypic changes which further provides support for the implication of radical species in the processes of muscle ageing. The overall aim of the work carried out in this thesis was; i) to develop specific techniques to determine changes in superoxide within the cytosolic and mitochondrial compartment of skeletal muscle, ii) to identify the major sites for superoxide generation in skeletal muscle and iii) to identify the reactive species that are involved in the accelerated loss of muscle mass in the homozygotic SOD1 knockout mouse model and to characterize the changes in redox status and adaptive responses that occur in muscles from the SOD1 knockout mice. The results of carried out in this thesis indicated that the superoxide sensitive fluorescent probes dihydroethidium and MitoSOX Red were capable of selectively detecting changes in superoxide within the cytosolic and mitochondrial matrix of skeletal muscle, respectively. Specific pathway inhibitors and immunolocalisation techniques showed that the major sub-cellular sites contributing to cytosolic superoxide changes in skeletal muscle both at rest and during contractions were the NAD(P)H oxidases. Finally with the use of single isolated muscle fibres from the flexor digitorum brevis muscle, it was concluded that formation of peroxynitrite in muscle fibres was a major effect of lack of SOD1 in SOD1 null mice, which may contribute to fibre loss in this model. Techniques developed in this study to monitor real-time changes in superoxide in the mitochondrial and cytosolic compartment of muscle fibres provided a useful tool to i) examine the sub-cellular pathways that are involved in the regulation of superoxide at rest and during contractile activity in skeletal muscle and to ii) determine the role of superoxide in skeletal muscle degeneration observed in SOD1 knockout mice. These results may have widespread implications for the understanding of diverse scientific areas, including the responses of muscle to exercise training, age-related loss of muscle mass and function, as well as inflammatory or degenerative muscle diseases, such as the muscular dystrophies that are associated with increased levels of oxidative damage.

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Jawaid, 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.

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The morphology of NMJ was quantified in soleus and EDL muscles during postnatal development. Differences were extensively quantified in adults by measuring various parameters (e.g. junctional area, terminal area, width/length ratio, fragmentation of the terminal, shape coefficient). The fluorescent marker FMI-43 was used to label the presynaptic synaptic vesicles in the terminals, and postsynaptic acetylcholine receptors were labelled with fluorescent Rh α-bungarotoxin. Fibre type proportions and fibre diameter were also studied to see if there is any relation between NMJ morphology and fibre type proportion of fibre diameter. Fibre types in both muscles were studied by using histochemistry and immunohistochemistry. The results demonstrate that NMJ morphologies are very similar initially, except for shape coefficient. Marked changes in NMJ morphological parameters occur in the third postnatal week, when both muscles diverge from their common neonatal activity pattern. Fibre type proportion, initially were slow in both muscles. After onset of the adult activity pattern, the rearrangement in fibre proportions makes soleus predominantly slow- and EDL a fast-twitch muscle. Fibre diameter is always greater in soleus. Fibre diameter increased in both muscles but only after the onset of adult activity. Soleus fibres were wider but have longer synapses. Finally, width/length ratio was found to be a major discriminator between NMJ morphologies in the two muscles. In soleus muscle, but not EDL, a reasonable correlation between width/length ratio of NMJ morphology and fibre types was found. All differences appeared after the establishment of adult activity pattern, supporting the hypothesis. Comparison with other studies, however, suggests the effects of activity are probably indirect, via changes in fibre diameter.

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Nordlund, 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/.

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Pasniciuc, Silviu Valeriu. « Complex mechanisms of metabolic regulation in nonperfused muscle ». The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1049304386.

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Luk, 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/.

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Skeletal muscle satellite cells are important for muscle repairing and muscle mass growth. For a successful muscle regenerative process, satellite cells have to sequentially undergoing different stages of myogenic process, i.e. proliferative state and differentiation state. To support this process, the presence of different circulating factors, such as immune cells, cytokines, and hormones, at the appropriate time course is critical. Among these factors, hormones, such as testosterone, cortisol, and IGF-1, have shown to play an important role in satellite cell proliferation and differentiation. Studies investigated the effect of testosterone on satellite cell using a supraphysiological dose in human or in cell culture demonstrated that testosterone is critical in satellite cell myogenic process. Due to the anabolic effect of testosterone on muscle, studies had been focused on the physiological means to increase the circulating testosterone concentration in the body to maximize the muscle mass growth from resistance exercise. The acute and transient increase in testosterone has shown to be beneficial to muscle mass growth and strength gain; however, this change in physiological testosterone concentration on satellite cell myogenesis is not known. Therefore the purpose of this dissertation is to first determine the effect of acute change in exercise-induced hormones on satellite cell myogenic state, then to determine if testosterone promotes satellite cell proliferation.

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Puhke, 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.

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Thèses sur le sujet « Skeletal change »

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