Spelling suggestions: "subject:"1l1uscle, skeletal"" "subject:"arbuscle, skeletal""
11 |
An analysis of metabolic fluxes in contracting human skeletal muscle /Crowther, Gregory John. January 2002 (has links)
Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 115-132).
|
12 |
Regualtion of myogenesis and skeletal muscle size by the myostatin-Smad and mammalian Hippo signalling transduction pathwaysWatt, Kevin. January 2009 (has links)
Thesis (Ph.D.)--Aberdeen University, 2009. / Title from web page (viewed on Mar. 30, 2010). Includes bibliographical references.
|
13 |
Low-frequency muscle contraction increases microvascular blood volume in normal and insulin resistant states /Inyard, April Corinne. January 2008 (has links)
Thesis (Ph. D.)--University of Virginia, 2008. / Includes bibliographical references. Also available in electronic form as viewed 2/16/2009.
|
14 |
Regulation of myogenesis and skeletal muscle size by the myostatin-Smad and mammalian Hippo signalling transduction pathwaysWatt, Kevin January 2009 (has links)
The aims of this thesis were to 1) investigate the effect of SB431542 <i>in vitro</i> and <i>ex vivo</i> as a novel approach towards promoting the functional hypertrophy of skeletal muscle by inhibiting the myostatin-Smad pathway, 2) to investigate the expression and function of the Yes-associated protein (Yap) in skeletal muscle and C2C12 cells as a novel regulator of C2C12 differentiation and 3) to generate a GFP-RCASBP-hYAP1 S127A retrovirus to allow the study of the function of Yap in skeletal muscle differentiation <i>in vivo</i>. The results presented in this thesis show that SB431542 promotes the hypertrophy of C2C12 myotubes and mature <i>Xenopus</i> skeletal muscle fibres. However, SB431542 treatment also results in a reduction in specific force of mature <i>Xenopus</i> muscle fibres suggesting that SB431542 is not suitable as a treatment for skeletal muscle atrophy. These results also show that Yap is expressed in mouse skeletal muscle <i>in vivo</i> and that Yap is a novel regulator of C2C12 differentiation. Finally, these results descried the generation of a GFP-RCASBP-hYAP1 S127A retrovirus that can be used to assess the role of Yap <i>in vivo </i>during skeletal muscle formation in the chick embryo. Together, these results suggest that Yap is a novel regulator of C2C12 differentiation that should be studied as a potential therapeutic target in musculoskeletal diseases.
|
15 |
Skeletal muscle damage repair and adaptation to uphill and downhill running in humansKrafft, Ingrid January 1994 (has links)
A Dissertation Submitted to the Department of Physiology, University of the Witwatersrand, Johannesburg for the Degree of Master of Science. / Extensive disruption of muscle fibres has been shown to occur after short term eccentric exercise where high mechanical forces are generated. This study tested whether downhill running acts as a stimulus for inducing eccentric damage, and results in greater muscle damage and deterioration in muscular performance than an equal workload of uphill running. The study aimed at determining whether an adaptation or training eflect takes place such that the muscle is more resistant to the damaging effects of a repeated bout of the same exercise. In addition, the study aimed at determining whether the lower muscle volumes and forces of muscular contractions in females compared to males, makes females less susceptible to the damaging effects of eccentric contraction. / IT2018
|
16 |
Vasomotor responses of rat skeletal muscle arterioles to norepinephrine and adenosine /Aaker, Aaron Paul, January 2001 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2001. / "May 2001." Typescript. Vita. Includes bibliographical references (leaves 122-137). Also available on the Internet.
|
17 |
An investigation of the Coxsackie and Adenovirus Receptor in striated muscle /Shaw, Christian A. January 2006 (has links)
Since its identification in 1997 as the common receptor for Coxsackie and adenovirus (CAR) multiple lines of evidence argue in favor of CAR contributing to aspects of cell adhesion in addition to serving as a viral receptor. Nevertheless, a precise biological role for CAR remains to be identified suggesting the receptor may participate in a variety of cellular functions that reflect its tissue specific and developmentally regulated expression. This thesis elucidates aspects of CAR biology in mature striated muscle by providing studies that encompass (i) its physiological cellular/subcellular localization and expression in mature striated muscle (ii) its expression profile in human diseased skeletal muscle and (iii) the potential consequences of its sustained expression in mature striated muscle where its levels would otherwise be highly attenuated. / In non-diseased, mature striated muscle despite low and barely detectable levels of the CAR transcript (cardiac and skeletal muscle respectively), we identified CAR as a novel component of the neuromuscular junction and showed its expression to be isoform-specific in contrast to the intercalated discs, where both predominant CAR isoforms are detected. We then investigated the expression of CAR at the level of human skeletal muscle disease. From these studies we observed that in diseases characterized by active necrosis and regeneration, extrasynaptic CAR expression is detectable in regenerating fibers and co-expressed with other previously described markers of regeneration at a high degree of coincidence. Moreover, extrasynaptic CAR expression appears to be a highly reliable indicator of the regenerative process offering potential use at the diagnostic level. Following these investigations, our final studies involved assessing whether sustained CAR expression might affect the normal homeostasis in skeletal and cardiac muscle using a transgenic mouse model. We discovered that transgenic mice expressing sustained high levels of CAR (as seen in the CAR+/+ transgenics) develop a lethal necrotizing myopathy characterized by dual deficiencies in dystrophin and dysferlin, two proteins pivotal in maintaining plasmalemmal integrity, raising the possibility for a previously unrecognized cause of skeletal muscle dysfunction. / Collectively these findings argue that in non-diseased mature skeletal and cardiac muscle, CAR expression is restricted to the neuromuscular junction and cardiac intercalated discs but in diseases of skeletal muscle characterized by active necrosis and regeneration, extrasynaptic CAR expression is reexpressed at these sites of injury/repair. In addition they raise the possibility that sustained CAR expression in mature skeletal muscle may be associated with altered muscle homeostasis.
|
18 |
The role of exercise and exercise-related factors in the control of mitochondrial oxidative function /Walsh, Brandon, January 2002 (has links)
Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.
|
19 |
Tendon transfer mechanics and donor muscle properties : implications in surgical correction of upper limb muscle imbalance /Pontén, Eva, January 2003 (has links)
Diss. (sammanfattning) Umeå : University, 2003. / Härtill 5 uppsatser.
|
20 |
Ankle stretch reflexes during anticipatory postural adjustmentsVedula, Siddharth. January 2009 (has links)
Thesis (M.Eng.). / Written for the Dept. of Biomedical Engineering. Title from title page of PDF (viewed 2009/06/17). Includes bibliographical references.
|
Page generated in 0.067 seconds