Thesis (Ph. D.)--University of Missouri--Columbia, 2004. / "December 2004" Typescript. Vita. Includes bibliographical references (l. 180-210). Also issued on the Internet.

Background. In this thesis a novel method of skinning a mesh utilizing Nvidia’sTuring Mesh Shader pipeline is presented. Skinning a mesh is often performed with a Vertex Shader or a Compute Shader. By leveraging the strengths of the new pipeline it may be possible to further optimize the skinning process and increase performance, especially for more complex meshes. Objectives. The aim is to determine if the novel method is a suitable replacement for existing skinning implementations. The key metrics being studied is the total GPU frame time of the novel implementation in relation to the rest, and its total memory usage. Methods. Beyond the pre-existing implementations such as Vertex Shader skinning and Compute Shader skinning, two new methods using Mesh Shaders are implemented. The first implementation being a naive method that simply divides the mesh into meshlets and skins each meshlet in isolation. The proposed novel common influences method instead takes the skinning data, such as the joint influences of each vertex, into account when generating meshlets. The intention is to produce meshlets where all vertices are influenced by the same joints, allowing for information to be moved from a per vertex basis to a per meshlet basis. Allowing for fewer fetches to occur in the shader at run-time and potentially better performance. Results. The results indicate that utilizing Mesh Shaders results in approximately identical performance compared to Vertex Shader skinning, (which was observed to be the fastest of the previous implementations) with the novel implementation being marginally slower due to the increased number of meshlets generated. Mesh Shading has the potential to be faster if optimizations unique to the new shaders are employed. Despite producing more meshlets, the novel implementation is not significantly slower and is faster at processing individual meshlets compared to the naive approach. The novel Common Influences implementation spends between 15-22% less time processing each meshlet at run-time compared to the naive solution. Conclusions. Ultimately the unique capabilities of Mesh Shaders allow for potential performance increases to be had. The proposed novel Common Influences method shows promise due to it being faster on a per meshlet basis, but more work must be done in order to reduce the number of meshlets generated. The Mesh Shading pipeline is as of writing very new and there is a lot of potential for future work to further enhance and optimize the work presented in this thesis. More work must be done in order to make the meshlet generation more efficient so that the run-time workload is reduced as much as possible. / Bakgrund. I denna avhandling presenteras en ny metod för att deformera en modell med hjälp av den nya Mesh Shader funktionaliteten som är tillgänglig i Nvidias nya Turing arkitektur. Deformering av modeller utförs just nu oftast med så kallade Vertex eller Compute Shaders. Genom att nyttja styrkan hos den nya arkitekturen så kan det vara möjligt att ytterligare optimera deformeringsprocessen och på så sätt öka prestandan. Speciellt i samband där mer komplexa modeller används. Syfte. Syftet är att avgöra om den nya metoden är en lämplig ersättning av de nuvarande implementationerna. De viktigaste aspekterna som studeras är den totala GPU-exekveringstiden per bild som renderas av den nya metoden i förhållande till resterande, samt dess totala minnesanvändning. Metod. Utöver de befintliga implementeringarna, såsom Vertex Shader deformering och Compute Shader deformering, implementeras två nya metoder som använder Mesh Shaders. Den första implementeringen är en naiv metod som helt enkelt delar modellen i mindre delar, så kallade meshlets och deformerar varje meshlet i isolering. Den föreslagna nya common influences metoden tar i stället hänsyn till deformeringsdatan som tillhör modellen, såsom de gemensamma inverkningarna av varje vertex, vid generering av meshlets.  Avsikten är att producera meshlets där alla vertriser påverkas av samma leder i modellens skelett, vilket gör det möjligt att flytta informationen från en per vertris basis till en per meshlet basis. Detta tillåter att färre hämtningar sker på grafikkortet vid körning och vilket kan potentiellt ge bättre prestanda. Resultat. Resultaten indikerar att utnyttjandet av Mesh Shaders resulterar i ungefär samma prestanda jämfört med Vertex Shader deformering, (som observerades vara den snabbaste av de existerande implementationerna) samt att den orginella implementationen är marginellt långsammare på grund av ett högre antal meshlets genereras. Mesh Shading har potential till att bli snabbare om optimeringar somär unika till den nya arkitekturen används. Trots att man producerar fler meshlets,är den nya metoden inte markant långsammare och är snabbare med att bearbeta meshlets individuellt jämfört med den naiva implementationen. Den orginella implementationen spenderar mellan 15-22% mindre tid per meshlet vid körtid jämfört med den naiva lösningen. Slutsatser. I slutändan så erbjuder Mesh Shaders unika nya möjligheter till optimeringar som kan leda till potentiellt bättre prestanda. Den föreslagna nya Common Influences-metoden är lovande på grund av att den är snabbare per meshlet, men mer arbete måste utföras för att minska antalet genererade meshlets. Mash Shaders och Turing arkitekturen är vid skrivande stund fortfarande väldigt nya och det finns mycket potential för framtida arbeten att yterrligare förbättra och optimera det arbete som presenteras i denna avhandling. Mer arbete måste utföras för att göra meshletgenereringen effektivare så att arbetet som måste utföras under körtid minskas så mycket som möjligt.

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This work presents an automatic cost-analysis system for an implicitly parallel skeletal programming language. Although deducing interesting dynamic characteristics of parallel programs (and in particular, run time) is well known to be an intractable problem in the general case, it can be alleviated by placing restrictions upon the programs which can be expressed. By combining two research threads, the “skeletal” and “shapely” paradigms which take this route, we produce a completely automated, computation and communication sensitive cost analysis system. This builds on earlier work in the area by quantifying communication as well as computation costs, with the former being derived for the Bulk Synchronous Parallel (BSP) model. We present details of our shapely skeletal language and its BSP implementation strategy together with an account of the analysis mechanism by which program behaviour information (such as shape and cost) is statically deduced. This information can be used at compile-time to optimise a BSP implementation and to analyse computation and communication costs. The analysis has been implemented in Haskell. We consider different algorithms expressed in our language for some example problems and illustrate each BSP implementation, contrasting the analysis of their efficiency by traditional, intuitive methods with that achieved by our cost calculator. The accuracy of cost predictions by our cost calculator against the run time of real parallel programs is tested experimentally. Previous shape-based cost analysis required all elements of a vector (our nestable bulk data structure) to have the same shape. We partially relax this strict requirement on data structure regularity by introducing new shape expressions in our analysis framework. We demonstrate that this allows us to achieve the first automated analysis of a complete derivation, the well known maximum segment sum algorithm of Skillicorn and Cai.

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

Despite the normally robust regenerative capacity of muscle tissue, extensive soft tissue damage often results in a functional loss that cannot be restored using classic reconstruction techniques. Although implanted biomaterials are capable of mechanically transmitting force generated from the remaining tissue, cellular repopulation, reinnervation and revascularization of the injured area is necessary to achieve complete functional restoration. Using an in vivo tissue engineering model, a 1.0 x 1.0 cm portion of the lateral gastrocnemius (LGAS) of Lewis rats was removed and replaced with a muscle-derived extracellular matrix (ECM). Constructs were seeded with bone marrow-derived (BMSCs) or adipose-derived stem cells (ADSCs) and the peroneal nerve was relocated over the implanted ECM. Creation of the defect resulted in a functional impairment of the LGAS, only capable of producing 85.1 ± 4.1% of the force generated in the contralateral LGAS following ECM implantation. A significant increase in specific tension (SPo) was seen in all groups following the nerve relocation procedure when compared to their corresponding cellular treatment without nerve relocation (p < 0.05). Histological quantification revealed significant increases in cellular content and blood vessel density in the top and bottom regions of ECM implants seeded with BMSCs (p < 0.05). The nerve relocation procedure significantly increased these same variables within the middle region of the ECM when compared to all groups lacking this treatment (p < 0.05). The presence of regenerating myofibers was immunofluorescently confirmed using antibodies against desmin, myosin heavy chain and laminin, while their developmental state was substantiated by the presence of central nuclei. These data corroborate a therapeutic effect of BMSCs on skeletal muscle regeneration within the ECM implant that was not seen following ADSC injection. Furthermore, the nerve relocation procedure stimulated an increased cellular and vascular growth within the middle region of the construct, likely the cause of improved functional output. / text

Skeletal muscle protein synthesis is regulated by the mammalian target of rapamycin (mTOR) signaling pathway. The first objective was to optimize the methodological procedures for assessing mTOR signaling in horses. The response of mTOR signaling (P-Akt Ser473, P-S6K1 Thr389, P-rpS6 Ser235/26 & 240/244, and P-4EBP1 Thr37/46 by Western blotting techniques) to meal consumption was determined at three gluteal muscle biopsy depths (6, 8, and 10 cm), and the repeatability of the contralateral side at 8 cm during 5 days of repeated biopsies. There was no effect (P > 0.05) of sampling side or biopsy depth on mTOR signaling in mature horses. During repeated biopsies there was an increase (P < 0.05) in downstream (P-S6K1 Thr389, P-rpS6 Ser235/236 & 240/244 and P-4EBP1 Thr389) mTOR signaling in response to feeding. The second objective was to characterize alterations in mTOR signaling throughout the equid lifespan. Adolescent horses (yearlings and two year olds) studied in the postprandial had a lowered (P < 0.05) activation of downstream mTOR signaling with aging. There was a lower (P < 0.05) abundance of P-S6K1 Thr389 in aged horses (23.5 years old) than in mature horses (11 years old) during the post-absorptive state. The final objective was to assess mTOR signaling during acute and chronic inflammation. Acute inflammation occurred during 5 days of repeated biopsies, and chronic inflammation is characteristic of the aged. During acute inflammation, characterized by increased muscle mRNA expression of inflammatory cytokines, there was an increase (P < 0.05) in downstream mTOR signaling. Chronic inflammation resulted in a decrease (P < 0.05) in the abundance of P-S6K1 Thr389. Phenylbutazone was administered to reduce (P < 0.05) acute and chronic inflammation in muscle. Phenylbutazone administration during acute inflammation reduced (P < 0.05) the activation of downstream mTOR signaling and trended to increase (P = 0.09) P-S6K1 Thr389 abundance during chronic inflammation. Whole-body protein synthesis determined using isotope infusion techniques increased (P < 0.05) when chronic inflammation was reduced due to phenylbutazone administration. This research provides new standards for muscle biopsy collection when examining mTOR signaling, and insight into management and feeding practices for adolescent and aging horses.

Skeletal muscle regeneration is a multifaceted process requiring the spatial and temporal coordination of myogenesis as well as angiogenesis. While these processes are often studied independently, recent evidence from our lab has shown that the resident adult stem cell population within skeletal muscle, called satellite cells, begins secreting soluble growth factors likely to contribute to the proangiogenic response. The overall aim of this study is to investigate the role of pro-angiogenic factors secreted by satellite cells during skeletal muscle regeneration. Results from the study indicate that Hepatocyte Growth Factor (HGF) is a critical protein for the proangiogenic effect of satellite cells. It was also shown that in hypoxic environments, such as those seen in an injury state, it appears that satellite cells decrease their proangiogenic effect if oxygen levels fall below a threshold level. This decrease in pro-angiogenic effect in the hypoxic environment appears to be due to the decrease in HGF expression and protein secretion and is not compensated for by the increase in Vascular Endothelial Growth Factor secretion also seen in the hypoxic response. Furthermore, the regulation of HGF in these hypoxic conditions appears to be in part due to increased levels of hypoxia inducible factor, which are acting on the hypoxia response element site found on the HGF promoter. In the last set of experiments, this injury response was further investigated as the effect of satellite cell mediated angiogenesis was examined in the disease state of muscular dystrophy. Here, we also observed a reduction in angiogenesis from media conditioned by satellite cells from dystrophic muscle compared to healthy muscle. Overall, this study further strengthens the case for satellite cells as important mediators of the angiogenic response in regenerating muscle and may serve as a potential site for therapeutic intervention in the future.

Cold-water immersion (CWI) is a common recovery modality used to facilitate restoration of pre-exercise muscle force generation and soreness following high-intensity exercise. Although it is commonly used by athletes and commonly studied in sport science, evidence is equivocal regarding its efficacy. We compared 4 CWI protocols (10 or 30 minutes at 10 or 20°C) of different durations and temperatures with passive rest for their effects on drop jump and squat jump height, inflammation (IL-6, IL-10, IL-8, MPO, IL-1β, TNFα, IFNγ, GM-CSF, IL-2), and ratings of soreness/impairment following high-intensity intermittent sprint-exercise. CWI for 10 minutes at 10°C promoted restoration of force generation, while CWI for 30 minutes at 10°C was associated with lower ratings of soreness/impairment, but higher plasma IL-8 and MPO at 2 hours post-exercise. Overall, minor functional benefits of CWI for 10 minutes at 10°C were observed, while longer duration CWI protocols may increase post-exercise inflammation.

Cold-water immersion (CWI) is a common recovery modality used to facilitate restoration of pre-exercise muscle force generation and soreness following high-intensity exercise. Although it is commonly used by athletes and commonly studied in sport science, evidence is equivocal regarding its efficacy. We compared 4 CWI protocols (10 or 30 minutes at 10 or 20°C) of different durations and temperatures with passive rest for their effects on drop jump and squat jump height, inflammation (IL-6, IL-10, IL-8, MPO, IL-1β, TNFα, IFNγ, GM-CSF, IL-2), and ratings of soreness/impairment following high-intensity intermittent sprint-exercise. CWI for 10 minutes at 10°C promoted restoration of force generation, while CWI for 30 minutes at 10°C was associated with lower ratings of soreness/impairment, but higher plasma IL-8 and MPO at 2 hours post-exercise. Overall, minor functional benefits of CWI for 10 minutes at 10°C were observed, while longer duration CWI protocols may increase post-exercise inflammation.