Дисертації з теми "GlycoGag"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 дисертацій для дослідження на тему "GlycoGag".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Переглядайте дисертації для різних дисциплін та оформлюйте правильно вашу бібліографію.
Bertelli, Cinzia. "Antiviral activity and retroviral counteraction of SERINC genes." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/321392.
Повний текст джерелаSyed, Noor Afshan. "Regulation of glycogen synthase and glycogen phosphorylase by insulin in HepG2 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63926.pdf.
Повний текст джерелаMartin, Jennifer Louise. "Molecular interactions involving glycogen phosphorylase." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253306.
Повний текст джерелаGhosh, Paritosh. "De Novo Glycogen Biosynthesis by a Glycogen Primer Complex in the Obliquely Striated Skeletal Muscle of Ascaris suum." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc935639/.
Повний текст джерелаKaris, Nils David. "Design and Synthesis of 1,3-Disubstitiuted-2-Pyridones as a New Class of Glycogen Phosphorylase Inhibitors." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/365791.
Повний текст джерелаThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Eskitis Institute for Cell and Molecular Therapies
Science, Environment, Engineering and Technology
Full Text
Street, Ian Philip. "Protein - carbohydrate interactions in glycogen phosphorylase." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25049.
Повний текст джерелаScience, Faculty of
Chemistry, Department of
Graduate
Stambolic, Vuk. "Regulation of glycogen synthase kinase-3." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0003/NQ27730.pdf.
Повний текст джерелаFraser, Bernadine Heather. "Glycogen and glucose metabolism in cardioprotection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ34764.pdf.
Повний текст джерелаHenning, Sarah Louise. "Myocardial glycogen metabolism and its regulation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61107.pdf.
Повний текст джерелаBarford, D. "Crystallographic studies on glycogen phosphorylase b." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233473.
Повний текст джерелаMcLaughlin, P. J. "Crystallographic studies on glycogen phosphorylase b." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370290.
Повний текст джерелаBichard, Claire J. F. "Synthesis of potential glycogen phosphorylase inhibitors." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260115.
Повний текст джерелаHu, Shu-Hong. "Crystallographic studies on activated glycogen phosphorylase." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291283.
Повний текст джерелаStambolic, Vuk. "Regulation of glycogen synthase kinase-3." Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.nlc-bnc.ca/obj/s4/f2/dsk2/tape16/PQDD%5F0003/NQ27730.pdf.
Повний текст джерелаHiguita, Juan Carlos. "Molecular consequences of cellular UDP-glucose deficiency /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-901-3/.
Повний текст джерелаHannigan, Linda L. (Linda Lucile). "Purification and characterization of glycogen synthase from Ascaris suum." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc798067/.
Повний текст джерелаMitchell, Edward Peter. "Cryocrystallographic and mechanistic studies on glycogen phosphorylase." Thesis, University of Oxford, 1994. https://ora.ox.ac.uk/objects/uuid:d562f4f6-0a93-43a6-ad74-d480697d1b8c.
Повний текст джерелаNitschke, Felix. "Phosphorylation of polyglycans, especially glycogen and starch." Phd thesis, Universität Potsdam, 2013. http://opus.kobv.de/ubp/volltexte/2013/6739/.
Повний текст джерелаPflanzen und Tiere speichern Glukose in hochmolekularen Kohlenhydraten, um diese bei Bedarf unter anderem zur Gewinnung von Energie zu nutzen. Amylopectin, der größte Bestandteil des pflanzlichen Speicherkohlenhydrats Stärke, und das tierische Äquivalent Glykogen sind chemisch betrachtet ähnlich, denn sie bestehen aus verzweigten Ketten, deren Bausteine (Glukosylreste) auf identische Weise miteinander verbunden sind. Zudem kommen in beiden Kohlenhydraten kleine aber ähnliche Mengen von Phosphatgruppen vor, die offenbar eine tragende Rolle in Pflanzen und Tieren spielen. Ist in Pflanzen der Einbau oder die Entfernung von Phosphatgruppen in bzw. aus Stärke gestört, so ist oft der gesamte Stärkestoffwechsel beeinträchtigt. Dies zeigt sich unter anderem in der übermäßigen Akkumulation von Stärke und in Wachstumsverzögerungen der gesamten Pflanze. Beim Menschen und anderen Säugern beruht eine schwere Form der Epilepsie (Lafora disease) auf einer Störung des Glykogenstoffwechsels. Sie wird durch das erblich bedingte Fehlen eines Enzyms ausgelöst, das Phosphatgruppen aus dem Glykogen entfernt. Während die Enzyme, die für die Entfernung des Phosphats aus Stärke und Glykogen verantwortlich sind, hohe Ähnlichkeit aufweisen, ist momentan die Ansicht weit verbreitet, dass der Einbau von Phosphat in beide Speicherkohlenhydrate auf höchst unterschiedliche Weise erfolgt. In Pflanzen sind zwei Enzyme bekannt, die Phosphatgruppen an unterschiedlichen Stellen in Glukosylreste einbauen (Kohlenstoffatome 6 und 3). In Tieren soll eine seltene, unvermeidbare und zufällig auftretende Nebenreaktion eines Enzyms, das eigentlich die Ketten des Glykogens verlängert (Glykogen-Synthase), den Einbau von Phosphat bewirken, der somit als unwillkürlich gilt und weithin als „biochemischer Fehler“ (mit fatalen Konsequenzen bei ausbleibender Korrektur) betrachtet wird. In den Glukosylresten des Glykogens sollen ausschließlich die C-Atome 2 und 3 phosphoryliert sein. Die Ergebnisse dieser Arbeit zeigen mittels zweier unabhängiger Methoden, dass Glykogen auch am Glukosyl-Kohlenstoff 6 phosphoryliert ist, der Phosphatposition, die in der Stärke am häufigsten vorkommt. Die Tatsache, dass in dieser Arbeit Phosphat neben Stärke auch erstmals an Glukosylresten von anderen pflanzlichen Kohlenhydraten (wasserlösliche Heteroglykane) nachgewiesen werden konnte, lässt vermuten, dass Phosphorylierung ein generelles Phänomen bei Polysacchariden ist. Des Weiteren wiesen die Ergebnisse darauf hin, dass Phosphat im Glykogen, wie auch in der Stärke, einem bestimmten Zweck dient, der im Zusammenhang mit der Regulation von Kettenverzweigung steht, und dass kein zufälliges biochemisches Ereignis für den Einbau verantwortlich sein kann. Aufgrund der grundlegenden Ähnlichkeiten im Stärke- und Glykogenstoffwechsel, liegt es nahe, dass die Phosphorylierung von Glykogen, ähnlich der von Stärke, ebenfalls durch spezifische Enzyme bewirkt wird. Ein besseres Verständnis der Mechanismen, die der Glykogen-Phosphorylierung zugrunde liegen, kann neue Möglichkeiten der Behandlung von Lafora disease aufzeigen.
Duke, Elizabeth Mary Helen. "X-ray diffraction studies on glycogen phosphorylase." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336092.
Повний текст джерелаKensley, Joy A. "Glycogen metabolism in Corynebacterium glutamicum ATCC 13032." Doctoral thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/4279.
Повний текст джерелаCorynebacterium glutamicum is a Gram-positive facultative aerobe particularly known for its industrial application in the synthesis of amino acids, such as L-glutamate and Llysine. The central metabolic pathways of this organism has been an area of much research by many groups. Linked to glycolysis is the synthesis of glycogen, previously considered a storage molecule of excess glucose. No information concerning the role of glycogen or its metabolism in C. glutamicum was known, and the aim of this work was to elucidate glycogen metabolism in this industrially important organism.
Allen, Tara J. "Characterization of vascular smooth muscle oxidative metabolism using ¹³C-isotopomer analysis of glutamate." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9988641.
Повний текст джерелаPuthanveetil, Prasanth Nair. "Glucocorticoid and its effect on cardiac glucose utilization." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5038.
Повний текст джерелаWatson, Kimberly Ann. "Crystallographic studies on phosphorylase : sugar recognition properties." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259849.
Повний текст джерелаBruce, Mark. "Amino acid metabolism during exercise and recovery in human subjects." Thesis, Loughborough University, 2001. https://dspace.lboro.ac.uk/2134/33569.
Повний текст джерелаGreen, Andrew R. "Interaction of phosphorylase and glycogen synthase in the defective control of glycogen metabolism in hepatocytes from the Zucker fatty rat." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413954.
Повний текст джерелаLees, Simon J. "The effects of fatigue on glycogen, glycogen phosphorylase, and calcium uptake associated with the sarcoplasmic reticulum of rat skeletal muscle." Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/35506.
Повний текст джерелаSkeletal muscle fatigue can be defined as the inability to produce a desired amount of force. Fatigue can not only limit athletic performance and rehabilitation, but it can affect one's ability to perform every day activity as well. Despite extensive investigation of muscle fatigue, little is known about the exact mechanisms that result in decreased muscle performance. It likely involves several factors that are themselves dependent upon activation patterns and intensity. The process of excitation-contraction (EC) coupling is of particular importance with respect to regulation of force production. The release of calcium (Ca2+) from the sarcoplasmic reticulum (SR), which is stimulated by the depolarization of the sarcolemma, causes muscle contraction. The SR Ca2+-adenosine triphosphatase (ATPase) drives the translocation of two Ca2+ ions into the SR, utilizing the energy derived from the hydrolysis of one adenosine triphosphate (ATP) molecule. The process of SR Ca2+ uptake causes muscle relaxation. It has been proposed that both glycogen and glycolytic enzymes are associated with the SR membrane (SR-glycogenolytic complex). Interestingly, glycogen phosphorylase, an enzyme involved in glycogen breakdown, seems to be associated with the SR-glycogenolytic complex through its binding to glycogen. The presence of the SR-glycogenolytic system may serve to locally regenerate ATP utilized by the SR Ca2+-ATPase.
The purpose of the present study was to investigate the effects of prolonged muscle contraction on glycogen concentration, glycogen phosphorylase content and activity, and maximum Ca2+ uptake rate associated with the SR. Tetanic contractions, elicited once per second for 15 minutes, significantly reduced glycogen associated with SR to 5.1% of control from 401.17 ± 79.81 to 20.46 ± 2.16 mg/mg SR protein (p⠤0.05). The optical density of glycogen phosphorylase from SDS-PAGE was significantly reduced to 21.2% of control (p⠤0.05). Activity of glycogen phosphorylase, in the direction of glycogen breakdown, was significantly reduced to 4.1% of control (p⠤0.05). Pyridoxal 5'-phosphate (PLP) concentration, a quantitative indicator of glycogen phosphorylase content, was significantly reduced to 3.3% of control (£ 0.05). Maximum SR Ca2+ uptake rates were significantly reduced to 80.8% of control (£ 0.05). These data suggest reduced glycogen and glycogen phosphorylase may be involved, either directly or indirectly, in a mechanism that causes decreased SR Ca2+ uptake normally found in fatigue.
Master of Science
au, R. Jacob@central murdoch edu, and Robin Henry Jacob. "Optimising the concentration of glycogen in lamb meat." Murdoch University, 2003. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20040513.153312.
Повний текст джерелаVarvill, Katherine Mary. "X-ray crystallographic studies on glycogen phosphorylase b." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352921.
Повний текст джерелаMung, Kwan-long, and 蒙君朗. "Regulation of glycogen phosphorylase in hypoxic cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/211148.
Повний текст джерелаpublished_or_final_version
Biochemistry
Master
Master of Philosophy
Pascoe, David D. "Glycogen synthesis in skeletal muscle following resistive exercise." Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/720309.
Повний текст джерелаHuman Performance Laboratory
Halse, Reza. "Control of glycogen synthesis in cultured human muscle." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310172.
Повний текст джерелаRusbridge, Nicholas Mercer. "Tryptic proteolysis of glycogen phosphorylase b in vitro." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317367.
Повний текст джерелаMcConchie, Stephen Mark. "Molecular heterogeneity of human muscle glycogen phosphorylase deficiency." Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317266.
Повний текст джерелаJiang, Xianguo. "Investigating adrenoceptor regulation of the astroglial glycogen reserve." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40130.
Повний текст джерелаХарченко, Каріна Олександрівна, and Олександра Юріївна Кушнір. "Glycogen in the liver of streptozotocin diabetic rats." Thesis, 39th International Medical Scientific Congress, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11214.
Повний текст джерелаPimentel, Helena Isabel da Costa Antunes. "Glycogen synthase kinase 3ß modulation in axonal regeneration." Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/5284.
Повний текст джерелаA espinal medula de mamíferos adultos não possui capacidade de regeneração ao contrário do nervo periférico lesionado. De forma a compreender os mecanismos que potenciem a regeneração do sistema nervoso central, o modelo de lesão condicionante foi usado. Neste, uma lesão no ramo periférico dos neurónios da raiz dorsal cerca de uma semana antes de uma lesão no ramo central dos mesmos neurónios, promove a regeneração do último. Através de abordagens proteómicas concluiu-se que a Glycogen Synthase Kinase 3β (GSK3β) e proteínas que interagem com esta, estavam diferencialmente regulados após lesão condicionante, explicando possivelmente o maior potencial regenerativo nesta condição. Com este projecto, pretendemos compreender o mecanismo de regulação da GSK3β que leva à regeneração axonal. Primeiro observámos nos neurónios da raiz dorsal, um aumento da fosforilação da Akt (a cinase que inactiva a GSK3β através de fosforilação da S9), um aumento da pGSK3β(S9) (forma inactiva) e diminuição dos níveis de pGSK3β(Y216) (forma activa) após lesão condicionante validando os resultados da proteómica. Relativamente à espinal medula (local de lesão), verificou-se a diminuição de pGSK3β(Y216) após lesão condicionante em comparação com a lesão na espinal medula sugerindo que a GSK3β se encontra inibida após lesão condicionante por modulação deste resíduo. Relativamente aos substratos da GSK3β, na espinal medula a fosforilação do CRMP2 encontra-se diminuída e os níveis de pMAP1b encontram-se aumentados após lesão condicionante. De forma a perceber o papel da fosforilação da GSK3β(Y216) na regeneração axonal tratámos culturas de neurónios da raiz dorsal condicionados com ácido lisofosfatídico, um indutor da fosforilação da GSK3β(Y216), o qual reduziu o efeito de condicionamento. Para além disso, o inibidor VII (inibidor da GSK3) provocou um aumento da extensão axonal em neurónios adultos da raiz dorsal possivelmente por diminuição da fosforilação da GSK3β(Y216). Analisámos também o mecanismo responsável pela modulação da fosforilação da GSK3β(Y216). Os nossos resultados sugerem que a Fyn seja um bom candidato, uma vez que observámos na espinal medula níveis aumentados da forma inactiva da Fyn após lesão condicionante. De forma a determinar o papel da GSK3β in vivo, a regeneração axonal foi avaliada utilizando ratinhos GSK3βS9A knockin (KI). Tanto as culturas de neurónios da raiz dorsal de ratinhos GSK3βS9A KI não lesionados como após condicionamento, tiveram crescimento axonal semelhante à dos ratinhos wild type mostrando que a modulação da GSK3β através de fosforilação da GSK3β(S9) não é necessária para o efeito de condicionamento. Os nossos resultados sugerem que a fosforilação da GSK3β(Y216) tem um papel importante na regeneração axonal apesar de a literatura se focar no mecanismo inibitório da fosforilação da GSK3β(S9). A identificação da importância que a GSK3β possa ter no potenciamento da regeneração axonal após lesão condicionante, pode ser positiva no desenvolvimento de novas terapias para lesões na espinal medula.
The adult mammalian spinal cord fails to regenerate, contrarily to the injured peripheral nerve. In order to shed light on the mechanisms enabling central nervous system axonal regeneration, the conditioning lesion model was used. In this model, an injury in the peripheral branch of the dorsal root ganglia (DRG), approximately one week prior to an injury in the central branch of the DRG, promotes regeneration of the latter. To identify putative candidates differentially regulated in the DRG following conditioning lesion in comparison to spinal cord injury (SCI) alone, two proteomic approaches were used. From these analysis, Glycogen Synthase Kinase 3β (GSK3β) and interacting proteins, were identified as being differentially regulated following conditioning lesion, possibly explaining the increased regeneration in this condition. In this study we aimed to understand how GSK3β is modulated in order to promote axonal regeneration. We observed in the DRG increased levels of pAkt (the kinase that inactivates GSK3β through S9 phosphorylation), an increase of pGSK3β(S9) (inactive form) and decreased pGSK3β(Y216) (active form) levels in the conditioning lesion model, validating the proteomic results. Concerning the spinal cord injury site, we observed a decrease in pGSK3β(Y216) after conditioning lesion when compared to SCI, suggesting that the GSK3β activity is downregulated through modulation of this residue. Regarding the GSK3β substrates, CRMP2 phoshorylation levels are decreased and MAP1b is increasingly phosphorylated following conditioning lesion when compared with SCI alone in the spinal cord injury site. In order to evaluate the role of GSK3β(Y216) phosphorylation in axonal regeneration we treated conditioned DRG neurons with lysophosphatidic acid, an inducer of Y216 phosphorylation, which reduced the conditioning effect. On the other hand, the GSK3 inhibitor VII increased axon growth of adult DRG neurons possibly through a decrease of GSK3β(Y216) phosphorylation. We also analysed the mechanism responsible for the modulation of GSK3β(Y216) phosphorylation. Our results suggest that Fyn is a good candidate as we observed increased levels of the inactive form of Fyn after conditioning lesion in the spinal cord injury site. To evaluate the role of GSK3β in vivo, we assessed axonal regeneration in GSK3βS9A knockin (KI) mice. Both uninjured and conditioned DRG neuronal cultures from GSK3βS9A KI mice had similar neurite outgrowth to cultures performed with wild type mice showing that modulation of GSK3β through GSK3β(S9) phosphorylation is not required for the conditioning effect. In summary, our results suggest that GSK3β(Y216) phosphorylation has an important role in axonal regeneration, though the literature focuses on the inhibitory mechanism of GSK3β(S9) phosphorylation. Determining the role of GSK3β in the promotion of axonal regeneration after conditioning lesion, might impact in the development of new therapies for SCI.
Sucic, Joseph F. "Regulation of glycogen phosphorylase genes in Dictyostelium discoideum." Diss., This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-06062008-170101/.
Повний текст джерелаSeibold, Gerd Michael. "Charakterisierung des Glycogen- und Maltosestoffwechsels von Corynebacterium glutamicum." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-63818.
Повний текст джерелаJacob, Robin Henry. "Optimising the concentration of glycogen in lamb meat." Thesis, Jacob, Robin Henry (2003) Optimising the concentration of glycogen in lamb meat. PhD thesis, Murdoch University, 2003. https://researchrepository.murdoch.edu.au/id/eprint/110/.
Повний текст джерелаJacob, Robin Henry. "Optimising the concentration of glycogen in lamb meat." Jacob, Robin Henry (2003) Optimising the concentration of glycogen in lamb meat. PhD thesis, Murdoch University, 2003. http://researchrepository.murdoch.edu.au/110/.
Повний текст джерелаFerguson, Donna Catherine. "Skeletal Muscle and Hepatic Glycogen Content in Birds." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146240.
Повний текст джерелаSemiz, Sabina. "Effects of diabetes, insulin, and vanadium on regulation of glycogen synthesis : roles of glycogen synthase kinase-3 and protein phosphatase-1." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61172.pdf.
Повний текст джерелаNaperalsky, Michael E. "Effect of post-exercise environmental temperature on glycogen resynthesis." The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-06052009-115319/.
Повний текст джерелаMunoz, Nicole. "Glucosamine reduces glycogen storage in L6 skeletal muscle cells." Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Fall2007/n_munoz_112507.pdf.
Повний текст джерелаForsyth, Robert J. "The contribution of astrocyte glycogen to brain energy homeostasis." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361387.
Повний текст джерелаChao, Feng Zhi. "The role of myocardial glycogen in the ischaemic heart." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/21139.
Повний текст джерелаWilliamson, Brian. "Cloning and characterization of glycogen synthase from Dictyostelium discoideum." Diss., Virginia Tech, 1995. http://hdl.handle.net/10919/40221.
Повний текст джерелаBatts, Timothy Wayne. "The Effect of Glycogen Depletion on Sarcoplasmic Reticulum Function." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/31095.
Повний текст джерелаMaster of Science
Gardner, Graham Edwin. "Nutritional regulation of glycogen metabolism in cattle and sheep." Thesis, Gardner, Graham Edwin ORCID: 0000-0001-7499-9986 (2001) Nutritional regulation of glycogen metabolism in cattle and sheep. PhD thesis, Murdoch University, 2001. https://researchrepository.murdoch.edu.au/id/eprint/41881/.
Повний текст джерелаBenedict, Michael A. "Reliability in the measurement of muscle fiber composition and the histrochemical staining for glycogen." Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/722240.
Повний текст джерелаSchool of Physical Education