Thesis (M.Sc. (Forensic Science))--Mahidol University, 1982.

Thesis (Ph. D.)--University of Michigan, 1929. / "By Robert H. Wilson and Howard B. Lewis." "Reprinted from the journal of biological chemistry, vol. LXXXIV, no. 2 ... November, 1929; vol. LXXXV, no. 2 ... January, 1930." Bibliography: p. 531, 569.

Thesis (Ph.D.)--University of Melbourne, Dept. of Paediatrics, Faculty of Medicine, Dentistry and Health Sciences, 2010. / Typescript. Includes bibliographical references (p. 101-111)

Made available in DSpace on 2014-06-11T19:23:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-08-15Bitstream added on 2014-06-13T19:49:46Z : No. of bitstreams: 1 virgilio_s_me_araiq_parcial.pdf: 346426 bytes, checksum: b52f7a11a59780ad34a571ead7eb48c6 (MD5) Bitstreams deleted on 2015-06-03T11:42:46Z: virgilio_s_me_araiq_parcial.pdf,. Added 1 bitstream(s) on 2015-06-03T11:44:11Z : No. of bitstreams: 1 000713098_20150815.pdf: 331522 bytes, checksum: 24d4cb0ce1bd6719c247a8fd735ff6d2 (MD5) Bitstreams deleted on 2015-08-17T11:07:13Z: 000713098_20150815.pdf,. Added 1 bitstream(s) on 2015-08-17T11:07:57Z : No. of bitstreams: 1 000713098.pdf: 1996543 bytes, checksum: 874f4dd2c6c18ce24b3770e47bc254d6 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / O fungo filamentoso Neurospora crassa é um organismo modelo utilizado na compreensão de diversos aspectos da biologia dos eucariotos, e tem sido usado, em nosso laboratório, para estudos celulares básicos, como os mecanismos bioquímicos e moleculares envolvidos na regulação do metabolismo de glicogênio. Uma análise sistemática realizada com uma coleção de linhagens mutantes em genes codificadores de fatores de transcrição permitiu identificar várias proteínas potencialmente envolvidas na regulação do metabolismo do glicogênio neste organismo. Algumas linhagens mutantes apresentaram alterações no perfil de acúmulo de glicogênio e na expressão dos genes que codificam as enzimas glicogênio sintase (gsn) e glicogênio fosforilase (gpn) quando comparadas à linhagem selvagem. Dentre estas, duas linhagens mutantes em genes que codificam para a proteína RCO-1 (regulator of conidiation-1) e para uma proteína hipotética foram selecionadas para o presente estudo, levando em consideração que ambas linhagens também apresentaram variações na progressão do ciclo celular quando analisadas por citometria de fluxo. Como a proteína RCO-1 é uma provável parceira da proteína RCM-1 (regulator of conidiation and morphology-1), então a linhagem mutante no gene codificador de RCM-1 foi incluída neste trabalho. Portanto, foi feita a caracterização de um fator de transcrição anotado como proteína hipotética e de dois cofatores transcricionais RCO-1 e RCM-1, ortólogos ao complexo corepressor Tup1-Ssn6 de Saccharomyces cerevisiae. As proteínas RCO-1, RCM-1 e a codificada pela ORF NCU09739 estão envolvidas na regulação do metabolismo do glicogênio, atuando na regulação da expressão dos genes gsn e/ou gpn. Estas mesmas proteínas também são necessárias para o crescimento e desenvolvimento normal do... / The filamentous fungus Neurospora crassa is a model organism used to understand various aspects of eukaryotic biology. It has been used, in our laboratory, in basic cellular studies, such as the biochemical and molecular mechanisms involved in the regulation of glycogen metabolism. A systematic analysis performed with a collection of mutant strains in genes encoding transcription factors led to the identification of proteins likely involved in the regulation of glycogen metabolism in this organism. Some mutant strains showed changes in the glycogen accumulation profile and in the expression of the genes encoding the enzymes glycogen synthase (gsn) and glycogen phosphorylase (gpn) when compared to the wild-type strain. Among these, two mutant strains in the genes encoding RCO-1 (regulator of conidiation-1) and a hypothetical proteins were selected for the present study. Both strains presented variations in cell cycle progression when analyzed by flow cytometry. RCO-1 protein is likely a partner of RCM-1 (regulator of conidiation and morphology-1) protein, thus the mutant strain in the gene encoding RCM-1 was included in this work. Therefore, we performed the characterization of a transcription factor annotated as a hypothetical protein and the two transcriptional cofactors RCO-1 and RCM-1, orthologs of the Saccharomyces cerevisiae corepressor complex Tup1-Ssn6. RCO-1, RCM-1 and the product of the ORF NCU09739 are involved in the regulation of glycogen metabolism, acting in the regulation of gsn and/or gpn gene expression. The same proteins are necessary for growth and normal development of the fungus, since the mutant strains showed changes in hyphae length, pigmentation and conidiation. Gene expression analysis showed that the NCU09739 gene was highly expressed at the beginning of the conidia germination, showing the importance... (Complete abstract click electronic access below)

Thesis (Masters Diploma (Medical Technology)--Cape Technikon, Cape Town, 1995 / The objective of the present study vvas primarily to determine vvhether modifications to the existing osmium tetroxide/potassium ferrocyanide method could be used as a general ultrastructural glycogen stain and whether this glycogen, vvhen so contrasted, differed in appearance in different tumours, such as Evving's sarcoma, Leiomyosarcoma, Rhabdomyosarcoma and Hepatocellular carcinoma. Normal skeletal muscle and liver were used to obtain a standard for the appearance of glycogen, and then, with diagnostic criteria in mind, the four glycogen-rich tumours, mentioned above vvere examined to determine the appearance, distribution and amount of glycogen present in them. Modifications to the osmium tetroxide/potassium ferrocyanide (OPF) method consisted of raising the concentration of the ferrocyanide, and using no en bloc or thin section staining by any uranyl salt solutions, because solutions of uranyl salts leaches glycogen from tissue. This procedure resulted in extremely electron-dense intracellular glycogen being retained, vvhich aided diagnosis of the these tumours. At high magnification. (>X30000) there vvas no morphological difference betvveen the glycogen particles in the various tumours, so these particles as such could not be used as a diagnostic criterion. Existing methods for the demonstration of myeloperoxidase and platelet peroxidase vvere modified to obtain more precise localization of the diaminobenzidine (DAB) reaction product. Different anti-coagulants, one of which was heparin and a modified fixation procedure vvas follovved.

Juvenile C. errans do not feed on particulate matter and yet they can survive, apparently unchanged, for several months before maturing into the adult stage which feeds on the eggs of Cancer magister. The significance of glycogen as an energy source for maintenance of the juvenile form was investigated.

Indiana University-Purdue University Indianapolis (IUPUI) / Pompe disease (PD) is a rare metabolic myopathy characterized by loss of acid alpha-glucosidase (GAA), the enzyme responsible for breaking down glycogen to glucose within the lysosomes. PD cells accumulate massive quantities of glycogen within their lysosomes, and as such, PD is classified as a “lysosomal storage disease” (LSD). GAA-deficient cells also exhibit accumulation of autophagic debris. Symptoms of severe infantile PD include extreme muscle weakness, hypotonia, and hypertrophic cardiomyopathy, resulting in death before one year of age. Certain LSDs are currently being successfully treated with enzyme replacement therapy (ERT), which involves intravenous infusion of a recombinant enzyme to counteract the endogenous deficiency. ERT has been less successful in PD, however, due to ineffective delivery of the recombinant enzyme. Alternatively, specific genes deletion may reduce lysosomal glycogen load, and could thus be targeted in PD therapy development. Absence of malin (EPM2B) or laforin (EPM2A) has been proposed to impair autophagy, which could reduce lysosomal glycogen levels. Additionally, deficiency of Stbd1 has been postulated to disable lysosomal glycogen import. Furthermore, Ptg deficiency was previously reported to abrogate Lafora body formation and correct neurological abnormalities in Lafora disease mouse models and could have similar effects on PD pathologies. The goal of this study was to characterize the effects of homozygous disruption of Epm2a, Epm2b, Stbd1, and Ptg loci on total glycogen levels in PD mouse model heart tissue, as in severe infantile PD, it is accumulation of glycogen in the heart that results in fatal hypertrophic cardiomyopathy. Gaa-/- mice were intercrossed with Epm2a-/-, Epm2b-/-, Stbd1-/-, and Ptg-/- mice to generate wildtype (WT), single knockout, and double knockout mice. The results indicated that Gaa-/- hearts accumulated up to 100-fold more glycogen than the WT. These mice also displayed cardiac hypertrophy. However, deficiency of Epm2a, Epm2b, Stbd1, or PTG in the Gaa-/- background did not reveal changes of statistical significance in either heart glycogen or cardiac hypertrophy. Nevertheless, since total glycogen was measured, these deficiencies should not be discarded in future discussions of PD therapy, as increasing sample sizes and/or distinguishing cytosolic from lysosomal glycogen content may yet reveal differences of greater significance.

No description available.

A complex which synthesized glycogen de novo has been purifiedfrom Ascaris suum. This complex (GS-2) consists of a 66 KDa protein, a 140 KDa protein, and a>330 KDa glycoprotein.

The fungal cell wall serves as the interface between the organism and its environment. Complex carbohydrates are a major component of the cell wall, , glucan, mannan and chitin. β-Glucan is a pathogen associated molecular pattern (PAMP) composed of β-(1 → 3,1 → 6)-linked glucopyranosyl repeat units. This PAMP plays a key role in fungal structural integrity and immune recognition. Glycogen is an α-(1 → 4,1 → 6)-linked glucan that is an intracellular energy storage carbohydrate. We observed that glycogen was co-extracted during the isolation of β-glucan from SC5314. We hypothesized that glucan and glycogen may form a macromolecular species that links intracellular glycogen with cell wall β-(1 → 3,1 → 6)-glucan. To test this hypothesis, we examined glucan-glycogen extracts by multi-dimensional NMR to ascertain if glycogen and β-glucan were interconnected. H NMR analyses confirmed the presence of glycogen and β-glucan in the macromolecule. Diffusion Ordered SpectroscopY (DOSY) confirmed that the β-glucan and glycogen co-diffuse, which indicates a linkage between the two polymers. We determined that the linkage is not via peptides and/or small proteins. Our data indicate that glycogen is covalently linked to β-(1 → 3,1 → 6) glucan via the β -(1 → 6)-linked side chain. We also found that the glucan-glycogen complex was present in , and , but was not present in or hyphal glucan. These data demonstrate that glucan and glycogen form a novel macromolecular complex in the cell wall of and other species This new and unique structure expands our understanding of the cell wall in species.