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Teses / dissertações sobre o tema "Thiamine deficiency"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 25 de julho de 2025

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1

Hazell, Alan Stewart. "The pathophysiology of pyrithiamine-induced thiamine deficiency encephalopathy." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28776.

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Pyrithiamine-induced thiamine deficiency (PTD) in the rat results in a metabolic disorder associated with selective cerebral vulnerability. The basis of the histological lesions that develop in areas that include the thalamus, medial geniculate, and inferior colliculus is undetermined but an underlying glutamate-mediated form of excitotoxicity may be responsible. This work examines the possibility that PTD leads to changes in extracellular glutamate concentration, membrane polarization status, and gene expression consistent with a decreased ability to maintain homeostatic integrity.<br>At the

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2

Larkin, James Robert. "The role of the kidney in diabetic thiamine deficiency." Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/34560/.

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Diabetes is a chronic epidemic compounded by a burden of vascular complications including diabetic nephropathy. Diabetic nephropathy affects ~40% of patients and is characterised by increased urinary albumin excretion and decreased glomerular filtration rate. Diabetic patients exhibit ~75% decreased plasma thiamine concentration, linked to increased renal thiamine clearance. In streptozotocin-induced diabetic rats, decreased plasma thiamine concentration was also associated with a reduction in expression and activity of transketolase. Transketolase is a thiamine pyrophosphate-dependent enzyme

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3

Molnar, Lydia. "Thiamine in a wet pet food application." Thesis, Kansas State University, 2017. http://hdl.handle.net/2097/35454.

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Master of Science<br>Department of Grain Science and Industry<br>Greg Aldrich<br>Since 2010, there have been seven recalls related to thiamine deficiency in cat food products (FDA, 2017; FSA, 2017). Cats have a high requirement of thiamine (5.6 mg/kg), and deficiencies can lead to death within a month if not treated (AAFCO, 2017). A few studies have been published regarding the impact of retort processing on thiamine loss in canned pet food but no work has been reported on heat penetration in other containers (pouches and trays). Therefore, our objectives were to determine the effect of contai

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4

Navarro, Darren. "Region-selective effects of thiamine deficiency on cerebral metabolism in pyrithiamine-treated rats." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115904.

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Pyrithiamine-induced thiamine deficiency in rats is a well-established animal model of Wernicke's Encephalopathy (WE). This thesis project, submitted as four articles, presents an examination of metabolic events that contribute to the selective neuronal lesions observed in the medial thalamus (MT) of thiamine-deficient (TD) rat. In addition, the phenomenon of glucose-precipitated worsening of neurological status in WE patients (Wallis et al., 1978; Watson et al., 1981) is explored.<br>Lactate accumulation is known to occur selectively in regions of the TD brain, which ultimately express neuron

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5

Yates, Jodye. "Diazepam administration during acute thiamine deficiency attenuates subsequent neuropathology and spatial-memory deficits in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape15/PQDD_0004/MQ39449.pdf.

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6

Kozel, Carrie L. "Early Feeding In Lake Trout Fry (salvelinus Namaycush) As A Mechanism For Ameliorating Thiamine Deficiency Complex." ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/685.

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Recruitment failure of lake trout (Salvelinus namaycush) in the Great Lakes has been attributed in part to the consumption of alewife (Alosa pseudoharengus) by adult lake trout, leading to Thiamine Deficiency Complex (TDC) and early mortality in fry. The current understanding of thiamine deficiency in lake trout fry is based on information from culture and hatchery settings, which do not represent conditions fry experience in the wild and may influence the occurrence of TDC. In the wild, lake trout fry have access to zooplankton immediately following hatching; previous studies found that wild

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7

Alexander-Kaufman, Kimberley Louise. "Proteomics of the human alcoholic brain: Implications for the pathophysiology of alcohol-related brain damage." The University of Sydney, 2008. http://hdl.handle.net/2123/2692.

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Doctor of Philosophy (PhD)<br>Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. The

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8

Alexander-Kaufman, Kimberley Louise. "Proteomics of the human alcoholic brain: Implications for the pathophysiology of alcohol-related brain damage." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2692.

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Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were t

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9

Soares, Susana Patrícia Veloso. "Paretic syndrome in gulls (Laridae) in the south of Portugal." Master's thesis, Universidade de Lisboa. Faculdade de Medicina Veterinária, 2014. http://hdl.handle.net/10400.5/6554.

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Dissertação de Mestrado Integrado em Medicina Veterinária<br>RIAS, a Portuguese wildlife rehabilitation centre located in Algarve, has been admitting a substantial high number of seagulls, since its opening in October of 2009, with consistent clinical presentations pertaining to a paretic syndrome without cues of a particular disease. This preliminary study describes the clinical signs and microbiological, parasitological, toxicological and pathologic findings of paretic gulls received between 2009 and 2012. It tries to understand if there is an association between the manifestation of th

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10

Vindedzis, Sally Ann. "The relationship between low blood thiamin levels in diabetes to thiamin intake and diabetic control." Thesis, Curtin University, 2008. http://hdl.handle.net/20.500.11937/248.

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Mild thiamin deficiency is prevalent in diabetes, and high dose thiamin ameliorates some diabetic complications, but there are no definitive studies addressing thiamin intake, diabetes control and thiamin status in diabetes. Subjects were 113 people with diabetes (58 type 1, 55 type 2), 43 with and 70 without thiamin supplementation. Dietary thiamin was estimated by 24-hour recall, diabetes control by HbA1c. Age, BMI, albumin excretion, activity level and smoking status did not correlate with red cell thiamin (RCT) in either group. RCT correlated with serum thiamin (ST) (p < 0.01). In those un

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11

Vindedzis, Sally Ann. "The relationship between low blood thiamin levels in diabetes to thiamin intake and diabetic control." Curtin University of Technology, School of Public Health, 2008. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=118316.

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Mild thiamin deficiency is prevalent in diabetes, and high dose thiamin ameliorates some diabetic complications, but there are no definitive studies addressing thiamin intake, diabetes control and thiamin status in diabetes. Subjects were 113 people with diabetes (58 type 1, 55 type 2), 43 with and 70 without thiamin supplementation. Dietary thiamin was estimated by 24-hour recall, diabetes control by HbA1c. Age, BMI, albumin excretion, activity level and smoking status did not correlate with red cell thiamin (RCT) in either group. RCT correlated with serum thiamin (ST) (p < 0.01). In those un

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12

Cathcart, Angela Elizabeth. "Monitoring seasonal changes in factors affecting thiamin status in a Gambian village." Thesis, University of Ulster, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267822.

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13

Jhala, Shivraj. "Regulation of excitotoxicity in thiamine deficiency : role of glutamate transporters." Thèse, 2012. http://hdl.handle.net/1866/9720.

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L’excitotoxicité est un mécanisme physiopathologique majeur impliqué dans la pathogenèse de la déficience en thiamine (DT). Dans les régions cérébrales vulnérables à la DT, on observe une mort cellulaire induite par excitotoxicité dont l’origine semble être la conséquence d’une perturbation du métabolisme énergétique mitochondrial, d’une dépolarisation membranaire soutenue et d’une diminution de l’absorption du glutamate par les astrocytes suite à la diminution de l’expression des transporteurs EAAT1 et EAAT2. Il est clairement établi que le glutamate joue un rôle central dans l’excitotoxicité

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14

Chen, Shiang-Chin, and 陳香瑾. "Studies of the cellular responses to thiamine deficiency in cortical neuron cells." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/91856500593915104284.

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碩士<br>國立陽明大學<br>生物化學研究所<br>92<br>Vitamin B1 (Thiamine) plays a critical role in energy and oxidative metabolism, its deficiency can result in abnormal oxidative degradation of nutrients. By treatment of cells with the thiamine antagonist amprolium as a means of inducing thiamine deficiency, we showed that thiamine deficiency elicited apoptosis in cultured cortical neuronal cells. The apoptosis was accompanied by the activation of caspases 3, 8, and 9 and a two-fold increase of reactive oxygen species (ROS) was detected. Treatment of cells with ROS inhibitors, NAC and vitamin C, did not prevent

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15

(9722096), Avril M. Harder. "Declining populations in changing environments: adaptive responses, genetic diversity, and conservation." Thesis, 2020.

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<p>Many salmonid populations are supported through captive breeding programs in which hatchery production supplies fish for reintroduction or supplementation efforts. In Lake Champlain, Atlantic salmon (Salmo salar) are the subject of a reintroduction effort that is complicated by the occurrence of thiamine (vitamin B1) deficiency in adult salmon returning to spawn. This deficiency results in high offspring mortality rates that must be mitigated by hatchery interventions (reviewed in Chapter 1). I used an experimental transcriptomics approach coupled with survival analyses to assess genetic va

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16

Azar, Ashraf. "Metabolomics analysis in rats with thiamine deficiency identifies key metabolites in vulnerable brain regions and suggests neural stem progenitor cells play a role in ameliorating metabolic dysfunction." Thèse, 2015. http://hdl.handle.net/1866/13866.

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La documentation scientifique fait état de la présence, chez l’adulte, de cellules souches et progénitrices neurales (CSPN) endogènes dans les zones sous-ventriculaire et sous-granulaire du cerveau ainsi que dans le gyrus denté de l’hippocampe. De plus, un postulat selon lequel il serait également possible de retrouver ce type de cellules dans la moelle épinière et le néocortex des mammifères adultes a été énoncé. L’encéphalopathie de Wernicke, un trouble neurologique grave toutefois réversible qui entraîne un dysfonctionnement, voire une défaillance du cerveau, est causée principalement par u

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17

Azizi, Namini Parastoo. "The Prevalence of Thiamin Deficiency in Ambulatory Patients with Heart Failure." Thesis, 2011. http://hdl.handle.net/1807/29469.

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Thiamin is a required coenzyme in the production of energy to fuel myocardial contraction. Therefore, thiamin deficiency (TD) may contribute to myocardial weakness by limiting the available energy for myocyte contraction. Previous studies report a wide range for the prevalence of TD in patients with heart failure (HF) (3% to 91%). These trials are limited by their small sample size, indirect measurement of thiamin status, exclusion criteria, and their focus on hospitalized patients. Therefore, this study determined the prevalence of TD in a large (n=100) group of ambulatory patients with HF, u

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18

Shangari, Nandita. "Interdependent toxicity mechanisms of oxidative stress, thiamin deficiency and alpha-oxoaldehydes." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=449961&T=F.

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19

Olivard, Sarah. "Studies on Uptake of Thiamin Analogs by a Thiamin Deficient E. coli Mutant Strain." Thesis, 2012. http://hdl.handle.net/1969.1/148374.

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Thiamin transport in Escherichia coli is a model system to establish the tolerance of derivatives for transport into the cell. Since little is known about what types of thiamin derivatives may be successfully taken into the cell through the transport system, a series of thiamin derivatives are synthesized. A thiamin amino analog is synthesized and tested to determine the use of the analog as an alternate source of thiamin for growth of an E. coli thiamin mutant. Formate, acetate, and benzoate thiamin esters are synthesized and tested as alternate sources for growth of an E. coli thiamin mutant

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20

Hanninen, Stacy Ann. "The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure." 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=81161&T=F.

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21

Beauchesne, Élizabeth. "Stress oxydatif cérébrovasculaire et rupture de la barrière hémato-encéphalique dans le syndrome de Wernicke-Korsakoff expérimental." Thèse, 2010. http://hdl.handle.net/1866/4913.

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Le syndrome de Wernicke-Korsakoff (SWK) est un désordre neuropsychiatrique causé par la déficience en thiamine (DT). Dans la DT expérimentale comme dans le SWK, on observe une mort neuronale et des hémorragies dans certaines régions précises du diencéphale et du tronc cérébral. Les lésions diencéphaliques du SWK sont particulièrement sévères et entraînent souvent des séquelles amnésiques permanentes. Le lien entre la dysfonction métabolique induite par la DT et la mort neuronale n’est pas connu. Des rapports précédents ont démontré que la perméabilité de la barrière hémato-encéphalique (BHE) é

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