Academic literature on the topic 'Thiamine deficiency'
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Journal articles on the topic "Thiamine deficiency"
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Pan, Xiaohua, Xuemei Nan, Liang Yang, Linshu Jiang, and Benhai Xiong. "Thiamine status, metabolism and application in dairy cows: a review." British Journal of Nutrition 120, no. 5 (July 10, 2018): 491–99. http://dx.doi.org/10.1017/s0007114518001666.
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AbstractAs the co-enzyme of pyruvate dehydrogenase andα-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows. Apart from feedstuff, microbial thiamine synthesis in the rumen is the main source for dairy cows. However, the amount of ruminal thiamine synthesis, which is influenced by dietary N levels and forage to concentrate ratio, varies greatly. Notably, when dairy cows are overfed high-grain diets, subacute ruminal acidosis (SARA) occurs and results in thiamine deficiency. Thiamine deficiency is characterised by decreased ruminal and blood thiamine concentrations and an increased blood thiamine pyrophosphate effect to >45 %. Thiamine deficiency caused by SARA is mainly related to the increased thiamine requirement during high grain feeding, decreased bacterial thiamine synthesis in the rumen, increased thiamine degradation by thiaminase, and decreased thiamine absorption by transporters. Interestingly, thiamine deficiency can be reversed by exogenous thiamine supplementation in the diet. Besides, thiamine supplementation has beneficial effects in dairy cows, such as increased milk and component production and attenuated SARA by improving rumen fermentation, balancing bacterial community and alleviating inflammatory response in the ruminal epithelium. However, there is no conclusive dietary thiamine recommendation for dairy cows, and the impacts of thiamine supplementation on protozoa, solid-attached bacteria, rumen wall-adherent bacteria and nutrient metabolism in dairy cows are still unclear. This knowledge is critical to understand thiamine status and function in dairy cows. Overall, the present review described the current state of knowledge on thiamine nutrition in dairy cows and the major problems that must be addressed in future research.
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Richter, Catherine A., Allison N. Evans, Maureen K. Wright-Osment, James L. Zajicek, Scott A. Heppell, Stephen C. Riley, Charles C. Krueger, and Donald E. Tillitt. "Paenibacillus thiaminolyticus is not the cause of thiamine deficiency impeding lake trout (Salvelinus namaycush) recruitment in the Great Lakes." Canadian Journal of Fisheries and Aquatic Sciences 69, no. 6 (June 2012): 1056–64. http://dx.doi.org/10.1139/f2012-043.
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Thiamine (vitamin B1) deficiency is a global concern affecting wildlife, livestock, and humans. In Great Lakes salmonines, thiamine deficiency causes embryo mortality and is an impediment to restoration of native lake trout ( Salvelinus namaycush ) stocks. Thiamine deficiency in fish may result from a diet of prey with high levels of thiaminase I. The discoveries that the bacterial species Paenibacillus thiaminolyticus produces thiaminase I, is found in viscera of thiaminase-containing prey fish, and causes mortality when fed to lake trout in the laboratory provided circumstantial evidence implicating P. thiaminolyticus. This study quantified the contribution of P. thiaminolyticus to the total thiaminase I activity in multiple trophic levels of Great Lakes food webs. Unexpectedly, no relationship between thiaminase activity and either the amount of P. thiaminolyticus thiaminase I protein or the abundance of P. thiaminolyticus cells was found. These results demonstrate that P. thiaminolyticus is not the primary source of thiaminase activity affecting Great Lakes salmonines and calls into question the long-standing assumption that P. thiaminolyticus is the source of thiaminase in other wild and domestic animals.
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Skelton, William P., and Nadine K. Skelton. "Thiamine deficiency neuropathy." Postgraduate Medicine 85, no. 8 (June 1989): 301–6. http://dx.doi.org/10.1080/00325481.1989.11700760.
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GOMES, Marleide da Mota, and Marcos Raimundo Gomes de FREITAS. "Probable first report of a motor deafferentation syndrome in the Paraguayan War." Arquivos de Neuro-Psiquiatria 79, no. 6 (June 2021): 554–56. http://dx.doi.org/10.1590/0004-282x-anp-2020-0479.
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ABSTRACT The Paraguayan War ended 150 years ago. Back then, there were outbreaks of combatants’ limb weakness and tingling related to "palustrian cachexia", not clearly funded at the time on nutritional deficiency, the use of native flora to feed troops, and alcoholism. We report a case of a soldier with ascending paralysis, mental confusion and finally tetraplegia with preserved oculomotricity. This would probably be a case of locked-in syndrome (LIS) due to Gayet-Wernicke's encephalopathy consequent to thiamine deficiency. The role of thiamine in the peripheral or central nervous system expression was shown decades later to be related to poor diet, or use of foods containing thiaminase or thiamine antagonists, worsened by the fact that the bodily stores of thiamine are restricted, and deficits may grow fast.
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Lonsdale, Derrick. "A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives." Evidence-Based Complementary and Alternative Medicine 3, no. 1 (2006): 49–59. http://dx.doi.org/10.1093/ecam/nek009.
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Thiamin(e), also known as vitamin B1, is now known to play a fundamental role in energy metabolism. Its discovery followed from the original early research on the ‘anti-beriberi factor’ found in rice polishings. After its synthesis in 1936, it led to many years of research to find its action in treating beriberi, a lethal scourge known for thousands of years, particularly in cultures dependent on rice as a staple. This paper refers to the previously described symptomatology of beriberi, emphasizing that it differs from that in pure, experimentally induced thiamine deficiency in human subjects. Emphasis is placed on some of the more unusual manifestations of thiamine deficiency and its potential role in modern nutrition. Its biochemistry and pathophysiology are discussed and some of the less common conditions associated with thiamine deficiency are reviewed. An understanding of the role of thiamine in modern nutrition is crucial in the rapidly advancing knowledge applicable to Complementary Alternative Medicine. References are given that provide insight into the use of this vitamin in clinical conditions that are not usually associated with nutritional deficiency. The role of allithiamine and its synthetic derivatives is discussed. Thiamine plays a vital role in metabolism of glucose. Thus, emphasis is placed on the fact that ingestion of excessive simple carbohydrates automatically increases the need for this vitamin. This is referred to as high calorie malnutrition.
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Bourassa, Megan, and Gilles Bergeron. "Advances from the International Thiamine Alliance." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 814. http://dx.doi.org/10.1093/cdn/nzaa053_019.
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Abstract Objectives Thiamine deficiency disorders, including beriberi, remain a pressing public health problem. Without rapid recognition of symptoms and treatment, it is often fatal, especially in infants, and can have lasting neurological effects for survivors. Thus our objective is to create an alliance of country representatives, public health professionals, physicians and researchers who can quantify the prevalence of thiamine deficiency disorders globally and create control and prevention strategies. Methods The first meeting of this international thiamine alliance was held in November 2019 to discuss the prevalence of thiamine deficiency disorders and devise strategies to improve thiamine status in at-risk populations. Results This alliance creates the first community of practice for thiamine deficiency. As a result of this meeting and recent data, there is growing recognition that thiamine deficiency is not localized to small areas within Southeast Asia, but covers a much broader area to include much of South and Central Asia, including areas of Kashmir and Assam in India and Bhutan. Challenges in diagnosing thiamine deficiency based on symptoms or biomarkers have been major barriers to recognizing thiamine deficiency disorders. Conclusions This group is now working to improve assessments of thiamine deficiency and raising awareness among the public health and medical professionals in areas where the diets are low in thiamine to ensure that its diagnosis is not overlooked. In areas with a known prevalence of thiamine deficiency, efforts are underway to increase dietary intake of thiamine, provide supplements especially to pregnant and lactating women, and fortify foods to improve thiamine status. Funding Sources Bill & Melinda Gates Foundation.
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van Snippenburg, Wouter, Mariet G. J. Reijnders, Jose G. M. Hofhuis, Rien de Vos, Stephan Kamphuis, and Peter E. Spronk. "Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients." Journal of Intensive Care Medicine 32, no. 9 (July 20, 2016): 559–64. http://dx.doi.org/10.1177/0885066616659429.
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Introduction: Thiamine is an essential cofactor in carbohydrate metabolism, and deficiency can therefore cause various organ dysfunctions. Little is known about the prevalence and possible worsening of thiamine deficiency in critically ill patients. In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores. Materials and Methods: An observational prospective cohort study was carried out in a medical–surgical ICU in a general teaching hospital in Apeldoorn, the Netherlands. All adults who were treated during that time with intensive insulin therapy were included. Deficiency was defined as a thiamine level <100 nmol/L. No thiamine supplementation was administered except for normal amounts present in standard enteral feeding. Results: A total of 58 patients were available for analysis. Median thiamine level at admission was 111 nmol/L. Deficiency was present in 39.7% of patients and was significantly associated with the presence of gastrointestinal pathology and with recent surgery. Thiamine levels increased a median of 14 nmol/L in 48 hours. Only 3.4% of patients showed a predefined relevant decline in thiamine levels. Conclusion: Intensive insulin therapy does not appear to cause or worsen thiamine deficiency. However, based on the high prevalence of deficiency at admission, it might be warranted to supplement thiamine in all patients admitted to the ICU, especially when there is an underlying gastrointestinal disease or recent surgery.
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Sweet, Rebecca L., and Jason A. Zastre. "HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency." International Journal for Vitamin and Nutrition Research 83, no. 3 (June 1, 2013): 188–97. http://dx.doi.org/10.1024/0300-9831/a000159.
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It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.
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Mohamed, Ragaa Abd-Elsalam, Ibrahim Mohamed Abu Farag, Marwa Elhady, and Radwa Saeed Ibrahim. "Myocardial dysfunction in relation to serum thiamine levels in children with diabetic ketoacidosis." Journal of Pediatric Endocrinology and Metabolism 32, no. 4 (April 24, 2019): 335–40. http://dx.doi.org/10.1515/jpem-2018-0320.
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Abstract Background Thiamine deficiency is commonly reported in patients with diabetes especially during diabetic ketoacidosis (DKA) that could attribute to myocardial dysfunction in those patients. However, there is limited data regarding its relation to myocardial function among those patients. This study aimed to explore the association between myocardial function and serum thiamine levels in children with type 1 diabetes mellitus (DM). Methods This cross-sectional comparative study included 25 patients with DKA. Clinical data assessment, echocardiographic examination and measurement of serum high-sensitive troponin T (hs-cTnT) and thiamine levels were done. We also assessed the association between troponin levels, echocardiographic ventricular systolic and diastolic function and serum thiamine. Results Twenty-four percent of children with DKA had thiamine deficiency. DKA children with thiamine deficiency had significant acidosis and higher serum troponin levels and significant impairment of diastolic function than those without thiamine deficiency. The serum thiamine level had a significant positive correlation with the echocardiographic indices of diastolic function but negative correlation with troponin levels. Conclusions Thiamine deficiency is a common finding during the treatment of children with DKA, and this deficiency may be associated with myocardial dysfunction.
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Buranasakda, Marturod, and Ratrawee Pattanarattanamolee. "Thiamine Level in Out-of-hospital Cardiac Arrest Patients." Open Access Macedonian Journal of Medical Sciences 10, B (April 2, 2022): 1037–41. http://dx.doi.org/10.3889/oamjms.2022.8015.
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BACKGROUND: Thiamine deficiency is more common in critically ill patients. Administration of thiamine in cardiac arrest mice has improved survival and neurological outcomes. Evidence for thiamine deficiency in cardiac arrest humans is insufficient to support routine use of thiamine in cardiac arrest patients. AIM: This study aimed to determine thiamine blood levels in cardiac arrest patients to understand whether the presence of thiamine deficiency is common in cardiac arrest patients. METHODS: A prospective descriptive study from April 2017 to March 2018, on 24 adult out-of-hospital cardiac arrest patients. We used the high-performance liquid chromatography technique to determine whole blood thiamine pyrophosphate levels in cardiac arrest patients who arrived at the emergency department within 1 h of the onset of a cardiac arrest. RESULTS: The mean thiamine pyrophosphate level within 1 h of the onset of a cardiac arrest was 170.9 ± 56.7 nmol/L. Only one participant had thiamine deficiency according to the cut-off level for thiamine pyrophosphate in whole blood of <70 nmol/L. Fourteen patients had spontaneous return of circulation. Thiamine pyrophosphate levels were not different between the two groups of patients who had and did not have the return of spontaneous circulation at the emergency department. CONCLUSION: Little evidence was found to support thiamine deficiency as a feature among our cardiac arrest patients. A study with a larger population is required for more meaningful statistical analysis. As there is no consensus on cut-off level for thiamine deficiency diagnosis, the level of thiamine pyrophosphate in specific populations should be evaluated to establish reference values.
Dissertations / Theses on the topic "Thiamine deficiency"
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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.At the acute symptomatic stage, extracellular glutamate by concentration as determined microdialysis was found to be elevated in the thalamus but within normal limits in the non-vulnerable parietal cortex. This result suggests an involvement of glutamate in the pathogenesis of thiamine deficiency lesions. An in vivo examination of L-type voltage-sensitive calcium channel activity using quantitative autoradiography and ($ sp3$H) -nimodipine at the same stage of PTD revealed that increased activity was present in and localized to the thalamus, but was absent in areas resistant to histological damage. The finding indicates a likelihood of regional depolarization. Finally, induction of the proto-oncogene c-fos was detected in the thalamus and inferior colliculus with quantitative in situ hybridization analysis at the acute symptomatic stage, thereby confirming the association of PTD with depolarization-related events occurring in advance of the appearance of frank infarction.
Together, these results suggest that vulnerability in the thalamus may be determined by an inability to maintain spatial buffering of extracellular glutamate under energy-compromised conditions. Such an environment may be sufficient to set into motion event cascades in these cells that lead to the demise of the structure as a whole.
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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 and a critical component of the reductive pentose phosphate pathway, a metabolic pathway leading from glycolysis involved with the synthesis of ribose sugars. It is proposed that increasing the relative flux of glucose through the pentose phosphate pathway can ameliorate hyperglycaemic damage. This thesis investigates mechanisms mediating the increased renal thiamine clearance and the effects of thiamine therapy on type 2 diabetic patients with nephropathy. The hypothesis that hyperglycaemia increases flux through the hexosamine pathway, leading to increased O-glycosylation of the transcription factor Sp1 and subsequent decreased expression of thiamine transporters is investigated. Thiamine transporters in normal human kidney sections were found to be localised to the proximal tubule. Investigations in primary cultures of human proximal tubule epithelial cells and the HK-2 cell line have shown that there is a decreased expression (-48 to -80%) and abundance (-52 to -77%) of thiamine transporters in cells cultured in high glucose concentrations (26mM) with respect to low glucose concentrations (5 mM). There is only limited evidence supporting the involvement of the hexosamine pathway in these decreases. A double-blind, placebo-controlled study investigated the effect of thiamine supplementation on type 2 diabetic patients with microalbuminuria. Thiamine therapy restored plasma thiamine concentrations from 11nM to 98nM, exceeding the published median concentration observed in normal patients (64nM). After three months, thiamine therapy, but not placebo, caused a decrease in the urinary albumin excretion rate relative to baseline (-18 mg day-1). These results show promise for thiamine as a therapy for diabetic nephropathy.
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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 ScienceDepartment of Grain Science and Industry
Greg Aldrich
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 container size and type on thiamine retention during processing of cat food. Our hypothesis was that thiamine retention would be impacted by container size and type. To address this, a 2x3 factorial arrangement of treatments in which two container sizes (small: 89-104 mL vs medium: 163-207 mL) and three container types (can, pouch, and tray) were evaluated for B-vitamin losses and thermal process lethality of a wet pet food. A model wet cat loaf type formula was produced for all six experimental treatments and each was processed in duplicate over six-days. All ingredients including the vitamin premix (10x level) were thoroughly mixed, heated to 43ºC, and containers were manually filled. The filled and sealed containers were cooked in a retort (cans: SJ Reid Retort, Bellingham, WA; trays and pouches: FMC retort, Madera, CA) with thermocouples attached to the center of representative containers (n=14) in each batch. Software (Calsoft Systems, v. 5.0.5) was used to record the internal temperatures. The retort time was targeted to meet an F₀=8 at 121ºC and 21 PSI. Treatment sample were analyzed for included pH, moisture, crude protein, crude fat, ash, and B-vitamins. Results were analyzed using the GLM procedure in SAS (v. 9.4; Cary, NC) with means and interactions separated using Fisher LSD method by significant F and an α of 5%. The proximate composition and pH were similar (P > 0.10) among treatments. There was an interaction (P < 0.05) between container size and type for time to reach the F₀=8; wherein, the medium can and tray had the longest time (45.5 and 46.3 min, respectively); the small can and tray, and medium pouch were intermediate (35.4, 36.0, and 32.0 min, respectively); and the small pouch had the shortest time (36.0 min). There was no difference for either main effect of container type or size on heating lethality values (each main effect average F₀=10.3) and total lethality ranged from 12.7-16.7 min. Thiamine retention was lowest (70%) among the B-vitamins, and there was minimal loss throughout the process. The excess heating beyond F₀=8 may account for the dramatic impact on the retention of heat labile nutrients like thiamine. This may be more difficult to control in the newer packaging systems like pouches and trays.
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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.Lactate accumulation is known to occur selectively in regions of the TD brain, which ultimately express neuronal cell death (McCandless, 1982; Munujos et al., 1996). In Article 1, the metabolic origin and cellular localization of region-selective lactate accumulation in the MT of TD rats was studied using combined 1H and 13C nuclear magnetic resonance (NMR) spectroscopy. Parallel studies were performed to examine the effects of glucose loading on regional brain lactate synthesis in TD animals. Thiamine deficiency caused focal increases in the de novo synthesis of lactate via elevated glycolytic flux in the MT, while contribution via pyruvate recycling and the periphery remained nominal. Lactate levels remained unaltered in the frontal cortex (FC), a brain region that is spared in thiamine deficiency. Administration of a glucose load intensified the selective increases in lactate de novo synthesis and accumulation in the MT of TD rats, positing a role for lactic acidosis in the glucose-precipitated worsening of neurological status in TD patients. Accordingly, Article 2 addresses the effect of glucose loading on local cerebral pH in the vulnerable MT, compared to the FC, of TD rats. Administration of a glucose load resulted in detrimental decreases in regional pH selectively in the MT, implying that alterations of brain pH contribute to the pathogenesis of thalamic neuronal damage and consequent cerebral dysfunction in WE.
Region-specific alterations in the steady state levels of cerebral amino acid neurotransmitters have been well-documented in experimental animal models of thiamine deficiency (Butterworth et al., 1979; Butterworth & Heroux, 1989; Gaitonde et al., 1975; Plaitakis et al., 1979); however, the dynamics of these changes have never been systematically explored. In Article 3, we examined the metabolic fluxes through thiamine-dependent pyruvate dehydrogenase (PDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) using multinuclear NMR spectroscopy. Furthermore the cellular localization of the metabolic changes in relation to regional vulnerability to thiamine deficiency was addressed. Our studies clearly demonstrate that early decreases m metabolic flux through alpha-KGDH result in commensurate declines in aspartate concentrations in the MT of TD rats. Impairments to PDH flux manifest secondarily to the metabolic block at alpha-KGDH, likely due to depleted oxaloacetate pools. As a result of impaired pyruvate oxidation, declines in the de novo synthesis of glutamate and GABA ensue. The present findings also suggest that inhibition of flux through alpha-KGDH in TD brain occurs primarily in the neurons, while astrocytes possess compensatory mechanisms, i.e. the anaplerotic pathway, to replenish oxaloacetate concentrations via metabolic pathways that do not involve thiamine-dependent enzymes.
In Article 4, we investigated the regional effects of thiamine deficiency on the activity of thiamine-dependent branched-chain alpha-ketoacid dehydrogenase (BCKDH) and the resultant effects on regional cerebral branched-chain amino acid (BCAA) oxidation. Thiamine deficiency resulted in significant impairments in BCKDH activity; while parallel studies on enzyme distribution confirmed a lower oxidative capacity for BCAAs in the MT compared with the Fe.
The data presented in these four articles confirm and extend findings for the region-selective impairments in thiamine-dependent metabolic processes as the foundation of vulnerability of the MT to thiamine deficiency. In addition, glucose loading of TD rats exacerbates both lactic acidosis and impaired pyruvate oxidation in this vulnerable brain region, positing a role for these processes in the glucose-precipitated worsening of neurological status in TD patients. Impaired oxidative metabolism of glucose and BCAAs in the MT leads to the accumulation of potentially harmful metabolic intermediates, contributing to the mitochondrial dysfunction, cellular energy failure and ultimately neuronal cell death observed in thiamine deficiency.
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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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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 fry begin feeding before complete yolk-sac absorption. However, hatchery-raised fry are not provided with food until after yolk-sac absorption, long after the development of TDC. Zooplankton are a potential source of dietary thiamine for wild fry in the early life stages that has not previously been considered in the occurrence of thiamine deficiency. We postulated that wild-hatched fry could mitigate thiamine deficiency through early feeding on natural prey. Specifically, we hypothesized 1) feeding should increase thiamine concentrations relative to unfed fry and 2) feeding should increase survival relative to unfed fry. Feeding experiments were conducted on lake trout fry reared from eggs collected from Lake Champlain in 2014 and Cayuga Lake in 2015. A fully crossed experimental design was used to determine the effect of early feeding by lake trout fry in thiamine replete and thiamine deplete treatments before and after feeding. Overall, thiamine concentrations and survival did not significantly differ between fed and unfed fry. Thiamine concentrations increased from egg stage to hatching in both years, suggesting a potential source of thiamine, which had not previously been considered, was available to the lake trout eggs during development.
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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)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 then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.
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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 then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.
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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 unsupplemented, adequate dietary thiamin did not ensure normal RCT, with 15.7 % of subjects below the reference range. Supplementation to intake > 4 mg/d, was significantly associated with normal RCT (p = 0.028), with 97.7% of supplemented subjects having normal RCT. Supplementation was also significantly associated with elevated serum thiamin 24 hours post supplementation, contrary to other reports. HbA1c was not significantly associated with RCT. Conclusions: In diabetes, adequate dietary thiamin does not ensure normal red cell thiamin, but supplementation to > 4 mg/day does, raising questions about actual thiamin requirements in diabetes and supporting evidence that thiamin deficiency in diabetes is not primarily due to dietary deficiency. Diabetes control was not significantly related to thiamin status.
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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 VeterináriaRIAS, 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 this disease and the different species and age classes affected. It seeks to determine possible relations between the geographic distribution of the cases and specific potentially problematic areas or human activities. All in order to additionally determine a probable cause for this disease taking into consideration the species affected, region where the animals were rescued and diseases that could explain the findings observed like: Newcastle disease, Salmonellosis, Aspergillosis, Sarcocystosis, Botulism, Algal toxicosis, Copper/Lead/Mercury intoxication, Organophosphorus/Carbamate poisoning and Thiamine deficiency. Additionally, a treatment trial with three therapeutic protocols (activated charcoal, fluid therapy and thiamine supplementation) was attempted to evaluate their influence in the outcome of the rehabilitation process and their value as a tentative diagnostic tools. Accordingly, digital records of 780 gulls were analyzed, as well as, results of more specific diagnostic ancillary tests used in carcasses and tissue samples in the centre and submitted to the Faculty of Veterinary Medicine of the University of Lisbon. From the 780 admissions, 148 gulls (18,97%) were found to have this paretic syndrome while alive, with L.fuscus and sub-adults being probably the classes most affected (p=0,02;p=0,00005). All these gulls, upon admission, were thin and dehydrated and the most frequent clinical signs documented were: depressed mental status without loss of conscious (58,8%); diarrhoea (43,9%), flaccid cloacae (70,3%); generalized muscular weakness (48,6%), moderate muscular weakness (46,6%); posterior paresis (69,6%) and moderate paresis (71,6%). Approximately half of the 148 gulls died while in rehabilitation and gross necropsy findings of paretic gulls were also unspecific and overall inconsistent. However, a high number of these gulls including dead admissions had a thin-walled cloacae distended with diarrhoea and the intestines were also displaying compatible signs of inflammation: oedema, vascular congestion and fluid faeces (32/71). Evidences of opportunistic diseases or development of confounding ailments like probably Aspergillosis were also noted. The differences between the therapeutic protocols were irrelevant (p=0,7422) and could not diagnose this condition. No pathogenic agent (bacterial or parasitic) capable of causing this syndrome was identified in the carcasses submitted (n=9). The necropsy examination and histopathology lesions reported in the faculty were inconclusive as to the cause of the paresis. Lead and Copper levels, analyzed in 2 gulls, were below what is considered in the literature as indicative of toxic. Nevertheless, in one of the gulls submitted a liver sample was positive for the presence of an organophosphorus compound, which could be in accordance with the high association measured between the spatial distribution of the proportion of paretic cases and density of several crops per municipality (Rho>0,5;p<0,05). In this moment, the data here compiled and the results obtained are still insufficient to determine or exclude the diseases in discussion as causes of this syndrome. Inconsistent use of ancillary tests results, paucity in the knowledge of ethologic and ecologic features of these birds in this region, irregularities in the retrieval of sick birds and tourism are some of the factors that may be influencing these results and should be addressed in future investigations.
RESUMO - SÍNDROME PARÉSICO EM GAIVOTAS (LARIDAE) NO SUL DE PORTUGAL - RIAS, centro de recuperação de animais selvagens localizado no Algarve, desde a sua abertura em Outubro de 2009 tem recebido um número elevado de gaivotas com um quadro clinico consistente com paresia, sem causa conhecida. Este estudo preliminar descreve os sinais clínicos e achados microbiológicos, parasitológicos, toxicológicos e anatomo/histopatológicos de gaivotas com parésia recebidas entre 2009 e 2012. Tenta igualmente perceber se existe uma associação entre a manifestação desta doença e as diferentes classes de idade e espécies afectadas. Procura determinar relações possíveis entre a distribuição geográfica dos casos e áreas/actividades humanas especificas e potencialmente problemáticas na área em estudo. Tudo com o intuito adicional de descobrir a causa provável desta doença tendo em consideração as espécies afectadas, região onde foram resgatadas e doenças que poderiam explicar os achados reunidos: Doença de Newcastle;Salmonelose;Aspergilose;Sarcocistose;Botulismo;Fitotoxicose;Intoxicação por cobre, chumbo, mercúrio;Intoxicação por organofosforados/carbamatos e Deficiência em tiamina. Três protocolos terapêuticos (carvão activado, fluidoterapia e tiamina) foram igualmente testados para avaliar os respectivos efeitos no processo de reabilitação e o seu valor diagnóstico. Desta forma, foram analisados registos de 780 gaivotas em conjunto com resultados obtidos de métodos de diagnóstico auxiliar mais específicos de carcaças e amostras recolhidas e analisadas no centro ou enviadas para a Faculdade de Medicina Veterinária da Universidade de Lisboa. Das 780 admissões, 148 larídeos (18,97%) exibiam em vida este síndrome, sendo provavelmente as classes mais afectadas: L.fuscus e sub-adultos (p=0,02;p=0,00005). Todas as gaivotas afectadas encontravam-se magras e desidratadas, sendo os sinais clínicos mais frequentemente documentados: depressão do estado mental (58,8%); diarreia (43,9%), cloaca flácida (70,3%); fraqueza muscular generalizada (48,6%), fraqueza muscular moderada (46,6%); paresia dos posteriores (69,6%) e paresia moderada (71,6%). Aproximadamente metade destes animais morreu no decurso da reabilitação e as lesões encontradas em necrópsia foram igualmente inespecíficas e inconsistentes. Contundo, um elevado número destes animais, incluindo admissões de animais mortos, apresentavam recurrentemente cloacas com parede finas e distendidas por diarreia e os intestinos apresentavam também sinais compatíveis com inflamação (32/71). Achados de doenças oportunistas ou capazes de provocar sinais/lesões semelhantes foram também reportados (e.g. Aspergilose). As diferenças obtidas entre os diferentes protocolos foram consideradas irrelevantes (p=0,7422) e incapazes de diagnosticar esta doença. Nenhum agente patogénico (bacteriano ou parasita) capaz de causar parésia foi identificado nas carcaças enviadas (n=9) e resultados de análise anatomo-histopatologia das lesões encontradas foram inconclusivos quanto à causa deste síndrome. Níveis de chumbo e cobre, analizados em amostras de fígado de 2 animais, encontravam-se abaixo do que é considerado na literatura como indicativo de tóxico. No entanto, em uma amostra de fígado de uma das gaivotas enviadas foram detectados resíduos de um organofosforado,o que poderá ser concordante com a elevada associação medida entre a distribuição espacial da proporção de casos com parésia e a densidade de diversas culturas por município (Rho>0,5;p<0,05). Neste momento, toda a informação aqui compilada é ainda insuficiente para determinar ou excluir as doenças em discussão enquanto causas. O inconsistente uso de métodos de diagnóstico auxiliar, a escassez de informação relativa à etologia e ecologia destes animais nesta região, irregularidades na recolha de animais doentes e o turismo são alguns dos factores que podem estar a influenciar estes resultados e deverão ser tidos em conta no futuro.
Books on the topic "Thiamine deficiency"
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McCandless, David W. Thiamine deficiency and associated clinical disorders. New York: Humana Press, 2010.
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McCandless, David W. Thiamine Deficiency and Associated Clinical Disorders. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4.
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Beriberi, white rice, and vitamin B: A disease, a cause, and a cure. Berkeley, CA: University of California Press, 2000.
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Carpenter, Kenneth J. Beriberi, white rice, and vitamin B: A disease, a cause, and a cure. Berkeley, CA: University of California Press, 2000.
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Carpenter, Kenneth J. Beriberi, white rice, and vitamin B: A disease, a cause, and a cure. Berkeley, CA: University of California Press, 2000.
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McCandless, David W. Thiamine Deficiency and Associated Clinical Disorders. Humana Press, 2012.
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Marrs, Chandler, and Derrick Lonsdale. Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. Elsevier Science & Technology Books, 2017.
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Marrs, Chandler, and Derrick Lonsdale. Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. Elsevier Science & Technology Books, 2017.
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B1 (thiamine) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0007.
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Vitamin B1 (thiamine) is involved in nervous system and muscle function and is essential for carbohydrate metabolism. Deficiency is common in Asia, where diets are often high in thiamine-depleted polished rice and can be low in other food sources. Pregnancy imposes an increasing requirement for thiamine over the course of gestation, and deficiency can lead to widespread metabolic disturbances affecting the placenta and fetus. Nutritional deficiency for thiamine is rare in people who consume a moderately varied diet that contains whole grains. However, excessive vomiting in pregnancy can cause thiamine depletion, in which case antenatal vitamins containing thiamine and other B vitamins may be beneficial.
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Janssen, Mirian C. H., and Shamima Rahman. Pyruvate Dehydrogenase Complex Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0006.
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Pyruvate dehydrogenase complex (PDHc) deficiency usually first manifests at a young age and is rarely diagnosed in adulthood. The clinical picture varies from neonatal death with overwhelming lactic acidosis to a relatively benign course early in life. The three main presentations are congenital lactic acidosis, Leigh syndrome, and episodic ataxia. Treatment consists of a ketogenic diet and cofactor supplementation with thiamine. Successful therapy is rare.
Book chapters on the topic "Thiamine deficiency"
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Thurston, Jean Holowach, Richard E. Hauhart, John A. Dirgo, and David B. McDougal. "Thiamine Deficiency." In Cerebral Energy Metabolism and Metabolic Encephalopathy, 353–59. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-1209-3_15.
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Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, Arti N. Shah, Bharat K. Kantharia, Ulrich Salzer, Bodo Grimbacher, et al. "Thiamine Deficiency." In Encyclopedia of Molecular Mechanisms of Disease, 2044–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1733.
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McCandless, David W. "Early Thiamine Deficiency." In Thiamine Deficiency and Associated Clinical Disorders, 9–16. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4_2.
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Dias, Fernando Machado Vilhena, Aline Sanches Oliveira, Danilo Jorge da Silva, and Angela Maria Ribeiro. "Thiamine Deficiency and Poverty." In Handbook of Famine, Starvation, and Nutrient Deprivation, 1–22. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40007-5_83-1.
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Dias, Fernando Machado Vilhena, Aline Sanches Oliveira, Danilo Jorge da Silva, and Angela Maria Ribeiro. "Thiamine Deficiency and Poverty." In Handbook of Famine, Starvation, and Nutrient Deprivation, 1567–87. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55387-0_83.
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McCandless, David W. "Thiamine Deficiency in Mammals." In Thiamine Deficiency and Associated Clinical Disorders, 17–30. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4_3.
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Misra, U. K., and J. Kalita. "Thiamine deficiency neurological disorders." In Neurological Consequences of Nutritional Disorders, 29–46. First edition. | Boca Raton, FL : Taylor & Francis, 2021.: CRC Press, 2021. http://dx.doi.org/10.1201/9780429316401-3.
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McCandless, David W. "Thiamine Deficiency in Serious Illness." In Thiamine Deficiency and Associated Clinical Disorders, 131–43. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4_10.
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McCandless, David W. "Early Chemistry." In Thiamine Deficiency and Associated Clinical Disorders, 1–7. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4_1.
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McCandless, David W. "World Health Concerns." In Thiamine Deficiency and Associated Clinical Disorders, 145–49. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-311-4_11.
Full textConference papers on the topic "Thiamine deficiency"
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Shah, Avni, Karen Camero, Alvaro Serrano, Yair Erell, and John Li. "Infant with Thiamine Deficiency from a Rare Cause." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.632-a.
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Uchel, T., and U. F. Sofi. "Refractory Lactic Acidosis Due to Thiamine Deficiency from Metformin Toxicity." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2939.
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Costa, Virgínia Madureira, Iris Maria de Miranda Correia, Laís Michela Rodrigues Sales Arruda, José Leandro da Silva Menezes Diniz, Maria Tereza Corrêa de Araújo, Maysa Aiany Dias de Sousa Alves, Maria Fernanda Paes de Assis, et al. "The effectiveness of using thiamine in the Wernicke-Korsakoff syndrome." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.380.
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Introduction: The Wernicke-Korsakoff syndrome is a condition caused by thiamine (vitamin B1) deficiency in the brain, being a debilitating and potentially fatal factor. It is characterized by a classic triad: delirium, ophthalmoparesis and ataxia. Objectives: Analyze the possible effectiveness of using thiamine in the prognostic change of patients with the syndrome, as well as the ideal dose and identification of possible secondary outcomes of the use of thiamine. Methods: A systematic review made in March 2021, included studies published between 2011-2021. The descriptors selected according to the MeSH platform, were inserted in the SCIELO, Lilacs and PubMed databases, resulting in a total of 323 studies, of which only 8 were selected. Results: Among the 8 evaluated articles, 5 reinforce the effectiveness of thiamine therapy, with prognostic changes in those patients, and only 4 of these studies describe their clinical evolution, showing mostly a gradual regression of the ocular manifestations and ataxia, while neurological symptoms tend to develop later. Thus 62,5% of the articles show improvement of patients with these therapeutics. Other studies do not refer to the prognosis after the institution of the treatment. About the dose, it was observed that the therapeutic effectiveness was related to higher doses of thiamine. Conclusion: Most of the analyzed studies were favorable to the hypothesis of the early use of thiamine in regression of the symptoms. Regarding the most effective dose, the topic still needs studies with high scientific evidence, as it hasn’t yet been thoroughly discussed in the literature.
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Sweet, Rebecca, Lauren Lim, and Jason Zastre. "Abstract 5419: Thiamine deficiency induces HIF-1 α stabilization and target gene expression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5419.
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Siqueira, Fernando, Vanessa Siqueira, Lucas Falcão, Arthur Bezerra, and Carlos Silva. "THE INFLUENCE BETWEEN ALZHEIMER’S DISEASE AND HEALTHY EATING: A SYSTEMATIC REVIEW." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda062.
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Background: Alzheimer’s Disease (AD) is a neurodegenerative disease responsible for neuronal losses that affect mainly the cortex and hippocampus, which begin to shrink in size, damaging cognitive functions. This process affects cholinergic neurons, influencing acetylcholine (ACH) levels, a memoryrelated neurotransmitter. Glucose metabolism and low thiamine levels appear to be affected by AD. Consequently, diabetes becomes a disease associated with AD and the thiamine deficiency levels depress the use of glucose by the brain. Thus, nutrition may have a role in preventing dementia through the treatment and prevention. Objective: To summarize the knowledge about this topic by reviewing articles and analyzing if healthy eating influences the development of AD. Methods: Selection of articles from the Scielo database. Results: Inflammation contributes to the pathogenesis of AD. The effect observed in patients with adherence to the Mediterranean diet translates into a decrease in inflammatory markers at the plasma level. One of the symptoms, memory loss, can be prevented by a micronutrient named thiamine, a precursor of ACH, it is found in the leguminous. The Mediterranean diet has been shown to attribute a neuroprotective activity which goes with its anti-inflammatory effect. Conclusion: AD starts by its multifactorial etiology that consists of genotype and phenotype. Nutrition would be efficient as a preventive and a therapeutic alternative among other.
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Elyahu, A. Y., S. Huelskamp, and H. Poor. "Thiamine Deficiency Causing High-Output Heart Failure with Concomitant Vasoreactive Pulmonary Arterial Hypertension: A Case Report." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7290.
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"PV-004 - THE COMPLEXITY OF DUAL PATHOLOGY: REGARDING A CASE REPORT OF SEIZURES." In 24 CONGRESO DE LA SOCIEDAD ESPAÑOLA DE PATOLOGÍA DUAL. SEPD, 2022. http://dx.doi.org/10.17579/abstractbooksepd2022.pv004.
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Objectives: Wernicke's encephalopathy (WE) is a potentially reversible neuropsychiatric emergency caused by thiamine deficiency, whose classical triad consists of confusion, ataxia, and oculomotor dysfunction. The diagnosis is missed in 75-80% of cases and approximately 80% of untreated patients develop Korsakoff Syndrome, whereby recognition of nutritional deficiency or any portion of the triad should prompt treatment. We present a case of a 44-year-old Ukrainian man with suspected background of chronic alcohol abuse and psychiatric history of schizoaffective disorder, who presented with acute onset of confusion, psychomotor agitation, gait ataxia and nystagmus. Anamnesis was hampered by the language barrier and absence of past medical history and patient's alcoholic habits remained unclear. After suspicion of WE it was introduced thiamine and diazepam, with significant improvement. After discontinuation of diazepam, the patient presented with several episodes of tonic-clonic seizures. Starting from this case report, we pretend to discuss the differential diagnosis of seizures in dual pathology. Materials and methods: Clinical records and Pubmed search using the keywords: Wernicke’s Encephalopathy, Seizures, Alcohol, Benzodiazepines. Results and conclusions: Seizures are a common presentation of various conditions associated with alcohol use, whose differential diagnosis is difficult, especially in patients with dubious alcohol consumption. Alcohol abuse is a major precipitant of status epilepticus as seizure threshold is raised by alcohol drinking. Seizures may also occur during alcohol withdrawal for which treatment with benzodiazepines is recommended, however carefully, since both abrupt cessation and high-dose use are critical for the appearance of seizures. Although very rare, WE may also present with seizures, whereby overdiagnosis and overtreatment are preferred to prevent persistent neurocognitive impairments. At discharge the diagnostic discussion prevailed and the patient was medicated for seizures with clinical stabilization. The complexity of psychiatric diagnoses in dual pathology requires a longitudinal assessment for a better understanding of clinical conditions as illustrated here.
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Rüsch, Christina, Saskia Wortmann, Reka Kovacs-Nagy, Patrice Grehten, Johannes Häberle, Bea Latal, and Georg Stettner. "P 233. Thiamine Pyrophosphokinase Deficiency due to Mutations in the TPK1 Gene: A Rare, Treatable Neurodegenerative Disorder." In Abstracts of the 44th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675992.
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