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Artykuły w czasopismach na temat "Wernicke-Korsakoff Syndrome"
Kotov, S. V., A. I. Lobakov, E. V. Isakova, G. A. Stashuk i T. V. Volchenkova. "Wernicke–Korsakoff syndrome". Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 116, nr 7 (2016): 4. http://dx.doi.org/10.17116/jnevro2016116714-11.
Pełny tekst źródłaSchaefer, Sandra. "Wernicke?Korsakoff Syndrome". Journal of the American Academy of Nurse Practitioners 8, nr 9 (wrzesień 1996): 435–36. http://dx.doi.org/10.1111/j.1745-7599.1996.tb00692.x.
Pełny tekst źródłaSivolap, Yu P., i I. V. Damulin. "Wernicke–Korsakoff syndrome". Neurology, Neuropsychiatry, Psychosomatics, nr 4 (10.12.2014): 76. http://dx.doi.org/10.14412/2074-2711-2014-4-76-80.
Pełny tekst źródłaMCNAMARA, M. EILEEN, JOHN J. CAMPBELL i PATRICIA RYAN RECUPERO. "Wernicke-Korsakoff Syndrome". Journal of Neuropsychiatry and Clinical Neurosciences 3, nr 2 (maj 1991): 232. http://dx.doi.org/10.1176/jnp.3.2.232.
Pełny tekst źródłaZubaran, C., J. G. Fernandes i R. Rodnight. "Wernicke-Korsakoff syndrome." Postgraduate Medical Journal 73, nr 855 (1.01.1997): 27–31. http://dx.doi.org/10.1136/pgmj.73.855.27.
Pełny tekst źródłaBrockington, I. "Wernicke-Korsakoff syndrome". Archives of Women's Mental Health 9, nr 1 (22.12.2005): 58–59. http://dx.doi.org/10.1007/s00737-005-0112-x.
Pełny tekst źródłaMadeira, N., T. Santos i J. L. Pio-Abreu. "Wernicke-Korsakoff Syndrome: A Common Yet Elusive Diagnosis". European Psychiatry 24, S1 (styczeń 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71095-8.
Pełny tekst źródłaMushtaq, Raheel, Sheikh Shoib, Tabindah Shah, Mudasir Bhat, Randhir Singh i Sahil Mushtaq. "Unusual Presentation of Uncommon Disease: Anorexia Nervosa Presenting as Wernicke-Korsakoff Syndrome—A Case Report from Southeast Asia". Case Reports in Psychiatry 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/482136.
Pełny tekst źródłaPokale, Yogesh Jagannath, i Sunil G. Gupte. "A Case Report on Wernicke–Korsakoff Syndrome". MVP Journal of Medical Sciences 1, nr 1 (1.01.2014): 44. http://dx.doi.org/10.18311/mvpjms/2014/v1/i1/835.
Pełny tekst źródłaSwain, Sanjana Simansu, i Suhasin Ganta. "Korsakoff Syndrome: A Chronic Nutritional Deficiency Neuropsychiatric condition". YMER Digital 21, nr 05 (27.05.2022): 1217–33. http://dx.doi.org/10.37896/ymer21.05/d6.
Pełny tekst źródłaRozprawy doktorskie na temat "Wernicke-Korsakoff Syndrome"
Roland, Jessica Justine. "Hippocampal and striatal acetylcholine efflux during learning in diencephalic-lesioned rats". Diss., Online access via UMI:, 2005.
Znajdź pełny tekst źródłaAlexander-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.
Pełny tekst źródłaProteomics 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.
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.
Pełny tekst źródłaRoland, Jessica Justine. "Septohippocampal system modulation in an animal model of diencephalic amnesia". Diss., Online access via UMI:, 2008.
Znajdź pełny tekst źródłaAnzalone, Steven J. "Cholinergic cortical dysfunction in an animal model of diencephalic amnesia". Diss., Online access via UMI:, 2009.
Znajdź pełny tekst źródłaBeauchesne, 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.
Pełny tekst źródłaWernicke-Korsakoff syndrome (WKS) is a neuropsychiatric disorder caused by thiamine deficiency (TD). In experimental TD as in WKS, neuronal cell death and hemorrhages are observed in specific diencephalic and brainstem areas. Diencephalic lesions in WKS are especially severe and often lead to permanent amnesic symptoms. The link between TD-induced metabolic dysfunction and neuronal cell death is unknown. Previous reports have shown that blood-brain barrier (BBB) permeability was impaired and that this occurred prior to the onset of neuronal damage, suggesting a critical role for vascular dysfunction. Interendothelial tight junctions (TJs), the anatomical basis of the BBB, constitute a molecular network comprising occludin and zonula occludens (ZOs). This thesis shows a loss of expression and alterations in the morphology of these proteins in relation to BBB dysfunction in the thalamus of thiamine-deficient mice, providing an explanation for the presence of hemorrhages. Oxidative stress can lead to direct oxidative damage to TJ proteins and interfere with their regulation mechanisms. Also, nitric oxide (NO) can induce matrix metalloproteinase-9 (MMP-9) involved in the degradation of these proteins. Cerebral vascular endothelium (CVE) seems to be an important source of NO in TD, since endothelial nitric oxide synthase (eNOS) expression is selectively induced in vulnerable areas. NO can react with reactive oxygen species and form peroxynitrite, leading to endothelial oxidative/nitrosative stress. Results have show that eNOS gene deletion prevents cerebrovascular oxidative/nitrosative stress, immunoglobulins G (IgGs) extravasation and occludin and ZOs alterations in the thalamus of thiamine-deficient mice. Also, eNOS gene deletion prevents the induction of MMP-9 in CVE. Similar results have been obtained with the antioxidant N-acetylcysteine (NAC). Precise mechanisms by which reactive species alter TJ proteins are unknown. Caveolin-1, a major component of CVE caveolæ, is involved in the regulation of TJ protein expression, and is modulated by oxidative/nitrosative stress; alteration in caveolin-1 expression has been recently associated with BBB breakdown. The present results show that caveolin-1 expression is selectively altered in CVE of the thalamus of thiamine-deficient mice, and show that normalization of caveolin-1 expression by NAC is associated with the attenuation of BBB damage. Taken together, these results demonstrate a central role for cerebrovascular oxidative/nitrosative stress, especially coming from eNOS, in BBB TJ protein alterations via direct damage and via induction of MMP-9 and caveolin-1. As a result, BBB breakdown contributes to neuronal cell death in the thalamus, since prevention of cerebrovascular alterations by eNOS gene deletion and NAC significantly attenuates neuronal cell death. Early administration of antioxidants combined with thiamine should therefore be an important consideration for the treatment of WKS.
Jhala, Shivraj. "Regulation of excitotoxicity in thiamine deficiency : role of glutamate transporters". Thèse, 2012. http://hdl.handle.net/1866/9720.
Pełny tekst źródłaExcitotoxicity has been implicated as a major pathophysiological mechanism in the pathogenesis of thiamine deficiency (TD). Excitotoxic-mediated cell death is localized in areas of focal vulnerability in TD and may occur as a consequence of impairment in mitochondrial energy metabolism, sustained cell membrane depolarization and decreased uptake of glutamate by astrocytes due to the loss of excitatory amino acid transporters, (EAAT1 and EAAT2). Over the years, a number of studies have identified glutamate as being a major contributor to excitotoxicity in the pathophysiology of TD. Thus, downregulation of astrocytic glutamate transporters resulting in excitotoxicity is a key feature of TD and understanding the regulation of these transporters is essential to understanding the pathophysiology of the disorder. The objective of the present thesis project was to examine the underlying basis of astrocytic glutamate transporter regulation during TD encephalopathy. Major findings of the studies presented in this thesis project provide evidence for glutamate transporter abnormalities in TD animal models and astrocyte cultures exposed to TD. TD results in the loss of the glutamate transporter splice variant-1b (GLT-1b) in vulnerable areas of brain, i.e. thalamus and inferior colliculus, with no significant alteration in the mRNA levels of the transporters, suggesting that glutamate transporter regulation under conditions of TD is a posttranscriptional event. Studies using a specific inhibitor of the transcription factor, Nuclear factor-kappa B (NF-κB) and a nuclear enzyme poly (ADP)ribose polymerase-1 (PARP-1) provided evidence for the regulation of GLT-1 by PARP-1 dependent NF-κB signalling pathways. The major findings of this study suggested an increase in the activation of PARP-1 and NF-κB molecule in the vulnerable areas of TD rat brain and TD astrocyte cultures. Pharmacological inhibition of NF-κB showed an increase in the levels of GLT-1, while inhibition of PARP-1 using a specific PARP-1 inhibitor, DPQ inhibited the increased activation of NF-κB that was observed during TD. Overall results of this finding provided evidence for a mechanism involving PARP-1 activation in the regulation of glutamate transporters. Given the increased lactate accumulation as a classical feature of TD, we studied the effect of soluble factors produced by astrocytes on glutamate transporter function. Treatment of naïve astrocyte cultures with TD conditioned media resulted in decreased levels of GLT-1 and inhibition of glutamate uptake capacity concomitant with a loss of mitochondrial membrane potential. Administration of exogenous lactic acid produced a similar reduction in glutamate uptake to that resulting from conditioned media. However, lactic acid treatment did not result in a change in GLT-1 protein levels. In addition, the pro-inflammatory cytokine TNF-α was shown to be increased in astrocytes treated with TD along with elevated levels of the phospho-IκB fragment, indicative of increased activation of NFκB. Inhibition of NFκB led to an amelioration of the decrease in GLT-1 that occurs in TD, along with recovery of glutamate uptake. Thus, soluble factors released from astrocytes under conditions of metabolic impairment such as lactate and TNF-α impairment appear to exert a regulatory influence on glutamate transporter function. Ceftriaxone, a β-lactam antibiotic, has the ability to differentially stimulate GLT-1b (splice-variant) expression in the inferior colliculus in TD rats and under in vitro conditions with TD astrocyte cultures. Thus, ceftriaxone may be a potential therapeutic strategy in the regulation of glutamate transporter function during TD. In summary, excitotoxic cell death in TD occurs as a consequence of mitochondrial dysfunction associated with cerebral energy impairment and abnormal glutamate transporter status. A major underlying mechanism for glutamate transporter abnormalities is mediated by PARP-1 dependent NF-κB signaling pathways. In addition, metabolic inhibition with substantial production of lactate and TNF-α may be perhaps another mechanism responsible for glutamate transporter downregulation in TD.
Książki na temat "Wernicke-Korsakoff Syndrome"
1911-, Adams Raymond D., i Collins George H. 1927-, red. The Wernicke-Korsakoff syndrome and related neurologic disorders due to alcoholism and malnutrition. Wyd. 2. Philadelphia, PA: F.A. Davis Co., 1989.
Znajdź pełny tekst źródłaHealth, Beller. 2019 Wernicke-Korsakoff Syndrome: A Preventable Dementia. Independently Published, 2019.
Znajdź pełny tekst źródłaBriggs, John, Jerry Beller, Beller Health i Brain Research. Wernicke-Korsakoff Syndrome: The Best Science in Everyday Language! Independently Published, 2020.
Znajdź pełny tekst źródłaMisulis, Karl E., i E. Lee Murray. Nutritional Deficiencies and Toxicities. Redaktorzy Karl E. Misulis i E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0029.
Pełny tekst źródłaZidrix, Druew. Causes of Nystagmus: Benign Paroxysmal Positional Vertigo, Meniere's Disease, Multiple Sclerosis, Stroke, Tullio Phenomenon, Wernicke-Korsakoff Syndrome, Noonan, Aniridia, Head Trauma, Canavan Disease. Independently Published, 2021.
Znajdź pełny tekst źródłaKaren, Bellenir, red. Alcoholism sourcebook: Basic consumer health information about the physical and mental consequences of alcohol abuse, including liver disease, pancreatitis, Wernicke-Korsakoff syndrome (alcoholic dementia), fetal alcohol syndrome, heart disease, kidney disorders, gastrointestinal problems, and immune system compromise, and featuring facts about addiction, detoxification, alcohol withdrawal, recovery, and the maintenance of sobriety, along with a glossary and directories of resources for further help and information. Detroit: Omnigraphics, 2000.
Znajdź pełny tekst źródłaCzęści książek na temat "Wernicke-Korsakoff Syndrome"
Lafleche, Ginette, i Mieke Verfaellie. "Wernicke-Korsakoff Syndrome". W Encyclopedia of Clinical Neuropsychology, 2699–702. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1164.
Pełny tekst źródłaLafleche, Ginette, i Mieke Verfaellie. "Wernicke-Korsakoff Syndrome". W Encyclopedia of Clinical Neuropsychology, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1164-2.
Pełny tekst źródłaLafleche, Ginette, i Mieke Verfaellie. "Wernicke-Korsakoff Syndrome". W Encyclopedia of Clinical Neuropsychology, 3716–20. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1164.
Pełny tekst źródłaSharp, Christopher S., i Kimberly D. Nordstrom. "Wernicke-Korsakoff Syndrome". W Quick Guide to Psychiatric Emergencies, 147–50. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58260-3_27.
Pełny tekst źródłaGreenberg, David A., i Ivan Diamond. "Wernicke—Korsakoff Syndrome". W Alcohol and the Brain, 295–314. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-9134-1_12.
Pełny tekst źródłaAkhouri, Shweta. "Wernicke–Korsakoff Syndrome". W The Palgrave Encyclopedia of Critical Perspectives on Mental Health, 1–3. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-12852-4_74-1.
Pełny tekst źródłaBöhm, Markus, Thomas A. Luger, Cem Evereklioglu, Mark Berneburg, Thomas Schwarz, Irene Guerrini, Allan D. Thomson i in. "Wernicke Korsakoff Syndrome". W Encyclopedia of Molecular Mechanisms of Disease, 2239–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3231.
Pełny tekst źródłaTheisler, Charles. "Wernicke-Korsakoff Syndrome". W Adjuvant Medical Care, 359–60. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-352.
Pełny tekst źródłaKunze, Klaus, Michael A. DeGeorgia i Michael N. Diringer. "Wernicke’s Encephalopathy (Wernicke-Korsakoff Syndrome)". W Neurocritical Care, 840–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_76.
Pełny tekst źródłaHéroux, Maryse, i Roger F. Butterworth. "Animal Models of the Wernicke-Korsakoff Syndrome". W Animal Models of Neurological Disease, II, 95–131. Totowa, NJ: Humana Press, 1992. http://dx.doi.org/10.1385/0-89603-211-6:95.
Pełny tekst źródłaStreszczenia konferencji na temat "Wernicke-Korsakoff Syndrome"
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 i in. "The effectiveness of using thiamine in the Wernicke-Korsakoff syndrome". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.380.
Pełny tekst źródłaRodríguez, Derly Judaissy Díaz, Jeffrey Andrés Díaz Rodríguez, Diva Constanza Gil Forero i María Paula Pineda Díaz. "Wernicke-Korsakoff syndrome and other chronic neurological syndromes related to alcohol abuse: prevention in people without home". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.686.
Pełny tekst źródła"CHRONIC EFFECTS OF ALCOHOL. A CASE REPORT". W 23° Congreso de la Sociedad Española de Patología Dual (SEPD) 2021. SEPD, 2021. http://dx.doi.org/10.17579/sepd2021p021s.
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