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https://www.readbyqxmd.com/read/27638475/urinary-metabolic-profiling-by-1-h-nmr-spectroscopy-in-patients-with-cirrhosis-may-discriminate-overt-but-not-covert-hepatic-encephalopathy
#1
Mark J W McPhail, Sara Montagnese, Manuela Villanova, Hamza El Hadi, Piero Amodio, Mary M E Crossey, Roger Williams, I Jane Cox, Simon D Taylor-Robinson
To date urinary metabolic profiling has been applied to define a specific metabolic fingerprint of hepatocellular carcinoma on a background of cirrhosis. Its utility for the stratification of other complications of cirrhosis, such as hepatic encephalopathy (HE), remains to be established. Urinary proton nuclear magnetic resonance ((1)H-NMR) spectra were acquired and NMR data from 52 patients with cirrhosis (35 male; 17 female, median (range) age [60 (18-81) years]) and 17 controls were compared. A sub-set of 45 patients (33 male; 12 female, [60 (18-90) years, median model for end stage liver disease (MELD) score 11 (7-27)]) were fully characterised by West-Haven criteria, Psychometric Hepatic Encephalopathy Score (PHES) and electroencephalogram (EEG), and defined as overt HE (OHE, n = 21), covert HE (cHE, n = 7) or no HE (n = 17)...
September 17, 2016: Metabolic Brain Disease
https://www.readbyqxmd.com/read/27535221/the-n-terminus-of-the-prion-protein-mediates-functional-interactions-with-the-neuronal-cell-adhesion-molecule-ncam-fibronectin-domain
#2
Urška Slapšak, Giulia Salzano, Ladan Amin, Romany N N Abskharon, Gregor Ilc, Blaž Zupančič, Ivana Biljan, Janez Plavec, Gabriele Giachin, Giuseppe Legname
The cellular form of the prion protein (PrP(C)) is a highly conserved glycoprotein mostly expressed in the central and peripheral nervous systems by different cell types in mammals. A misfolded, pathogenic isoform, denoted as prion, is related to a class of neurodegenerative diseases known as transmissible spongiform encephalopathy. PrP(C) function has not been unequivocally clarified, and it is rather defined as a pleiotropic protein likely acting as a dynamic cell surface scaffolding protein for the assembly of different signaling modules...
October 14, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27486995/early-cord-metabolite-index-and-outcome-in-perinatal-asphyxia-and-hypoxic-ischaemic-encephalopathy
#3
C E Ahearne, N M Denihan, B H Walsh, S N Reinke, L C Kenny, G B Boylan, D I Broadhurst, D M Murray
BACKGROUND: A 1H-NMR-derived metabolomic index based on early umbilical cord blood alterations of succinate, glycerol, 3-hydroxybutyrate and O-phosphocholine has shown potential for the prediction of hypoxic-ischaemic encephalopathy (HIE) severity. OBJECTIVE: To evaluate whether this metabolite score can predict 3-year neurodevelopmental outcome in infants with perinatal asphyxia and HIE, compared with current standard biochemical and clinical markers. METHODS: From September 2009 to June 2011, infants at risk of perinatal asphyxia were recruited from a single maternity hospital...
2016: Neonatology
https://www.readbyqxmd.com/read/27341298/structural-transitions-in-full-length-human-prion-protein-detected-by-xenon-as-probe-and-spin-labeling-of-the-n-terminal-domain
#4
Sunilkumar Puthenpurackal Narayanan, Divya Gopalakrishnan Nair, Daniel Schaal, Marisa Barbosa de Aguiar, Sabine Wenzel, Werner Kremer, Stephan Schwarzinger, Hans Robert Kalbitzer
Fatal neurodegenerative disorders termed transmissible spongiform encephalopathies (TSEs) are associated with the accumulation of fibrils of misfolded prion protein PrP. The noble gas xenon accommodates into four transiently enlarged hydrophobic cavities located in the well-folded core of human PrP(23-230) as detected by [(1)H, (15)N]-HSQC spectroscopy. In thermal equilibrium a fifth xenon binding site is formed transiently by amino acids A120 to L125 of the presumably disordered N-terminal domain and by amino acids K185 to T193 of the well-folded domain...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27184108/the-protonation-state-of-histidine-111-regulates-the-aggregation-of-the-evolutionary-most-conserved-region-of-the-human-prion-protein
#5
Luis Fonseca-Ornelas, Markus Zweckstetter
In a group of neurodegenerative diseases, collectively termed transmissible spongiform encephalopathies, the prion protein aggregates into β-sheet rich amyloid-like deposits. Because amyloid structure has been connected to different prion strains and cellular toxicity, it is important to obtain insight into the structural properties of prion fibrils. Using a combination of solution NMR spectroscopy, thioflavin-T fluorescence and electron microscopy we here show that within amyloid fibrils of a peptide containing residues 108-143 of the human prion protein [humPrP (108-143)]-the evolutionary most conserved part of the prion protein - residue H111 and S135 are in close spatial proximity and their interaction is critical for fibrillization...
August 2016: Protein Science: a Publication of the Protein Society
https://www.readbyqxmd.com/read/26105442/pp120-hydatidiform-mole-as-a-cause-of-eclampsia-in-the-first-trimester-a-case-report
#6
S Ottanelli, S Simeone, C Serena, M P Rambaldi, A Villanucci, K Tavella, G Amunni, F Mecacci, G Mello
INTRODUCTION: The occurrence of preeclampsia before the 20th week of gestation is rare and it has been associated with hydatidiform molar pregnancy. OBJECTIVES: We describe a case of first trimester eclampsia which occurred in a patient with hydatidiform mole. METHODS: Case report. RESULTS: A 16-year-old woman came to emergency service for abdominal pain and vaginal bleeding. She had been suffering of vomiting after meals and complaining for abdominal mass for 2months, without consulting her physician...
July 2012: Pregnancy Hypertension
https://www.readbyqxmd.com/read/26043781/molecular-dynamics-studies-on-the-buffalo-prion-protein
#7
Jiapu Zhang, Feng Wang, Subhojyoti Chatterjee
It was reported that buffalo is a low susceptibility species resisting to transmissible spongiform encephalopathies (TSEs) (same as rabbits, horses, and dogs). TSEs, also called prion diseases, are invariably fatal and highly infectious neurodegenerative diseases that affect a wide variety of species (except for rabbits, dogs, horses, and buffalo), manifesting as scrapie in sheep and goats; bovine spongiform encephalopathy (BSE or "mad-cow" disease) in cattle; chronic wasting disease in deer and elk; and Creutzfeldt-Jakob diseases, Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia, and Kulu in humans etc...
2016: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/25959287/-1-h-nmr-brain-metabonomics-of-scrapie-exposed-sheep
#8
Paola Scano, Antonella Rosa, Alessandra Incani, Caterina Maestrale, Cinzia Santucciu, Daniela Perra, Sarah Vascellari, Alessandra Pani, Ciriaco Ligios
While neurochemical metabolite modifications, determined by different techniques, have been diffusely reported in human and mice brains affected by transmissible spongiform encephalopathies (TSEs), this aspect has been little studied in the natural animal hosts with the same pathological conditions so far. Herein, we investigated, by high resolution (1)H NMR spectroscopy and multivariate statistical data analysis, the brain metabolite profile of sheep exposed to a scrapie agent in a naturally affected flock...
July 2015: Molecular BioSystems
https://www.readbyqxmd.com/read/25735860/ammonia-metabolism-and-hyperammonemic-disorders
#9
REVIEW
Valerie Walker
Human adults produce around 1000 mmol of ammonia daily. Some is reutilized in biosynthesis. The remainder is waste and neurotoxic. Eventually most is excreted in urine as urea, together with ammonia used as a buffer. In extrahepatic tissues, ammonia is incorporated into nontoxic glutamine and released into blood. Large amounts are metabolized by the kidneys and small intestine. In the intestine, this yields ammonia, which is sequestered in portal blood and transported to the liver for ureagenesis, and citrulline, which is converted to arginine by the kidneys...
2014: Advances in Clinical Chemistry
https://www.readbyqxmd.com/read/25424547/ex-vivo-1-h-nuclear-magnetic-resonance-spectroscopy-reveals-systematic-alterations-in-cerebral-metabolites-as-the-key-pathogenetic-mechanism-of-bilirubin-encephalopathy
#10
Wenyi Hu, Xiaojie Cheng, Xinjian Ye, Liangcai Zhao, Yanan Huang, Huanle Zhu, Zhihan Yan, Xuebao Wang, Xiaojie Wang, Guanghui Bai, Hongchang Gao
BACKGROUND: Bilirubin encephalopathy (BE) is a severe neurologic sequelae induced by hyperbilirubinemia in newborns. However, the pathogenetic mechanisms underlying the clinical syndromes of BE remain ambiguous. Ex vivo (1)H nuclear magnetic resonance (NMR) spectroscopy was used to measure changes in the concentrations of cerebral metabolites in various brain areas of newborn 9-day-old rats subjected to bilirubin to explore the related mechanisms of BE. RESULTS: When measured 0...
2014: Molecular Brain
https://www.readbyqxmd.com/read/25268146/visualization-of-different-characteristics-of-cerebrospinal-fluid-with-acute-encephalopathy-and-febrile-seizures-using-pattern-recognition-analysis-of-1h-nmr
#11
Takeshi Asano, Keiko Hirakawa, Kaoru Koike, Youkichi Ohno, Osamu Fujino
BACKGROUND: In acute encephalopathy, deterioration of the condition can be rapid, and early intervention is essential to prevent progression of the disease. However, in the acute period, differentiating acute encephalopathy from febrile seizures is difficult. Thus, an early diagnostic marker has been sought to enable early intervention. Proton nuclear magnetic resonance ((1)H NMR) spectroscopy is used to study the chemical characteristics of biological fluids such as cerebrospinal fluid (CSF)...
January 2015: Pediatric Research
https://www.readbyqxmd.com/read/25034052/pathophysiology-of-brain-dysfunction-in-hyperammonemic-syndromes-the-many-faces-of-glutamine
#12
REVIEW
Roger F Butterworth
Ineffective hepatic clearance of excess ammonia in the form of urea, as occurs in urea cycle enzymopathies (UCDs) and in liver failure, leads to increases in circulating and tissue concentrations of glutamine and a positive correlation between brain glutamine and the severity of neurological symptoms. Studies using 1H/13C Nuclear Magnetic Resonance (NMR) spectroscopy reveal increased de novo synthesis of glutamine in the brain in acute liver failure (ALF) but increases of synthesis rates per se do not correlate with either the severity of encephalopathy or brain edema...
September 2014: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/24512824/increased-brain-lactate-is-central-to-the-development-of-brain-edema-in-rats-with-chronic-liver-disease
#13
Cristina R Bosoi, Claudia Zwingmann, Helen Marin, Christian Parent-Robitaille, Jimmy Huynh, Mélanie Tremblay, Christopher F Rose
BACKGROUND & AIMS: The pathogenesis of brain edema in patients with chronic liver disease (CLD) and minimal hepatic encephalopathy (HE) remains undefined. This study evaluated the role of brain lactate, glutamine and organic osmolytes, including myo-inositol and taurine, in the development of brain edema in a rat model of cirrhosis. METHODS: Six-week bile-duct ligated (BDL) rats were injected with (13)C-glucose and de novo synthesis of lactate, and glutamine in the brain was quantified using (13)C nuclear magnetic resonance spectroscopy (NMR)...
March 2014: Journal of Hepatology
https://www.readbyqxmd.com/read/24466704/-encephalopathy-caused-by-intravenous-potassium-permanganate-used-for-illegal-production-of-methcathinone-ephedrone-from-medicines-containing-pseudoephedrine
#14
REVIEW
Bogusław Habrat, Helena Baran-Furga, Halina Sienkiewicz-Jarosz, Jacek Sein Anand, Renata Poniatowska
Encephalopathy caused by manganese compounds used for illicit production of ephedrone (methcathinone) is described. The onset of disease could be observed after some months of regular intravenous use of ephedrone contaminated with manganese. In clinical picture dominate neurological signs and symptoms, mainly extrapyramidal syndromes: parkinsonism, tremor, muscle distonia, pro- and retropulsion. Some other symptoms may be observed: hypophonia or dysarthria, gain disturbances, impairment of precise movement, and micrographia...
2013: Przegla̧d Lekarski
https://www.readbyqxmd.com/read/24184221/molecular-dynamics-studies-on-the-nmr-and-x-ray-structures-of-rabbit-prion-proteins
#15
Jiapu Zhang, Yuanli Zhang
Prion diseases, traditionally referred to as transmissible spongiform encephalopathies (TSEs), are invariably fatal and highly infectious neurodegenerative diseases that affect a wide variety of mammalian species, manifesting as scrapie in sheep and goats, bovine spongiform encephalopathy (BSE or mad-cow disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob diseases, Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia, and kulu in humans, etc. These neurodegenerative diseases are caused by the conversion from a soluble normal cellular prion protein (PrP(C)) into insoluble abnormally folded infectious prions (PrP(Sc)), and the conversion of PrP(C) to PrP(Sc) is believed to involve conformational change from a predominantly α-helical protein to one rich in β-sheet structure...
February 7, 2014: Journal of Theoretical Biology
https://www.readbyqxmd.com/read/24059340/nmr-structural-studies-of-human-cellular-prion-proteins
#16
REVIEW
Ivana Biljan, Gregor Ilc, Gabriele Giachin, Giuseppe Legname, Janez Plavec
Prion diseases or transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative disorders associated with the conformational conversion of the cellular prion protein, PrP(C), into a pathological form known as prion or PrP(Sc). They can be classified into sporadic, inherited and infectious forms. Spontaneous generation of PrP(Sc) in inherited forms of prion diseases is caused by mutations in the human prion protein gene (PRNP). A major goal in prion biology is unraveling the molecular mechanism by which PrP(C) misfolds and leads to development of diseases...
2013: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/23966072/probing-early-misfolding-events-in-prion-protein-mutants-by-nmr-spectroscopy
#17
REVIEW
Gabriele Giachin, Ivana Biljan, Gregor Ilc, Janez Plavec, Giuseppe Legname
The post-translational conversion of the ubiquitously expressed cellular form of the prion protein, PrPC, into its misfolded and pathogenic isoform, known as prion or PrPSc, plays a key role in prion diseases. These maladies are denoted transmissible spongiform encephalopathies (TSEs) and affect both humans and animals. A prerequisite for understanding TSEs is unraveling the molecular mechanism leading to the conversion process whereby most α-helical motifs are replaced by β-sheet secondary structures. Importantly, most point mutations linked to inherited prion diseases are clustered in the C-terminal domain region of PrPC and cause spontaneous conversion to PrPSc...
2013: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/23931672/1h-nmr-derived-metabolomic-profile-of-neonatal-asphyxia-in-umbilical-cord-serum-implications-for-hypoxic-ischemic-encephalopathy
#18
Stacey N Reinke, Brian H Walsh, Geraldine B Boylan, Brian D Sykes, Louise C Kenny, Deirdre M Murray, David I Broadhurst
Neonatal hypoxic ischemic encephalopathy (HIE) is a severe consequence of perinatal asphyxia (PA) that can result in life-long neurological disability. Disease mechanisms, including the role and interaction of individual metabolic pathways, remain unclear. As hypoxia is an acute condition, aerobic energy metabolism is central to global metabolic pathways, and these metabolites are detectable using 1H NMR spectroscopy, we hypothesized that characterizing the NMR-derived umbilical cord serum metabolome would offer insight into the consequences of PA that lead to HIE...
September 6, 2013: Journal of Proteome Research
https://www.readbyqxmd.com/read/23650394/structural-plasticity-of-the-cellular-prion-protein-and-implications-in-health-and-disease
#19
Barbara Christen, Fred F Damberger, Daniel R Pérez, Simone Hornemann, Kurt Wüthrich
Two lines of transgenic mice expressing mouse/elk and mouse/horse prion protein (PrP) hybrids, which both form a well-structured β2-α2 loop in the NMR structures at 20 °C termed rigid-loop cellular prion proteins (RL-PrP(C)), presented with accumulation of the aggregated scrapie form of PrP in brain tissue, and the mouse/elk hybrid has also been shown to develop a spontaneous transmissible spongiform encephalopathy. Independently, there is in vitro evidence for correlations between the amino acid sequence in the β2-α2 loop and the propensity for conformational transitions to disease-related forms of PrP...
May 21, 2013: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/23647538/the-ph-triggered-conversion-of-the-prp-c-to-prp-sc
#20
REVIEW
Guo-Ping Zhou, Ri-Bo Huang
Transmissible spongiform encephalopathies (TSEs) are prion protein misfolding diseases that involve the accumulation of an abnormal β-sheet-rich prion protein aggregated form (PrP(sc)) of the normal α- helix-rich prion protein (PrP(c)) within the central nervous system (CNS) and other organs. On account of its large size and insolubility properties, characterization of PrP(c) is quite difficult. A soluble intermediate, called PrP(β) or β(o), exhibiting many of the same features as PrP(sc), can be generated using a combination of low pH and/or mild denaturing conditions...
2013: Current Topics in Medicinal Chemistry
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