Relevant bibliographies by topics / Glycation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Glycation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Glycation"

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Rabbani, Naila, Maryam Al-Motawa, and Paul J. Thornalley. "Protein Glycation in Plants—An Under-Researched Field with Much Still to Discover." International Journal of Molecular Sciences 21, no. 11 (May 30, 2020): 3942. http://dx.doi.org/10.3390/ijms21113942.

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Recent research has identified glycation as a non-enzymatic post-translational modification of proteins in plants with a potential contributory role to the functional impairment of the plant proteome. Reducing sugars with a free aldehyde or ketone group such as glucose, fructose and galactose react with the N-terminal and lysine side chain amino groups of proteins. A common early-stage glycation adduct formed from glucose is Nε-fructosyl-lysine (FL). Saccharide-derived reactive dicarbonyls are arginine residue-directed glycating agents, forming advanced glycation endproducts (AGEs). A dominant dicarbonyl is methylglyoxal—formed mainly by the trace-level degradation of triosephosphates, including through the Calvin cycle of photosynthesis. Methylglyoxal forms the major quantitative AGE, hydroimidazolone MG-H1. Glucose and methylglyoxal concentrations in plants change with the developmental stage, senescence, light and dark cycles and also likely biotic and abiotic stresses. Proteomics analysis indicates that there is an enrichment of the amino acid residue targets of glycation, arginine and lysine residues, in predicted functional sites of the plant proteome, suggesting the susceptibility of proteins to functional inactivation by glycation. In this review, we give a brief introduction to glycation, glycating agents and glycation adducts in plants. We consider dicarbonyl stress, the functional vulnerability of the plant proteome to arginine-directed glycation and the likely role of methylglyoxal-mediated glycation in the activation of the unfolded protein response in plants. The latter is linked to the recent suggestion of protein glycation in sugar signaling in plant metabolism. The overexpression of glyoxalase 1, which suppresses glycation by methylglyoxal and glyoxal, produced plants resistant to high salinity, drought, extreme temperature and other stresses. Further research to decrease protein glycation in plants may lead to improved plant growth and assist the breeding of plant varieties resistant to environmental stress and senescence—including plants of commercial ornamental and crop cultivation value.
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Thornalley, P. J. "The enzymatic defence against glycation in health, disease and therapeutics: a symposium to examine the concept." Biochemical Society Transactions 31, no. 6 (December 1, 2003): 1341–42. http://dx.doi.org/10.1042/bst0311341.

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Glycation of proteins, nucleotides and basic phospholipids by glucose, glyoxal, methylglyoxal, 3-deoxyglucosone and other saccharide derivatives is potentially damaging to the proteome and mutagenic. It is now recognized that there is an enzymatic defence against glycation – a group of enzymes that suppress the physiological levels of potent glycating agents and repair glycated proteins: glyoxalase I, aldehyde reductases and dehydrogenases, amadoriase and fructosamine 3-phosphokinase. The enzymatic defence against glycation influences morbidity and the efficiency of drug therapy in certain diseases. Improved understanding of the balance between glycation and the enzymatic anti-glycation defence will advance disease diagnosis and therapy.
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Khan, Hamda, Mohd Waseem, Mohammad Faisal, Abdulrahman A. Alatar, Ahmed A. Qahtan, and Saheem Ahmad. "Inhibitory Effect of Multimodal Nanoassemblies against Glycative and Oxidative Stress in Cancer and Glycation Animal Models." BioMed Research International 2021 (April 9, 2021): 1–17. http://dx.doi.org/10.1155/2021/8892156.

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In recent years, there has been a progress in the study of glycation reaction which is one the possible reason for multiple metabolic disorders. Glycation is a nonenzymatic reaction between nucleic acids, lipids, and proteins resulting into the formation of early glycation products that may further lead to the accumulation of advanced glycation end products (AGEs). The precipitation of AGEs in various cells, tissues, and organs is one of the factors for the initiation and progression of various metabolic derangements including the cancer. The AGE interaction with its receptor “RAGE” activates the inflammatory pathway; yet, the downregulation of RAGE and its role in these pathways are not clear. We explore the effect of anticancer novel nanoassemblies on AGEs to determine its role in the regulation of the expression of RAGE, NFƙB, TNF-α, and IFN-γ. This paper is based on the in vivo and in vitro study in glycation and lung cancer model systems. Upon the treatment of nanoassemblies in both the model systems, we observed a protective effect of nanoassemblies over the inhibition of glycative and oxidative stress via mRNA expression analysis. The mRNA expression results corroborated with the reactive oxygen species (ROS), carboxy-methyl-lysine (CML), and fluorescence studies. In this study, we found that the presence of common factors for glycation and lung cancer is oxidative and glycative stress. This oxidation and glycation might be responsible for the initiation of inflammation which may further lead to uncontrolled growth of cells leading to cancer. This can be a strong association between lung cancer and glycation reaction. The intervention of the anticancer and antiglycation effects of multimodal nanoassemblies throughout the study promises a new pathway for cancer research.
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Kumar, P. Anil, M. Satish Kumar, and G. Bhanuprakash Reddy. "Effect of glycation on α-crystallin structure and chaperone-like function." Biochemical Journal 408, no. 2 (November 14, 2007): 251–58. http://dx.doi.org/10.1042/bj20070989.

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The chaperone-like activity of α-crystallin is considered to play an important role in the maintenance of the transparency of the eye lens. However, in the case of aging and in diabetes, the chaperone function of α-crystallin is compromized, resulting in cataract formation. Several post-translational modifications, including non-enzymatic glycation, have been shown to affect the chaperone function of α-crystallin in aging and in diabetes. A variety of agents have been identified as the predominant sources for the formation of AGEs (advanced glycation end-products) in various tissues, including the lens. Nevertheless, glycation of α-crystallin with various sugars has resulted in divergent results. In the present in vitro study, we have investigated the effect of glucose, fructose, G6P (glucose 6-phosphate) and MGO (methylglyoxal), which represent the major classes of glycating agents, on the structure and chaperone function of α-crystallin. Modification of α-crystallin with all four agents resulted in the formation of glycated protein, increased AGE fluorescence, protein cross-linking and HMM (high-molecular-mass) aggregation. Interestingly, these glycation-related profiles were found to vary with different glycating agents. For instance, CML [Nϵ-(carboxymethyl)lysine] was the predominant AGE formed upon glycation of α-crystallin with these agents. Although fructose and MGO caused significant conformational changes, there were no significant structural perturbations with glucose and G6P. With the exception of MGO modification, glycation with other sugars resulted in decreased chaperone activity in aggregation assays. However, modification with all four sugars led to the loss of chaperone activity as assessed using an enzyme inactivation assay. Glycation-induced loss of α-crystallin chaperone activity was associated with decreased hydrophobicity. Furthermore, α-crystallin isolated from glycated TSP (total lens soluble protein) had also increased AGE fluorescence, CML formation and diminished chaperone activity. These results indicate the susceptibility of α-crystallin to non-enzymatic glycation by various sugars and their derivatives, whose levels are elevated in diabetes. We also describes the effects of glycation on the structure and chaperone-like activity of α-crystallin.
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Inagi, Reiko. "Glycative stress and glyoxalase in kidney disease and aging." Biochemical Society Transactions 42, no. 2 (March 20, 2014): 457–60. http://dx.doi.org/10.1042/bst20140007.

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Glycation is one of the important reactions regulating physiological state, and glycative stress, namely an overwhelming and unfavourable glycation state, is established as a pathological factor. Glycative stress is closely associated with not only various kidney diseases, but also kidney aging. Accumulating evidence, including studies in my laboratory, demonstrates that progression of renal tubular damage and its aging is correlated with the decrease in the activity of anti-glycative stress enzyme Glo1 (glyoxalase I) in the kidney. The reduction of glycative and oxidative stresses by Glo1 overexpression is beneficial for prevention of kidney disease and treatment, suggesting the novel therapeutic approaches targeting Glo1. The present review is focused on the impact of glycative stress and Glo1 on protein homoeostasis and discusses further the cross-talk between glycative stress and UPR (unfolded protein response), which controls the protein homoeostasis state.
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Khan, Mohd W. A., Ahmed A. Otaibi, Arwa F. M. Alhumaid, Abdulmohsen K. D. Alsukaibi, Asma K. Alshamari, Eida M. Alshammari, Salma A. Al-Zahrani, Ahmed Y. M. Almudyani, and Subuhi Sherwani. "Garlic Extract: Inhibition of Biochemical and Biophysical Changes in Glycated HSA." Applied Sciences 11, no. 22 (November 21, 2021): 11028. http://dx.doi.org/10.3390/app112211028.

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Glycation of various biomolecules contributes to structural changes and formation of several high molecular weight fluorescent and non-fluorescent, advanced glycation end products (AGEs). AGEs and glycation are involved in various health complications. Synthetic medicines, including metformin, have several adverse effects. Natural products and their derivatives are used in the treatment of various diseases due to their significant therapeutic qualities. Allium sativum (garlic) is used in traditional medicines because of its antioxidant, anti-inflammatory, and anti-diabetic properties. This study aimed to determine the anti-glycating and AGEs inhibitory activities of garlic. Biochemical and biophysical analyses were performed for in vitro incubated human serum albumin (HSA) with 0.05 M of glucose for 1, 5, and 10 weeks. Anti-glycating and AGEs inhibitory effect of garlic was investigated in glycated samples. Increased biochemical and biophysical changes were observed in glycated HSA incubated for 10 weeks (G-HSA-10W) as compared to native HSA (N-HSA) as well as glycated HSA incubated for 1 (G-HSA-1W) and 5 weeks (G-HSA-5W). Garlic extract with a concentration of ≥6.25 µg/mL exhibited significant inhibition in biophysical and biochemical changes of G-HSA-10W. Our findings demonstrated that garlic extract has the ability to inhibit biochemical and biophysical changes in HSA that occurred due to glycation. Thus, garlic extract can be used against glycation and AGE-related health complications linked with chronic diseases in diabetic patients due to its broad therapeutic potential.
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Das, Sourav, Sharat Sarmah, Zaved Hazarika, Mostofa Ataur Rohman, Pallavi Sarkhel, Anupam Nath Jha, and Atanu Singha Roy. "Targeting the heme protein hemoglobin by (−)-epigallocatechin gallate and the study of polyphenol–protein association using multi-spectroscopic and computational methods." Physical Chemistry Chemical Physics 22, no. 4 (2020): 2212–28. http://dx.doi.org/10.1039/c9cp05301h.

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Pawlukianiec, Cezary, Małgorzata Ewa Gryciuk, Kacper Maksymilian Mil, Małgorzata Żendzian-Piotrowska, Anna Zalewska, and Mateusz Maciejczyk. "A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies." Pharmaceuticals 13, no. 9 (September 10, 2020): 240. http://dx.doi.org/10.3390/ph13090240.

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Meloxicam is a non-steroidal anti-inflammatory drug, which has a preferential inhibitory effect to cyclooxyganase-2 (COX-2). Although the drug inhibits prostaglandin synthesis, the exact mechanism of meloxicam is still unknown. This is the first study to assess the effect of meloxicam on protein glyco-oxidation as well as antioxidant activity. For this purpose, we used an in vitro model of oxidized bovine serum albumin (BSA). Glucose, fructose, ribose, glyoxal and methylglyoxal were used as glycating agents, while chloramine T was used as an oxidant. We evaluated the antioxidant properties of albumin (2,2-di-phenyl-1-picrylhydrazyl radical scavenging capacity, total antioxidant capacity and ferric reducing antioxidant power), the intensity of protein glycation (Amadori products, advanced glycation end products) and glyco-oxidation (dityrosine, kynurenine, N-formylkynurenine, tryptophan and amyloid-β) as well as the content of protein oxidation products (advanced oxidation protein products, carbonyl groups and thiol groups). We have demonstrated that meloxicam enhances the antioxidant properties of albumin and prevents the protein oxidation and glycation under the influence of various factors such as sugars, aldehydes and oxidants. Importantly, the antioxidant and anti-glycating activity is similar to that of routinely used antioxidants such as captopril, Trolox, reduced glutathione and lipoic acid as well as protein glycation inhibitors (aminoguanidine). Pleiotropic action of meloxicam may increase the effectiveness of anti-inflammatory treatment in diseases with oxidative stress etiology.
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Sattar, Naila Abdul, Fatma Hussain, Tahira Iqbal, and Munir Ahmad Sheikh. "Determination of in vitro antidiabetic effects of Zingiber officinale Roscoe." Brazilian Journal of Pharmaceutical Sciences 48, no. 4 (December 2012): 601–7. http://dx.doi.org/10.1590/s1984-82502012000400003.

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Aqueous extracts of Zingiber officinale rhizomes were studied to evaluate their antidiabetic effects on protein glycation and on the diffusion of glucose in vitro in the present study. Zingiber officinale rhizome aqueous extract were examined at concentrations of 5, 10, 20 and 40 g/L. The antidiabetic effects were found to be dose-dependent. Antidiabetic potential of Zingiber officinale was mainly through inhibition of the glucose diffusion and to a limited extent by reducing the glycation. However, further studies are needed to determine in vitro effects of therapeutic potential by restraining postprandial glucose absorptions and plasma protein glycations in diabetic subjects.
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Biedrzycki, Grzegorz, Blanka Wolszczak-Biedrzycka, Justyna Dorf, Daniel Michalak, Małgorzata Żendzian-Piotrowska, Anna Zalewska, and Mateusz Maciejczyk. "Antioxidant and Anti-Glycation Potential of H2 Receptor Antagonists—In Vitro Studies and a Systematic Literature Review." Pharmaceuticals 16, no. 9 (September 8, 2023): 1273. http://dx.doi.org/10.3390/ph16091273.

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Background: Histamine H2 receptor antagonists are a group of drugs that inhibit gastric juice secretion in gastrointestinal diseases. However, there is evidence to suggest that H2 blockers have a broader spectrum of activity. The antioxidant properties of H2 blockers have not been fully elucidated, and their anti-glycation potential has not been studied to date. Therefore, this is the first study to compare the antioxidant and antiglycation potentials of the most popular H2 antagonists (ranitidine, cimetidine, and famotidine) on protein glycoxidation in vitro. Methods: Bovine serum albumin (BSA) was glycated using sugars (glucose, fructose, galactose, and ribose) as well as aldehydes (glyoxal and methylglyoxal). Results: In the analyzed group of drugs, ranitidine was the only H2 blocker that significantly inhibited BSA glycation in all tested models. The contents of protein carbonyls, protein glycoxidation products (↓dityrosine, ↓N-formylkynurenine), and early (↓Amadori products) and late-stage (↓AGEs) protein glycation products decreased in samples of glycated BSA with the addition of ranitidine relative to BSA with the addition of the glycating agents. The anti-glycation potential of ranitidine was comparable to those of aminoguanidine and Trolox. In the molecular docking analysis, ranitidine was characterized by the lowest binding energy for BSA sites and could compete with protein amino groups for the addition of carbonyl groups. H2 blockers also scavenge free radicals. The strongest antioxidant properties are found in ranitidine, which additionally has the ability to bind transition metal ions. The systematic literature review also revealed that the anti-glycation effects of ranitidine could be attributed to its antioxidant properties. Conclusions: Ranitidine showed anti-glycation and antioxidant properties. Further research is needed, particularly in patients with diseases that promote protein glycation.
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Dissertations / Theses on the topic "Glycation"

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Pun, Boon Li Pamela. "Mitochondrial glycation." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607726.

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Yeboah, Faustinus Kwabena. "Protein glycation reactions." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0029/NQ64699.pdf.

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Palma, Durán Susana Alejandra. "Protein glycation & chronic diseases." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8640/.

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Price, Claire. "Immunomodulation by Advanced Glycation End-Products." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508487.

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Olufemi, O. S. "Glycation of albumin, fibrinogen and haemoglobin." Thesis, University of Strathclyde, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382412.

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Davie, Sarah Jill. "Factors affecting the glycation of proteins." Thesis, University of Surrey, 1990. http://epubs.surrey.ac.uk/843818/.

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Forty-two non-diabetics whose glycated haemoglobin levels could not be explained by their levels of fasting glycaemia or glucose tolerance were identified as part of the Islington Diabetes Survey. Mean glycated haemoglobin levels that were high relative to their blood glucose levels (HIGH GLYCATORS) were found in 22 subjects whilst 20 subjects had low relative levels (LOW GLYCATORS). A repeat glucose tolerance test in 13 of the 42 subjects (7 high and 6 low glycators) showed that they remained categorised in the two groups four years after the discrepancy was identified. Mean blood glucose levels calculated from two 5-point diurnal profiles also failed to explain the glycated haemoglobin levels in the two groups. Further biochemical and haematological tests revealed that glycated albumin showed a better relationship with blood glucose levels than did glycated haemoglobin. Intra-erythrocyte glucose concentrations were significantly lower than the plasma glucose in the low glycators, whilst the levels of erythrocyte 2,3-diphosphoglycerate (a known catalyst of glycation) were significantly higher in the high glycators. These findings may partially explain the original discovery of low and high glycators. The effects of high fibre/low glucose and high glucose/low fibre diets on glycated proteins were studied in normal subjects. Only glycated albumin levels changed significantly, probably due to small changes in plasma glucose occurring on each diet, which were not mirrored by similar changes in the erythrocyte. When another group of normal subjects received 1 g vitamin C daily for three months, significant reductions in glycated albumin and glycated haemoglobin were observed, with the former being reduced to a greater extent. This suggests that vitamin C has the potential of being used therapeutically to reduce glycation. In conclusion, for normal subjects, glycated albumin is a more reliable indicator of blood glucose control than glycated haemoglobin.
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Esclapez, Marie-Claire. "La glycation des lipoproteines : conséquences physiopathologiques." Paris 5, 1994. http://www.theses.fr/1994PA05P062.

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Yu, Wendy Hsiao-Wen. "Advanced Glycation Endproducts In Periodontal Disease." Thesis, Faculty of Dentistry, 2006. http://hdl.handle.net/2123/4240.

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Indurthi, Venkata. "Interactions of the Receptor for Advanced Glycation End Products (Rage) with Advanced Glycation End Products (AGEs) and S100B." Diss., North Dakota State University, 2016. http://hdl.handle.net/10365/25817.

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RAGE is a multi-ligand pattern recognition receptor. RAGE can bind several damage associated molecular pattern proteins. RAGE- ligand interaction is pathophysiologically relevant to several major diseases including diabetes and certain cancers. RAGE inhibition has been reported to reduce morbidity in these disease states. However, to design better RAGE inhibitors it is necessary to understand the structural basis behind the RAGE-ligand interaction and currently this is not well understood. This thesis focuses on understanding the interaction of RAGE with two of its ligands; AGEs and S100B. AGEs are highly heterogeneous and are formed as a result of non-enzymatic glycation. A panel of AGEs were characterized in terms of their side chain modifications, thermal stability, secondary structure, aggregation and surface charge. These glycation induced changes were then correlated to RAGE binding. Building on these results the role of AGE-RAGE interaction in pancreatic cancer cell proliferation and migration was determined. Ribose modified BSA induced ROS formation, which then triggered NF-?B upregulation via RAGE induced ROS signaling. Ribose BSA increased pancreatic cell proliferation and migration. Anti-RAGE antibodies and RAGE inhibitors prevented AGE induced cellular effects. The role of ribose modified BSA was also determined in macrophage activation and pro-inflammatory cytokine release. Rapid internalization was observed of the ribose-BSA and confocal imaging revealed the internalization of the AGE compound into the lysosomes which lead to the ROS production, NF-?B activation and pro-inflammatory cytokine release in a RAGE independent signaling mechanism. Finally, the role of tryptophan residues of the V domain in domain stability and S100B binding was determined. We have generated single, double and triple tryptophan mutants of the V domain by site directed mutagenesis. The effect of Trp residues in the domain stability could not elucidated as no change was observed in the secondary structure of the mutants when compared to the wild type suggesting the plasticity of the V-domain. The fluorescence emission and life time properties of each Trp residue was determined. Our binding assays of the Trp Ala mutants indicate tighter binding of the S100B to the mutants. The S100-RAGE peptide structures suggest multi modal interaction of S100B-RAGE interaction.
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Kennedy, David M. "The effect of glycation on antibody function." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262111.

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Books on the topic "Glycation"

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Laurie, Coulston, and Australasian Association of Clinical Biochemists., eds. Diabetes, glycation and complications. Mt. Lawley, W.A: Australasian Association of Clinical Biochemists, 1996.

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Colaco, Camilo. The glycation hypothesis of atherosclerosis. New York: Springer, 1997.

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The glycation hypothesis of atherosclerosis. New York: Chapman & Hall, 1997.

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Abdel-Wahab, Yasserr Hassan Atef. Glycation of insulin: A novel aspect of pancreatic B-cell dysfunction contributing to glucose intolerance. [S.l: The Author], 1993.

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Park, Lisa. Advanced glycation endproducts and the development of accelerated atherosclerosis in diabetic apolipoprotein E deficient mice / c Lisa Park. [New Haven, Conn: s.n.], 1997.

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Rea, Carol Anne. Glycation and the production of reactive oxygen species: Possible link in the pathogenesis of the vascular complications of diabetes. Birmingham: University of Birmingham, 1991.

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Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.

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Ansari, Nadeem Ahmad. Closer Look at Glycation. Nova Science Publishers, Incorporated, 2021.

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Ansari, Nadeem Ahmad. Closer Look at Glycation. Nova Science Publishers, Incorporated, 2021.

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ZOFFOUN, Isaac. Peau: Collagène et Anti-Glycation. Independently Published, 2021.

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Book chapters on the topic "Glycation"

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Farris, Patricia K. "Skin Aging, Glycation and Glycation Inhibitors." In Cosmeceuticals and Cosmetic Practice, 173–83. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118384824.ch17.

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Rabbani, Naila, and Paul J. Thornalley. "Glycation of Proteins." In Analysis of Protein Post-Translational Modifications by Mass Spectrometry, 307–32. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781119250906.ch8.

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Takahashi, Motoko. "Glycation of Proteins." In Glycoscience: Biology and Medicine, 1–7. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54836-2_182-1.

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Takahashi, Motoko. "Glycation of Proteins." In Glycoscience: Biology and Medicine, 1339–45. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54841-6_182.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Glycation of Proteins." In Encyclopedia of Exercise Medicine in Health and Disease, 374. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2445.

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Simm, Andreas, and Alexander Navarrete Santos. "Advanced Glycation Endproducts." In Mechanisms Linking Aging, Diseases and Biological Age Estimation, 59–67. Boca Raton, FL : CRC Press, 2016. | “A science publishers book.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315371382-8.

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Biruete, Annabel, and Jaime Uribarri. "Advanced Glycation End Products." In Nutrition in Kidney Disease, 553–62. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44858-5_29.

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Ramasamy, Ravichandran, Shi Fang Yan, and Ann Marie Schmidt. "Glycation, Inflammation and RAGE." In Atherosclerosis, 27–41. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch3.

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Rabbani, Naila, and Paul J. Thornalley. "Advanced Glycation Endproducts (AGEs)." In Uremic Toxins, 293–304. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118424032.ch19.

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Lackner, K. J., and D. Peetz. "Advanced glycation end products." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_108-1.

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Conference papers on the topic "Glycation"

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Cohen, I., D. Burk, R. J. Fullertone, A. Veis, and D. Green. "NONENZYMATIC GLYCATI0N OF HUMAN BLOOD PLATELET PROTEINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644491.

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Atherothrombotic events are common in diabetics, and enhanced platelet function is thought to be partly responsible. Since excessive glycation occurs in many proteins of diabetic subjects, we decided to evaluate glycation of diabetic platelet proteins, and especially those proteins known to be involved in platelet aggregation. We believe this is the first report of nonenzy-matic glycation of platelet proteins from patients with poorly-controlled diabetes mellitus. Overall glycation was assessed by the extent of incorporation of [3H]BH4 into fructosyl lysine separated from whole platelet proteins following protein hydrolysis. We studied 12 diabetic patients, all of whom had severe atherothrombotic disease, and 13 normal controls. Fructosyl lysine eluted in the first major radioactive peak and represented 5.7 ± 1.0 S.D. of the total radioactivity in the normal whole platelet samples. Five of the 12 diabetics showed increased radioactive labeling of fructosyl lysine, without a clear pattern of correlation with the levels of glycation of hemoglobin and albumin (r = 0.33 and 0.17, respectively for hemoglobin and albumin). The pattern of glycation of the various platelet proteins in whole platelets, as determined by the incorporation of [3H]BH4 in proteins electrophoretically separated, does not clearly show a selectivity, although myosin and glycoproteins IIb and IIIa have relatively increased levels of [3H]BH4 incorporation. Artificially glycated platelet membranes exhibit glycation mainly in proteins corresponding to the electrophoretic mobility of myosin, glycoproteins IIb and IIIa and actin.Whether this glycation results in enhanced platelet function and specific loss of these platelets in vascular thrombi is still unclear. Trapping of highly glycated platelets in thrombi may be responsible for the poor correlation between the extent of platelet glycation and the elevated levels of glycated hemoglobin and albumin. (Supported in part by Grant AM13921-26 to A.V.)
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Ghazaryan, Ara A., Jo-Ya Tseng, Wen Lo, Yang-Fang Chen, Vladimir Hovhannisyan, Shean-Jen Chen, Hsin-Yuan Tan, and Chen-Yuan Dong. "Multiphoton imaging and quantification of tissue glycation." In SPIE BiOS, edited by Robert R. Alfano. SPIE, 2011. http://dx.doi.org/10.1117/12.874536.

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Lin, Chih-Ju, Jeon Woong Kang, Peter T. C. So, and Chen-Yuan Dong. "Analysis diffusion and glycation rate of artery in high concentration sugar condition via autofluorescence of advanced glycation end productions." In Diagnostic and Therapeutic Applications of Light in Cardiology 2020, edited by Kenton W. Gregory and Laura Marcu. SPIE, 2020. http://dx.doi.org/10.1117/12.2545589.

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Pugachenko, I. S., E. I. Nasybullina, O. V. Kosmachevskaya, and A. F. Topunov. "EFFECT OF NITROXYL ON MODIFICATION OF HEMOGLOBIN BY OXIDATION AND GLYCATION." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.215-219.

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Nitroxyl in biological systems can work as a classic antioxidant. It has been shown that ni-troxyl reduces the yield of free radical products in the reaction of hemoglobin with tert-butyl peroxide. Due to this, nitroxyl slows down the formation of non-enzymatic glycation products in the reaction of hemoglobin with methylglyoxal.
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Nasybullina, E. I., I. S. Pugachenko, O. V. Kosmachevskaya, and A. F. Topunov. "CARBONYL STRESS IN BACTERIA. ANTI-GLYCATION EFFECT OF NITROXYL ON ESCHERICHIA COLI CELLS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.211-215.

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Bacteria suffer carbonyl stress at sudden transition to high-level carbohydrate substrates or in a stationary phase. Methylglyoxal (MG) inhibited bacterial growth and increased advanced glycation end products. Nitroxyl prevented the toxic effect of MG in a low-aerated cell culture.
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Liang-yuan Xu, Gong Zhang, Yong Liu, Long Zhang, Ling Zhu, Xiao-lin Kong, Lu-sheng Wu, Simon liao, and Yi-kun Wang. "Apparatus for detecting advanced glycation Endproducts fluorescence of skin." In 2009 Canadian Conference on Electrical and Computer Engineering (CCECE). IEEE, 2009. http://dx.doi.org/10.1109/ccece.2009.5090252.

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Lazareva, Ekaterina N., and Valery V. Tuchin. "Monitoring of hemoglobin glycation using spectral and refraction measurements." In SPIE Proceedings, edited by Qingming Luo, Lihong V. Wang, Valery V. Tuchin, and Min Gu. SPIE, 2007. http://dx.doi.org/10.1117/12.741636.

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Muir, Rhona, Shareen Forbes, David J. Birch, and Olaf J. Rolinski. "Monitoring glycation using the intrinsic fluorescence of biological fluorophores." In UV and Higher Energy Photonics: From Materials to Applications 2022, edited by Gilles Lérondel, Yong-Hoon Cho, and Atsushi Taguchi. SPIE, 2022. http://dx.doi.org/10.1117/12.2631649.

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Cherkasova, Olga P., Maxim M. Nazarov, and Alexander P. Shkurinov. "Investigation of bovine serum albumin glycation by THz spectroscopy." In Saratov Fall Meeting 2015, edited by Elina A. Genina, Valery V. Tuchin, Vladimir L. Derbov, Dmitry E. Postnov, Igor V. Meglinski, Kirill V. Larin, and Alexander B. Pravdin. SPIE, 2016. http://dx.doi.org/10.1117/12.2229741.

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Otero de Joshi, Virginia, Narahari V. Joshi, Herminia Gil, William Velasquez, Silvia Contreras, and Glevis Marquez. "Assessment of nonenzymatic glycation in protein by FTIR spectroscopy." In BiOS '99 International Biomedical Optics Symposium, edited by Michael D. Morris. SPIE, 1999. http://dx.doi.org/10.1117/12.345408.

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Reports on the topic "Glycation"

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Boojar, Fargol, Sepideh Golmohamad, and Golnaz Tafreshi. Comparative Study on the Status of Glycation Precursors, Advanced Glycation End Products, and Cell Viability Under Effects of Kaempferol, Myricetin, and Azaleatin in HGC-27 Cell Line. Journal of Young Investigators, January 2019. http://dx.doi.org/10.22186/jyi.36.1.5-10.

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Ganju, Ramesh K. Receptor for Advanced Glycation End Products (RAGE) as a Novel Target for Inhibiting Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592353.

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Syed, Aleem. Spatial and temporal dynamics of receptor for advanced glycation endproducts, integrins, and actin cytoskeleton as probed with fluorescence-based imaging techniques. Office of Scientific and Technical Information (OSTI), January 2016. http://dx.doi.org/10.2172/1342583.

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