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Literatura académica sobre el tema "Glycosaminoglycans Metabolism"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 30 de enero de 2023

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Artículos de revistas sobre el tema "Glycosaminoglycans Metabolism"

Viola, Manuela, Timothy E. L. Douglas, Laura Alaniz, and Barbara Bartolini. "Glycosaminoglycans Metabolism." Biochemistry Research International 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/245792.

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Mironov, S. P., A. M. Gerasimov, L. N. Furtseva, A. G. Tikhomirov, D. O. Vasiliev, and R. V. Merkurieva. "Oxyprolinuria and Glycosaminoglycansuria in Achilles Tendon Ruptures." N.N. Priorov Journal of Traumatology and Orthopedics 5, no. 2 (June 15, 1998): 51–53. http://dx.doi.org/10.17816/vto104492.

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In 17 athlets and ballet dancers with Achilles tendon ruptures oxyprolinuria and urine content of hexuronic acid were studied. Considerable increase of collagen and glycosaminoglycans decay products was detected. The results of differential spectrophotometry showed that urine glycosaminoglycanes presented by proteoglycans. It was assumed that Achilles tendon ruptures could be caused by excessive mechanical load and/or lack of the connective tissue metabolism. The authors consider that further study of oxyprolinuria as well as enzyme-substrate systems of glycosaminoglycans are perspective for the detection of trauma risk group.

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Koźma, Ewa M., Kornelia Kuźnik-Trocha, Katarzyna Winsz-Szczotka, Grzegorz Wisowski, Paweł Olczyk, Katarzyna Komosińska-Vassev, Mariusz Kasperczyk, and Krystyna Olczyk. "Significant Remodeling Affects the Circulating Glycosaminoglycan Profile in Adult Patients with both Severe and Mild Forms of Acute Pancreatitis." Journal of Clinical Medicine 9, no. 5 (May 1, 2020): 1308. http://dx.doi.org/10.3390/jcm9051308.

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Acute pancreatitis (AP) manifests itself either as a mild, self-limiting inflammation or a severe, systemic inflammatory process that is associated with various complications and a high mortality rate. It is unknown whether these two forms of the disease can differ in the profile of circulating glycosaminoglycans, which are molecules with huge biological reactivity due to a high density of negative electric charge. Plasma glycosaminoglycans were characterized/quantified in 23 healthy controls, 32 patients with mild AP, and 15 individuals with severe disease using electrophoresis with enzymatic identification (chondroitin sulfate and heparan sulfate) or an ELISA-based test (hyaluronan). Moreover, the correlations between the glycosaminoglycan levels and clinical parameters were evaluated. Both forms of AP showed similar remodeling of the plasma profile of the sulfated glycosaminoglycans. In contrast, only in the patients with mild AP was the level of circulating hyaluronan significantly decreased as compared to the healthy controls. Both forms of AP are associated with systemic changes in the metabolism of glycosaminoglycans. However, the alterations in hyaluronan metabolism may contribute to the disease evolution. The circulating hyaluronan may have some clinical value to predict the severity of AP and to evaluate the clinical status of patients with severe AP.

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Wolf, Hanna, Andrea Graßmann, Romina Bester, André Hossinger, Christoph Möhl, Lydia Paulsen, Martin H. Groschup, Hermann Schätzl, and Ina Vorberg. "Modulation of Glycosaminoglycans Affects PrPScMetabolism but Does Not Block PrPScUptake." Journal of Virology 89, no. 19 (July 22, 2015): 9853–64. http://dx.doi.org/10.1128/jvi.01276-15.

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ABSTRACTMammalian prions are unconventional infectious agents composed primarily of the misfolded aggregated host prion protein PrP, termed PrPSc. Prions propagate by the recruitment and conformational conversion of cellular prion protein into abnormal prion aggregates on the cell surface or along the endocytic pathway. Cellular glycosaminoglycans have been implicated as the first attachment sites for prions and cofactors for cellular prion replication. Glycosaminoglycan mimetics and obstruction of glycosaminoglycan sulfation affect prion replication, but the inhibitory effects on different strains and different stages of the cell infection have not been thoroughly addressed. We examined the effects of a glycosaminoglycan mimetic and undersulfation on cellular prion protein metabolism, prion uptake, and the establishment of productive infections in L929 cells by two mouse-adapted prion strains. Surprisingly, both treatments reduced endogenous sulfated glycosaminoglycans but had divergent effects on cellular PrP levels. Chemical or genetic manipulation of glycosaminoglycans did not prevent PrPScuptake, arguing against their roles as essential prion attachment sites. However, both treatments effectively antagonizedde novoprion infection independently of the prion strain and reduced PrPScformation in chronically infected cells. Our results demonstrate that sulfated glycosaminoglycans are dispensable for prion internalization but play a pivotal role in persistently maintained PrPScformation independent of the prion strain.IMPORTANCERecently, glycosaminoglycans (GAGs) became the focus of neurodegenerative disease research as general attachment sites for cell invasion by pathogenic protein aggregates. GAGs influence amyloid formationin vitro. GAGs are also found in intra- and extracellular amyloid deposits. In light of the essential role GAGs play in proteinopathies, understanding the effects of GAGs on protein aggregation and aggregate dissemination is crucial for therapeutic intervention. Here, we show that GAGs are dispensable for prion uptake but play essential roles in downstream infection processes. GAG mimetics also affect cellular GAG levels and localization and thus might affect prion propagation by depleting intracellular cofactor pools.

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Kittlick, P. D. "Inflammation, glycolytic metabolism, and glycosaminoglycans." Experimental pathology 30, no. 1 (January 1986): 1–19. http://dx.doi.org/10.1016/s0232-1513(86)80051-2.

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Bower, L., C. Warren, and G. Manley. "Human Serum and Urine Glycosaminoglycans in Health and in Patients with Chronic Renal Failure." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 29, no. 2 (March 1992): 190–95. http://dx.doi.org/10.1177/000456329202900212.

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Quantitation of uronic acid precipitable by cetylpyridinium chloride (CPC) and electrophoretic separation of glycosaminoglycans were performed on sera from patients with chronic renal failure and compared to normal controls. Serum CPC-precipitable uronic acid (CpUA) levels in patients with renal failure were significantly higher (mean 13·7 mg/L, range 7·1–23·6 mg/L) than normal controls (mean 9·6 mg/L, range 5·1–13·9 mg/L) due to increased concentrations of low sulphated chondroitin sulphate. A positive correlation between serum CpUA and creatinine was found in renal failure patients. Urine CpUA excretion was raised in renal failure patients compared to normal controls with an increased excretion of chondroitin sulphate (Ch-S) of reduced electrophoretic mobility. Heparan sulphate (HS), a major glycosaminoglycan in normal urine, was absent from the urine of these patients. The possible origin of urine glycosaminoglycans and the role of the kidney in glycosaminoglycan metabolism are discussed.

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Kahaly, G., C. Stover, J. Beyer, and E. Otto. "In vitro synthesis of glycosaminoglycans in endocrine ophthalmopathy." Acta Endocrinologica 127, no. 5 (November 1992): 397–402. http://dx.doi.org/10.1530/acta.0.1270397.

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The effects of humoral and cell-mediated immunity on the glycosaminoglycan synthesis of retrobulbar fibroblasts was evaluated in patients with endocrine ophthalmopathy. After incubation with IgG and sera, secreted glycosaminoglycans, radiolabeled with D-6-3H-glucosamine and 35sulfate, were precipitated with cetylpyridinium chloride and ethanol. Hyaluronic acid synthesis of human retrobulbar fibroblasts after incubation with sera and IgG and after co-culture with lymphocytes was assessed by means of a radiometric test. Patients' IgG, compared to controls', accounted for a higher secretory stimulation of porcine retrobulbar fibroblasts (as measured by cetylpyridinium chloride precipitation) after 24 and 48 h. Contrasting with 24 h incubation time, glycosaminoglycan values after 48 h were increased two to threefold. Patients' and controls' sera caused earlier and stronger, yet indistinguishable glycosaminoglycan production. Non-sulfated hyaluronic acid was the preponderant glycosaminoglycan secreted into the media by retrobulbar fibroblasts. As assessed with the radiometric test, incubation with patients' and controls' sera and IgG did not reveal a significant difference in stimulating the hyaluronic synthesis of patients' and controls' retrobulbar fibroblasts. When measuring the hyaluronic acid synthesis of controls' and patients' retrobulbar fibroblasts after co-cultivation of lymphocytes, however, patients' lymphocytes had a marked ability to increase the hyaluronic acid concentration compared to controls' lymphocytes. The hyaluronic acid concentration after incubation of a patient's retrobulbar fibroblasts with autologous lymphocytes was markedly more elevated than the intrinsic hyaluronic acid production of retrobulbar fibroblasts. In conclusion, though a significant in vitro influence of patients' IgG and sera on the glycosaminoglycan release of both porcine and human (patients' as well as controls') retrobulbar fibroblasts could not be observed in this study, the indications of a marked stimulatory influence of lymphocytes on the hyaluronic acid secretion of retrobulbar fibroblasts demand further investigation.

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Chang, Chih-Cheng, Tien-Chun Chang, Shine CS Kao, Yea-Fhey Kuo, and Li-Fei Chien. "Pentoxifylline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves' ophthalmopathy and pretibial myxoedema." Acta Endocrinologica 129, no. 4 (October 1993): 322–27. http://dx.doi.org/10.1530/acta.0.1290322.

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Excessive amounts of glycosaminoglycans accumulate in the extraocular muscles of patients with Graves' ophthalmopathy and in the affected skin of patients with pretibial myxoedema. It is widely accepted that fibroblasts are the sources of glycosaminoglycan synthesis. Pentoxifylline, an analogue of the methylxanthine theobromine, inhibits the proliferation and certain biosynthetic activities of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders. Our objective was to determine whether pentoxifylline has similar effects on fibroblasts derived from patients with Graves' ophthalmopathy and pretibial myxoedema and could serve as a candidate for the treatment of these manifestations. Fibroblasts from the extraocular muscles of two patients with Graves' ophthalmopathy and normal extraocular muscles of two subjects with strabismus, as well as the affected skin of two patients with pretibial myxoedema were cultured in vitro in the presence and absence of pentoxifylline to assay its effect on the proliferation of fibroblasts and their production of glycosaminoglycans. In subconfluent fibroblast cultures, pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation. In confluent fibroblast cultures both in the presence and absence of serum, exposure to pentoxifylline similarly resulted in a dose-dependent inhibition of glycosaminoglycan synthesis for all these different kinds of fibroblasts. These findings may form the rationale for a clinical trial using pentoxifylline for the treatment of Graves' ophthalmopathy and pretibial myxoedema.

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Bondar', I. A., and V. V. Klimontov. "Glycosaminoglycans and diabetic nephropathy." Problems of Endocrinology 50, no. 2 (April 15, 2004): 29–34. http://dx.doi.org/10.14341/probl11392.

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Diabetic nephropathy (DN) is one of the leading places in the structure of mortality of patients with diabetes mellitus (DM) in Russia and abroad. Despite intensive study, the causes and development mechanisms of this complication are not finally clear. Most often, diabetic kidney damage is seen as the result of a complex interaction of metabolic, hemodynamic, genetic and other mechanisms. At the same time, the majority of researchers give the leading role to hyperglycemia and the metabolic disorders triggered by it. The latter include intensification of non-enzymatic glycation processes, activation of protein kinase C and polyol shunt, oxidative and carbonyl stress, hyperlipidemia, an imbalance of transcription factors and cytokines, and collagen metabolic disturbances. The role of these factors in the formation of DN has been reflected in a number of recent reviews.

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KAHALY, G., M. SCHULER, A. C. SEWELL, G. BERNHARD, J. BEYER, and U. KRAUSE. "URINARY GLYCOSAMINOGLYCANS IN Graves'OPHTHALMOPATHY." Clinical Endocrinology 33, no. 1 (July 1990): 35–44. http://dx.doi.org/10.1111/j.1365-2265.1990.tb00463.x.

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Tesis sobre el tema "Glycosaminoglycans Metabolism"

Lewis, Martin David. "Human lysosomal sulphate transport." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phl6752.pdf.

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Addendum inserted at back Includes bibliographical references (leaves 266-287). 1. Introduction -- 2. Materials and general methods -- 3. Characterisation and partial purification of the lysosomal sulphate transporter -- 4. Identification of proteins involved in lysosomal sulphate transport -- 5. The relationship between a sulphate anion transporter family and the lysosomal sulphate transporter -- 6. Investigation of sulphate transport in human skin fibroblasts -- 7. Concluding remarks

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Freeman, Craig. "The lysosomal degradation of heparan sulphate : a comparative study of the physical and catalytic properties of the heparan sulphate degradative enzymes /." Title page, contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phf855.pdf.

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Nigro, Julie. "The role of PPAR-α ligands (fibrates) in the regulation of vascular smooth muscle proteoglycan synthesis and structure as a contributor to reduced lipoprotein binding and the development of atherosclerosis". Monash University, Dept. of Medicine, 2004. http://arrow.monash.edu.au/hdl/1959.1/5464.

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Leroux, Mélanie. "Production de glycosaminoglycanes par voie microbiologique et enzymatique." Thesis, Université Grenoble Alpes (ComUE), 2019. http://www.theses.fr/2019GREAV024.

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Les glycosaminoglycanes (GAGs) sont des polymères de sucres linéaires, présents chez tous les animaux. Certaines bactéries pathogènes synthétisent également des polysaccharides identiques ou très similaires aux GAGs humains. Cette thèse a porté en particulier sur la synthèse de la chondroïtine sulfate et de l’héparosan qui font partie de cette famille de polysaccharides. L’intérêt pour ces deux GAGs est grandissant dans l’industrie pharmaceutique du fait des nombreuses applications médicales qu’ils pourraient permettre. La chondroïtine sulfate est d’ores et déjà extraite de tissus animaux ce qui peut engendrer des problèmes sanitaires, notamment des contaminations virales ou aux prions. En revanche, le procédé de production pour l’héparosan reste à mettre en place. Il est donc nécessaire de développer des procédés de production pour ces deux molécules. La synthèse enzymatique est une voie particulièrement prometteuse pour la production de la chondroïtine sulfate et de l’héparosan, et a fait l’objet de ce travail de thèse Glycosaminoglycans (GAGs) are long linear polysaccharide chains, found in all animals. Some pathogenic bacteria also synthesize polysaccharides identical or similar to human GAGs. This thesis deals with chondroitin sulfate and heparosan syntheses, members of the GAGs family. There is a growing interest in these two GAGs in the pharmaceutical industry due to numerous potential applications they offer. Chondroitin sulfate is currently extracted from animal tissues which can lead to sanitary problems such as viral or prion contaminations. On the other hand, a production process still needs to be developed for heparosan. Therefore, it is necessary to develop new methods for the production of these two polymers. Enzymatic synthesis, which is a promising alternative for the production of chondroitin sulfate and heparosan, was the subject of this thesis

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Lucon, Marcos. "Avaliação do metabolismo de glicosaminoglicanos em pacientes portadores de cistite intersticial." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5153/tde-06022013-164806/.

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Introdução: a cistite intersticial é doença crônica do trato urinário inferior cujos sintomas são: aumento da freqüência urinária, nictúria, dor pélvica ou perineal que piora com a repleção vesical e melhora com a micção. A etiopatogenia não é totalmente conhecida, mas há indícios de que os glicosaminoglicanos e proteoglicanos que revestem o urotélio vesical possam participar da sua gênese. A perda destes componentes protetores facilitaria o contato de íons e solutos presentes na urina com as porções mais profundas do urotélio desencadeando e perpetuando um processo inflamatório local. Para tentar entender seu metabolismo, investigamos o comportamento dos glicosaminoglicanos na urina e no tecido (biópsia do urotélio vesical) de pacientes portadoras de cistite intersticial e de incontinência urinária de esforço genuína. Casuística e métodos: o perfil e expressão gênica de glicosaminoglicanos no tecido, e o perfil dos glicosaminoglicanos da urina de 11 pacientes com cistite intersticial foram comparados aos de 11 pacientes com incontinência urinária de esforço. A análise estatística foi feita através de teste T e Anova, considerando significativos valores p<0,05. Resultados: verificamos que pacientes com cistite intersticial excretam menor concentração de glicosaminoglicanos na urina do que as portadoras de incontinência urinária de esforço (0,45 ± 0,11 x 0,62 ± 0,13 g/mg creatinina, p<0,05), porém sem redução do conteúdo de glicosaminoglicanos no urotélio. Na imunofluorescência o urotélio de pacientes com cistite intersticial mostrou maior marcação de TGF-beta, decorim (um proteoglicano de condroitim/dermatam sulfato), fibronectina e de ácido hialurônico. Foi identificada menor expressão gênica (PCR em tempo real) das sintases e uma hialuronidase do ácido hialurônico no urotélio das cistites intersticiais. Conclusão: a combinação desses resultados sugere que os glicosaminoglicanos podem estar relacionados ao processo contínuo de inflamação e remodelamento do urotélio disfuncional presente na cistite intersticial. O estudo da expressão gênica pode representar uma altenativa para o entendimento da doença. Introduction: interstitial cystitis is a chronic disease of the lower urinary tract whose symptoms are: increased urinary frequency, nocturia, perineal or pelvic pain that worses with bladder filling and improves with urination. The pathogenesis is not fully known, but there is evidence that proteoglycans and glycosaminoglycans lining the bladder urothelium can participate in its genesis. The loss of these protective compounds facilitate the contact of ions and solutes in the urine with deeper portions of bladder wall triggering and perpetuating a local inflammatory process. We investigated GAG behavior in urine and tissue (biopsy of bladder urothelium) of patients with IC/PBS and genuine stress urinary incontinence (SUI) in an attempt to better understand its metabolism. Patients and Methods: gene expression and glycosaminoglycans profile in tissue, and glycosaminoglycans profile in urine of 11 patients with interstitial cystitis were compared to 11 patients with pure urinary stress incontinence. Statistical analysis were performed using t Student test and Anova, considering significant when p<0,05. Results: patients with interstitial cystitis excreted lower concentration of glycosaminoglycans in urine when compared to those with pure urinary stress incontinence (respectively 0.45 + 0.11 x 0.62 + 0.13 mg/mg creatinine, p< 0.05). However, there was no reduction of the content of glycosaminoglycans in the urothelium of both patients. The immunofluorescence study showed that patients with interstitial cystitis had a stronger staining of TGF-beta, decorin (a proteoglycan of chondroitin/dermatan sulfate), fibronectin and hyaluronic acid. We were able to indentify by real-time PCR lower gene expression of hyaluronic acid synthases and hyaluronidase in the urothelium of patients with interstitial cystitis. Conclusion: the results suggest that glycosaminoglycans may be related to the ongoing process of inflammation and remodeling of the dysfunctional urothelium that is present in the interstitial cystitis. The study of the gene expression may represent an alternative to understand the disease

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Robert, Joe͏̈lle. "Influence de divers constituants de la matrice extracellulaire sur le comportement de cellules dermiques d'embryon de poulet cultivées in vitro." Grenoble 1, 1988. http://www.theses.fr/1988GRE10110.

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Donida, Bruna. "Investigação dos biomarcadores de estresse oxidativo e inflamação em pacientes portadores de mucopolissacaridose tipo IVA submetidos à terapia de reposição enzimática." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/158766.

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A Mucopolissacaridose tipo IVA (MPS IVA), é uma doença lisossômica de depósito ocasionada pela degradação deficiente dos glicosaminoglicanos (GAG) queratan sulfato e condroitin-6-sulfato devido à deficiência da enzima N-acetilgalactosamina 6-sulfatase. Como a fisiopatologia desta doença ainda não está totalmente elucidada e muitos estudos vêm demonstrando o envolvimento do estresse oxidativo e inflamação na patogênese de outros tipos de mucopolissacaridoses, o objetivo principal deste trabalho foi investigar os parâmetros de estresse oxidativo e mediadores inflamatórios em pacientes MPS IVA sob terapia de reposição enzimática (TRE). Foram analisadas amostras de urina e sangue de pacientes MPS IVA sob TRE (n=17) e controles saudáveis pareados por idade (n=10-14). Os pacientes apresentaram diminuição significativa nos níveis de defesas antioxidantes, medida através dos níveis de glutationa reduzida (GSH), e aumento da enzima superóxido dismutase (SOD) em eritrócitos. Em relação ao dano a biomoléculas, foi observado nos pacientes um aumento de lipoperoxidação (aumento dos níveis de isoprostanos urinários) e de dano oxidativo a proteínas (aumento dos níveis urinários de di-tirosina e diminuição dos grupamentos sulfidrila no plasma) comparativamente aos controles. Nossos resultados também mostraram que os pacientes MPS IVA sob TRE apresentaram maior dano ao DNA, sendo este dano de origem oxidativa e atingindo bases purínicas e pirimidínicas. Além disso, os pacientes apresentaram níveis significativamente aumentados de interleucina-6 e esta, por sua vez, apresentou correlação negativa com GSH, mostrando uma possível relação entre inflamação e estresse oxidativo nesta doença. Considerando que os níveis de GAG urinários ainda se encontravam elevados nos pacientes em comparação com o grupo controle, pode-se supor que os mesmos estejam, pelo menos em parte, correlacionados com os danos oxidativos encontrados nestes pacientes. Os dados encontrados no presente trabalho sugerem que pacientes MPS IVA sob TRE apresentam uma condição pró-inflamatória e oxidativa e que a suplementação com antioxidantes em combinação com a TRE deve ser investigada com o intuito de melhorar a qualidade de vida dos pacientes. Cabe ressaltar que este é o primeiro estudo em pacientes que relaciona MPS IVA com estresse oxidativo e inflamação. The Mucopolysaccharidosis type IVA (MPS IVA) is a lysosomal storage disease caused by impaired degradation of keratan sulfate and chondroitin-6-sulfate glycosaminoglycans (GAG), due to a deficiency on the enzyme N-acetylgalactosamine-6-sulfatase. Since the pathophysiology of this disease is still not totally elucidated and many studies demonstrated the involvement of oxidative stress and inflammation in the pathogenesis of other mucopolysaccharidoses types, the principal objective of this study was to investigate oxidative stress parameters and inflammatory mediators in MPS IVA patients under enzyme replacement therapy (ERT). Urine anda blood samples of MPS IVA patients under ERT (n= 17) and healthy age-matched controls (n= 10-14) were evaluated. Patients presented a significant decrease in antioxidant defenses levels, assessed by reduced glutathione (GSH), and increased superoxide dismutase (SOD) activity in erythrocytes. With regard to the biomolecules damage, was observed that patients presented lipid peroxidation (increase of isoprostanes urinary levels) and protein damage (increase of di-tyrosine urinary levels and decrease of sulfhydryl groups in plasma), when compared to controls. Our results showed higher DNA damage levels in MPS IVA patients compared to control group, in both pyrimidines and purines bases. The pro-inflammatory cytokine interleukin 6 (IL-6) was significantly increased in patients and showed an inverse correlation with GSH levels, showing a possible link between inflammation and oxidative stress in MPS IVA disease. Considering that GAG urinary level were still high in ERT patients compared to the control group, we propose that GAG are, at least in part, related with oxidative damage found in MPS IVA patients. The data presented suggest that pro-inflammatory and pro-oxidant states occur in MPS IVA patients under ERT, and the supplementation of antioxidants in combination with ERT can be investigated with the purpose of improving the patient’s life quality. To the best of our knowledge, this is the first study in patients relating MPS IVA with oxidative stress and inflammation.

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Franco, Renata Nogueron. "Biomarcadores do metabolismo da cartilagem e sua relação com as alterações morfológicas, inflamatórias e funcionais: um estudo sobre a lesão condral secundária em joelhos humanos." Universidade Federal de São Carlos, 2011. https://repositorio.ufscar.br/handle/ufscar/5131.

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Made available in DSpace on 2016-06-02T20:18:15Z (GMT). No. of bitstreams: 1 3931.pdf: 5591864 bytes, checksum: b4873ba462675328d3fc2005b8032afb (MD5) Previous issue date: 2011-02-28 Osteoarthritis (OA), a degenerative joint disease, is one of the most frequent causes of pain in the musculoskeletal system and of the inability to work in Brazil and the world. It is a multifactor, chronic disease, leading to progressive functional inability. It can arise as a result of injuries to structures such as the anterior crossed ligament and/or meniscus (post-traumatic OA), which, in this case, can affect individuals in any age range. The development of osteoarthritis includes multiple changes in the extracellular cartilage matrix, altering the normal morphological configuration of the joint involved, leading to a lack of equilibrium between the synthesis and degradation of products in this matrix. Although OA is not considered primordially as an inflammatory disease, inflammation of the joint has been shown to be a potential amplifier of the degenerative process. Thus the objective of the present study was to analyze potential biological markers in the serum and synovial fluid, and then correlate them with one another and with the morphological, inflammatory and functional alterations found in individuals with chronic injury of the anterior crossed ligament (ACL). The following techniques were used in the study: zymography, to determine the activity of the metallopeptidases 2 and 9 (MMP-2 and MMP-9); an immune-enzymatic assay (ELISA) to determine the presence of systemic and local cytokines; and a manual count of inflammatory cells (mononuclear and polymorphonuclear) by optical microscopy and spectrophotometry, in order to analyze for sulfated glycosaminoglycans (GAGs). The results indicated joint and systemic inflammation in chronic injury of the ACL by the detection of systemic and local cytokines, by the activity of MMP-9 and by the inflow of neutrophils. There were interactions between systemic and local cytokines, in which a cytokine did not always exert the same function in the serum as in the synovial fluid. The interleucines (IL) connected to degradation of the cartilage in chronic injury of the ACL were IL-12, IL-6 and IL-8, and those connected to pain and loss of function were IL-6 and IL-9. In counterpart, MMP-2 showed a negative correlation with the damage to the cartilage. It was concluded that the molecules studied had potential as biomarkers, since alterations were suggestive of injury and degradation of the cartilage. In addition, after the traumatic event resulting in rupture of the ACL, the ambient remained chronically inflamed and this inflammation was crucial for the high index of posttraumatic OA. A osteoartrite (OA), doença articular degenerativa, é uma das causas mais freqüentes de dor do sistema músculo-esquelético e de incapacidade para o trabalho no Brasil e no mundo. É uma doença crônica, multifatorial, que leva a uma incapacidade funcional progressiva. Pode surgir em decorrência de lesões em estruturas como ligamento cruzado anterior e/ou meniscos (OA pós-traumática), e neste caso, pode afetar indivíduos em qualquer faixa etária. O desenvolvimento da osteoartrite inclui múltiplas mudanças na matriz extracelular da cartilagem, o que altera a configuração morfológica normal da articulação envolvida, levando a um desequilíbrio entre a síntese e degradação dos produtos desta matriz. Apesar da OA não ser considerada primordialmente como uma doença inflamatória, a inflamação articular tem demonstrado um potencial amplificador do processo degenerativo. Sendo assim, o objetivo deste trabalho foi analisar potenciais marcadores biológicos no soro e no líquido sinovial, e em seguida correlacioná-los uns com os outros e com as alterações morfológicas, inflamatórias e funcionais encontradas em sujeitos com lesão crônica do ligamento cruzado anterior (LCA). Para este estudo foram utilizadas técnicas de: zimografia, para verificar a atividade das metalopeptidases 2 e 9 (MMP-2 e MMP-9); Ensaio imunoenzimático (ELISA), para constatar a presença das citocinas sistêmicas e locais; contagem manual de células inflamatórias (mononucleares e polimorfonucleares) por microscopia óptica e espectrofotometria para a análise dos glicosaminoglicanos sulfatados (GAGs). Os resultados apontaram para uma inflamação articular e sistêmica na lesão crônica do LCA, pela detecção de citocinas sistêmicas e locais, pela atividade das MMP-9 e pelo influxo de neutrófilos. Houve interações entre citocinas sistêmicas e locais, nas quais nem sempre uma citocina exerce a mesma função no soro e no líquido sinovial. As interleucinas (IL) ligadas à degradação da cartilagem na lesão crônica do LCA foram IL-12, IL-6 e IL-8 e as ligadas à dor e a perda de função foram IL-6 e IL-8. Em contrapartida, a MMP-2 apresentou correlação negativa com os danos na cartilagem. Conclui-se que, as moléculas estudadas apresentam potencial como biomarcadores, sendo suas alterações sugestivas de lesão e degradação da cartilagem. E ainda, que após o evento traumático responsável pelo rompimento do LCA, o ambiente permanece inflamado cronicamente e que esta inflamação é crucial para o alto índice de OA pós-traumática.

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Lewis, Martin D. "Human lysosomal sulphate transport / Martin David Lewis." 2001. http://hdl.handle.net/2440/21672.

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Addendum inserted at back Includes bibliographical references (leaves 266-287). xxiv, 289 leaves, [2] leaves of plates : ill. ; 30 cm. Title page, contents and abstract only. The complete thesis in print form is available from the University Library. Thesis (Ph.D.)--University of Adelaide, Dept. of Paediatrics, 2001

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Freeman, Craig. "The lysosomal degradation of heparan sulphate : a comparative study of the physical and catalytic properties of the heparan sulphate degradative enzymes / by Craig Freeman." Thesis, 1991. http://hdl.handle.net/2440/19747.

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Copies of author's previously published articles inserted Includes bibliographic references 2 v. (various foliations) : ill ; 30 cm. Summary: Studies the enzymology of some of the nine lysosomal exo-enzyme activities which act together to degrade the more highly sulphated regions of the glycosaminoglycans heparin and heparan sulphate. A deficiency of any one of these enzyme activities can result in one of the lysosomal storage disorders collectively known as the Mucopolysaccharidoses (MPS) Thesis (Ph.D.)--University of Adelaide, Dept. of Paediatrics, 1991

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Libros sobre el tema "Glycosaminoglycans Metabolism"

The role of proteoglycans and glycosaminolglycans in aging. Basel: Karger, 1994.

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(Editor), Vittorio Zambotti, ed. Glycolipids, Glycoproteins, and Mucopolysaccharides of the Nervous System. Springer, 1995.

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Frawley, Geoff. Mucopolysaccharidoses. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0064.

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The mucopolysaccharidoses (MPS) are a group of seven chronic progressive diseases caused by deficiencies of 11 different lysosomal enzymes required for the catabolism of glycosaminoglycans (GAGs). Hurler syndrome (MPS IH) is an autosomal recessive storage disorder caused by a deficiency of α‎-L-iduronidase. Hunter syndrome (MPS II) is an X-linked recessive disorder of metabolism involving the enzyme iduronate-2-sulfatase. Many of the MPS clinical manifestations have potential anesthetic implications. Significant airway issues are particularly common due to thickening of the soft tissues, enlarged tongue, short immobile neck, and limited mobility of the cervical spine and temporomandibular joints. Spinal deformities, hepatosplenomegaly, airway granulomatous tissue, and recurrent lung infections may inhibit pulmonary function. Odontoid dysplasia and radiographic subluxation of C1 on C2 is common and may cause anterior dislocation of the atlas and spinal cord compression.

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Capítulos de libros sobre el tema "Glycosaminoglycans Metabolism"

Linhardt, R. J., D. Loganathan, A. Al-Hakim, and S. A. Ampofo. "Structure and Metabolism of Glycosaminoglycans." In New Trends in Haemostasis, 12–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-84318-1_2.

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Kreysel, H. W., and H. P. Nissen. "Glycosaminoglycan Metabolism." In Hair and Hair Diseases, 255–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74612-3_11.

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Jones, Simon, and Frits A. Wijburg. "Glycosaminoglycans and Oligosaccharides Disorders: Glycosaminoglycans Synthesis Defects, Mucopolysaccharidoses, Oligosaccharidoses and Sialic Acid Disorders." In Inborn Metabolic Diseases, 765–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-63123-2_41.

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Fluharty, Arvan L. "Diseases of Glycosaminoglycan and Proteoglycan Metabolism." In Connective Tissue Disease, 491–521. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003210016-25.

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Kopper, László, József Timár, András Jeney, and Károly Lapis. "Glycosaminoglycan (GAG) Metabolism as a Potential Target to Prevent Metastasis Formation." In Advances in Experimental Medicine and Biology, 367–75. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-5037-6_40.

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HARDINGHAM, TIM. "Proteoglycans and Glycosaminoglycans." In Dynamics of Bone and Cartilage Metabolism, 85–98. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012088562-6/50006-6.

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HARDINGHAM, T. "Proteoglycans and Glycosaminoglycans." In Dynamics of Bone and Cartilage Metabolism, 85–98. Elsevier, 2006. http://dx.doi.org/10.1016/b9-78-012088-5/62650-0066.

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Lachmann, Robin H. "Disorders of Carbohydrate Metabolism." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 1893–901. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0234.

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Sugar molecules play many roles in metabolism. Glucose is an essential source of energy in the body, but carbohydrates also have important structural and signalling functions as constituents of glycoproteins, glycolipids, and glycosaminoglycans. Disorders of carbohydrate metabolism, although caused be defects in individual enzymes, are best viewed as disorders of metabolic pathways. Their tissue pathology can be due to deficiency of a product of metabolism, but just as often it is due to accumulation of toxic molecules which cannot be metabolized. In this chapter, a number of monogenic diseases will be described which involve the monosaccharides glucose, galactose, and fructose, and their roles in intermediary metabolism. The many other inherited metabolic diseases which affect the formation of glycosylated macromolecules (the congenital disorders of glycosylation) or their breakdown (lysosomal storage disorders) will not be discussed.

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Cervós-Navarro, Jorge, and Henry Urich. "Disorders of Glycosaminoglycan Metabolism (Mucopolysaccharidoses)." In Metabolic and Degenerative Diseases of the Central Nervous System, 110–36. Elsevier, 1995. http://dx.doi.org/10.1016/b978-012165250-0/50004-0.

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Actas de conferencias sobre el tema "Glycosaminoglycans Metabolism"

Vannucchi, S., F. Pasquali, P. Bianchi-ni, and M. Ruggiero. "BINDING AND METABOLISM OF HEPARIN BY ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644187.

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In this study we show that bovineadrenal capillary endothelial cells(BACE) contain heparin (HP); this HP has been found associated with the cell surface (i.e; trypsin-removable^and intracellularly. How-ever, experiments with [ sjsodium sulfate labelling, demonstrate that BACE cells donot synthesize HP de novo, but they uptake it from serum. We have studied binding, uptake, and metabolism odifferent molecular weight-HPs: 13 Kd-HP from bovine source, 14 Kd-HP from porcine source, 4.5 Kd, and 2.5-HP fragments. Comparison among different HPs, was carried out by calculating the IC from competition curves for [3HJ- HP. Binding of labelled-HP to BACE cells was specificand saturable. Dextran sulfate and glycosaminoglycans did not compete for binding; only heparan sulfate showed some competition. Binding of different HPs was strictly dependent on their molecular weight; 2.5 Kd- HP was unable to bind to cells, although sulfation degree of this fragment and of unfractionated HP was almost identical. Therefore, we assume that a specific oligosaccharide sequence could be responsible for HP binding to BACE cells; this hypothetical "binding sequence" could then be lost in very low molecular weight-HP fragments. BACE cells are also able to internalize HP, and they release its low molecular weight degradation products into culture medium. Thus we suggest that endothelial cells might represent a site for the metabolism of endogenous and exogenous HP in vivo.

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Smith, Robert Lane. "Mechanical Loading and Articular Cartilage Metabolism." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2520.

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Abstract Articular cartilage provides diarthrodial joints with a loading-bearing surface that ensures functional motility. The physical characteristics of articular cartilage originate with the highly organized matrix of extracellular macromolecules that provide structural elements to the tissue. The matrix specialization rests with specific proteins produced by the cartilage cells, the chondrocytes that undergo extensive post-translational modification through addition of sulfated glycosaminoglycan and oligosaccharides. The matrix proteins fall into three major categories, the collagens, the proteoglycans and the glycoproteins, with each group contributing unique properties to cartilage form and function.

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