Academic literature on the topic 'Desmosine'

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Journal articles on the topic "Desmosine"

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McClintock, Dana E., Barry Starcher, Mark D. Eisner, B. Taylor Thompson, Doug L. Hayden, Gwynne D. Church, and Michael A. Matthay. "Higher urine desmosine levels are associated with mortality in patients with acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L566—L571. http://dx.doi.org/10.1152/ajplung.00457.2005.

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Desmosine is a stable breakdown product of elastin that can be reliably measured in urine samples. We tested the hypothesis that higher baseline urine desmosine would be associated with higher mortality in 579 of 861 patients included in the recent Acute Respiratory Distress Syndrome Network trial of lower tidal volume ventilation ( 1 ). We also correlated urine desmosine levels with indexes of disease severity. Finally, we assessed whether urine desmosine was lower in patients who received lower tidal volumes. Desmosine was measured by radioimmunoassay in urine samples from days 0, 1, and 3 of the study. The data were expressed as a ratio of urine desmosine to urine creatinine to control for renal dilution. The results show that higher baseline ( day 0) urine desmosine-to-creatinine concentration was associated with a higher risk of death on adjusted analysis (odds ratio 1.36, 95% confidence interval 1.02–1.82, P = 0.03). Urine desmosine increased in both ventilator groups from day 0 to day 3, but the average rise was higher in the 12-ml/kg predicted body weight group compared with the 6-ml/kg predicted body weight group ( P = 0.053, repeated-measures model). In conclusion, patients with acute lung injury ventilated with lower tidal volumes have lower urine desmosine levels, a finding that may reflect reduced extracellular matrix breakdown. These results illustrate the value of evaluating urinary biological markers that may have prognostic and pathogenetic significance in acute lung injury.
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Starcher, Barry, and Marti Scott. "Fractionation of Urine to Allow Desmosine Analysis by Radioimmunoassay." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 29, no. 1 (January 1992): 72–78. http://dx.doi.org/10.1177/000456329202900111.

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The present study was designed to re-evaluate the radioimmunoassay for desmosine in urine, which is currently used as a measure of elastin metabolism. Using ion exchange chromatography, gel filtration and affinity chromatography it was shown that at least five other compounds in hydrolysates of human urine competed for desmosine in the RIA. Fractionating the urine prior to hydrolysis with acetone removed one of the major contaminants. The other contaminants could subsequently be removed by extracting the urine hydrolysate with a mixture of chloroform/ethanol (60:40). Samples from nine normal adult urines showed that an average of 45% of the RIA competing material in unfractionated urine was not desmosine. The final extracted residue retained all of the desmosine and only 16% of the original solids. The average adult urine contains approximately 50 pmol desmosine/mg creatinine, reflecting a daily turnover of between 3 and 4 mg of elastin per day.
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Murakami, Yuko, Rina Suzuki, Hiroto Yanuma, Jiangtao He, Shuren Ma, Gerard M. Turino, Yong Y. Lin, and Toyonobu Usuki. "Synthesis and LC-MS/MS analysis of desmosine-CH2, a potential internal standard for the degraded elastin biomarker desmosine." Org. Biomol. Chem. 12, no. 48 (2014): 9887–94. http://dx.doi.org/10.1039/c4ob01438c.

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Hirose, Mika, Reiko Yokoo, Daisuke Watanabe, Rina Suzuki, Miho Tanigawa, and Toyonobu Usuki. "Synthesis of Multi‐Deuterated Desmosine." ChemistrySelect 5, no. 13 (April 2020): 3843–46. http://dx.doi.org/10.1002/slct.202000507.

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Schräder, Christoph U., Andrea Heinz, Petra Majovsky, and Christian E. H. Schmelzer. "Fingerprinting Desmosine-Containing Elastin Peptides." Journal of The American Society for Mass Spectrometry 26, no. 5 (January 21, 2015): 762–73. http://dx.doi.org/10.1007/s13361-014-1075-9.

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Pai, V., A. Guz, G. J. Phillips, N. T. Cooke, D. C. S. Hutchison, and T. D. Tetley. "Urinary desmosine, elastolysis, and lung disease." Metabolism 40, no. 2 (February 1991): 139–45. http://dx.doi.org/10.1016/0026-0495(91)90164-r.

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Janssen, Rob, Jef Serré, Ianthe Piscaer, Ruben Zaal, Henny van Daal, Carolien Mathyssen, Pieter Zanen, Jody M. W. van den Ouweland, and Wim Janssens. "Post hoc analysis of a randomised controlled trial: effect of vitamin D supplementation on circulating levels of desmosine in COPD." ERJ Open Research 6, no. 4 (October 2020): 00128–2019. http://dx.doi.org/10.1183/23120541.00128-2019.

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BackgroundVitamin D supplementation lowers exacerbation frequency in severe vitamin D-deficient patients with COPD. Data regarding the effect of vitamin D on elastin degradation are lacking. Based on the vitamin's anti-inflammatory properties, we hypothesised that vitamin D supplementation reduces elastin degradation, particularly in vitamin D-deficient COPD patients. We assessed the effect of vitamin D status and supplementation on elastin degradation by measuring plasma desmosine, a biomarker of elastin degradation.MethodsDesmosine was measured every 4 months in plasma of 142 vitamin D-naïve COPD patients from the Leuven vitamin D intervention trial (100 000 IU vitamin D3 supplementation every 4 weeks for 1 year).ResultsNo significant association was found between baseline 25-hydroxyvitamin D (25(OH)D) and desmosine levels. No significant difference in desmosine change over time was found between the placebo and intervention group during the course of the trial. In the intervention arm, an unexpected inverse association was found between desmosine change and baseline 25(OH)D levels (p=0.005).ConclusionsVitamin D supplementation did not have a significant overall effect on elastin degradation compared to placebo. Contrary to our hypothesis, the intervention decelerated elastin degradation in vitamin D-sufficient COPD patients and not in vitamin D-deficient subjects.
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Sekhon, H. S., and W. M. Thurlbeck. "Lung growth in hypobaric normoxia, normobaric hypoxia, and hypobaric hypoxia in growing rats. I. Biochemistry." Journal of Applied Physiology 78, no. 1 (January 1, 1995): 124–31. http://dx.doi.org/10.1152/jappl.1995.78.1.124.

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Adaptive changes in cellular and connective tissue components of the lung after chronic exposure to reduced ambient oxygen and/or pressure were studied. Four-week-old male Sprague-Dawley rats were randomly divided into five groups (n = 12 each): 1) general control, room air (GC); 2) hypobaric normoxic; 3) normobaric hypoxic; 4) hypobaric hypoxic; and 5) weight-matched control, restricted food intake (WMC; weight matched to hypobaric hypoxic animals). Lung growth (lung weight and DNA, RNA, protein, hydroxyproline, and desmosine contents) diminished in WMC compared with GC. Somatic growth decreased in hypobaric and normobaric hypoxic rats compared with GC. Lung weight; DNA, RNA, protein, hydroxyproline, and desmosine contents; and RNA/DNA, protein/DNA, and desmosine/DNA ratios increased in both hypobaric and normobaric hypoxic rats compared with WMC. Hydroxyproline and desmosine contents and the hydroxyproline/DNA ratio were significantly higher in hypobaric than normobaric hypoxic rats. Hypobaric normoxia caused a slight somatic growth reduction, but biochemical parameters of lung growth remained unaffected. In conclusion, in growing animals, despite inhibition of lung growth due to reduced food consumption, accelerated lung growth in hypobaric or normobaric hypoxia occurs by hyperplastic and hypertrophic changes. Hypobaric normoxia does not affect lung growth, but connective tissue proteins accumulate slightly more in hypobaric hypoxia than in hypoxia alone.
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Zay, K., S. Loo, C. Xie, D. V. Devine, J. Wright, and A. Churg. "Role of neutrophils and α1-antitrypsin in coal- and silica-induced connective tissue breakdown." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 2 (February 1, 1999): L269—L279. http://dx.doi.org/10.1152/ajplung.1999.276.2.l269.

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Mineral dusts produce emphysema, and administration of dust to rats results in the rapid appearance of desmosine and hydroxyproline in lavage fluid, confirming that dusts directly induce connective tissue breakdown. To examine the role of neutrophils and α1-antitrypsin (α1-AT) in this process, we instilled silica or coal into normal rats or rats that had been pretreated with antiserum against neutrophils. One day after dust exposure, lavage fluid neutrophils and desmosine and hydroxyproline levels were all elevated; treatment with antiserum against neutrophils reduced neutrophils by 75%, desmosine by 40–50%, and hydroxyproline by 25%. By 7 days, lavage fluid neutrophils and desmosine level had decreased, whereas macrophages and hydroxyproline level had increased. By ELISA analysis, lavage fluid α1-AT levels were increased four- to eightfold at both times. On Western blot, some of the α1-AT appeared as degraded fragments, and by HPLC analysis, 5–10% of the methionine residues were oxidized. At both times, lavage fluid exhibited considerably elevated serine elastase inhibitory capacity and also showed elevations in metalloelastase activity. We conclude that, in this model, connective tissue breakdown is initially driven largely by neutrophil-derived proteases and that markedly elevated levels of functional α1-AT do not prevent breakdown, thus providing in vivo support for the concept of quantum proteolysis proposed by Liou and Campbell (T. G. Liou and E. J. Campbell. Biochemistry 34: 16171–16177, 1995). Macrophage-derived proteases may be of increasing importance over time, especially in coal-treated animals.
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TETLEY, T. D., G. J. PHILLIPS, A. GUZ, and B. FOX. "The Blotchy Mouse, Lung Desmosine, and Emphysema." Annals of the New York Academy of Sciences 624, no. 1 (May 1991): 358. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17048.x.

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Dissertations / Theses on the topic "Desmosine"

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Hopkins, Gemma V. "The mechanism of desmosome internalisation." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493936.

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Desmosomes are intercellular adhesive junctions providing architectural integrity to tissues that are subject to mechanical stress. During wound healing downregulation of desmosomal adhesion is necessary to facilitate tissue remodeling. Ultrastructural observations suggest that downregulation may occur by internalisation of whole desmosomes but the mechanism of downregulation is not understood. Protein kinase C alpha (PKCα) has been shown to colocalise with desmosomes at the wound edge and to modulate their adhesion. This thesis investigates the internalisation of desmosomes with particular reference to the roles of the cytoskeleton and PKC.
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Tan, Celia I. C. "A radiological and biochemical perspective on ageing and degeneration of the human thoracic intervertebral disc." University of Western Australia. School of Surgery and Pathology, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0059.

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Disc degenerative changes are directly or indirectly associated with spinal pain and disability. Literature revealed a high prevalence of disc degeneration in the thoracic region, however thoracic MRI degeneration trends and information on disc biochemical matrix constituents are limited for thoracic discs compared to lumbar and cervical discs. The objective of this thesis was to use MRI to investigate the prevalence of disc degenerative changes affecting the human thoracic spine, and to determine the factors affecting spinal disc biochemical matrix. A 3-point subjective MRI grading scale was used to grade the films. The feasibility of using archived formalin-fixed cadaver material was investigated to analyse collagen and elastin crosslinks. The prevalence of degenerative changes in human thoracic discs and vertebrae (T1 to T12) was determined retrospectively from an audit of 216 MRI cases, using sagittal T1- and T2-weighted MR images. In a subsequent series of ex-vivo studies, human thoracic discs and LF from 26 formalin-fixed and two fresh spines, involving all thoracic levels, were examined macroscopically to determine the degeneration status. Subsequently, disc and ligament tissues were analysed biochemically for collagen (pyridinoline and deoxypyridinoline) and elastin (desmosine and isodesmosine) crosslinks. These crosslinks were extracted from hydrolysed samples by cellulose partition chromatography, and analysed by reverse-phase HPLC. Collagen content was determined using its hydroxyproline content, and proteoglycan content was assayed using a modified DMB assay for chondroitin sulphate. Finally the MRI and macroscopic assessments of thoracic discs, were compared with the biochemical data from two fresh cadaver thoracic spines. The 3-point MRI grading scale had a high inter- (k = 0.57 to 0.78) and intra-rater (k = 0.71 to 0.87) reliability. There were no significant differences in the collagen and elastin content and extent of collagen crosslinks between formalin fixed and unfixed ligament and disc tissues, after 25 weeks of formalin fixation. From the in-vivo MRI series of investigations (n = 216 MRI films), the prevalence of thoracic disc degenerative and vertebral morphological changes revealed significant age, gender and spinal level trends (p < 0.05).Generally, males had a higher propensity for disc degeneration in contrast to females, especially older females, where the trend showed a higher prevalence of osteophytes and vertebral body changes. In particular, the mid and lower thoracic levels have a higher prevalence of degenerative changes, except for osteophytes and anterior vertebral wedging. With increased age, there was a concomitant increase in anterior wedging and bi-concavity and disc degenerative changes except for end-plates. The biochemical investigations on the ex-vivo series of formalin-fixed thoracic discs (n = 303) also revealed significant changes in the disc matrix due to degeneration status, age, gender and spinal regional factors. With increased age, normal disc matrices have significantly lower collagen content and extent of pyridinoline (p < 0.001). In contrast, the degenerated disc matrix revealed significantly higher collagen content and extent of deoxypyridinoline (p < 0.05). These findings suggest that an altered matrix existed in normal ageing discs, which render the disc prone to injury and degeneration over the life span. The higher collagen and deoxypyridinoline in degenerated disc matrices reflects an increase in chondrocyte synthesis, and is also a novel finding, suggesting that they may be used as markers of ageing and degeneration processes. The biochemical investigations on another series of ex-vivo spinal LF tissues (n = 364), revealed that this had a lower collagen and pyridinoline, but significantly higher elastin and deoxypyridinoline compared to spinal discs (p < 0.05). Elastin crosslinks however were difficult to detect in spinal discs, being present in negligible amounts in a few lumbar discs. The elastin crosslinks in the LF were not significantly affected by age, but were significantly higher in calcified, and female ligamentum tissues, and also in the lumbar region (p < 0.05). These MRI prevalence findings enhanced our knowledge of vertebral body and disc degeneration trends in the thoracic region and contributed to the interpretation of MR images for pathology in the human thoracic spine. Information on the associated collagenous and elastic changes in the disc and ligamentum matrices provide original data and insight on the pathogenesis of degeneration in the disc matrix from a biochemical perspective, highlighting gender, age and spinal level influences on the matrix tensile strength and cellular synthetic activities.
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Winfield, Kaye R. "Extraction of desmosines from urine : an indicator for inflammatory lung damage." University of Western Australia. School of Paediatrics and Child Health, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0059.

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[Truncated abstract] Urinary desmosines have been proposed as a biomarker for inflammatory lung damage. Desmosine, a breakdown product of elastin, is an effective marker of the degradation of elastin and has been studied in many disease scenarios where there is acute and chronic lung inflammation. Lung matrix degradation has been proven in vitro and in vivo with many experiments showing that the excess proteases degrades lung matrix. The secretion of proteases by neutrophils is an innate response of the body to the invasion by micro organisms and when secreted in excess, the protective anti-protease mechanism is swamped. Chronic inflammation and persistent infection eventually leads to bronchiectasis and respiratory failure. Urinary desmosine has been shown to be elevated in respiratory conditions with acute and chronic inflammation . . . Urinary desmosine levels in a large cohort of healthy children have been established using this method and predictive Z-score formulae have been developed to use in children with lung disease. Exploration of these scores in children with CF have shown that the levels of urinary desmosine appear to be sensitive to the clinical setting, where high urinary desmosine levels were present during exacerbation and significantly reduced when treated for infection with antibiotic therapy and physiotherapy. The study of young children under the age of seven was undertaken to determine if the urinary desmosine levels could indicate when lung damage was occurring and to determine what mechanisms might be involved. Since there appeared to be no apparent relationship between elevated desmosines and proteases in the lung in young children with CF, further studies are required to define the mechanisms behind increased elastin metabolism in those children.
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Winfield, Kaye R. "Extraction of desmosines from urine : an indicator for inflammatory lung damage /." Connect to this title, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0059.

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Lloyd, Susan. "Calcium-independent desmosome adhesion : aquisition, maintenance and modulation." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295856.

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Measures, H. R. "A study of desmosome formation in kidney epithelial cells." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234435.

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Cabral, Rita Meira e. Cruz de Vasconcelos. "The role of desmoplakin and plakoglobin in desmosome associated disease." Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/2413.

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Desmosomes are intercellular junctions that connect intermediate filaments (IFs) of adjacent cells within tissues, generating a large and mechanically resilient network. Desmosomes are prominent in epithelia and the myocardium. Their importance for maintenance of the strength and flexibility of these tissues is underlined by mutations in desmosomal genes which compromise skin or heart and in some instances both. This thesis is focused on two obligate plaque proteins of the desmosome, desmoplakin (DP) and plakoglobin (PG), and their role in disease of skin and heart. A novel homozygous nonsense mutation, p.S24X, in the gene encoding PG, JUP, was identified in three non-consanguineous Argentinean patients, resulting in skin fragility, palmoplantar keratoderma (PPK) and woolly hair with no symptoms of cardiomyopathy. p.S24X mRNA was readily detected and an alternative AUG codon translates an N-terminally truncated PG, which is expressed in patient and parental skin samples at barely detectable levels. At the same time another novel homozygous mutation, c.468G>A, was identified in JUP causing a very similar phenotype in two Kuwaiti siblings and resulting also in very low levels of PG in the skin. These results suggest that PG is essential for maintenance of skin integrity, but not for normal heart development in children. The gene encoding DP, DSP, produces two alternative splice variants, DPI and DPII. A novel DP alternative splice isoform, DPIb, is described. As shown by RT-PCR, DSPIb is expressed in several epithelial and cardiovascular tissues and is the only DSP isoform detected in the aorta. Western blotting proteins from HaCaT and K1 cells identified this novel isoform, which has been previously missed due to its similarity in size to DPII. DPIb may help compensate defects in patients with DSPI-specific mutations. The molecular mechanisms of three different DSP mutations leading to skin disease or skin disease associated with cardiomyopathy were investigated. Mutations causing DPI/DPII haploinsufficiency and DPI knock-out lead to decreased expression levels of the desmosomal proteins DSC2, DSC3 and PKP1 in an experimental system using HaCaT keratinocytes. Expression of a mutant DSPI construct harbouring a dominant 30 bp insertion results in the formation of large DPI aggregates at the cell membrane of HaCaT cells. The spectrum of DSP and JUP mutations which cause different clinical phenotypes is discussed.
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ZORILA, FLORESCU SILVANA MARIA. "Alteration du profil d'expression des composants desmosomaux et des jonctions adherentes dans les carcinomes epidermoides de l'oropharynx et leur valeur predictive : etude in vivo et in vitro." Paris 7, 2001. http://www.theses.fr/2001PA07GA02.

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DEPONDT, JOEL. "Evaluation prospective des cytokeratines et des composants desmosomaux comme marqueurs diagnostiques et pronostiques des carcinomees epidermoides de l'oropharynx." Paris 7, 2000. http://www.theses.fr/2000PA07GA01.

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Asimaki, Angeliki. "Arrhythmogenic right ventricular cardiomyopathy, a disease of the desmosome : genetic and functional studies." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1443947/.

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Mutation analysis of the recognized ARVC genes and of further candidate genes was performed on a large cohort of ARVC patients. Several novel mutations were identified and three further desmosomal genes were linked to the disease: plakophilin2, desmocollin2 and desmoglein2. Heart and skin samples from ARVC patients were subjected to microscopic examination and immunohistochemistry to study the effect of the newly-identified mutations on the structure of cell adhesion complexes.;The functional effects of a particular novel mutation were thoroughly examined in vitro. S39_K40insS is the first dominant ARVC-causing plakoglobin mutation to be reported. Yeast-two hybrid analysis was used to investigate the effect of S39_K40insS on the proteins interactions established by plakoglobin. A HEK293 cell line stably expressing the mutant protein was generated and used to study the effects of S39_K40insS on desmosomal structure, cell proliferation, cell death, subcellular localization and expression levels of proteins involved in adhesion and signalling and cellular responses to defined mechanical load. A recombinant adenovirus expressing the mutant protein was generated and used to transfect neonatal rat ventricular cardiomyocytes, whose behaviour and responses were subsequently analysed. The functional consequences of S39_K40insS were compared with those of PK215del2, a previously reported recessive plakoglobin mutation known to underlie Naxos disease, a syndromic form of ARVC.;These results point towards novel mechanisms of disease pathogenesis, that apart from weakened cell-cell adhesion involve altered protein turnover kinetics and defects in signalling pathways. Similar studies should improve our understanding of ARVC and provide a more accurate diagnostic algorithm.
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Books on the topic "Desmosine"

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Wise, Irene Ann. Modulation of desmosome adhesion by intercellular signals involving protein kinase C. Manchester: University of Manchester, 1996.

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Syrris, Petros, and Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0359.

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Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder of the heart muscle which is typically inherited in an autosomal dominant manner. It is believed to be familial in over 50% of cases. A recessive mode of inheritance has also been reported in syndromic cases with cardiocutaneous features. The classic form of the disorder is considered to be ‘a disease of the desmosome’ as pathogenic variants have been identified in five genes encoding key desmosomal proteins: plakoglobin, desmoplakin, plakophilin-2, desmoglein-2, and desmocollin-2. Mutations in these genes account for 30–50% of ARVC cases. A further eight non-desmosomal genes have also been implicated in the pathogenesis of the disorder but only account for rare cases. Studies of patients with ARVC-associated gene mutations have revealed marked genetic heterogeneity and very limited genotype–phenotype correlation. Disease expression often varies significantly amongst individuals carrying the same mutation. It has been proposed that the presence of more than one sequence variant is required to determine overt clinical disease and patients with multiple variants have a more severe phenotype compared to single variant carriers. Identification of a potentially pathogenic variant comprises a major criterion in the diagnosis of ARVC but informative integration of genetic testing into clinical practice remains challenging. Gene testing should be used to identify asymptomatic family members at risk and only aids diagnosis in cases of high suspicion for ARVC, along with other evident features of the disease already present. However, genetic findings should be used with caution in clinical practice and their interpretation must be performed in expert centres.
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Book chapters on the topic "Desmosine"

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Mattey, D. L., A. Suhrbier, E. Parrish, and D. R. Garrod. "Recognition, Calcium and the Control of Desmosome Formation." In Novartis Foundation Symposia, 49–77. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513408.ch4.

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Kolegraff, Keli, Porfirio Nava, and Asma Nusrat. "Specialized Intercellular Junctions in Epithelial Cells: The Tight Junction and Desmosome." In Cellular Domains, 321–37. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118015759.ch19.

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Waller, G. R., C. F. Yang, L. F. Chen, C. H. Su, R. M. Liou, S. C. Wu, C. C. Young, et al. "Can Soyasaponin I and Mono- and Bi- Desmosides Isolated from Mungbeans Serve as Growth Enhancers in Mungbeans and Lettuce?" In Advances in Experimental Medicine and Biology, 123–39. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0413-5_11.

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"Desmosin." In Springer Reference Medizin, 675. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_310998.

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"Desmosome." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 493. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4335.

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"Desmosinol." In Natural Compounds, 41. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-0537-5_91.

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"Desmosin to Dextransulfate." In RÖMPP Lexikon Chemie, edited by Jürgen Falbe and Manfred Regitz. Stuttgart: Georg Thieme Verlag, 1997. http://dx.doi.org/10.1055/b-0036-135449.

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"van Deemter-Gleichung to Desmosin." In RÖMPP Lexikon Chemie, edited by Jürgen Falbe and Manfred Regitz. Stuttgart: Georg Thieme Verlag, 1997. http://dx.doi.org/10.1055/b-0036-135448.

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Lie, Pearl P. Y., C. Yan Cheng, and Dolores D. Mruk. "The Biology of the Desmosome-Like Junction." In International Review of Cell and Molecular Biology, 223–69. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-385859-7.00005-7.

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Beggs, Reena R., William F. Dean, and Alexa L. Mattheyses. "dSTORM Imaging and Analysis of Desmosome Architecture." In Methods in Molecular Biology. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/7651_2020_325.

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Conference papers on the topic "Desmosine"

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Spanbroek, Michiel, Jody Van den Ouweland, Twan Beijers, Henny Van Daal, Richard Dekhuijzen, and Rob Janssen. "Short-term stability of the mature elastin degradation biomarker plasma desmosine and influence of smoking on plasma desmosine levels." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3973.

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Lindberg, Claes, Henrik Lindberg, Sven Kjellström, Gunnar Engström, Maria Gerhardsson de Verdier, Ulf Nihlén, Magnus Dahlbäck, Magnus Svartengren, Martin Anderson, and Kristina F. Semb. "Urinary Desmosine Excretion Is Strongly Influenced By Age And Gender." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5959.

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Syed, Maaz, Zaid Iskander, Alexander Fletcher, Samuel Debono, Marc Dweck, Jeffrey T. J. Huang, Calvin Chin, David Newby, and Anna Maria Choy. "BS7 Plasma desmosine as a biomarker in acute aortic syndrome." In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.205.

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Huang, Jeffrey T. J., Elena Kuzmanova, Alison Dicker, Holly Keir, Simon Finch, Stefano Aliberti, Thomas Fardon, and James Chalmers. "Desmosine is a predictor of long-term cardiovascular mortality in bronchiectasis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4718.

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Mordi, Ify, Rachael Forsythe, Matthew Bown, Chim Lang, David Newby, Corry Gellatly, Calvin Chin, et al. "65 The novel plasma biomarker desmosine, a marker of elastin breakdown, is an independent predictor of abdominal aortic aneurysm events independent of aneurysm size." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.65.

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Iskandar, Zaid, Jeffrey Huang, Lynn Miller, Calvin Chin, Ify Mordi, Catherine Mcwilliam, David Goudie, et al. "126 Urinary desmosine, a biomarker of elastin degradation is significantly elevated and associated with maximum aortic root size and aortic Z-scores in patients with bicuspid aortic valve." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.123.

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Baron, Maayan, and Trey Ideker. "Abstract 178: Desmosome mutations in melanoma promote cellular proliferation and disease progression." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-178.

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Sheu, Jim J., Brian Y. Kuo, Chia-Cheng Wu, Jacky Yang, and Chih-Mei Chen. "Abstract 4504: Functional roles of KRT6-KRT14 fusion variant 7 in desmosome remodeling and cell spreading/migration." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4504.

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