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144 results on '"Little, C. B."'

1. A consensus-based framework for conducting and reporting osteoarthritis phenotype research

Author

van Spil, W. E., Bierma-Zeinstra, S. M. A., Deveza, L. A., Arden, N. K., Bay-Jensen, A.-C., Kraus, V. Byers, Carlesso, L., Christensen, R., Van Der Esch, M., Kent, P., Knoop, J., Ladel, C., Little, C. B., Loeser, R. F., Losina, E., Mills, K., Mobasheri, A., Nelson, A. E., Neogi, T., Peat, G. M., Rat, A.-C., Steultjens, M., Thomas, M. J., Valdes, A. M., and Hunter, D. J.

Published
2020
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10. A consensus-based framework for conducting and reporting osteoarthritis phenotype research

Author

van Spil, W. E. (W. E.), Bierma-Zeinstra, S. M. (S. M. A.), Deveza, L. A. (L. A.), Arden, N. K. (N. K.), Bay-Jensen, A.-C. (A.-C.), Byers Kraus, V. (V.), Carlesso, L. (L.), Christensen, R. (R.), Van Der Esch, M. (M.), Kent, P. (P.), Knoop, J. (J.), Ladel, C. (C.), Little, C. B. (C. B.), Loeser, R. F. (R. F.), Losina, E. (E.), Mills, K. (K.), Mobasheri, A. (A.), Nelson, A. E. (A. E.), Neogi, T. (T.), Peat, G. M. (G. M.), Rat, A.-C. (A.-C.), Steultjens, M. (M.), Thomas, M. J. (M. J.), Valdes, A. M. (A. M.), Hunter, D. J. (D. J.), van Spil, W. E. (W. E.), Bierma-Zeinstra, S. M. (S. M. A.), Deveza, L. A. (L. A.), Arden, N. K. (N. K.), Bay-Jensen, A.-C. (A.-C.), Byers Kraus, V. (V.), Carlesso, L. (L.), Christensen, R. (R.), Van Der Esch, M. (M.), Kent, P. (P.), Knoop, J. (J.), Ladel, C. (C.), Little, C. B. (C. B.), Loeser, R. F. (R. F.), Losina, E. (E.), Mills, K. (K.), Mobasheri, A. (A.), Nelson, A. E. (A. E.), Neogi, T. (T.), Peat, G. M. (G. M.), Rat, A.-C. (A.-C.), Steultjens, M. (M.), Thomas, M. J. (M. J.), Valdes, A. M. (A. M.), and Hunter, D. J. (D. J.)

Abstract

Background: The concept of osteoarthritis (OA) heterogeneity is evolving and gaining renewed interest. According to this concept, distinct subtypes of OA need to be defined that will likely require recognition in research design and different approaches to clinical management. Although seemingly plausible, a wide range of views exist on how best to operationalize this concept. The current project aimed to provide consensus-based definitions and recommendations that together create a framework for conducting and reporting OA phenotype research. Methods: A panel of 25 members with expertise in OA phenotype research was composed. First, panel members participated in an online Delphi exercise to provide a number of basic definitions and statements relating to OA phenotypes and OA phenotype research. Second, panel members provided input on a set of recommendations for reporting on OA phenotype studies. Results: Four Delphi rounds were required to achieve sufficient agreement on 11 definitions and statements. OA phenotypes were defined as subtypes of OA that share distinct underlying pathobiological and pain mechanisms and their structural and functional consequences. Reporting recommendations pertaining to the study characteristics, study population, data collection, statistical analysis, and appraisal of OA phenotype studies were provided. Conclusions: This study provides a number of consensus-based definitions and recommendations relating to OA phenotypes. The resulting framework is intended to facilitate research on OA phenotypes and increase combined efforts to develop effective OA phenotype classification. Success in this endeavor will hopefully translate into more effective, differentiated OA management that will benefit a multitude of OA patients.

Published
2020

26. Aggrecanase versus matrix metalloproteinases in the catabolism of the interglobular domain of aggrecan in vitro

Author

Little, C B, Flannery, C R, Hughes, C E, Mort, J S, Roughley, P J, Dent, C, and Caterson, B

Subjects
Cartilage, Articular, Extracellular Matrix Proteins, Swine, Gene Expression, In Vitro Techniques, Matrix Metalloproteinases, Protein Structure, Tertiary, Endopeptidases, Matrix Metalloproteinase 13, Osteoarthritis, Animals, Humans, Cattle, Lectins, C-Type, Matrix Metalloproteinase 3, Proteoglycans, Aggrecans, Collagenases, RNA, Messenger, Research Article, Glycosaminoglycans
Abstract

The importance of aggrecanase versus matrix metalloproteinase (MMP) enzymic activities in the degradation of aggrecan in normal and osteoarthritic (OA) articular cartilage in vitro was studied in order to further our understanding of the potential role of these two enzyme activities in aggrecan catabolism during the pathogenesis of cartilage degeneration. Porcine and bovine articular cartilage was maintained in explant culture for up to 20 days in the presence or absence of the catabolic stimuli retinoic acid, interleukin-1 or tumour necrosis factor-alpha. Release of proteoglycan from cartilage was measured as glycosaminoglycan (GAG) release using a colorimetric assay. Analysis of proteoglycan degradation products, both released into culture media and retained within the cartilage matrix, was performed by Western blotting using antibodies specific for the N- and C-terminal neoepitopes generated by aggrecanase- and MMP-related catabolism of the interglobular domain of the aggrecan core protein (IGD). In addition, studies determining the mRNA expression for MMP-3 and MMP-13 in these same cultures were undertaken. These analyses indicated that all three catabolic agents stimulated the release of >80% of the GAG from the articular cartilage over 4 days. The degree of GAG release corresponded to an increase in aggrecanase-generated aggrecan catabolites released into the media and retained within the cartilage. Importantly, there was no evidence for the release of MMP-generated aggrecan metabolites into the medium, nor the accumulation of MMP-generated catabolites within the tissue in these same cultures. Expression of the mRNAs for two MMPs known to be capable of degrading the aggrecan IGD, MMP-3 and MMP-13, was detected. However, increased expression of these MMPs was not correlated with aggrecan degradation. Analyses using porcine cartilage, cultured with or without catabolic stimulation for 12 h to 20 days, indicated that primary cleavage of the IGD by aggrecanase was responsible for release of aggrecan metabolites at both the early and late time points of culture. Cultures of late-stage OA human articular cartilage samples indicated that aggrecanase activity was upregulated in the absence of catabolic stimulation when compared with normal porcine or bovine cartilage. In addition, even in this late-stage degenerate cartilage, aggrecanase and not MMP activity was responsible for the release of the majority of aggrecan from the cartilage. This study demonstrates that the release of aggrecan from both normal and OA cartilage in response to catabolic stimulation in vitro involves a primary cleavage by aggrecanase and not MMPs.

Published
1999

30. Immunolocalization and distribution of proteoglycans in carious dentine.

Author

Stankoska, K, Sarram, L, Smith, S, Bedran‐Russo, AK, Little, CB, Swain, MV, Bertassoni, LE, Bedran-Russo, A K, Little, C B, Swain, M V, and Bertassoni, L E

Subjects
PROTEOGLYCANS, DENTIN, COLLAGEN, PROTEOMICS, GLYCOPROTEINS, DENTAL caries, IMMUNOHISTOCHEMISTRY, POLYSACCHARIDES
Abstract

Background: Collagen type I, proteoglycans (PG) and non-collagenous proteins represent important building blocks of the dentine matrix. While different PGs have been identified in dentine, changes in the distribution of these macromolecules with the progression of caries have been poorly characterized. The aim of this study was to compare the immunolocalization of three small collagen-binding PGs (biglycan, fibromodulin and lumican) as well as collagen (types I and VI) in healthy versus carious dentine.Methods: Longitudinal demineralized sections of extracted teeth were stained with antibodies recognizing specific PG core proteins and collagens, as well as glycosaminoglycans (GAGs) with toluidine blue.Results: In healthy dentine, PGs appeared to be more abundant near the tubule walls and directly under the cusps. Conversely, in carious dentine, specific locations appeared to be more prone to PG degradation than others. These degradation patterns were well correlated with the progression of caries into the tissue, and also appeared to trigger interesting morphological changes in the tissue structure, such as the deformation of dentine tubules near highly infected areas and the lower concentration of PG in tertiary dentine.Conclusions: This study presents new insights into the involvement of PGs in the progression of caries. [ABSTRACT FROM AUTHOR]

Published
2016
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34. What constitutes an "animal model of osteoarthritis"--the need for consensus?

Author

Little CB, Zaki S, Little, C B, and Zaki, S

Abstract

Objective: To review the use of animal models of osteoarthritis (OA) with regard to their utility for investigation of the mechanisms and regulation of structural pathology and pain.Methods: PubMed searches were conducted using separate clusters of terms to retrieve articles on (i) models of structural joint damage in genetically-modified (GM) mice, and (ii) models of OA joint pain. The papers were reviewed to investigate whether there was evidence that the research outcome was dependent on the model used.Results: Out of a total of 109 separate GM mice strains identified in which an effect on OA was reported, 15 had been studied using more than one arthritis model. In 10/15 the same effect of the GM on arthritis was reported in at least two different models. In 5/15 the effect of the GM on arthritis structural pathology was different, and sometimes opposite, when comparing two or more induction methods. A total of 112 publications were retrieved in which pain/disability was examined in a model suggested to represent OA. The induction methods used most commonly to study "OA pain" were distinct from those most often used to investigate the pathophysiology and regulation of structural joint damage. Four papers directly comparing pain mechanisms in different models were identified, with 3/4 describing differences in nociceptive pathways.Conclusions: The available data indicates that the molecular mechanisms of both joint structural damage and pain may be distinct in animal models of OA induced or initiated by different means. This suggests the need to continue using multiple OA animal models but that the subsequent interpretation of the data and its extrapolation to the human condition must be more precise. [ABSTRACT FROM AUTHOR]

Published
2012
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36. n-3 fatty acids specifically modulate catabolic factors involved in articular cartilage degradation.

Author

Curtis, C L, Hughes, C E, Flannery, C R, Little, C B, Harwood, J L, and Caterson, B

Abstract

This study describes specific molecular mechanisms by which supplementation with n-3 fatty acids (i.e. those present in fish oils) can modulate the expression and activity of degradative and inflammatory factors that cause cartilage destruction during arthritis. Our data show that incorporation of n-3 fatty acids (but not other polyunsaturated or saturated fatty acids) into articular cartilage chondrocyte membranes results in a dose-dependent reduction in: (i) the expression and activity of proteoglycan degrading enzymes (aggrecanases) and (ii) the expression of inflammation-inducible cytokines (interleukin (IL)-1alpha and tumor necrosis factor (TNF)-alpha) and cyclooxygenase (COX-2), but not the constitutively expressed cyclooxygenase COX-1. These findings provide evidence that n-3 fatty acid supplementation can specifically affect regulatory mechanisms involved in chondrocyte gene transcription and thus further advocate a beneficial role for dietary fish oil supplementation in alleviation of several of the physiological parameters that cause and propogate arthritic disease.

Published
2000

39. Differential expression of aggrecanase and matrix metalloproteinase activity in chondrocytes isolated from bovine and porcine articular cartilage.

Author

Hughes, C E, Little, C B, Büttner, F H, Bartnik, E, and Caterson, B

Abstract

The release of aggrecan catabolites from cartilage is an early event in the pathogenesis of degenerative joint diseases. The enzymes involved in this process are unknown, controversial, and the subject of intense investigation. In this paper we have utilized a recombinant substrate containing the interglobular domain (IGD) of aggrecan to study specifically aggrecanase versus matrix metalloproteinase (MMP) catabolism in this domain of aggrecan. Our studies have shown that (i) there are species differences in the expression of latent versus active MMP activity on the aggrecan IGD; (ii) interleukin-1alpha exposure induces both aggrecanase and MMP activities, whereas retinoic acid induces only aggrecanase activity and inhibits the MMP activity on the aggrecan IGD; (iii) activators of latent MMP activity (p-aminophenylmercuric acetate and trypsin) significantly reduce aggrecanase activity; (iv) the time course of the appearance of aggrecanase versus the MMP catabolism of aggrecan IGD differs; (v) aggrecanase is a protease with metalloprotease characteristics; however (vi) the physiological (tissue) inhibitors of MMPs show weak inhibition (TIMP-1) or no inhibition (TIMP-2) of aggrecanase activity. Collectively, these studies show that aggrecanase and MMP catabolism of the aggrecan IGD are independent and uncoupled.

Published
1998

43. Chemiluminescence from Organic Reactions. Formation of Diphenoyl Peroxide as an Intermediate.

Author

ILLINOIS UNIV AT URBANA DEPT OF CHEMISTRY, Little,C B, Schuster,G B, ILLINOIS UNIV AT URBANA DEPT OF CHEMISTRY, Little,C B, and Schuster,G B

Abstract

Visible, long-lasting chemiluminescence results when diphenic anhydride and p-nitroperoxybenzoic acid in THF are treated with powdered KOH in the presence of a catalytic chemiluminescence (CIEEL) activator. This chemiluminescent process is presumed to involve in situ generation of diphenoyl peroxide, which then undergoes chemiluminescent decomposition by the CIEEL mechanism. Carboxylate 4, the precursor to diphenoyl peroxide in this reaction, was generated by an entirely different route from peroxide 5. (Author)

Published
1985

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