The role of cyclic climatic regimes and riparian vegetation: a qualitative and quantitative study into the cause of river bank slope instability and channel widening on the Macdonald River, New South Wales.

Numerous case studies have demonstrated the catastrophic nature of channel change experienced on the Macdonald River, a tributary of the Hawkesbury-Nepean River, New South Wales. However, there is an absence of studies that clearly state how and why the channel changed as dramatically as it did. As a consequence, the magnitude of, and ultimate controls on the changes to the Macdonald River’s form and processes are not fully appreciated. In this study, a comparison is undertaken on the three existing river morphology perspectives with respect to the Macdonald River. The Warner and Erskine Perspective states the sole importance of the cyclic hydro-climatic conditions of the FDR and DDRs on river morphology. The Brierely and co-workers Perspective states the sole importance of anthropogenic influence in the catchment and on the banks on river morphology. The Intermediate Perspective of Hubble and co-workers considers both existing and conflicting perspectives and states the importance of both cyclic climatic regimes and anthropogenic activity in the catchment and particularly on the river banks, in determining river morphology. Resultantly, a selection of Hubble and co-workers Perspective is made to classify the Macdonald River’s morphology. It is clear, from the analysis of historical aerial photographs, archival sketches, photographs and historical documentation, that riparian vegetation was absent from the banks of the Macdonald River from 1941 as a result of land-clearing practices from the early 19th Century. The banks of the Macdonald River would not have experienced this ‘catastrophic’ channel change between 1949 and 1955 had riparian vegetation remained on the banks. Riparian vegetation has been found to increase the soil-shear strength and hence the stability of river bank slopes, in particularly on the Upper Nepean and the Macdonald Rivers in New South Wales, where vulnerable sands to silty-sands predominate the bank material. This has been further proved with geochemical bank stability modeling

Citrullination of synovial proteins in murine models of rheumatoid arthritis

Item does not contain fulltextOBJECTIVE: Antibodies directed to citrulline-containing proteins are highly specific for rheumatoid arthritis (RA) and can be detected in up to 80% of patients with RA. Citrulline is a nonstandard amino acid that can be incorporated into proteins only by posttranslational modification of arginine by peptidylarginine deiminase (PAD) enzymes. The objective of this study was to investigate the presence of anticitrulline antibodies, PAD enzymes, and citrullinated antigens in mouse models of both acute and chronic destructive arthritis: streptococcal cell wall (SCW)-induced arthritis and collagen-induced arthritis (CIA), respectively. METHODS: Synovial tissue biopsy specimens were obtained from naive mice, mice with CIA, and mice with SCW-induced arthritis. The expression of messenger RNA (mRNA) for PAD enzymes was analyzed by reverse transcriptase-polymerase chain reaction; the presence of PAD proteins and their products (citrullinated proteins) was analyzed by Western blotting and by immunolocalization. The presence of anticitrullinated protein antibodies was investigated by an anti-cyclic citrullinated peptide (anti-CCP) enzyme-linked immunosorbent assay (ELISA) and an ELISA using in vitro citrullinated fibrinogen. RESULTS: In both mouse models, PAD type 2 (PAD2) mRNA was present in the synovium but was not translated into PAD2 protein. In contrast, PAD4 mRNA, although absent from healthy synovium, was readily transcribed and translated by polymorphonuclear neutrophils infiltrating the synovial tissue during inflammation. As a consequence, several synovial proteins were subjected to citrullination. One of these proteins was identified as fibrin, which has been reported to be citrullinated also in synovium of patients with RA. Although generation of citrullinated antigens during synovial inflammation in the mice was eminent, no anti-CCP antibodies could be detected. CONCLUSION: Citrullination of synovial antigens is an active process during joint inflammation in both mice and humans, but the induction of autoantibodies directed to these proteins is a more specific phenomenon, detectable only in human RA patients

Dual role of IL-12 in early and late stages of murine collagen type II arthritis

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Anticytokine treatment of established type II collagen-induced arthritis in DBA/1 mice: a comparative study using anti-TNFalpha, anti-IL-1alpha/beta, and IL-1Ra

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Blockade of endogenous IL-12 results in suppression of murine streptococcal cell wall (SCW) arthritis by enhancement of IL-10 and IL-1ra

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Regulatory role of IL-10 in joint inflammation and cartilage destruction in murine SCW arthritis. More therapeutic benefit with IL-4/IL-10 combination therapy than with IL-10 treatment alone.

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Localization of insulin-like growth factor-1 receptor in human normal and osteoarthritic cartilage in relation to proteoglycan synthesis and content

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Protection against cartilage and bone destruction by systemic IL-4 treatment in established murine type II collagen-induced arthritis

Contains fulltext : 134228.pdf (publisher's version ) (Open Access)11 p

Anticytokine treatment of established type II collagen-induced arthritis in DBA/1 mice: a comparative study using anti-TNFalpha, anti-IL-1alpha/beta and IL-1Ra.

Contains fulltext : 69834.pdf (publisher's version ) (Closed access)OBJECTIVE: To examine the role of tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha), and IL-1 beta in collagen-induced arthritis (CIA), immediately after onset and during the phase of established arthritis. METHODS: Male DBA/1 mice with collagen-induced arthritis were treated with antibodies against murine TNF alpha and IL-1 alpha/beta at different time points of the disease. IL-1 receptor antagonist (IL-1Ra) was administered using Alzet osmotic minipumps. The effect of anticytokine treatment was monitored by visual scoring. Histology and cytokine reverse transcription polymerase chain reaction (RT-PCR) analyses were performed at the end of the treatment period. RESULTS: Anti-TNF alpha treatment showed efficacy shortly after onset of the disease, but had little effect on fully established CIA. Histologic analysis after early treatment revealed that anti-TNF alpha significantly reduced joint pathology, as determined by infiltration of inflammatory cells and cartilage damage. Anti-IL-1 alpha/beta treatment ameliorated both early and full-blown CIA. This clear suppression of established arthritis was confirmed by administration of high doses of IL-1Ra. Dose-response experiments showed that a continuous supply of 1 mg/day was needed for optimal suppression. Histologic analysis showed markedly reduced cartilage destruction both in the knee and the ankle joints. Autoradiography demonstrated full recovery of chondrocyte synthetic function of articular cartilage. In addition, we found that the IL-1 beta isoform plays a dominant role in established CIA. Profound suppression of CIA was observed with anti-IL-1 beta, although elimination of both IL-1 alpha and IL-1 beta still gave better protection. Analysis of messenger RNA with RT-PCR revealed that IL-1 beta was highly upregulated in synovium and cartilage at late stages of CIA, whereas anti-IL-1 beta treatment markedly reduced IL-1 beta message in the synovium. CONCLUSION: The present study identified different TNF alpha/IL-1 dependencies in various stages of CIA and revealed that blocking of TNF alpha does not necessarily eliminate IL-1. Continuous, high doses of IL-1Ra are needed to block CIA

Cholesterol accumulation caused by low density lipoprotein receptor deficiency or a cholesterol-rich diet results in ectopic bone formation during experimental osteoarthritis

Contains fulltext : 125532.pdf (publisher's version ) (Open Access)INTRODUCTION: Osteoarthritis (OA) is associated with the metabolic syndrome, however the underlying mechanisms remain unclear. We investigated whether low density lipoprotein (LDL) accumulation leads to increased LDL uptake by synovial macrophages and affects synovial activation, cartilage destruction and enthesophyte/osteophyte formation during experimental OA in mice. METHODS: LDL receptor deficient (LDLr-/-) mice and wild type (WT) controls received a cholesterol-rich or control diet for 120 days. Experimental OA was induced by intra-articular injection of collagenase twelve weeks after start of the diet. OA knee joints and synovial wash-outs were analyzed for OA-related changes. Murine bone marrow derived macrophages were stimulated with oxidized LDL (oxLDL), whereupon growth factor presence and gene expression were analyzed. RESULTS: A cholesterol-rich diet increased apolipoprotein B (ApoB) accumulation in synovial macrophages. Although increased LDL levels did not enhance thickening of the synovial lining, S100A8 expression within macrophages was increased in WT mice after receiving a cholesterol-rich diet, reflecting an elevated activation status. Both a cholesterol-rich diet and LDLr deficiency had no effect on cartilage damage; in contrast, ectopic bone formation was increased within joint ligaments (fold increase 6.7 and 6.1, respectively). Moreover, increased osteophyte size was found at the margins of the tibial plateau (4.4 fold increase after a cholesterol-rich diet and 5.3 fold increase in LDLr-/- mice). Synovial wash-outs of LDLr-/- mice and supernatants of macrophages stimulated with oxLDL led to increased transforming growth factor-beta (TGF-beta) signaling compared to controls. CONCLUSIONS: LDL accumulation within synovial lining cells leads to increased activation of synovium and osteophyte formation in experimental OA. OxLDL uptake by macrophages activates growth factors of the TGF-superfamily