Publications
149 results found
Behmoaras J, Smith J, D'Souza Z, et al., 2010, Genetic Loci Modulate Macrophage Activity and Glomerular Damage in Experimental Glomerulonephritis, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 21, Pages: 1136-1144, ISSN: 1046-6673
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- Citations: 22
Ashby DR, Gale DP, Busbridge M, et al., 2010, Erythropoietin administration in humans causes a marked and prolonged reduction in circulating hepcidin, HAEMATOLOGICA-THE HEMATOLOGY JOURNAL, Vol: 95, Pages: 505-508, ISSN: 0390-6078
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- Citations: 138
Smith J, McDaid JP, Bhangal G, et al., 2010, A Spleen Tyrosine Kinase Inhibitor Reduces the Severity of Established Glomerulonephritis, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 21, Pages: 231-236, ISSN: 1046-6673
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- Citations: 64
McAdoo SP, Tam FW, Pusey CD, 2010, Disease models of rapidly progressive glomerulonephritis, Drug Discovery Today: Disease Models, Vol: 7, Pages: 43-50, ISSN: 1740-6757
Rapidly progressive glomerulonephritis is a life-threatening clinical syndrome that accounts for a disproportionate number of patients requiring renal replacement therapy. The association with organ-specific and systemic autoimmunity is longstanding, but treatment with non-specific cytotoxic immunosuppression, first introduced in the 1970s, is still limited by its efficacy and toxicity. There are now accurate and reproducible rodent models of human diseases and investigation of these models has clarified many of the underlying mechanisms and unveiled targets for therapeutic manipulation that are being explored clinically. It is hoped that future work will lead to more effective, less toxic treatments for patients with renal and other autoimmune conditions. © 2010 Elsevier Ltd. All rights reserved.
Kazempour-Ardebili S, Lecamwasam VL, Dassanyake T, et al., 2009, Assessing glycemic control in maintenance hemodialysis patients with type 2 diabetes: Response to Riveline and Hadjadj, Diabetes Care, Vol: 32, ISSN: 0149-5992
Turner CM, Elliott JI, Tam FWK, 2009, P2 receptors in renal pathophysiology, PURINERGIC SIGNALLING, Vol: 5, Pages: 513-520, ISSN: 1573-9538
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- Citations: 14
Prasad S, McDaid JP, Tam FWK, et al., 2009, Pkd2 Dosage Influences Cellular Repair Responses following Ischemia-Reperfusion Injury, AMERICAN JOURNAL OF PATHOLOGY, Vol: 175, Pages: 1493-1503, ISSN: 0002-9440
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- Citations: 51
Kazempour Ardebili S, Lecamwasam VL, Dassanyake T, et al., 2009, Assessing Glycemic Control in Maintenance Hemodialysis Patients With Type 2 Diabetes, Diabetes Care, Vol: 32, Pages: 1137-1142, ISSN: 1935-5548
Tam FW, Riser BL, Meeran K, et al., 2009, Urinary monocyte chemoattractant protein 1 (MCP-1) and Connective tissue growth factor (CCN2) as prognostic markers for the progression of diabetic nephropathy., Cytokine.
Kazempour-Ardebili S, Lecamwasam VL, Dassanyake T, et al., 2009, Assessing Glycaemic Control in Maintenance Haemodialysis Patients with Type 2 Diabetes., Diabetes Care.
Taylor SRJ, Gonzalez-Begne M, Sojka DK, et al., 2009, Lymphocytes from P2X<sub>7</sub>-deficient mice exhibit enhanced P2X<sub>7</sub> responses, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 85, Pages: 978-986, ISSN: 0741-5400
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- Citations: 42
Taylor SRJ, Turner CM, Elliott JI, et al., 2009, P2X<sub>7</sub> Deficiency Attenuates Renal Injury in Experimental Glomerulonephritis, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 20, Pages: 1275-1281, ISSN: 1046-6673
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- Citations: 98
Ashby DR, Gale DP, Busbridge M, et al., 2009, Plasma hepcidin levels are elevated but responsive to erythropoietin therapy in renal disease, KIDNEY INTERNATIONAL, Vol: 75, Pages: 976-981, ISSN: 0085-2538
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- Citations: 235
Ashby D, Ford H, Wynne K, et al., 2009, Sustained appetite improvement in malnourished dialysis patients with daily subctanous ghrelin, Kidney International, Vol: 2, Pages: 199-206
Smith J, Lai PC, Behmoaras J, et al., 2007, Genes expressed by both mesangial cells and bone marrow-derived cells underlie genetic susceptibility to crescentic glomerulonephritis in the rat, J.Am.Soc.Nephrol., Vol: 18, Pages: 1816-1823
The Wistar-Kyoto (WKY) rat shows marked susceptibility to crescentic glomerulonephritis. In the model of nephrotoxic nephritis (NTN) that is induced by a small dose of nephrotoxic globulin, WKY rats developed crescents in 80 +/- 2% of glomeruli at day 10, whereas no crescents were seen in Lewis rats. This was associated with marked increase in monocyte chemoattractant protein-1 synthesis in WKY glomeruli. It was posited whether susceptibility depended on circulating cells or intrinsic renal cells. Bone marrow (BM) isografts from WKY to WKY or Lewis to Lewis did not affect susceptibility to NTN. When BM was transferred from WKY to Lewis rats, crescents developed in 35 +/- 9% of glomeruli 10 d after induction of NTN, indicating that susceptibility could be transferred by BM cells. However, crescents were also seen in WKY rats that were given Lewis marrow. For assessment of the contribution of intrinsic renal cells, kidneys from WKY or Lewis rats were transplanted into F1 animals. In NTN, the ratio of crescents in the transplanted kidney to the native kidney was significantly higher for WKY-to-F1 than for Lewis-to-F1 transplants, demonstrating that the kidney itself also influences susceptibility. Mesangial cell responses were then examined in the two strains. Mesangial cells that were derived from WKY rats synthesized significantly more monocyte chemoattractant protein-1 basally and after stimulation with heat-aggregated rabbit IgG or TNF-alpha. These results show that susceptibility to NTN in the WKY rat depends on both circulating and intrinsic renal cells and that there are genetic differences between the strains in mesangial responses to inflammatory stimuli
Malik AR, Little MA, Henriksson M, et al., 2007, Peritonitis, peritoneal inflammation and membrane permeability: a longitudinal study of dialysate and serum MCP-1 in stable patients on peritoneal dialysis, JOURNAL OF NEPHROLOGY, Vol: 20, Pages: 340-349, ISSN: 1121-8428
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- Citations: 11
Sheryanna A, Bhangal G, McDaid J, et al., 2007, Inhibition of p38 mitogen-activated protein kinase is effective in the treatment of experimental crescentic glomerulonephritis and suppresses monocyte chemoattractant protein-1 but not IL-1β or IL-6, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 18, Pages: 1167-1179, ISSN: 1046-6673
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- Citations: 63
Turner CM, Tam FWK, Lai P-C, et al., 2007, Increased expression of the pro-apoptotic ATP-sensitive P2X<sub>7</sub> receptor in experimental and human glomerulonephritis, NEPHROLOGY DIALYSIS TRANSPLANTATION, Vol: 22, Pages: 386-395, ISSN: 0931-0509
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- Citations: 67
Mosley K, Tam FWK, Edwards RJ, et al., 2006, Urinary proteomic profiles distinguish between active and inactive lupus nephritis, RHEUMATOLOGY, Vol: 45, Pages: 1497-1504, ISSN: 1462-0324
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- Citations: 70
Tam FWK, 2006, Current pharmacotherapy for the treatment of crescentic glomerulonephritis., Expert Opin Investig Drugs, Vol: 15, Pages: 1353-1369
Glomerulonephritis is an important cause of end-stage renal disease. Crescentic glomerulonephritis is the most severe form of glomerulonephritis and, if untreated, patients will develop renal failure within days or weeks of diagnosis. Current immunotherapy consists of corticosteroids, cytotoxic drugs and plasma exchange. Challenges include minimising toxicity of therapy, preventing relapse in antineutrophil cytoplasmic antibodies-associated vasculitis and finding an effective treatment for crescentic IgA nephropathy. There are opportunities for more specific therapies using monoclonal antibodies to T cells (and their co-stimulatory receptors), B cells and cytokines, or pharmacological inhibitors of signal transduction. Their efficacy and safety remain to be established with controlled clinical trials. Recent development of urinary cytokine measurement provides a noninvasive biomarker of renal disease activity, which is useful in monitoring response to therapy and assessing prognosis.
Ahmad S, Qureshi A, Brown EA, et al., 2006, CCL 18 and angiogenin: Novel cytokines present in PD fluid and involved in regulation of inflammation and fibrosis in the peritoneal membrane, 43rd Annual Congress of the European-Renal-Association/European-Dialysis-and-Transplant-Association (ERA-EDTA), Publisher: OXFORD UNIV PRESS, Pages: 490-490, ISSN: 0931-0509
Ahmad S, Frank JW, Tam FWK, et al., 2006, FDG PET scans in long term peritoneal dialysis patients may detect an inflammatory phase of encapsulating peritoneal sclerosis: Evidence from dialysate MCP-1 levels, 43rd Annual Congress of the European-Renal-Association/European-Dialysis-and-Transplant-Association (ERA-EDTA), Publisher: OXFORD UNIV PRESS, Pages: 490-490, ISSN: 0931-0509
Lai PC, Smith J, Bhangal G, et al., 2005, Interleukin-11 reduces renal injury and glomerular NF-Kappa B activity in murine experimental glomerulonephritis, Nephron Experimental Nephrology, Vol: 101, Pages: e146-e154, ISSN: 1660-2129
Khan SB, Cook HT, Bhangal G, et al., 2005, Antibody blockade of TNF-alpha reduces inflammation and scarring in experimental crescentic glomerulonephritis, Kidney International, Vol: 67, Pages: 1812-1820, ISSN: 0085-2538
Lai PC, Smith J, Bhangal G, et al., 2005, Interleukin-11 reduces renal injury and glomerular NF-Kappa B activity in murine experimental glomerulonephritis, NEPHRON EXPERIMENTAL NEPHROLOGY, Vol: 101, Pages: E146-E154, ISSN: 1660-2129
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- Citations: 15
Tam FWK, Sanders JS, George A, et al., 2004, Urinary monocyte chemoattractant protein-1 (MCP-1) is a marker of active renal vasculitis., Nephrol Dial Transplant
Barhamein MY, Tam FWK, Lai PC, et al., 2003, Urinary monocyte chemoattractant protein-1 (uMCP-1) is more useful than PDGF-BB or IFN-γ for monitoring activity of lupus nephritis (LN), 36th Annual Meeting of the American-Society-of-Nephrology, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: 148A-148A, ISSN: 1046-6673
Hammad TM, Tam FWK, Posey CD, et al., 2003, Urinary levels of monocyte chemoattractant protein-1 (MCP-1) as a marker of disease activity in ANCA associated vasculitis., 36th Annual Meeting of the American-Society-of-Nephrology, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: 758A-758A, ISSN: 1046-6673
Hammad TM, Tam FWK, Pusey CD, et al., 2003, Urinary levels of monocyte chemoattractant protein-1 (MCP-1) as a disease marker of disease activity in ANCA associated vasculitis, American Society of Nephrology 36th Meeting, Publisher: J Am Soc Nephrol
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