Publications
149 results found
Norden AGW, Lapsley M, Lee PJ, et al., 2002, Fragmentation of filtered proteins and implications for glomerular protein sieving in Fanconi syndrome., Kidney Int, Vol: 62, ISSN: 0085-2538
Tam FWK, 2002, Role of selectins in glomerulonephritis., Clin Exp Immunol, Vol: 129, Pages: 1-3, ISSN: 0009-9104
Lai PC, Cook HT, Smith J, et al., 2001, Interleukin-11 attenuates nephrotoxic nephritis in Wistar Kyoto rats, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 12, Pages: 2310-2320, ISSN: 1046-6673
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- Citations: 26
Norden AGW, Lapsley M, Lee PJ, et al., 2001, Glomerular protein sieving and implications for renal failure in Fanconi syndrome, KIDNEY INTERNATIONAL, Vol: 60, Pages: 1885-1892, ISSN: 0085-2538
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- Citations: 191
Larbi KY, Allen AR, Tam FWK, et al., 2000, VCAM-1 has a tissue-specific role in mediating interleukin-4-induced eosinophil accumulation in rat models: evidence for a dissociation between endothelial-cell VCAM-1 expression and a functional role in eosinophil migration, BLOOD, Vol: 96, Pages: 3601-3609, ISSN: 0006-4971
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- Citations: 16
Reynolds J, Tam FWK, Chandraker A, et al., 2000, CD28-B7 blockade prevents the development of experimental autoimmune glomerulonephritis, JOURNAL OF CLINICAL INVESTIGATION, Vol: 105, Pages: 643-651, ISSN: 0021-9738
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- Citations: 141
Tam FWK, Smith J, Agarwal S, et al., 2000, Type IV phosphodiesterase inhibitor is effective in prevention and treatment of experimental crescentic glomerulonephritis, NEPHRON, Vol: 84, Pages: 58-66, ISSN: 1660-8151
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- Citations: 18
Tam FWK, Smith J, Morel D, et al., 1999, Development of scarring and renal failure in a rat model of crescentic glomerulonephritis, NEPHROLOGY DIALYSIS TRANSPLANTATION, Vol: 14, Pages: 1658-1666, ISSN: 0931-0509
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- Citations: 61
Lai PC, Cook HT, Tam FWK, et al., 1999, Recombinant interleukin-11 is effective in ameliorating glomerulonephritis in Wistar-Kyoto rats., KIDNEY INTERNATIONAL, Vol: 55, Pages: 2579-2579, ISSN: 0085-2538
Karkar AM, Smith J, Tam FWK, et al., 1999, Prevention of acute inflammation and crescent formation in experimental crescentic nephritis by blocking tumour necrosis factor-α (TNF-α)., KIDNEY INTERNATIONAL, Vol: 55, Pages: 2103-2104, ISSN: 0085-2538
Cook HT, Singh SJ, Wembridge DE, et al., 1999, Interleukin-4 ameliorates crescentic glomerulonephritis in Wistar Kyoto rats, KIDNEY INTERNATIONAL, Vol: 55, Pages: 1319-1326, ISSN: 0085-2538
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- Citations: 41
McGinty A, Tam FWK, Cook HT, et al., 1999, Suppressors of cytokine signalling (SOCS): Expression by mesangial cells and regulation by cytokine and growth factors., Publisher: FEDERATION AMER SOC EXP BIOL, Pages: A39-A39, ISSN: 0892-6638
Waddington SN, Mosley K, Cook HT, et al., 1998, Arginase AI Is upregulated in acute immune complex-induced inflammation, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 247, Pages: 84-87, ISSN: 0006-291X
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- Citations: 35
Waddington SN, Tam FWK, Cook HT, et al., 1998, Arginase activity is modulated by IL-4 and HOArg in nephritic glomeruli and mesangial cells, AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, Vol: 274, Pages: F473-F480, ISSN: 1931-857X
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- Citations: 40
Waddington SN, Tam FWK, Cook HT, et al., 1998, Arginase activity is modulated by IL-4 and HOArg in nephritic glomeruli and mesangial cells, American Journal of Physiology - Renal Physiology, Vol: 274, ISSN: 1931-857X
Arginase shares a common substrate, L-arginine, with nitric oxide synthase (NOS). Both enzymes are active at inflammatory sites. To understand regulation of arginase and its relationship to nitric oxide (NO) production, we studied effects of N(G)-hydroxy-L-arginine (HOArg) and interleukin-4 (IL- 4) on urea and NO2/- synthesis by glomeruli during rat immune glomerulonephritis and compared these with macrophages and glomerular mesangial cells (MC). In nephritic glomeruli, elicited macrophages, and MC stimulated with IL-1 and adenosine 3',5'-cyclic monophosphate agonists, increased arginase and induced NOS activity was found. Urea production was inhibited by HOArg and increased by IL-4. NO inhibition [N(G)-monomethyl-L- arginine (L-NMMA)] increased arginase activity in nephritic glomeruli and macrophages but not MC. NO2/- synthesis was inhibited by L-NMMA and IL-4. It was increased with HOArg under conditions of NO inhibition. In contrast, in normal glomeruli and basal MC, where there was no induced NO synthesis, IL-4 had no effect on arginase activity, whereas HOArg consistently reduced it in glomeruli only. Type II arginase (Arg II) mRNA was detected in normal glomeruli; nephritic glomeruli expressed both Arg I and Arg II mRNAs. This is the first demonstration of arginase modulation in glomeruli and MC and of the expression of arginase isoforms in glomeruli. The differential responses to two endogenous compounds generated by inflammation suggest this may be part of coordinated regulation of arginase and inducible NOS in immune injury, whereby arginase is inhibited during high-output NO production and stimulated with NO suppression. This, together with control of arginase and NOS isoforms, may be important in controlling the balance of inflammatory and repair mechanisms.
Tam FWK, Smith J, Karkar AM, et al., 1997, Interleukin-4 ameliorates experimental glomerulonephritis and up-regulates glomerular gene expression of IL-1 decoy receptor, KIDNEY INTERNATIONAL, Vol: 52, Pages: 1224-1231, ISSN: 0085-2538
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- Citations: 40
Karkar AM, Smith J, Tam FWK, et al., 1997, Abrogation of glomerular injury in nephrotoxic nephritis by continuous infusion of interleukin-6, KIDNEY INTERNATIONAL, Vol: 52, Pages: 1313-1320, ISSN: 0085-2538
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- Citations: 34
Boulton R, Woodman A, Calnan D, et al., 1997, Nonparenchymal cells from regenerating rat liver generate interleukin-1 alpha and -1 beta: A mechanism of negative regulation of hepatocyte proliferation., HEPATOLOGY, Vol: 26, Pages: 49-58, ISSN: 0270-9139
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- Citations: 90
Morel D, Tam FWK, Smith J, et al., 1996, Glomerular expression of RANTES and recruitment of CD8+ cells in crescentic glomerulonephritis in WKY rats., JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 7, Pages: A2322-A2322, ISSN: 1046-6673
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- Citations: 1
Tam FWK, Smith J, Morel D, et al., 1996, Type IV phosphodiesterase inhibitor is effective in both prevention and treatment of progressive experimental glomerulonephritis., JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 7, Pages: A2376-A2376, ISSN: 1046-6673
Wang Y, Pratt JR, Tam FW, et al., 1996, Up-regulation of type 1 plasminogen activator inhibitor messenger RNA with thrombotic changes in renal grafts., Transplantation, Vol: 61, Pages: 684-689, ISSN: 0041-1337
Small vessel thrombosis is a prominent feature in kidneys undergoing vascular rejection. Type I and type 2 plasminogen activator inhibitors (PAI-1 and PAI-2, respectively) are known to mediate thrombosis. To examine the potential role of PAI-1 and PAI-2 in the mediation of vascular injury, the relationship and the time course of gene expression of PAI-1 and PAI-2 with the thrombotic changes in renal grafts were investigated in an unmodified rejection model in rats. Orthotopic renal transplantation was performed from Lewis to dark agouti (DA) rats and from DA to DA isografts; untreated normal rat kidneys were used as controls. The rats were killed on days 1-9 posttransplantation (n=18 in each allograft and isograft group). The grafts were analyzed by histopathology, in situ mRNA hybridization and Northern blot methods. The results show that PAM mRNA was first detected at day 4, when the thrombotic changes in the grafts were first seen, and that this relationship persisted during the time course observed to day 9. There was no detectable PAI-1 mRNA in the control groups and no PAI-2 in either group. In situ hybridization showed that PAI-1 positive cells were predominantly located in the cortical interstitium, consistent with the distribution of interstitial microthrombi. These results provide experimental evidence that the thrombotic changes in rejecting allografts are associated with the up-regulation of PAI-1 in the donor tissue, whereas PAI-2, from our results, does not seem to influence these changes. The data are consistent with a role for PAI-1 in the pathogenesis of vascular rejection.
Tam FWK, Karkar AM, Smith J, et al., 1996, Differential expression of macrophage inflammatory protein-2 and monocyte chemoattractant protein-1 in experimental glomerulonephritis, KIDNEY INTERNATIONAL, Vol: 49, Pages: 715-721, ISSN: 0085-2538
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- Citations: 49
Karkar AM, Tam FW, Steinkasserer A, et al., 1995, Modulation of antibody-mediated glomerular injury in vivo by IL-1ra, soluble IL-1 receptor, and soluble TNF receptor., Kidney Int, Vol: 48, Pages: 1738-1746, ISSN: 0085-2538
The severity of glomerular injury in the heterologous phase of NTN is dependent on proinflammatory cytokines including TNF alpha and IL-1 beta, and can be enhanced by LPS. We have previously shown that passive immunization against IL-1 beta and TNF partially abrogated the LPS effect in this model. In the present work, we have assessed the effects on glomerular injury of blocking and binding of IL-1 to its receptor by rh IL-1 receptor antagonist (IL-1ra) and by neutralizing IL-1 and TNF with rm soluble IL-1 receptor type1 (sIL-1Rt1) and rh sTNF receptor (sTNFr p55), respectively. Pretreatment with either IL-1ra, sIL-1Rt1, or sTNFr partially abrogated the effects of LPS and reduced albumin excretion from 45 +/- 8, 66 +/- 9, and 101 +/- 17 mg/24 hr at 13 +/- 4 (P < 0.02), 14 +/- 4 (P < 0.001), and 21 +/- 7 mg/24 hr (P < 0.001), respectively. Similarly, these inhibitors reduced the prevalence of glomerular capillary thrombi and the intensity of glomerular neutrophil infiltration. Glomerular thrombosis was reduced from 18 +/- 3%, 28 +/- 5%, and 25 +/- 7% to 3 +/- 2% (P < 0.002), 6 +/- 2% (P < 0.001), and 3 +/- 2 (P < 0.001), respectively, and glomerular neutrophil infiltration was reduced from 46 +/- 3, 54 +/- 2, 59 +/- 8 to 19 +/- 2 (P < 0.001), 25 +/- 2 (P < 0.001), and 28 +/- 2 neutrophils/50 glomeruli in section, respectively. Coadministration of both soluble receptors of IL-1 and TNF caused a further decrease in glomerular injury. The protective effect was also noticed at four hours after induction of nephritis, and even when these inhibitors were administered after the LPS injection and at the same time of induction of nephritis. All three treatments reduced circulating TNF concentration (down to 20%, 34%, and 0%, respectively) but without detectable glomerular TNF gene expression. Glomerular IL-1 beta mRNA levels were also reduced by 41%, 53%, and 67%, respectively, when assessed by densitometric analysis of Northern blots. In contrast, the
Largen PJ, Tam FW, Rees AJ, et al., 1995, Rat mesangial cells have a selective role in macrophage recruitment and activation., Exp Nephrol, Vol: 3, Pages: 34-39, ISSN: 1018-7782
In proliferative glomerulonephritis glomeruli are the target of an inflammatory reaction involving macrophage recruitment and activation. We examined the role of mesangial cells in this process. Supernatants from basal, IL-1, IFN-tau or LPS-stimulated rat mesangial cells (MCS) were tested for chemotactic, colony-stimulating and activation effects on macrophages in vitro. IL-1-stimulated MCS produced a macrophage chemoattractant (p = 0.007 compared with basal MCS) and MCP-1 mRNA was detected in IL-1-stimulated mesangial cells. LPS or IL-1-stimulated MCS produced colony-stimulating activity (LPS p < 0.05, IL-1 p < 0.01, compared with basal MCS or control supernatant, CS). Macrophage activation, assessed by nitric oxide generation, was suppressed. This evidence from functional bioassays supports a selective role for mesangial cells in the control of macrophage-induced glomerular injury, whereby activated mesangial cells participate in the recruitment and proliferation of infiltrating macrophages, and suppresses at least one field of macrophage activation, namely nitric oxide generation.
TAM FWK, SMITH J, CASHMAN SJ, et al., 1994, GLOMERULAR EXPRESSION OF INTERLEUKIN-1 RECEPTOR ANTAGONIST AND INTERLEUKIN-1-BETA GENES IN ANTIBODY-MEDIATED GLOMERULONEPHRITIS, AMERICAN JOURNAL OF PATHOLOGY, Vol: 145, Pages: 126-136, ISSN: 0002-9440
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- Citations: 35
Karkar AM, Tam FW, Proudfoot AE, et al., 1993, Modulation of antibody-mediated glomerular injury in vivo by interleukin-6., Kidney Int, Vol: 44, Pages: 967-973, ISSN: 0085-2538
We have shown previously that pretreatment with small doses of bacterial lipopolysaccharide (LPS), human recombinant interleukin-1 beta (hrIL-1 beta) and human recombinant tumor necrosis factor-alpha (hrTNF) increase injury in the heterologous phase of nephrotoxic nephritis (NTN). All three pretreatments induce synthesis of interleukin-6 (IL-6) which in some systems down-regulates synthesis of IL-1 and TNF. We have now investigated the influence of IL-6 on injury in both heterologous and autologous phases of NTN in rats. Injection of hrIL-6 in doses sufficient to induce hepatic synthesis of acute phase proteins (assessed by plasma alpha 2-macroglobulin concentration) had no effect on glomerular injury in the heterologous phase of NTN (albuminuria in NTAb alone 9 +/- 6; LPS/NTAb 34 +/- 10 and IL-6/NTAb 2 +/- 1 mg/24 hr, P < 0.001, Wilcoxon test). In contrast, IL-6 pretreatment partially abrogated the effect of LPS on albumin excretion (NTAb 4 +/- 2; LPS/NTAb 85 +/- 11 and IL-6/LPS/NTAb 32 +/- 6 mg/24 hr, P < 0.002), percentage of glomerular capillary thrombi (3 +/- 1%; 39 +/- 8%; and 6 +/- 1%, P < 0.001) and glomerular neutrophil infiltrate (29 +/- 3; 58 +/- 5; and 34 +/- 2 neutrophils/50 glomeruli in section, P < 0.001, respectively) at 24 hours. The effect of IL-6 was also evident four hours after induction of nephritis and was associated with a marked reduction in glomerular concentration of mRNA for IL-1 beta and TNF, without change in that of tubulin. Serum TNF concentrations were also significantly reduced at four hours in IL-6 treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
TAM FWK, CLAGUE J, DIXON CMS, et al., 1992, INHALED PLATELET-ACTIVATING-FACTOR CAUSES PULMONARY NEUTROPHIL SEQUESTRATION IN NORMAL HUMANS, AMERICAN REVIEW OF RESPIRATORY DISEASE, Vol: 146, Pages: 1003-1008, ISSN: 0003-0805
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- Citations: 25
ROSS CN, TAM FWK, WINTER RJD, et al., 1990, ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES AND SUBGLOTTIC STENOSIS, LANCET, Vol: 335, Pages: 1231-1232, ISSN: 0140-6736
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- Citations: 9
Tam FWK, Pusey CD, The role of T lymphocytes in extracapillary glomerulonephritis, JOURNAL OF NEPHROLOGY, Vol: 8, Pages: 305-315, ISSN: 1121-8428
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- Citations: 8
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