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  • 1
    Electronic Resource
    Electronic Resource
    Reactions of .pi.-sulfuranes (ylides) with aromatic carbonium ions (1973)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 95 (1973), S. 1285-1295 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00785a046
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  • 2
    Electronic Resource
    Electronic Resource
    Catalytic and photolytic decomposition of 1-chloro-4-diazoalkenes (1972)
    s.l. : American Chemical Society
    The @journal of organic chemistry 37 (1972), S. 3133-3139 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00985a021
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  • 3
    Electronic Resource
    Electronic Resource
    Cardiovascular risk in dialysis patients: A comparison of risk factors and cardioprotective therapy between 1996 and 2001 (2003)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 8 (2003), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY:  Cardiovascular disease (CVD) is the major cause of mortality in dialysis patients. Aspirin, beta-blockers, statins, and angiotensin-converting enzyme (ACE) inhibitors reduce CVD mortality in the general population, as may angiotensin II receptor antagonists. The prevalence of cardiovascular risk factors and usage rates of cardioprotective agents in end-stage renal failure are unknown. A retrospective, cross-sectional study of dialysis patients was performed to compare: (i) prevalence of cardiovascular risk factors (age, hypertension, hyperlipidaemia, diabetes mellitus, and smoking); (ii) use of cardioprotective agents; and (iii) prevalence of cardiovascular disease between the time-points: 1996 (n = 262) versus 2001 (n = 369). We found an increase in the risk factors of age (53.6 ± 14.9 years in 1996 vs 58.4 ± 14.3 in 2001; P 〈 0.001) and hyperlipidaemia (45 vs 51.8%; P 〈 0.001) between the two time-points, with a reduction in the prevalence of smoking (14.5 vs 8.1%; P = 0.016). There was no difference in the prevalence of cardiovascular disease (37.4 vs 40.7%; P = 0.44). Cardioprotective agents were underutilized, with improvement in prescribing practice between 1996 and in 2001, especially in the usage of statins (21.4 vs 38.7% in 2001; P = 0.019). In conclusion, CVD is the primary cause of mortality in our dialysis patients. Although traditional cardiovascular risk factors affect the majority of the dialysis population, underutilization of cardioprotective agents is common. Proof of efficacy of these agents in this population of enormous risk is urgently required.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2003.00157.x
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  • 4
    Electronic Resource
    Electronic Resource
    Historical controlled trial of OKT3 versus basiliximab induction therapy in simultaneous pancreas–renal transplantation (2003)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 8 (2003), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY:  Simultaneous pancreas–kidney (SPK) transplant recipients are at high immunological risk of rejection. Antibody induction is beneficial but lymphocyte-depleting therapy is associated with a high incidence of side-effects. We performed a historical controlled trial to compare OKT3 versus anti-CD25 antibody (basiliximab) induction therapy with regard to patient, kidney and pancreas survival, as well as to examine for any differences in acute rejection, graft function, and infective complications. Twenty-eight consecutive SPK transplants were performed at the Monash Medical Centre between December 1997 and November 2001. Anti CD3 monoclonal antibody (OKT3) was used prior to March 2000 (n = 12) and basiliximab was used after (n = 16), both in combination with cyclosporin, mycophenolate, and prednisolone. A retrospective comparison of outcomes was performed. At 6 months, patient (100 vs 100%), kidney (91.7 vs 91.7%) and pancreas (75 vs 83.3%) survival were similar in the OKT3 and basiliximab groups, respectively. A minority of subjects in each group remained free from rejection (42% basiliximab vs 25% on OKT3, P = NS). Renal function was superior in the basiliximab group (mean calculated creatinine clearance 79.4 ± 11.9 vs 54.5 ± 15.9 mL/min for  basiliximab vs OKT3, P 〈 0.001). The incidence of major opportunistic infection was lower in basiliximab-treated patients (9 vs 50% in the OKT3 group, P = 0.033). Basiliximab was associated with similar 6-month patient, kidney and pancreas survival, superior renal function and less opportunistic infection as compared with OKT3 induction therapy in SPK transplants. Basiliximab is at least as effective and is safer than OKT3 for induction therapy in SPK transplantation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2003.00158.x
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  • 5
    Electronic Resource
    Electronic Resource
    Combined interleukin 1 and tumour necrosis factor α blockade in rat crescentic anti-glomerular basement membrane glomerulonephritis (2001)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 6 (2001), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: Studies in experimental models have established that blockade of either interleukin 1 (IL-1) or tumour necrosis factor α (TNF-α) is effective in suppressing crescentic glomerulonephritis. However, it is not known whether simultaneous blockade of both cytokines will provide additional disease suppression compared with that produced by single cytokine blockade. We have addressed this question in a study of accelerated crescentic anti-glomerular basement membrane (GBM) glomerulonephritis in the rat. Groups of six animals were treated with an IL-1 receptor antagonist (IL-1ra), TNF-α-binding protein (TNFbp), IL-1ra + TNFbp (combined) or saline (control) from the time of anti-GBM serum injection until being killed, 10 days later. Saline-treated animals developed crescentic glomerulonephritis with tubulointerstitial damage, heavy proteinuria and renal impairment. Compared with saline, treatment with either IL-1ra or TNFbp alone resulted in significant suppression of crescent formation (3.0% and 3.3%, respectively, vs. 21.0%; both P 〈 0.001 vs. control), tubulointerstitial leucocytic infiltration (262 ± 31 and 282 ± 32 cells/mm2 vs. 481 ± 71 cells/mm2; both P 〈 0.001 vs. control) and proteinuria (167 ± 44 and 164 ± 23 mg/24 h vs. 279 ± 36 mg/24 h; both P 〈 0.001 vs. control) and prevented the loss of renal function. Combined IL-1ra and TNFbp treatment resulted in a virtually identical degree of disease suppression as individual cytokine blockade in terms of crescent formation (2.7%), interstitial leucocytic infiltration (274 ± 45 cells/mm2), proteinuria (190 ± 18 mg/24 h) and renal function preservation. In conclusion, this study has demonstrated that blockade of either IL-1 or TNF-α alone substantial suppresses experimental crescentic glomerulonephritis to a similar extent to that achieved by simultaneous blockade of both cytokines. These findings provide a rationale for the use of cytokine monotherapy, rather than multiple cytokine blockade, in the treatment of human crescentic glomerulonephritis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2001.00056.x
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  • 6
    Electronic Resource
    Electronic Resource
    Intrarenal synthesis of IL-6 in IgA nephropathy (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 3 (1997), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Recent in vitro studies have shown the synthesis of interleukin-6 (IL-6) in glomerular mesangial and epithelial cells, and suggested the involvement of IL-6 in mesangial proliferative glomerulonephritis. However, the expression site of IL-6 mRNA in renal tissue of IgA nephropathy (IgAN), the most common chronic mesangial proliferative glomerulonephritis, remains obscure. to localize IL-6 mRNA in renal biopsy specimens of IgAN, we used nonradioactive in situ hybridization (ISH) developed in our laboratory, sensitive in detecting individual cells positive for a specific mRNA. In some sections, periodic acid-Schiff staining was performed after ISH in order to identify the topographical relation between IL-6 mRNA positive cells and glomerular basement membrane and mesangial area. In situ hybridization for IL-6 mRNA and immunohistochemistry for CD3 and CD68, markers for lymphocytes and monocytes, respectively, were also performed on serial sections to examine the contribution of infiltrated mononuclear cells to cells positive for IL-6 mRNA in glomeruli. Glomerular resident cells, including glomerular mesangial and epithelial cells and cells of Bowman's capsule, as well as tubular epithelial cells and infiltrated mononuclear cells expressed IL-6 mRNA. We also compared the localization of IL-6 mRNA and protein and showed different distribution between the gene product and protein. the expression of IL-6 mRNA correlated with the degree of mesangial cell proliferation and tubulointerstitial changes. Our results indicate that IL-6 is synthesized in renal tissues of IgAN and suggest that the increased IL-6 expression may be important in the pathogenesis of IgAN.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1997.tb00265.x
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  • 7
    Electronic Resource
    Electronic Resource
    The XIVth International Congress of Nephrology: Incorporating the VIIth Asian Pacific Congress of Nephrology and the 33rd Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 2 (1996), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1996.tb00115.x
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  • 8
    Electronic Resource
    Electronic Resource
    EGF and EGF-receptor expression in rat anti-Thy-1 mesangial proliferative nephritis (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 1 (1995), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Epidermal growth factor (EGF) is a potent mesangial cell and tubular epithelial cell mitogen. Based upon the novel finding that rat mesangial cells express EGF mRNA and protein in vitro, we investigated whether renal EGF production was involved in mesangial proliferation and concomitant tubular epithelial proliferation in rat anti-Thy-1 mesangial proliferative nephritis. During the period of mesangial proliferation in anti-Thy-1 nephritis (days 4–14) no EGF immunoreactive material was detected within the glomerulus. Epidermal growth factor-receptor (EGF-R) expression, which is strong on podocytes in normal glomeruli, was notably absent from focal areas of proliferating mesangial cells, suggesting that EGF available from the circulation was not involved in mesangial cell proliferation. Concomitant with the transient decline in creatinine clearance on day 8 of disease, there was mild tubular injury and a significant increase in cortical tubular proliferation as assessed by expression of the proliferating cell nuclear antigen (PCNA). Double immunohistochemistry staining found that the increased cortical tubular proliferation on day 8 occurred in EGF− tubules, but not EGF+ tubules. In contrast, there was an increase in proliferation of EGF+ tubules, but not EGF− tubules, on day 28. Renal EGF mRNA and protein expression was down-regulated over days 1-14, with a rebound in expression on day 28 which correlated with proliferation of EGF+ tubules. Tubular EGF-R expression, which is most clearly seen on EGF+ tubules in normal rat kidney, was unchanged over the disease course. the potential role of EGF in tubular proliferation in normal and diseased states is discussed. In summary, this study finds no evidence to implicate EGF in mesangial cell proliferation in rat anti-Thy-1 nephritis, even though mesangial cells can express EGF in vitro, and suggests that EGF may regulate proliferation of tubular epithelial cells in different stages of disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1995.tb00013.x
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  • 9
    Electronic Resource
    Electronic Resource
    Determinants of native arteriovenous fistula blood flow (2004)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 9 (2004), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Determinants of native arteriovenous fistula (AVF) placement have been well studied. Little is known on whether these factors impact on subsequent blood flow (Qa) in the mature AVF.Methods:  Arteriovenous fistula Qa and cardiac index (CI) were determined by ultrasound dilution. Multiple linear regression was used to assess independent predictors of AVF Qa.Results:  Of the 148 patients available for the analysis, 68% were male, with 61% using a radiocephalic AVF. Aetiology of renal disease was: 38% glomerulonephritis (GN), 22% diabetes mellitus (DM), 9% hypertension/ischaemic (HTN) and 31% other. Thirty per cent had coronary artery disease (CAD), 10% cerebrovascular disease and 11% peripheral vascular disease (PVD). Median (iqr) Qa was 1185 mL/min (790–1650) and CI was 3.15 L/min per 1.73 m2 (2.60–3.93). On univariable analysis, log CI (0.98, P 〈 0.001), age (−0.1 per 10 years, P = 0.002), access position (upper vs lower 0.26, P = 0.003, PVD (−0.35, P = 0.015), CAD (−0.25, P = 0.008), and primary renal disease (DM vs GN, −0.35, P = 0.003, HTN vs GN, −0.34, P = 0.04) were associated with Qa. On multivariable analysis, CI (0.84, P 〈 0.001), access position (upper vs lower, 0.17, P = 0.018) and primary renal disease (DM vs GN, −0.26, P = 0.005, and HTN vs GN, −0.26, P = 0.038) remained significant predictors of AVF Qa.Conclusion:  Once established, CI, AVF position and primary renal disease (hypertension/ischaemic and diabetes) are the major determinants of AVF Qa while female gender, CAD, PVD and body mass index were not significant determinants of Qa in this cohort.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.2004.00257.x
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  • 10
    Electronic Resource
    Electronic Resource
    Role of interleukin-10 in rat mesangioproliferative glomerulonephritis (2003)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 8 (2003), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: Interleukin-10 (IL-10) has been recognized as a growth factor for rat mesangial cells in vitro; however, its role in mesangioproliferative glomerulonephritis is unknown. We studied the expression of IL-10 mRNA in the rat anti-Thy-1 model of mesangioproliferative glomerulonephritis (experiment 1) and, subsequently, the effects of blocking IL-10 during anti-Thy-1 nephritis using the IL-10 inhibitor, AS101 (experiment 2). In experiment 1, PCR analysis failed to detect IL-10 mRNA in normal rat kidney, however, a clear signal for IL-10 mRNA was evident on day 6 of anti-Thy-1 nephritis. In situ hybridization showed IL-10 mRNA expression in focal glomerular areas in anti-Thy-1 nephritis. Combined in situ hybridization and immunohistochemistry showed that glomerular IL-10 mRNA was expressed by both macrophages and mesangial cells. In experiment 2, treatment with AS101 significantly downregulated renal IL-10 gene expression, as demonstrated by semiquantitative PCR. However, the induction of glomerular hypercellularity, mesangial proliferation (PCNA+ cells), mesangial cell activation (α-SMA expression) and macrophage accumulation (ED1+ cells) seen in saline-treated anti-Thy-1 nephritis was unaffected by AS101 treatment. In conclusion, renal IL-10 gene expression is upregulated during pathological mesangial cell proliferation in rats with anti-Thy-1 nephritis. However, the inability of IL-10 suppression with AS101 to prevent anti-Thy-1 disease suggests that IL-10 is not essential for pathological mesangial cell proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2003.00125.x
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