Paediatrics (RCH) - Research Publications
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ItemDeclining lung cancer mortality of young Australian women despite increased smoking is linked to reduced cigarette 'tar' yields.(Springer Science and Business Media LLC, 2001-02-02)Lung cancer data were examined to determine whether the mortality rates of young Australian women have continued to increase in line with the proportions of them who have smoked tobacco. Trends in annual age-specific lung cancer mortality were estimated for 1965-1998. Age-specific mortality rates and age-adjusted ratios of mortality rates were calculated for birth cohorts. Proportions of smokers in those cohorts were estimated from results of eight national surveys of smoking, and their mean ages of commencement and years of smoking were assessed from surveys of smokers in two states. Lung cancer mortality rates of 20-44-year-old Australian women peaked in 1986. Age-adjusted mortality rates are lower for women born in the 1950s and 1960s than for women born in the 1940s, despite higher proportions of smokers, younger age of commencement and longer duration of smoking by age 30 years in the more recent cohorts. Increased smoking has not resulted in higher lung cancer mortality for Australian women born in the 1950s and 1960s. Reductions in tar yields of Australian-made cigarettes, which would have affected primarily those born after the 1940s, may be responsible.
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ItemNo Preview AvailableEleven years of sexual discovery.(Springer Science and Business Media LLC, 2001)A report on Novartis Foundation Symposium 244 "The Genetics and Biology of Sex Determination", London, UK, 1-3 May 2001.
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ItemDIABLO promotes apoptosis by removing MIHA/XIAP from processed caspase 9(ROCKEFELLER UNIV PRESS, 2001-02-05)MIHA is an inhibitor of apoptosis protein (IAP) that can inhibit cell death by direct interaction with caspases, the effector proteases of apoptosis. DIABLO is a mammalian protein that can bind to IAPs and antagonize their antiapoptotic effect, a function analogous to that of the proapoptotic Drosophila molecules, Grim, Reaper, and HID. Here, we show that after UV radiation, MIHA prevented apoptosis by inhibiting caspase 9 and caspase 3 activation. Unlike Bcl-2, MIHA functioned after release of cytochrome c and DIABLO from the mitochondria and was able to bind to both processed caspase 9 and processed caspase 3 to prevent feedback activation of their zymogen forms. Once released into the cytosol, DIABLO bound to MIHA and disrupted its association with processed caspase 9, thereby allowing caspase 9 to activate caspase 3, resulting in apoptosis.
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ItemNo Preview AvailableAntibodies to MMP-cleaved aggrecan.(Humana Press, 2001)
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ItemPost-immunisation gastritis and Helicobacter infection in the mouse:: a long term study(BRITISH MED JOURNAL PUBL GROUP, 2001-10)BACKGROUND AND AIMS: Helicobacter pylori is a major cause of peptic ulcers and gastric cancer. Vaccine development is progressing but there is concern that immunisation may exacerbate Helicobacter induced gastritis: prophylactic immunisation followed by challenge with H felis or H pylori can induce a more severe gastritis in mice than seen with infection alone. The aim of this study was to investigate the relationship between immunity to Helicobacter infection and post-immunisation gastritis. METHODS: (1) C57BL/6 mice were prophylactically immunised before challenge with either H felis or H pylori. Histopathology and colonisation were assessed one month post-challenge. (2) C57BL/6 mice were prophylactically immunised against H felis infection and gastritis assessed up to 18 months post-challenge. RESULTS: Prophylactic immunisation induced a reduction in bacterial colonisation following H felis challenge which was associated with increased severity of active gastritis with neutrophil infiltration and atrophy. However, immunised mice challenged with H pylori SS1 had little evidence of pathology. Long term follow up showed that post-immunisation gastritis was evident at three months. However, from six months onwards, although immunised/challenged mice still developed gastritis, there was no significant difference between inflammation in these mice and infected controls. Post-immunisation gastritis was not associated with the serum antibody response. Immunisation prevented the formation of secondary lymphoid aggregates in the gastric tissue. CONCLUSION: The H felis mouse model of post-immunisation gastritis is the most extreme example of this type of pathology. We have shown in this model that post-immunisation gastritis is a transient event which does not produce long term exacerbation of pathology.
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ItemHelicobacter-induced expression of Bcl-XL in B lymphocytes in the mouse model:: A possible step in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma(WILEY-LISS, 2001-06-01)Primary gastric mucosa-associated lymphoid tissue (MALT) lymphoma may develop from chronic infection with Helicobacter sp. in the mouse model. The mechanisms of pathogenesis remain unclear. Regulation of B-cell proliferation and death are important features to investigate. Proteins encoded by bcl-2 family genes, e.g., Bcl-X(L), regulate apoptosis; and alterations in the expression of these genes can contribute to the development of cancer. Our aim was to determine the role of Bcl-X(L) in B lymphocytes in the development of gastric MALT lymphoma associated with Helicobacter infection using the BALB/c mouse model. We analyzed 37 animals with Helicobacter-associated MALT (n = 25), low-grade MALT lymphoma (n = 10) and high-grade lymphoma (n = 2), investigating the in vivo distribution of Bcl-X(L) in B cells/B-lymphoma cells using immunohistochemical analysis. In vitro cultivation of B cells/B-lymphoma cells was employed to perform RT-PCR analysis of Bcl-X(L) mRNA expression after cell stimulation with Helicobacter antigen. We found significant Bcl-X(L) protein expression in B lymphocytes within MALT and low-grade MALT lymphoma, whereas there was no and minimal expression, respectively, of Bcl-X(L) in the 2 high-grade MALT lymphoma cases. Expression of bcl-X(L) mRNA in B lymphocytes was up-regulated in vitro upon Helicobacter-antigen stimulation and associated with prolonged cell survival. These findings support the hypothesis that Bcl-X(L) plays a role in the pathogenesis of B-cell MALT lymphoma by providing cell-survival signals and by triggering the acquisition of MALT.
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ItemSevere Bordetella holmesii infection in a previously healthy adolescent confirmed by gene sequence analysis(UNIV CHICAGO PRESS, 2001-07-01)We describe an immunocompetent adolescent who presented with exceptionally severe Bordetella holmesii infection, including previously undescribed manifestations. Sequelae included a severe restrictive lung defect due to pulmonary fibrosis.