Celebrating the past : the growth of amateur history in South Australia / Kerrie Round.

Bibliography: leaves 356-375.2 v. (v,375 ; [166] leaves) ; 30 cm.Thesis (Ph.D.)--University of Adelaide, Dept. of History, 199

Anti-cartel or anti-foreign? Australian attitudes to anti-competitive behaviour before the first World War

More than a century elapsed between Australia's first legislative attempts to modify anticompetitive behaviour (the Australian Industries Preservation Act 1906) and its most recent efforts to criminalise price fixing (Trade Practices Amendment (Cartel Conduct and Other Measures) Act 2009). After a burst of activity in the first decade of Federation, the intervening years saw only sporadic interest by governments to promote competitive markets, with limited impact until the late 1960s. This paper assesses the first period of Australia's attempts to promote competition. It traces the political, economic and social environments of anticompetitive business behaviour in Australia from 1901 up to World War I. We suggest that Australia's initial forays into regulating cartels were motivated more by protectionist aims than by efforts to increase competition, which in part also explains the next half-century of legislative apathy towards anti-competitive legislation.

Yantu-gongcheng-xuebao : shuangyuekan = Chinese journal of geotechnical engineering

The polarized reorganization of the T cell membrane and intracellular signaling molecules in response to T cell receptor (TCR) engagement has been implicated in the modulation of T cell development and effector responses. In siRNA-based studies Dlg1, a MAGUK scaffold protein and member of the Scribble polarity complex, has been shown to play a role in T cell polarity and TCR signal specificity, however the role of Dlg1 in T cell development and function in vivo remains unclear.Here we present the combined data from three independently-derived dlg1-knockout mouse models; two germline deficient knockouts and one conditional knockout. While defects were not observed in T cell development, TCR-induced early phospho-signaling, actin-mediated events, or proliferation in any of the models, the acute knockdown of Dlg1 in Jurkat T cells diminished accumulation of actin at the IS. Further, while Th1-type cytokine production appeared unaffected in T cells derived from mice with a dlg1 germline-deficiency, altered production of TCR-dependent Th1 and Th2-type cytokines was observed in T cells derived from mice with a conditional loss of dlg1 expression and T cells with acute Dlg1 suppression, suggesting a differential requirement for Dlg1 activity in signaling events leading to Th1 versus Th2 cytokine induction. The observed inconsistencies between these and other knockout models and siRNA strategies suggest that 1) compensatory upregulation of alternate gene(s) may be masking a role for dlg1 in controlling TCR-mediated events in dlg1 deficient mice and 2) the developmental stage during which dlg1 ablation begins may control the degree to which compensatory events occur.These findings provide a potential explanation for the discrepancies observed in various studies using different dlg1-deficient T cell models and underscore the importance of acute dlg1 ablation to avoid the upregulation of compensatory mechanisms for future functional studies of the Dlg1 protein

Characterization of in vivo Dlg1 deletion on T cell development and function.

BackgroundThe polarized reorganization of the T cell membrane and intracellular signaling molecules in response to T cell receptor (TCR) engagement has been implicated in the modulation of T cell development and effector responses. In siRNA-based studies Dlg1, a MAGUK scaffold protein and member of the Scribble polarity complex, has been shown to play a role in T cell polarity and TCR signal specificity, however the role of Dlg1 in T cell development and function in vivo remains unclear.Methodology/principal findingsHere we present the combined data from three independently-derived dlg1-knockout mouse models; two germline deficient knockouts and one conditional knockout. While defects were not observed in T cell development, TCR-induced early phospho-signaling, actin-mediated events, or proliferation in any of the models, the acute knockdown of Dlg1 in Jurkat T cells diminished accumulation of actin at the IS. Further, while Th1-type cytokine production appeared unaffected in T cells derived from mice with a dlg1 germline-deficiency, altered production of TCR-dependent Th1 and Th2-type cytokines was observed in T cells derived from mice with a conditional loss of dlg1 expression and T cells with acute Dlg1 suppression, suggesting a differential requirement for Dlg1 activity in signaling events leading to Th1 versus Th2 cytokine induction. The observed inconsistencies between these and other knockout models and siRNA strategies suggest that 1) compensatory upregulation of alternate gene(s) may be masking a role for dlg1 in controlling TCR-mediated events in dlg1 deficient mice and 2) the developmental stage during which dlg1 ablation begins may control the degree to which compensatory events occur.Conclusions/significanceThese findings provide a potential explanation for the discrepancies observed in various studies using different dlg1-deficient T cell models and underscore the importance of acute dlg1 ablation to avoid the upregulation of compensatory mechanisms for future functional studies of the Dlg1 protein

T cell polarization and migration are not hindered by the loss of <i>dlg1</i>.

<p>(A) <i>dlg1^wt;GT</i> or <i>dlg1^ko;GT</i> activated T lymphoblasts were stained with CD43 or CD44 and assessed for protein polarization (<i>left panel</i>). The percentage polarization of CD43 and CD44 to the T cell uropod was determined by scoring 45 cells in two independent experiments (<i>right panel, top and bottom</i>). (B) <i>dlg1^flox/flox or dlg1^flox/flox:CD4^cre</i> CD4⁺ T cells were allowed to conjugate with anti-TCR antibody coated beads for 20 minutes, fixed and stained with the indicated antibodies. The indicated proteins were scored for localization to the DPC (<i>left panel</i>) or IS (<i>right panel</i>). 50–100 conjugates were scored for F-actin localization to the T cell/APC interface in each of 2–3 independent experiments (<i>right panel</i>). Data represent mean +/− StDev. Differences were not statistically significant for any sample pair. (C) <i>dlg1^wt;GT</i> or <i>dlg1^ko;GT</i> activated T lymphoblasts were subjected to time-lapse microscopy and assessed for random migration (<i>top panels</i>). Total distance was determined from DIC images acquired at 1 min intervals by tracking a total of 30 cells over a 30 min period (<i>bottom panels</i>). Data are representative of n = 2 experiments. (D) A modified Boyden chamber was used to assess the percent of <i>dlg1^flox/flox</i> or <i>dlg1^flox/flox:CD4^cre</i> T cells which migrated in response to no chemokine, CXCL12, or CCL19 over 2 hours and was calculated as the ratio of the total cells, to cells that migrated * = p≤0.05. (E) The percentage of Jurkat cells transfected with either empty vector or shDlg1 which migrated in response to no chemokine or CXCL12 for 2 hours was calculated as: number of cells migrated/total number of cells. n.s. = no significiant difference.</p

An acute, but not germline or conditional, loss of <i>dlg1</i> impairs receptor-mediated actin polymerization.

<p>(A) <i>dlg1^flox/flox</i> or <i>dlg1^flox/flox:CD4^cre</i> CD4⁺ T cells were allowed to conjugate with anti-TCR antibody-coated beads for 20 minutes and stained for actin with rhodamine-phalloidin (<i>top panel</i>). At least 50 cells were scored for actin localization to the T cell/bead interface (<i>bottom panel</i>). (B) Expanded T cells from <i>dlg1^wt;BG</i> or <i>dlg1^ko;BG</i> mice were restimulated with plate-bound anti-CD3 and anti-CD28 antibodies for 5 or 15 minutes. Cells were stained with a combination of anti-CD4, anti-CD8, and FITC-phalloidin and assessed by FACS to determine the relative level of induced actin polymerization in CD4⁺ (<i>top panel</i>) and CD8⁺ (<i>bottom panel</i>) T cell populations. These data are representative of 2 independent experiments, n≥4 for WT and KO samples. (C) Whole cell lysates from Jurkat cells expressing empty vector (empty) or Dlg1 shRNA were immunoblotted with antibodies against Dlg1 or GAPDH, as indicated. (D) Jurkat T cells (green) were transfected with either pCMS3.eGFP.H1p empty vector or pCMS3.eGFP.H1p containing a shDlg1 target sequence. Cells were stimulated with SEE-pulsed (or untreated) Raji B cells (blue) and stained with rhodamine-phalloidin (red) (<i>left panel</i>). At least 50 conjugates were scored for F-actin localization to the T cell/APC interface in each of two independent experiments (<i>right panel</i>). Data represent mean +/− StDev. n.s., not statistically significant.</p