James Cook University (JCU) enrolled its first cohort of 64 in 2000 into a 6-year undergraduate m... more James Cook University (JCU) enrolled its first cohort of 64 in 2000 into a 6-year undergraduate medical program aimed at producing graduates capable of meeting the needs of North Queensland, Australia, with a focus on rural, remote, Indigenous and tropical health. The school's 1465 graduates over 13 cohorts who have a pattern of practice likely to meet the region's health needs. The JCU course was the first new Australian medical program for 25 years. The number of Australian medical schools has since doubled, while enrollments have almost tripled. JCU's course features innovations such as dispersed, community-based education, rurally-focused selection, extended rural placements, and an emphasis on community needs - which are all now mainstream. This paper traces developments at JCU over the past decade, illustrating parallels with the broader Australian scene. Maintaining quality and educational integrity while numbers grow is challenging. The course has undergone modes...
We examined how increasing patient and health care professional (HCP) engagement with SMBG can im... more We examined how increasing patient and health care professional (HCP) engagement with SMBG can improve management of patients with diabetes. We propose that SMBG is still underutilised in Australia despite the use of test strips increasing by 6.3% per year.
Introduction: Research was conducted to assess the effectiveness of a new innovative teaching met... more Introduction: Research was conducted to assess the effectiveness of a new innovative teaching methodology to better prepare students for their end of year clinical examinations. Methods: All Year 2 medical students were administered a survey immediately following the new teaching methodology, and another survey one week after their end-of-year clinical examination. Results: Post new teaching methodology, >80% of students agreed (response rate=96%) that the sessions benefited them by: strengthening the link between theory and practice; building their confidence in preparing for ‘real’ patient encounters; improving their problem-solving skills regarding differential diagnosis; and, improving their skills regarding delivering a focused physical examination. Following the end-of-year clinical examinations, 80% of student respondents (response rate = 40%) reported the new teaching methodology helped them get a better score on their clinical examinations, and 93% thought the teaching m...
Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, includi... more Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, including hydroxyoctadecadienoic acids (HODEs). These stable oxidation products of linoleic acid (LA) are abundant in atherosclerotic plaque and activate PPARγ and GPR132. We investigated the mechanisms through which HODEs regulate apoptosis. The effect of HODEs on THP-1 monocytes and adherent THP-1 cells were compared with other C18 fatty acids, LA and α-linolenic acid (ALA). The number of cells was reduced within 24 hours following treatment with 9-HODE (p < 0.01, 30 μM) and 13 HODE (p < 0.01, 30 μM), and the equivalent cell viability was also decreased (p < 0.001). Both 9-HODE and 13-HODE (but not LA or ALA) markedly increased caspase-3/7 activity (p < 0.001) in both monocytes and adherent THP-1 cells, with 9-HODE the more potent. In addition, 9-HODE and 13-HODE both increased Annexin-V labelling of cells (p < 0.001). There was no effect of LA, ALA, or the PPARγ agonist rosiglitazone (1 μM), but the effect of HODEs was replicated with apoptosis-inducer camptothecin (10 μM). Only 9-HODE increased DNA fragmentation. The pro-apoptotic effect of HODEs was blocked by the caspase inhibitor DEVD-CHO. The PPARγ antagonist T0070907 further increased apoptosis, suggestive of the PPARγ-regulated apoptotic effects induced by 9-HODE. The use of siRNA for GPR132 showed no evidence that the effect of HODEs was mediated through this receptor. 9-HODE and 13-HODE are potent--and specific--regulators of apoptosis in THP-1 cells. Their action is PPARγ-dependent and independent of GPR132. Further studies to identify the signalling pathways through which HODEs increase apoptosis in macrophages may reveal novel therapeutic targets for atherosclerosis.
James Cook University (JCU) enrolled its first cohort of 64 in 2000 into a 6-year undergraduate m... more James Cook University (JCU) enrolled its first cohort of 64 in 2000 into a 6-year undergraduate medical program aimed at producing graduates capable of meeting the needs of North Queensland, Australia, with a focus on rural, remote, Indigenous and tropical health. The school's 1465 graduates over 13 cohorts who have a pattern of practice likely to meet the region's health needs. The JCU course was the first new Australian medical program for 25 years. The number of Australian medical schools has since doubled, while enrollments have almost tripled. JCU's course features innovations such as dispersed, community-based education, rurally-focused selection, extended rural placements, and an emphasis on community needs - which are all now mainstream. This paper traces developments at JCU over the past decade, illustrating parallels with the broader Australian scene. Maintaining quality and educational integrity while numbers grow is challenging. The course has undergone modes...
We examined how increasing patient and health care professional (HCP) engagement with SMBG can im... more We examined how increasing patient and health care professional (HCP) engagement with SMBG can improve management of patients with diabetes. We propose that SMBG is still underutilised in Australia despite the use of test strips increasing by 6.3% per year.
Introduction: Research was conducted to assess the effectiveness of a new innovative teaching met... more Introduction: Research was conducted to assess the effectiveness of a new innovative teaching methodology to better prepare students for their end of year clinical examinations. Methods: All Year 2 medical students were administered a survey immediately following the new teaching methodology, and another survey one week after their end-of-year clinical examination. Results: Post new teaching methodology, >80% of students agreed (response rate=96%) that the sessions benefited them by: strengthening the link between theory and practice; building their confidence in preparing for ‘real’ patient encounters; improving their problem-solving skills regarding differential diagnosis; and, improving their skills regarding delivering a focused physical examination. Following the end-of-year clinical examinations, 80% of student respondents (response rate = 40%) reported the new teaching methodology helped them get a better score on their clinical examinations, and 93% thought the teaching m...
Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, includi... more Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, including hydroxyoctadecadienoic acids (HODEs). These stable oxidation products of linoleic acid (LA) are abundant in atherosclerotic plaque and activate PPARγ and GPR132. We investigated the mechanisms through which HODEs regulate apoptosis. The effect of HODEs on THP-1 monocytes and adherent THP-1 cells were compared with other C18 fatty acids, LA and α-linolenic acid (ALA). The number of cells was reduced within 24 hours following treatment with 9-HODE (p < 0.01, 30 μM) and 13 HODE (p < 0.01, 30 μM), and the equivalent cell viability was also decreased (p < 0.001). Both 9-HODE and 13-HODE (but not LA or ALA) markedly increased caspase-3/7 activity (p < 0.001) in both monocytes and adherent THP-1 cells, with 9-HODE the more potent. In addition, 9-HODE and 13-HODE both increased Annexin-V labelling of cells (p < 0.001). There was no effect of LA, ALA, or the PPARγ agonist rosiglitazone (1 μM), but the effect of HODEs was replicated with apoptosis-inducer camptothecin (10 μM). Only 9-HODE increased DNA fragmentation. The pro-apoptotic effect of HODEs was blocked by the caspase inhibitor DEVD-CHO. The PPARγ antagonist T0070907 further increased apoptosis, suggestive of the PPARγ-regulated apoptotic effects induced by 9-HODE. The use of siRNA for GPR132 showed no evidence that the effect of HODEs was mediated through this receptor. 9-HODE and 13-HODE are potent--and specific--regulators of apoptosis in THP-1 cells. Their action is PPARγ-dependent and independent of GPR132. Further studies to identify the signalling pathways through which HODEs increase apoptosis in macrophages may reveal novel therapeutic targets for atherosclerosis.
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