Contemporary issues in dental education in Australia

Australia has witnessed a proliferation of dental workforce training opportunities over the last 15 years, including dentists, dental therapists, dental hygienists and prosthetists. The reasons for this have not been examined critically. Universities have welcomed the opportunities to increase the student base but do not seem to have examined the advisability of continued expansion or its impact on the delivery and costs of health services. Nor have they enquired expressly whether they have any responsibility in these matters. Public health benefits should constitute a significant element of curriculum design. There seems to have been a general acceptance of the premise that more is necessarily better. Ironically, these developments have occurred in the face of significant recurrent cost increments and serious academic staff shortages. The schools have responded with alterations to curriculum content. Student cohort composition, course structures, educational focus, postgraduate training and research have been affected. The primary purpose of this review is to highlight the issues which currently drive workforce training and curriculum content and to suggest that some current practices should be re-examined as a starting point for setting defined common objectives within the Australian dental educational spectrum. Salient issues which require examination include course standards and accreditation, workforce mix, dental health demands, public service obligations and staffing profiles.     

Interaction between blood type,smoking and factor V Leiden mutation and risk of venous thromboembolism: a Danish case‐cohort study

See also Lowe GDO. Epidemiology of venous thromboembolism: the need for large (including prospective) studies and meta‐analyses. This issue, pp 2186–8 and Rosendaal FR. Etiology of venous thrombosis: the need for small original studies. This issue, pp 2189–90.     

A School-Based,Family-Centered Intervention to Prevent Substance Use: The Family Check-Up

Background/Objectives: The Family Check-Up (FCU) is a selected intervention model that can be delivered in contexts such as schools that serve at-risk children and families. It is grounded in developmental theory and targets salient risk factors for the development of later problem behavior such as substance use, family management deficits, deviant peer affiliations, and problem behavior at school. Methods: The FCU model has been implemented in schools across several randomized trials. The model includes the development of a family resource center in the schools and interventions that target youth at risk for problem behavior and substance use. Results: Twenty years of research associated with the FCU have produced outcomes that show that the model is effective for enhancing family management skills, reducing risk behavior, and reducing the long-term risk for substance use in adolescence. Conclusions and Scientific Significance: Implications for public policy and the delivery of interventions to prevent substance use in public schools and communities are discussed.     

Recombinant human megakaryocyte growth and development factor stimulates thrombocytopoiesis in normal nonhuman primates

Megakaryocyte growth and development factor (MGDF) is a novel cytokine that binds to the c-mpl receptor and stimulates megakaryocyte development in vitro and in vivo. This report describes the ability of recombinant human (r-Hu) MGDF to affect megakaryocytopoiesis in normal nonhuman primates. r-HuMGDF was administered subcutaneously to normal, male rhesus monkeys once per day for 10 consecutive days at dosages of 2.5, 25, or 250 micrograms/kg of body weight. Bone marrow and peripheral blood were assayed for clonogenic activity and peripheral blood counts were monitored. Circulating platelet counts increased significantly (P < .05) for all doses within 6 days of r-HuMGDF administration and reached maximal levels between day 12 and day 14 postcytokine administration. The 2.5, 25.0, and 250.0 micrograms/kg/d doses elicited peak mean platelet counts that were 592%, 670%, and 449% of baseline, respectively. Bone marrow-derived clonogenic data showed significant increases in the concentration of megakaryocyte (MEG)- colony-forming unit (CFU) and granulocyte-erythroid-macrophage- megakaryocyte (GEMM)-CFU, whereas that of granulocyte-macrophage (GM)- CFU and burst-forming unit-erythroid (BFU-e) remained unchanged during the administration of r-HuMGDF. These data show that r-HuMGDF is a potent stimulator of thrombocytopoiesis in the normal nonhuman primate.     

Expression of CD27 and its ligand, CD70, on chronic lymphocytic leukemia B cells

Crosslinking the CD27 antigen on T cells provides a costimulatory signal that, in concert with T-cell receptor crosslinking, can induce T- cell proliferation and cellular immune activation. We find that chronic lymphocytic leukemia (CLL) B cells from most patients coexpress both membrane-bound and soluble CD27, along with its newly identified ligand, CD70. The expression of soluble CD27 may preclude leukemic B cells from stimulating T cells via CD70, thereby potentially impairing their ability to function as effective antigen-presenting cells. We find that leukemic B-cell expression of soluble and membrane-bound CD27 can be downmodulated through a CD40-dependent signal. This signal also induces enhanced expression of CD70 on both normal and leukemic B cells. We find that tumor necrosis factor (TNF)-alpha, or the Th1 cytokine interferon (IFN)-gamma, also can induce downmodulation of CD27, whereas Th2-associated cytokines interleukin-4 (IL-4) or IL-10 can enhance leukemic B-cell expression of this accessory molecule. The modulation of CD27 induced by these conditions is accompanied by reciprocal changes in the expression levels of CD70, suggesting that these accessory molecules may be engaged in reciprocal receptor-ligand downmodulation. Consistent with this, we observe that co-culture of CLL B cells with transfected murine plasmacytoma cells that express human CD70 affects downmodulation of CD27 and enhanced expression of CD70 on leukemic B cells, but does not affect expression of CD27 mRNA. However, we find that CD40-crosslinking, in addition to reducing the level of CD27 protein, also reduces leukemic B-cell expression of CD27 mRNA. This argues that the changes in the expression levels of CD27 following CD40-signaling are not simply due to induced increases in the expression levels of CD70. Finally, we demonstrate that reciprocal changes in expression of CD27 and CD70 may contribute to the enhanced antigen-presenting capacity of CLL B cells after CD40-dependent leukemic B-cell activation. These findings expand the understanding of the regulation of costimulatory molecules important in antigen presentation and also have implications for the immunobiology of and therapy for CLL.