Simulation‐based education (SBE) is a rapidly developing method of supplementing and enhancing the clinical education of medical students. Clinical situations are simulated for teaching and learning purposes, creating opportunities for deliberate practice of new skills without involving real patients. Simulation takes many forms, from simple skills training models to computerised full‐body mannequins, so that the needs of learners at each stage of their education can be targeted. Emerging evidence supports the value of simulation as an educational technique; to be effective it needs to be integrated into the curriculum in a way that promotes transfer of the skills learnt to clinical practice. Currently, SBE initiatives in Australia are fragmented and depend on local enthusiasts; Health Workforce Australia is driving initiatives to develop a more coordinated national approach to optimise the benefits of simulation.

OBJECTIVE-Mutations in the human HNF4A gene encoding the hepatocyte nuclear factor (HNF)-4␣ are known to cause maturity-onset diabetes of the young (MODY), which is characterized by autosomal-dominant inheritance and impaired glucose-stimulated insulin secretion from pancreatic ␤-cells. HNF-4␣ has a key role in regulating the multiple transcriptional factor networks in the islet. Recently, heterozygous mutations in the HNF4A gene were reported to cause transient hyperinsulinemic hypoglycemia associated with macrosomia.RESEARCH DESIGN AND METHODS-Three infants presented with macrosomia and severe hypoglycemia with a positive family history of MODY. The hypoglycemia was confirmed to be due to hyperinsulinism, and all three patients required diazoxide therapy to maintain normoglycemia. Two of the three infants are still requiring diazoxide therapy at 8 and 18 months, whereas one of them had resolution of hyperinsulinemic hypoglycemia at 32 months of age.RESULTS-Sequencing of the HNF4A gene identified heterozygous mutations in all three families. In family 1, a frameshift mutation L330fsdel17ins9 (c.987 1003del17ins9; p.Leu330fs) was present in the proband; a mutation affecting the conserved A nucleotide of the intron 2 branch site (c.264 -21AϾG) was identified in the proband of family 2; and finally a nonsense mutation, Y16X (c.48CϾG, p.Tyr16X), was found in the proband of family 3. (1,2). HNF-4␣ is a transcription factor of the nuclear hormone receptor superfamily and is expressed in liver, kidney, gut, and pancreatic islets (3). It plays a key role in the regulation of pancreatic insulin secretion. Loss-of-function HNF4A mutations have been identified in maturity-onset diabetes of the young (MODY) families in both coding and regulatory regions of the gene, including the P2 promoter region, which is suggested to be the primary transcriptional start site used in ␤-cells (4,5). MODY is characterized by an autosomal-dominant inheritance pattern and impaired glucose-stimulated insulin secretion from pancreatic ␤-cells (4). CONCLUSIONS-HeterozygousThe finding of transient mild hyperinsulinemic hypoglycemia is unexpected, since heterozygous mutations in the HNF4A gene lead to loss of glucose-induced insulin secretion with glucose intolerance in these patients. We now extend the observations of two previous studies (1,2) and report that heterozygous HNF4A mutations can cause macrosomia with severe and persistent hyperinsulinemic hypoglycemia as well as MODY in three families. RESEARCH DESIGN AND METHODSPatient 1. Patient 1 was born at 39 weeks' gestation with a birth weight of 5.9 kg after a vaginal delivery. The delivery was complicated with a prolonged second stage and shoulder dystocia. After delivery, the baby developed severe symptomatic hypoglycemia (jitteriness and irritability with a blood glucose concentration of 0.8 mmol/l). He required a continuous infusion of 25% dextrose delivering 25 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 glucose, as well as an infusion of glucagon to maintain normoglycemia. Biochemical analysis showed an in...

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Tight glycaemic control reduces the risk of development and progression of organ complications in people with type 1 or type 2 diabetes. In this position statement, the Australian Diabetes Society recommends a general target glycated haemoglobin (HbA1c) level of ≤ 7.0% for most patients. This position statement also provides guidelines for the individualisation of glycaemic targets to a tighter or lesser degree, with a recommended target HbA1c level of ≤ 6.0% in some people, or up to ≤ 8.0% in others. Individualisation of the HbA1c target is based on patient‐specific factors, such as the type of diabetes and its duration, pregnancy, diabetes medication being taken, presence of cardiovascular disease, risk of and problems from hypoglycaemia, and comorbidities. Management of diabetes also includes: adequate control of other cardiovascular risk factors, including weight, blood pressure and lipid serum levels; antiplatelet therapy; and smoking cessation.