Design, implementation and evaluation of a new core learning objectives curriculum for a urology clerkship.

PURPOSE: Until recently, medical students at the University of Wisconsin School of Medicine and Public Health participated in a traditional 2-week urology clerkship. We hypothesized that a new curriculum with core learning objectives and student oriented didactic sessions would increase learning and satisfaction compared to a traditional clerkship. MATERIALS AND METHODS: Between July 2008 and June 2009, 55 medical students completed the urology clerkship following the traditional curriculum. Between July 2009 and June 2010, 51 students followed the core learning objectives curriculum. We compared the curriculum outcomes using objective and subjective measures. Overall student participation was 90%, with 95 of 106 students completing both assessment tools. RESULTS: The objective scores of the students following the core learning objectives were higher than those of the students following the traditional curriculum. The t test to evaluate the difference between the 2 curricula was statistically significant (t = 2.845, df = 93, p <0.05). Subjective scores for the core learning objectives group were lower in all but 1 category. Student perception of knowledge attainment for the core learning objectives cohort was higher than that of the traditional cohort, but none of the subjective scores was statistically significant. CONCLUSIONS: This study demonstrated that a core learning objectives curriculum was associated with higher objective test scores compared to a traditional model, suggesting that the core learning objectives curriculum increased student learning compared to the traditional curriculum. However, the core learning objectives cohort did not show greater satisfaction than students following the traditional curriculum.

The time course of glutamate in the synaptic cleft.

The peak concentration and rate of clearance of neurotransmitter from the synaptic cleft are important determinants of synaptic function, yet the neurotransmitter concentration time course is unknown at synapses in the brain. The time course of free glutamate in the cleft was estimated by kinetic analysis of the displacement of a rapidly dissociating competitive antagonist from N-methyl-D-aspartate (NMDA) receptors during synaptic transmission. Glutamate peaked at 1.1 millimolar and decayed with a time constant of 1.2 milliseconds at cultured hippocampal synapses. This time course implies that transmitter saturates postsynaptic NMDA receptors. However, glutamate dissociates much more rapidly from alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Thus, the time course of free glutamate predicts that dissociation contributes to the decay of the AMPA receptor-mediated postsynaptic current.

Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons.

The modulation of Ca2+ currents by the excitatory neurotransmitter glutamate and its analogs was investigated in hippocampal neurons in culture. In the presence of glutamate receptor-gated ion channel antagonists, all of the analogs tested caused either a small reversible depression or had no effect on the Ca2+ current. However, in neurons dialyzed with GTP gamma S, quisqualate and glutamate but not NMDA, kainate, AMPA, or L-APB caused marked and irreversible depressions of the Ca2+ current. This inhibition was only observed if Ca2+ was present in either the internal or external medium. Intracellular H-7, staurosporine, IP3, cAMP, cGMP, or calmodulin inhibitors failed to prevent the quisqualate-induced Ca2+ current inhibition. These observations are consistent with an interaction between a G protein-coupled glutamate receptor and Ca2+ channels.

Synaptic excitation mediated by glutamate-gated ion channels.

Excitatory synaptic transmission in the central nervous system relies predominantly on stimulation of L-glutamate-gated ion channels in postsynaptic membranes. Activation of these channels not only mediates millisecond to millisecond signalling but can also have long term influences on synaptogenesis and synaptic plasticity. Recent work has resolved some longstanding problems involving the identity of the transmitter, the postsynaptic localization of the receptor subtypes, and the time course of the transmitter in the synaptic cleft.

Upregulation of surface alpha4beta2 nicotinic receptors is initiated by receptor desensitization after chronic exposure to nicotine.

It is hypothesized that desensitization of neuronal nicotinic acetylcholine receptors (nAChRs) induced by chronic exposure to nicotine initiates upregulation of nAChR number. To test this hypothesis directly, oocytes expressing alpha4beta2 receptors were chronically incubated (24-48 hr) in nicotine, and the resulting changes in specific [3H]nicotine binding to surface receptors on intact oocytes were compared with functional receptor desensitization. Four lines of evidence strongly support the hypothesis. (1) The half-maximal nicotine concentration necessary to produce desensitization (9.7 nM) was the same as that needed to induce upregulation (9.9 nM). (2) The concentration of [3H]nicotine for half-maximal binding to surface nAChRs on intact oocytes was also similar (11.1 nM), as predicted from cyclical desensitization models. (3) Functional desensitization of alpha3beta4 receptors required 10-fold higher nicotine concentrations, and this was mirrored by a 10-fold shift in concentrations necessary for upregulation. (4) Mutant alpha4beta2 receptors that do not recover fully from desensitization, but not wild-type channels, were upregulated after acute (1 hr) applications of nicotine. Interestingly, the nicotine concentration required for half-maximal binding of alpha4beta2 receptors in total cell membrane homogenates was 20-fold lower than that measured for surface nAChRs in intact oocytes. These data suggest that cell homogenate binding assays may not accurately reflect the in vivo desensitization affinity of surface nAChRs and may account for some of the previously reported differences in the efficacy of nicotine for inducing nAChR desensitization and upregulation.

Time-dependent changes in central nicotinic acetylcholine channel kinetics in excised patches.

The behavior of nicotinic acetylcholine receptor (nAChR) channels in acutely isolated habenula neurons was examined by rapidly applying nicotinic agonists to outside-out membrane patches. At negative membrane potentials, applications of 100 microM nicotine routinely produced macroscopic currents due to the opening of a large number of channels. During the continuous application of the agonist, the number of open nAChR channels decreased exponentially, i.e. receptor desensitization. A progressive loss in the number of channels contributing to the peak current was observed with time following outside-out patch excision, i.e. receptor rundown. In addition to rundown there was a time-dependent increase in the rate of desensitization and a concomitant slowing in the rate of recovery from desensitization. The extent of rundown and the changes in desensitization were coupled to the time after patch excision and were not dependent on ligand activation of nicotinic channels.

Nicotinic acetylcholine receptor subunit mRNA expression and channel function in medial habenula neurons.

Relationships between nicotinic acetylcholine receptor (nAChR) channel function and nAChR subunit mRNA expression were explored in acutely isolated rat medial habenula (MHb) neurons using a combination of whole-cell recording and single cell RT-PCR techniques. Following amplification using subunit-specific primers, subunits could be categorized in one of three ways: (i) present in 95-100% cells: alpha3, alpha4, alpha5, beta2 and beta4; (ii) never present: alpha2; and (iii) sometimes present ( approximately 40% cells): alpha6, alpha7 and beta3. These data imply that alpha2 subunits do not participate in nAChRs on MHb cells, that alpha6, alpha7 and beta3 subunits are not necessary for functional channels but may contribute in some cells, and that nAChRs may require combinations of all or subsets of alpha3, alpha4, alpha5, beta2 and beta4 subunits. Little difference in the patterns of subunit expression between nicotine-sensitive and insensitive cells were revealed based on this qualitative analysis, implying that gene transcription per se may be an insufficient determinant of nAChR channel function. Normalization of nAChR subunit levels to the amount of actin mRNA, however, revealed that cells with functional channels were associated with high levels (>0.78 relative to actin; 11/12 cells) of all of the category (i) subunits: alpha3, alpha4, alpha5, beta2 and beta4. Conversely, one or more of these subunits was always low (<0.40 relative to actin) in all cells with no detectable response to nicotine. Thus the formation of functional nAChR channels on MHb cells may require critical levels of several subunit mRNAs.

Alpha3beta4 subunit-containing nicotinic receptors dominate function in rat medial habenula neurons.

Regional-specific differences in nicotinic acetylcholine receptors (nAChRs) were examined using the whole-cell patch clamp technique in rat medial habenula (MHb) slices. The majority of cells in the ventral two thirds of the MHb responded robustly to local pressure application of nAChR agonists. Mean agonist potency profiles in the middle and ventral thirds of the MHb were similar: cytisine was the most potent agonist and DMPP the weakest, consistent with a significant contribution of the beta4 subunit to functional nAChRs in all areas of the MHb. In acutely isolated MHb neurons, the alpha3beta4-selective toxin alpha-CTx-AuIB (1 microM) reversibly blocked approximately 75% of the nicotine-induced currents, as expected for cells solely expressing alpha3beta4 nAChRs. However, the alpha3beta2-selective toxin, alpha-CTx-MII (100 nM), blocked a variable fraction (0-90%) of the MHb nicotinic response implying that beta2 subunits may contribute to some functional receptors. We suggest that the effects of alpha-CTx-MII may arise from interaction with alpha3beta2beta4 subunit-containing nAChRs. This idea is supported by the findings (1) that alpha-CTx-MII antagonizes receptors comprised of alpha3, beta2 and beta4 subunits in Xenopus oocytes, and (2) that a mutant alpha-CTx-MII toxin[H12A], which blocks alpha3beta2beta4 receptors but not alpha3beta2 or alpha3beta4 nAChRs, also reduces nicotinic currents in some MHb neurons. Overall these data imply that most functional nAChRs on MHb cells contain at least alpha3 and beta4 subunits, and that a variable subpopulation additionally contains the beta2 subunit.

Symposium overview: mechanism of action of nicotine on neuronal acetylcholine receptors, from molecule to behavior.

Nicotine has long been known to interact with nicotinic acetylcholine (ACh) receptors since Langley used it extensively to chart sympathetic ganglia a century ago. It has also been used as an effective insecticide. However, it was not until the 1990s that the significance of nicotine was increasingly recognized from the toxicological, pharmacological, and environmental points of view. This is partly because studies of neuronal nicotinic ACh receptors are rapidly emerging from orphan status, fueled by several lines of research. Since Alzheimer's disease is known to be associated with down-regulation of cholinergic activity in the brain, a variety of nicotine derivatives are being tested and developed for treatment of the disease. Public awareness of the adverse effects of nicotine has reached the highest level recently. Since insect resistance to insecticides is one of the most serious issues in the pest-control arena, it is an urgent requirement to develop new insecticides that act on target sites not shared by the existing insecticides. The neuronal nicotinic ACh receptor is one of them, and new nicotinoids are being developed. Thus, the time is ripe to discuss the mechanism of action of nicotine from a variety of angles, including the molecular, physiological, and behavioral points of view. This Symposium covered a wide area of nicotine studies: genetic, genomic, and functional aspects of nicotinic ACh receptors were studied, as related to anthelmintics and insecticides; interactions between ethanol and nicotine out the ACh receptor were analyzed, in an attempt to explain the well-known heavy drinker-heavy smoker correlation; the mechanisms that underlie the desensitization of ACh receptors were studied as related to nicotine action; selective pharmacological profiles of nicotine, and descriptions of some derivatives were described; and chronic nicotine infusion effects on memory were examined using animal models.

Ketamine blocks an NMDA receptor-mediated component of synaptic transmission in rat hippocampus in a voltage-dependent manner.

We have examined the voltage dependence of the effects of ketamine on synaptic currents in hippocampal CA1 neurons in vitro under conditions where there is a large N-methyl-D-aspartate (NMDA) receptor mediated component of the response. Ketamine reduced inward currents to a greater extent than outward currents of a corresponding size. D-2-Amino-5-phosphonovalerate (APV) substantially reduced the residual outward currents recorded in ketamine, but had only a small effect on the residual inward ones. It is concluded that in this system the action of ketamine in blocking synaptically evoked NMDA receptor-mediated currents shows some voltage dependence.

Intracellular demonstration of an N-methyl-D-aspartate receptor mediated component of synaptic transmission in the rat hippocampus.

Rat hippocampal CA1 pyramidal neurones were monosynaptically activated via stimulation of the Schaffer collateral-commissural pathway. On changing from a 1 mM Mg2+-containing to a Mg2+-free medium there was a pronounced prolongation of the intracellularly recorded excitatory postsynaptic potential. This effect was reversibly abolished by the selective N-methyl-D-aspartate (NMDA) antagonist, D-2-amino-5-phosphonovalerate (APV). We propose that Mg2+ normally prevents expression of NMDA receptor-mediated responses during low-frequency stimulation. During a period of tetanic stimulation, however, cells may depolarize sufficiently to allow a significant NMDA component of the response to be manifest. This could then initiate long-term potentiation.

Optical properties of poly(2,6-dimethyl-1,4-phenylene oxide) film and its potential for a long-term solar ultraviolet dosimeter.

The optical properties of poly(2,6-dimethyl-1,4-phenylene oxide) (PPO) film have been characterized in order to develop an alternative method for UV dosimetry with a focus on long-term human exposure measurements. The dynamic range of PPO film was found to extend to 2 MJ m(-2) of broadband UV exposure independently of film thickness, providing an exposure range of roughly four summer days at subtropical latitudes. The sensitivity of the film to UV exposure was positively related to film thickness in the 20-40 microm range. Films of 40 microm thickness proved to be the most suitable for long-term human UV exposure measurements. The temperature independence of the response of 40 microm PPO film was established from 1.5 degrees C to 50 degrees C within a dosimeter response uncertainty of 6.5%. Dose-rate independence was also demonstrated within 8% of the mean dosimeter response. The spectral response approximates the CIE erythemal action spectrum between 300 and 340 nm, with a peak response at 305 nm. A large deviation from this action spectrum was observed at shorter wavelengths. Investigation of the angular response in both the azimuth and altitude planes showed a cosine error of less than 6.2% between 0 degrees and 40 degrees, and did not exceed 13.3% at any angle greater than 40 degrees. These results indicate that PPO film satisfies the requirements for use as a UV dosimeter, and may be employed in long-term human exposure measurements.

Acetylcholine receptor desensitization induced by nicotine in rat medial habenula neurons.

1. The activation and desensitization properties of nicotinic acetylcholine receptor (nAChR) channels were examined in acutely isolated medial habenula (MHb) neurons using whole cell patch-clamp recordings. nAChR-mediated currents were evoked by applying known concentrations of nicotinic agonists using rapid solution exchange techniques. 2. At a membrane potential of -60 mV, nAChR currents were observed above a concentration of approximately 100 mM nicotine. The peak current amplitude at low doses of agonist was proportional to the square of the concentration of nicotine, indicating that at least two molecules of agonist were required for channel opening. The concentration of nicotine required for half-maximal nAChR activation was estimated as 77 microM from a complete concentration-response curve. 3. During the continuous activation (2-5 s) of nAChRs by high concentrations of nicotine (300 microM), the current desensitized rapidly and extensively. The desensitization phase was described by the sum of two exponentials, with time constants of 210 and 1,435 ms. The fast component comprised 74% of the desensitizing phase of the current. Recovery from desensitization induced by 2- s applications of 300 microM nicotine was also fast and could be reasonably well described by a single exponential with a time constant of approximately 800 ms. Both the time courses of desensitization and recovery from desensitization were slightly slower at positive membrane potentials. 4. Incubation of neurons with low concentrations of nicotine (100 nM-10 microM) caused a slowly developing but pronounced desensitization of the nAChRs. In these cases desensitization was assessed from the reduction in the amplitude of the peak nicotinic current induced by repetitively applied pulses of a higher test concentration of agonist. A 5-min continuous exposure to 1 microM nicotine reduced the amplitude of the acetylcholine (30 microM, 1 s) test response to < 30% of its control value. As with higher concentrations of nicotine, the onset of the desensitization induced by 1 microM nicotine was biexponential, with fast and slow time constants of 15 s and 1.74 min, respectively. Recovery from the desensitization induced by these longer applications of nicotine was much slower than that observed with the brief pulses of high concentrations of nicotine. The concentration required for half-maximal desensitization after a 5-min incubation was approximately 300 nM. 5. Peak nAChR currents were approximately 85% smaller at +40 mV compared with -40 mV. The receptors that do not open at positive potentials desensitize almost as well as they would at negative potentials after channel opening.(ABSTRACT TRUNCATED AT 400 WORDS)

Improving pneumococcal vaccination coverage among older people in Victoria.

Although pneumococcal vaccine is recommended by the National Health and Medical Research Council and is cost-effective in preventing invasive pneumococcal disease, it is the only vaccine on the standard schedule that is not nationally funded through public health grants to the States. In Victoria, the Department of Human Services has provided free pneumococcal vaccine to people aged 65 years and over since 1998. Pneumococcal vaccination was given in conjunction with the annual influenza vaccination program; 28.5% of the eligible cohort (95% CI, 24.8%-32.1%) received pneumococcal vaccine in 1998, giving an estimated cumulative coverage of 42% (13.4% had received it in 1997). We expect coverage will continue to increase over time, but revaccination every five years will present a substantial financial burden; access to vaccine is critical to improving coverage. Our experience in Victoria suggests that a nationally funded program, administered similarly to the influenza vaccination program, would dramatically increase pneumococcal vaccination coverage at a national level.

NMDA channel behavior depends on agonist affinity.

We have compared the kinetic properties of NMDA receptor channels activated by exogenous agonists with those activated synaptically. Short (4 msec) applications of L-glutamate to outside-out patches from hippocampal neurons evoked currents that decayed with a double exponential time course that was controlled by both the unbinding rate of agonist and receptor desensitization. Lower-affinity agonists evoked NMDA receptor-activated currents that had faster rates of decay and recovered from desensitization more quickly, consistent with the idea that agonists which dissociate faster allow the receptor to reach a desensitized state less often. Both synaptic and patch responses could be well fitted with a simple kinetic model comprised of two independent but identical binding sites, one open state, one closed state, and one desensitized state, all doubly liganded. Provided that the agonist has a slow unbinding rate relative to the rates into the open and desensitized states (e.g., L-glutamate), this model predicts a response with two decay phases and can thus account for the synaptic response. Since the unbinding rate is the critical determinant of the time course, different affinity transmitters would affect such properties as excitatory postsynaptic current (EPSC) duration. Of the known endogenous excitatory amino acids, only L-glutamate has an affinity for the NMDA receptor consistent with the time course of the EPSC recorded between hippocampal neurons in culture.

Spectral ultraviolet albedo of roofing surfaces and human facial exposure.

Spectral field measurements were used to quantify the ultraviolet (UV) spectral albedos of four different metallic roofing surfaces. The effect of the albedos of two of these surfaces on erythemal exposure to human facial anatomical sites was quantified by UV dosimetry. The albedos of all roofing surfaces were greater than the albedo of grass. Little SZA dependence was observed for any of the surfaces. The albedos of the coloured metallic corrugated surfaces were strongly dependent on wavelength in the UVA, increasing from 3 to 12%. Facial erythemal measurements showed significant exposure enhancements over the galvanised corrugated surface compared to grass. The undersides of the chin and nose received exposure enhancements over the galvanised corrugated surface of about 1290 and 190%, respectively, of the exposure of these sites over grass. It is concluded that the albedo of the galvanised surfaces are higher than those of the coloured surfaces by at least 20%, and higher than grass by at least 27%. Consequently, normally shaded facial anatomical sites receive substantially higher UV exposures over these galvanised surfaces compared to grass.

Synaptic activation of N-methyl-D-aspartate receptors in the Schaffer collateral-commissural pathway of rat hippocampus.

1. The involvement of N-methyl-D-aspartate (NMDA) receptors in the response to single-shock (0.033 Hz) stimulation of the Schaffer collateral-commissural pathway in hippocampal slices has been investigated using current- and voltage-clamp techniques. 2. In the presence of Mg2+ (1 or 2 mM) at membrane potentials near rest, the selective NMDA antagonist D-2-amino-5-phosphonovalerate (APV) had no effect on the excitatory postsynaptic potential (EPSP) and the biphasic inhibitory postsynaptic potential (IPSP) evoked by Schaffer collateral-commissural stimulation. The recurrent IPSP evoked by antidromic stimulation of alvear fibres was also unaffected by APV. 3. The introduction of a Mg2+-free perfusate led, at high stimulus intensity, to an orthodromically evoked epileptiform discharge but little change in the recurrent IPSP. APV suppressed a large proportion of the enhanced response in Mg2+-free perfusate. 4. EPSPs and excitatory postsynaptic currents (EPSCs) evoked in Mg2+-free perfusate invariably had both APV-resistant and APV-sensitive components. Both synaptic components had similar thresholds and latencies to onset. The APV-sensitive component had a long time to peak and long duration. 5. Under current-clamp conditions in Mg2+-containing medium, an APV-sensitive component was recorded at membrane potentials of between -30 and -10 mV, but not at potentials more negative than -55 mV. 6. Under voltage-clamp, but not current-clamp, conditions in Mg2+-containing medium, a small APV-sensitive component was recorded at resting membrane potentials and increased with membrane depolarization. The difference between the current- and voltage-clamp data is attributed to the hyperpolarizing influence of conjointly activated IPSPs. 7. In the presence of Mg2+ and picrotoxin, a dual-component EPSC was recorded between -30 and +30 mV in all cells examined. The APV-resistant and APV-sensitive components had similar latencies to onset. They both had reversal potentials of between -8 and 0 mV. The APV-sensitive component had a longer latency to peak and duration than the APV-resistant component. 8. It is suggested that NMDA receptors can contribute a low-threshold and long-duration monosynaptic component of the response evoked by low-frequency stimulation of the Schaffer collateral-commissural pathway. However, under physiological conditions significant expression of this component is prevented by concurrently activated IPSPs which rapidly hyperpolarize neurones into a region where Mg2+ substantially blocks NMDA channels.

Frequency-dependent N-methyl-D-aspartate receptor-mediated synaptic transmission in rat hippocampus.

1. The effects of the N-methyl-D-aspartate (NMDA) antagonist, D-2-amino-5-phosphonovalerate (APV) were examined on synaptic responses evoked by high-frequency stimulation of the Schaffer collateral-commissural pathway, in the presence of Mg2+ (1 or 2 mM) and functional synaptic inhibition. 2. The synaptic response evoked by 100 Hz stimulation comprised fast excitatory postsynaptic potentials (EPSPs) evoked by each shock and a slow depolarization. APV reduced the size of the depolarization without depressing the fast EPSPs. 3. The mean (+/- 1 S.E.) amplitude of the APV-sensitive component (3.0 +/- 0.3 mV), evoked by 100 Hz stimulation at membrane potentials near rest, was invariably smaller than the first fast EPSP (9.8 +/- 0.7 mV). Both of these synaptic components had similar thresholds and increased in amplitude as the stimulus intensity was raised. There was a positive correlation between the amplitude of the two components (r = 0.57, P less than 0.01). 4. The amplitude of the APV-sensitive component was positively correlated (r = 0.97, P less than 0.05) with the frequency of stimulation during the trains (between 10 and 100 Hz). The threshold frequency for evoking an APV-sensitive component was approximately 10 Hz. 5. In contrast to the fast EPSPs the amplitude of the APV-sensitive component increased with depolarization, and decreased with hyperpolarization, of a neurone from its resting membrane potential. The component was no longer present in some cells which had been hyperpolarized sufficiently. 6. It is suggested that during high-frequency stimulation a neurone may become depolarized for a sufficient time to reduce the Mg2+ block of NMDA channels. This enables the NMDA receptor system to contribute transiently to the synaptic response, despite the inhibitory synaptic mechanisms which prevent its activation during single-shock stimulation. The characteristics of the NMDA receptor-mediated synaptic response may explain properties relating to the induction of long-term potentiation (LTP).

Home vaccination for children behind in their immunisation schedule: a randomised controlled trial.

OBJECTIVE: To ascertain the effectiveness of a home vaccination service for children behind in their vaccination schedule. DESIGN: Randomised controlled trial of nurse-administered vaccination at home. Children were allocated at random to the intervention or the control group before any contact with the parents was made. SETTING: 10 council areas in north-west metropolitan Melbourne defined by 56 postcode zones. Six-week intervention period from November 1996. PARTICIPANTS: 405 children--all those in the study area (n = 2610) 90 days late (age 9 months) for their third diphtheria-tetanus-pertussis/poliomyelitis/Haemophilus influenzae type B (DTP/OPV/Hib) vaccination, or 120 days late (age 16 months) for their measles-mumps-rubella (MMR) vaccination, according to the Australia Childhood Immunisation Register. MAIN OUTCOME MEASURES: Number of children completing DTP/OPV/Hib or MMR during the intervention period, and number up to date before intervention. RESULTS: Verification of vaccination status with the parents revealed that 123 (60%) of the children in the intervention group and 113 (56%) of those in the control group were up to date with their vaccinations, leaving a study population of 81 (intervention group) and 88 (control group). Vaccination was achieved in 46 (57%) intervention children and 24 (27%) control children (risk ratio [RR], 2.08; 95% CI, 1.4-3.1; P < 0.001). For DTP/OPV/Hib, 18/32 (56%) intervention children and 12/36 (33%) control children were vaccinated, (P = 0.06). For MMR, 28/49 (57%) and 12/52 (23%) children were vaccinated, respectively (P < 0.001). Home vaccinations were completed with 26 families (including five siblings). The average cost per child vaccinated as a result of the home program was $92.52. CONCLUSION: Home vaccination for children behind in their immunisation schedule is an effective, acceptable and relatively cheap method of completing recommended vaccinations. We recommend that a home vaccination program be widely implemented and made available, particularly for disadvantaged families.