The economics of awards, status and performance: the John Bates Clark Medal and the Fellowship of the Econometric Society

This thesis investigates whether receiving an important award in academia raises recipients’ subsequent research productivity and status compared to a synthetic control group of non-recipient scholars with similar previous research performance. It examines the case of being awarded the John Bates Clark Medal and becoming a Fellow of the Econometric Society finding evidence of positive incentive and status effects that raise both productivity and citation levels.

Directing democracy : competing interests and contested terrain in the John Lewis Partnership

The John Lewis Partnership is one of Europe’s largest models of employee ownership and has been operating a form of employee involvement and participation since its formation in 1929. It is frequently held up as a model of best practice (Cathcart, 2013) and has been described as a ‘workers’ paradise’ (Stummer and Lacey, 2001). At the beginning of 2012, the Deputy Prime Minister of the UK unveiled plans to create a ‘John Lewis Economy’ (Wintour, 2012). As John Lewis is being positioned at the heart of political and media discussions in the UK about alternatives to the corporate capitalist model of enterprise, it is vital that more is known about the experience of employee involvement and participation within the organisation. This article explores the ways in which the practice of employee involvement and participation has changed in John Lewis as a result of competing employee and managerial interests. Its contribution is a contemporary exploration of participation in the John Lewis Partnership and an examination of the ways in which management and employees contested the meaning and practice of employee involvement and participation as part of a ‘democracy project’, which culminated in significant changes and degeneration of the democratic structures.

The John Lewis model reveals the tensions and paradoxes at the heart of workplace democracy

Politicians of all parties have been keen to promote the ‘John Lewis model’ of industrial organisation, emphasising its features of employee ownership and workplace democracy. Dr Abby Cathcart’s research into the company shows that management and workers have different visions of what ‘partnership’ means, with ongoing struggle taking place via the organisation’s democratic structures. This, she argues, has stark implications for other organisations with partnership models that are less robust.

Repeated intrauterine exposures to inflammatory stimuli attenuated transforming growth factor-β signaling in the ovine fetal lung

Background: Bronchopulmonary dysplasia (BPD) is one of the most common complications after preterm birth and is associated with intrauterine exposure to bacteria. Transforming growth factor-β (TGFβ) is implicated in the development of BPD. Objectives: We hypothesized that different and/or multiple bacterial signals could elicit divergent TGFβ signaling responses in the developing lung. Methods: Time-mated pregnant Merino ewes received an intra-amniotic injection of lipopolysaccharide (LPS) and/or Ureaplasma parvum serovar 3 (UP) at 117 days' and/or 121/122 days' gestational age (GA). Controls received an equivalent injection of saline and or media. Lambs were euthanized at 124 days' GA (term = 150 days' GA). TGFβ1, TGFβ2, TGFβ3, TGFβ receptor (R)1 and TGFβR2 protein levels, Smad2 phosphorylation and elastin deposition were evaluated in lung tissue. Results: Total TGFβ1 and TGFβ2 decreased by 24 and 51% after combined UP+LPS exposure, whereas total TGFβ1 increased by 31% after 7 days' LPS exposure but not after double exposures. Alveolar expression of TGFβR2 decreased 75% after UP, but remained unaltered after double exposures. Decreased focal elastin deposition after single LPS exposure was prevented by double exposures. Conclusions: TGFβ signaling components and elastin responded differently to intrauterine LPS and UP exposure. Multiple bacterial exposures attenuated TGFβ signaling and normalized elastin deposition.

Review : "Ghosts...of the Civil Dead" -- John Hillcoat

Synopsis and review of the Australian prison film Ghosts...of the Civil Dead (John Hillcoat, 1988). Drawing heavily from the book In the Belly of the Beast by American author and long-term prisoner Jack Henry Abbott, as well as from the historical and philosophical work of Michel Foucault (the credits include ‘Foucault Authority – Simon During’), Ghosts… Of the Civil Dead is a searing critique of the so-called ‘new generation’ prison system developed in the United States and recently introduced in Australia. Director John Hillcoat and producer Evan English conducted extensive research for the film, including spending time at the National Institute of Corrections, a think tank in Colorado, and visiting numerous institutions like the ‘new Alcatraz’ at Marion Illinois and other maximum security prisons across the United States. Using a mix of professionals and non-actors, including former prisoners and prison guards, the ‘story’ was workshopped during a lengthy rehearsal period with many actual events and experiences of participants incorporated into the film. The end result deliberately blurs the line between American and Australian prison experience to make the political point that what had happened in the US – from where many events and characters, and much of the architecture and design of the prison are drawn – was beginning to happen in Australia. The film emphasises the vicious cycle of institutionalisation, and highlights the role state authorities play in manufacturing, provoking and manipulating violence and fear both in prisons and in wider society as a means to augment policing and surveillance of the population, to oppress the working classes, and to maintain the political status quo...

Late Oligocene to Middle Miocene rifting and synextensional magmatism in the southwestern Sierra Madre Occidental, Mexico : the beginning of the Gulf of California rift

Although Basin and Range–style extension affected large areas of western Mexico after the Late Eocene, most consider that extension in the Gulf of California region began as subduction waned and ended ca. 14–12.5 Ma. A general consensus also exists in considering Early and Middle Miocene volcanism of the Sierra Madre Occidental and Comondú Group as subduction related, whereas volcanism after ca. 12.5 Ma is extension related. Here we present a new regional geologic study of the eastern Gulf of California margin in the states of Nayarit and Sinaloa, Mexico, backed by 43 new Ar-Ar and U-Pb mineral ages, and geochemical data that document an earlier widespread phase of extension. This extension across the southern and central Gulf Extensional Province began between Late Oligocene and Early Miocene time, but was focused in the region of the future Gulf of California in the Middle Miocene. Late Oligocene to Early Miocene rocks across northern Nayarit and southern Sinaloa were affected by major approximately north-south– to north-northwest– striking normal faults prior to ca. 21 Ma. Between ca. 21 and 11 Ma, a system of north-northwest–south-southeast high angle extensional faults continued extending the southwestern side of the Sierra Madre Occidental. Rhyolitic domes, shallow intrusive bodies, and lesser basalts were emplaced along this extensional belt at 20–17 Ma. Rhyolitic rocks, in particular the domes and lavas, often show strong antecrystic inheritance but only a few Mesozoic or older xenocrysts, suggesting silicic magma generation in the mid-upper crust triggered by an extension induced basaltic infl ux. In northern Sinaloa, large grabens were occupied by huge volcanic dome complexes ca. 21–17 Ma and filled by continental sediments with interlayered basalts dated as 15–14 Ma, a stratigraphy and timing very similar to those found in central Sonora (northeastern Gulf of California margin). Early to Middle Miocene volcanism occurred thus in rift basins, and was likely associated with decompression melting of upper mantle (inducing crustal partial melting) rather than with fluxing by fluids from the young and slow subducting microplates. Along the eastern side of the Gulf of California coast, from Farallón de San Ignacio island offshore Los Mochis, Sinaloa, to San Blas, Nayarit, a strike distance of >700 km, flat lying basaltic lavas dated as ca. 11.5–10 Ma are exposed just above the present sea level. Here crustal thickness is almost half that in the unextended core of the adjacent Sierra Madre Occidental, implying signifi cant lithosphere stretching before ca. 11 Ma. This mafic pulse, with subdued Nb-Ta negative spikes, may be related to the detachment of the lower part of the subducted slab, allowing an upward asthenospheric flow into an upper mantle previously modified by fluid fluxes related to past subduction. Widespread eruption of very uniform oceanic island basalt–like lavas occurred by the late Pliocene and Pleistocene, only 20 m.y. after the onset of rifting and ~9 m.y. after the end of subduction, implying that preexisting subduction-modified mantle had now become isolated from melt source regions. Our study shows that rifting across the southern-central Gulf Extensional Province began much earlier than the Late Miocene and provided a fundamental control on the style and composition of volcanism from at least 30 Ma. We envision a sustained period of lithospheric stretching and magmatism during which the pace and breadth of extension changed ca. 20–18 Ma to be narrower, and again after ca. 12.5 Ma, when the kinematics of rifting became more oblique.

Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate

The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (P < 0.05) with migraine. Two SNPs, rs73532286 and rs6426929, separated by approximately 0.1 kb, displayed complete LD (r 2 = 1.00, D′ = 1.00, D′ 95% CI = 0.96–1.00). In all cases, the minor allele led to a decrease in migraine risk (beta coefficient = 0.286–0.315), suggesting that common gene variants confer an increased risk of migraine in the Norfolk pedigree. This effect may be explained by founder effect in this genetic isolate. This study provides evidence for association of variants in the KCNN3 ion channel gene with migraine susceptibility in the Norfolk genetic isolate with the rarer allelic variants conferring a possible protective role. This the first comprehensive analysis of this potential candidate gene in migraine and also the first study that has utilised the unique Norfolk Island large pedigree isolate to implicate a specific migraine gene. Studies of additional variants in KCNN3 in the Norfolk pedigree are now required (e.g. polyglutamine variants) and further analyses in other population data sets are required to clarify the association of the KCNN3 gene and migraine risk in the general outbred population.

The effects of vitamin supplementation and MTHFR (C677T) genotype on homocysteine-lowering and migraine disability

BACKGROUND: Migraine is a prevalent and debilitating disease that may, in part, arise because of disruption in neurovascular endothelia caused by elevated homocysteine. This study examined the homocysteine-lowering effects of vitamin supplementation on migraine disability, frequency and severity and whether MTHFRC677T genotype influenced treatment response. METHODS: This was a randomized, double-blind placebo, controlled trial of 6 months of daily vitamin supplementation (i.e. 2 mg of folic acid, 25 mg vitamin B6, and 400 microg of vitamin B12) in 52 patients diagnosed with migraine with aura. FINDINGS: Vitamin supplementation reduced homocysteine by 39% (approximately 4 mumol/l) compared with baseline, a reduction that was greater then placebo (P=0.001). Vitamin supplementation also reduced the prevalence of migraine disability from 60% at baseline to 30% after 6 months (P=0.01), whereas no reduction was observed for the placebo group (P>0.1). Headache frequency and pain severity were also reduced (P<0.05), whereas there was no reduction in the placebo group (P>0.1). In this patient group the treatment effect on both homocysteine levels and migraine disability was associated with MTHFRC677T genotype whereby carriers of the C allele experienced a greater response compared with TT genotypes (P<0.05). INTERPRETATION: This study provides some early evidence that lowering homocysteine through vitamin supplementation reduces migraine disability in a subgroup of patients. Larger trials are now warranted to establish whether vitamin therapy is a safe, inexpensive and effective prophylactic option for treatment of migraine and whether efficacy is dependant on MTHFRC677T genotype.

Phenotypical characterisation of the isolated Norfolk Island population focusing on epidemiological indicators of cardiovascular disease

Objectives Only 193 people from Pitcairn Island, all descended from 9 ‘Bounty’ mutineers and 12 Tahitian women, moved to the uninhabited Norfolk Island in 1856. Our objective was to assess the population of Norfolk Island, several thousand km off the eastern coast of Australia, as a genetic isolate of potential use for cardiovascular disease (CVD) gene mapping. Methods A total of 602 participants, approximately two thirds of the island’s present adult population, were characterized for a panel of CVD risk factors. Statistical power and heritability were calculated. Results Norfolk Islander’s possess an increased prevalence of hypertension, obesity and multiple CVD risk factors when compared to outbred Caucasian populations. 64% of the study participants were descendents of the island’s original founder population. Triglycerides, cholesterol, and blood pressures all had heritabilities above 0.2. Conclusions The Norfolk land population is a potentially useful genetic isolate for gene mapping studies aimed at identifying CVD risk factor quantitative trait loci (QTL).

Clinically-indicated replacement versus routine replacement of peripheral venous catheters

BACKGROUND: US Centers for Disease Control guidelines recommend replacement of peripheral intravenous (IV) catheters no more frequently than every 72 to 96 hours. Routine replacement is thought to reduce the risk of phlebitis and bloodstream infection. Catheter insertion is an unpleasant experience for patients and replacement may be unnecessary if the catheter remains functional and there are no signs of inflammation. Costs associated with routine replacement may be considerable. This is an update of a review first published in 2010. OBJECTIVES: To assess the effects of removing peripheral IV catheters when clinically indicated compared with removing and re-siting the catheter routinely. SEARCH METHODS: For this update the Cochrane Peripheral Vascular Diseases (PVD) Group Trials Search Co-ordinator searched the PVD Specialised Register (December 2012) and CENTRAL (2012, Issue 11). We also searched MEDLINE (last searched October 2012) and clinical trials registries. SELECTION CRITERIA: Randomised controlled trials that compared routine removal of peripheral IV catheters with removal only when clinically indicated in hospitalised or community dwelling patients receiving continuous or intermittent infusions. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted data. MAIN RESULTS: Seven trials with a total of 4895 patients were included in the review. Catheter-related bloodstream infection (CRBSI) was assessed in five trials (4806 patients). There was no significant between group difference in the CRBSI rate (clinically-indicated 1/2365; routine change 2/2441). The risk ratio (RR) was 0.61 but the confidence interval (CI) was wide, creating uncertainty around the estimate (95% CI 0.08 to 4.68; P = 0.64). No difference in phlebitis rates was found whether catheters were changed according to clinical indications or routinely (clinically-indicated 186/2365; 3-day change 166/2441; RR 1.14, 95% CI 0.93 to 1.39). This result was unaffected by whether infusion through the catheter was continuous or intermittent. We also analysed the data by number of device days and again no differences between groups were observed (RR 1.03, 95% CI 0.84 to 1.27; P = 0.75). One trial assessed all-cause bloodstream infection. There was no difference in this outcome between the two groups (clinically-indicated 4/1593 (0.02%); routine change 9/1690 (0.05%); P = 0.21). Cannulation costs were lower by approximately AUD 7.00 in the clinically-indicated group (mean difference (MD) -6.96, 95% CI -9.05 to -4.86; P ≤ 0.00001). AUTHORS' CONCLUSIONS: The review found no evidence to support changing catheters every 72 to 96 hours. Consequently, healthcare organisations may consider changing to a policy whereby catheters are changed only if clinically indicated. This would provide significant cost savings and would spare patients the unnecessary pain of routine re-sites in the absence of clinical indications. To minimise peripheral catheter-related complications, the insertion site should be inspected at each shift change and the catheter removed if signs of inflammation, infiltration, or blockage are present. OBJECTIVES: To assess the effects of removing peripheral IV catheters when clinically indicated compared with removing and re-siting the catheter routinely. SEARCH METHODS: For this update the Cochrane Peripheral Vascular Diseases (PVD) Group Trials Search Co-ordinator searched the PVD Specialised Register (December 2012) and CENTRAL (2012, Issue 11). We also searched MEDLINE (last searched October 2012) and clinical trials registries. SELECTION CRITERIA: Randomised controlled trials that compared routine removal of peripheral IV catheters with removal only when clinically indicated in hospitalised or community dwelling patients receiving continuous or intermittent infusions. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted data. MAIN RESULTS: Seven trials with a total of 4895 patients were included in the review. Catheter-related bloodstream infection (CRBSI) was assessed in five trials (4806 patients). There was no significant between group difference in the CRBSI rate (clinically-indicated 1/2365; routine change 2/2441). The risk ratio (RR) was 0.61 but the confidence interval (CI) was wide, creating uncertainty around the estimate (95% CI 0.08 to 4.68; P = 0.64). No difference in phlebitis rates was found whether catheters were changed according to clinical indications or routinely (clinically-indicated 186/2365; 3-day change 166/2441; RR 1.14, 95% CI 0.93 to 1.39). This result was unaffected by whether infusion through the catheter was continuous or intermittent. We also analysed the data by number of device days and again no differences between groups were observed (RR 1.03, 95% CI 0.84 to 1.27; P = 0.75). One trial assessed all-cause bloodstream infection. There was no difference in this outcome between the two groups (clinically-indicated 4/1593 (0.02%); routine change 9/1690 (0.05%); P = 0.21). Cannulation costs were lower by approximately AUD 7.00 in the clinically-indicated group (mean difference (MD) -6.96, 95% CI -9.05 to -4.86; P ≤ 0.00001). AUTHORS' CONCLUSIONS: The review found no evidence to support changing catheters every 72 to 96 hours. Consequently, healthcare organisations may consider changing to a policy whereby catheters are changed only if clinically indicated. This would provide significant cost savings and would spare patients the unnecessary pain of routine re-sites in the absence of clinical indications. To minimise peripheral catheter-related complications, the insertion site should be inspected at each shift change and the catheter removed if signs of inflammation, infiltration, or blockage are present.

TUNEL analysis of DNA fragmentation in mouse unfertilized oocytes : the effect of microorganisms within human follicular fluid collected during IVF cycles

Recently we reported the presence of bacteria within follicular fluid. Previous studies have reported that DNA fragmentation in human spermatozoa after in vivo or in vitro incubation with bacteria results in early embryo demise and a reduced rate of ongoing pregnancy, but the effect of bacteria on oocytes is unknown. This study examined the DNA within mouse oocytes after 12 hours’ incubation within human follicular fluids (n = 5), which were collected from women undergoing in vitro fertilization (IVF) treatment. Each follicular fluid sample was cultured to detect the presence of bacteria. Terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) was used to label DNA fragmentation in ovulated, non-fertilized mouse oocytes following in vitro incubation in human follicular fluid. The bacteria Streptococcus anginosus and Peptoniphilus spp., Lactobacillus gasseri (low-dose), L. gasseri (high-dose), Enterococcus faecalis, or Propionibacterium acnes were detected within the follicular fluids. The most severe DNA fragmentation was observed in oocytes incubated in the follicular fluids containing P. acnes or L. gasseri (high-dose). No DNA fragmentation was observed in the mouse oocytes incubated in the follicular fluid containing low-dose L. gasseri or E. faecalis. Low human oocyte fertilization rates (<29%) were associated with extensive fragmentation in mouse oocytes (80–100%). Bacteria colonizing human follicular fluid in vivo may cause DNA fragmentation in mouse oocytes following 12 h of in vitro incubation. Follicular fluid bacteria may result in poor quality oocytes and/or embryos, leading to poor IVF outcomes.

Ross River virus evolution : implications for vaccine development

Ross River virus is a mosquito-borne alphavirus that causes approximately 5000 cases of epidemic polyarthritis in Australia each year and has direct medical-associated costs of approximately US$15 million annually. While mosquito control programs are able, at best, to contain rather than prevent this disease, natural infection with Ross River virus confers lifelong protection against subsequent clinical infection. A killed-virus vaccine has been developed, which is in Phase III clinical trials. Analyses of intra-host genetic diversity and of long-term evolutionary changes in Ross River virus populations suggest that antigenic variation is unlikely to pose a threat to the efficacy of this vaccine.

Caffeine ingestion and cycling power output in a low or normal muscle glycogen state

Purpose Commencing selected workouts with low muscle glycogen availability augments several markers of training adaptation compared with undertaking the same sessions with normal glycogen content. However, low glycogen availability reduces the capacity to perform high-intensity (>85% of peak aerobic power (V·O2peak)) endurance exercise. We determined whether a low dose of caffeine could partially rescue the reduction in maximal self-selected power output observed when individuals commenced high-intensity interval training with low (LOW) compared with normal (NORM) glycogen availability. Methods Twelve endurance-trained cyclists/triathletes performed four experimental trials using a double-blind Latin square design. Muscle glycogen content was manipulated via exercise–diet interventions so that two experimental trials were commenced with LOW and two with NORM muscle glycogen availability. Sixty minutes before an experimental trial, subjects ingested a capsule containing anhydrous caffeine (CAFF, 3 mg-1·kg-1 body mass) or placebo (PLBO). Instantaneous power output was measured throughout high-intensity interval training (8 × 5-min bouts at maximum self-selected intensity with 1-min recovery). Results There were significant main effects for both preexercise glycogen content and caffeine ingestion on power output. LOW reduced power output by approximately 8% compared with NORM (P < 0.01), whereas caffeine increased power output by 2.8% and 3.5% for NORM and LOW, respectively, (P < 0.01). Conclusion We conclude that caffeine enhanced power output independently of muscle glycogen concentration but could not fully restore power output to levels commensurate with that when subjects commenced exercise with normal glycogen availability. However, the reported increase in power output does provide a likely performance benefit and may provide a means to further enhance the already augmented training response observed when selected sessions are commenced with reduced muscle glycogen availability. It has long been known that endurance training induces a multitude of metabolic and morphological adaptations that improve the resistance of the trained musculature to fatigue and enhance endurance capacity and/or exercise performance (13). Accumulating evidence now suggests that many of these adaptations can be modified by nutrient availability (9–11,21). Growing evidence suggests that training with reduced muscle glycogen using a “train twice every second day” compared with a more traditional “train once daily” approach can enhance the acute training response (29) and markers representative of endurance training adaptation after short-term (3–10 wk) training interventions (8,16,30). Of note is that the superior training adaptation in these previous studies was attained despite a reduction in maximal self-selected power output (16,30). The most obvious factor underlying the reduced intensity during a second training bout is the reduction in muscle glycogen availability. However, there is also the possibility that other metabolic and/or neural factors may be responsible for the power drop-off observed when two exercise bouts are performed in close proximity. Regardless of the precise mechanism(s), there remains the intriguing possibility that the magnitude of training adaptation previously reported in the face of a reduced training intensity (Hulston et al. (16) and Yeo et al.) might be further augmented, and/or other aspects of the training stimulus better preserved, if power output was not compromised. Caffeine ingestion is a possible strategy that might “rescue” the aforementioned reduction in power output that occurs when individuals commence high-intensity interval training (HIT) with low compared with normal glycogen availability. Recent evidence suggests that, at least in endurance-based events, the maximal benefits of caffeine are seen at small to moderate (2–3 mg·kg-1 body mass (BM)) doses (for reviews, see Refs. (3,24)). Accordingly, in this study, we aimed to determine the effect of a low dose of caffeine (3 mg·kg-1 BM) on maximal self-selected power output during HIT commenced with either normal (NORM) or low (LOW) muscle glycogen availability. We hypothesized that even under conditions of low glycogen availability, caffeine would increase maximal self-selected power output and thereby partially rescue the reduction in training intensity observed when individuals commence HIT with low glycogen availability.

Ross River virus arthritis

“Epidemics” of a benign disease causing polyarthralgia and rash were first described in Australia in 1927.63 Following the recovery of the causative agent and the advent of serologic tests able to diagnose Ross River virus infection, epidemic polyarthritis has been recognized as endemic in Australia and has occurred as epidemics in numerous Pacific nations. Approximately 4000 cases of epidemic polyarthritis are reported in Australia each year, with a peak of 7800 cases in 1996. Some confusion has been generated recently by use of the term Ross River fever to describe clinical Ross River virus infections because fever does not develop in more than half of those with clinical disease.59 Additional confusion has been generated by efforts to describe any polyarthritis caused by an Australian arbovirus as epidemic polyarthritis. The term epidemic polyarthritis should be used to describe only clinical disease caused by Ross River virus.

Murray Valley Encephalitis

Outbreaks of an acute, severe, encephalitic illness, clinically similar to Japanese and St. Louis encephalitis, occurred in rural areas of southeastern Australia in 1917, 1918, 1922, 1925, 1951, and 1974[1,9,14-16] and in north and northwestern Australia in 1981, 1993, and 2000.[8,12,41] Approximately 420 cases were reported in these nine outbreaks.[41] They are thought to represent a single entity for which various names (Australian X disease, Murray Valley encephalitis, Australian encephalitis) have been used. Twenty-two cases were diagnosed in the 5 years between 2007 and 2011; three were fatal, and one of the fatalities occurred in a Canadian tourist on return from a holiday in northern Australia. Case-fatality rates, as high as 70 percent in the early years,[9,11] declined to 20 percent in the 1974 outbreak and have remained at about this level since then.[5,10,12] However, significant residual neurologic disability occurs in as many as 50 percent of survivors.[10,12] The presence of this disease in Papua New Guinea was confirmed in 1956.[20] The causative virus was transmitted to experimental animals as early as 1918,[6,11] although those strains could not be maintained. The definitive isolation and characterization of Murray Valley encephalitis virus in 1951[19] led to epidemiologic studies that suggested its survival in bird-mosquito cycles in northern Australia but not in the area of epidemic occurrence in southern Australia.[1] Murray Valley encephalitis is caused by Murray Valley encephalitis virus. In an effort to dissociate a disease from a specific locality, the term Australian encephalitis was proposed by residents of Murray Valley for the disease caused by Murray Valley encephalitis virus. Some researchers subsequently have attempted to expand the term Australian encephalitis to include encephalitis caused by any Australian arbovirus. Because the term Australian encephalitis has no scientific validity and is ambiguous, it should not be used.