Bactericidal action of positive and negative ions in air

In recent years there has been renewed interest in the use of air ionisers to control of the spread of airborne infection. One characteristic of air ions which has been widely reported is their apparent biocidal action. However, whilst the body of evidence suggests a biocidal effect in the presence of air ions the physical and biological mechanisms involved remain unclear. In particular, it is not clear which of several possible mechanisms of electrical origin (i.e. the action of the ions, the production of ozone, or the action of the electric field) are responsible for cell death. A study was therefore undertaken to clarify this issue and to determine the physical mechanisms associated with microbial cell death. In the study seven bacterial species (Staphylococcus aureus, Mycobacterium parafortuitum, Pseudomonas aeruginosa, Acinetobacter baumanii, Burkholderia cenocepacia, Bacillus subtilis and Serratia marcescens) were exposed to both positive and negative ions in the presence of air. In order to distinguish between effects arising from: (i) the action of the air ions; (ii) the action of the electric field, and (iii) the action of ozone, two interventions were made. The first intervention involved placing a thin mica sheet between the ionisation source and the bacteria, directly over the agar plates. This intervention, while leaving the electric field unaltered, prevented the air ions from reaching the microbial samples. In addition, the mica plate prevented ozone produced from reaching the bacteria. The second intervention involved placing an earthed wire mesh directly above the agar plates. This prevented both the electric field and the air ions from impacting on the bacteria, while allowing any ozone present to reach the agar plate. With the exception of Mycobacterium parafortuitum, the principal cause of cell death amongst the bacteria studied was exposure to ozone, with electroporation playing a secondary role. However in the case of Mycobacterium parafortuitum, electroporation resulting from exposure to the electric field appears to have been the principal cause of cell inactivation. The results of the study suggest that the bactericidal action attributed to negative air ions by previous researchers may have been overestimated

Publication records of Australian accounting and finance faculty promoted to full professor, set within an international context

Australian accounting and finance faculty promoted to full professor required a median 15 papers in ABDC‐listed journals, with 7 at the highest A*/A quality levels. Promotees were typically 44 years old, with 14 years' academic experience including 9 years post‐PhD. Neither gender nor whether promotion was internal/external seemed to affect promotion requirements. Finance professors typically had more publications than accounting professors, though not at the higher quality levels; however, accounting promotees had greater academic experience but a shorter period post‐PhD. Female promotees were typically older than males. Both the volume and quality of pre‐promotion publications have increased over time

Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels

Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P <10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P <5 x 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health.Peer reviewe

Momentum crashes: the Australian evidence

Previous studies report that significant alpha can be generated in various international equity markets by employing a momentum strategy — i.e. buying past winners and short selling past losers. However, the strategy sometimes crashes, generating large negative returns over one or more consecutive months. Using Australian data, this study generally confirms recent US findings that these crashes tend to occur following steep market declines and are characterised by large positive returns by the past Loser portfolio rather than large negative returns by the past Winner portfolio. This paper also identifies significant risk changes to a momentum strategy in bear markets but, unlike the US study, it does not find the strategy to exhibit option-like behaviour at the time of a momentum crash

Accounting and Finance: authorship and citation trends

Accounting and Finance (A&F) has experienced a surge in published research in the last decade. The analysis here reveals a marked increase in the number of published articles in A&F since 2003, a distinct trend for published papers to have a larger number of authors, a significant and stable contribution by the top 5 Australian accounting/finance departments, as well as a notable increase in contribution from non-US foreign universities, particularly those located in the UK, Canada, Hong Kong, Singapore and Spain. An analysis of citations indicates the increasing impact of A&F in recent years

The llusory Australian small firm premium

Previous research has found that the small firm premium which was prominent in the US and UK markets up until the late 1980s has disappeared from both markets. In contrast, studies continue to report an exceptionally strong and persistent small firm premium over time within the Australian market. However, our analysis finds that in practice there is no exploitable small firm premium in Australian stock returns