A screen for genes regulating neuroblast activity in Drosophila.

Following embryogenesis, the morphology of the CNS becomes dramatically remodelled to reflect the different locomotive and sensory requirements of the adult relative to the larva. This is largely achieved through the varying spatio-temporal proliferation patterns of the neural stem cell-like precursors (termed postembryonic neuroblasts: pNBs). Although both NB-autonomous and non-cell autonomous mechanisms have been identified, relatively few factors controlling this process are known. My studies focus on using genetic screening to identify new genes involved in this process. I executed two genetic screens, which were designed to complement each others limitations. The first of these involved screening using Mosaic Analysis with a Repressible Cell Marker (MARCM), to identify embryonic-lethal mutations that act in a cell-autonomous manner to produce under- or over-sized pNB clones. The second screen focused on the rarer class of pupal-lethal mutation, where homozygous mutant larvae were screened for abnormal morphology of the CNS. In total, we screened 4200 mutagenised lines on chromosome III, recovering 82 mutants with interesting phenotypes 68 from the MARCM screen and 14 from the pupal-lethal screen. These were divided into 69 complementation groups, 9 of which contained multiple alleles. These groups were subdivided into phenotypic classes, with 9 distinct classes recovered from the MARCM screen and 2 from the pupal-lethal screen. These were sub-categorised into CNS-specific or non-CNS specific, according to the absence or presence of a phenotype in the eye disc. I initially focused my studies on 9 of the pupal-lethal mutations, 5 of which I successfully mapped using chromosomal deficiencies, to 38-329Kb intervals. Two mutations showing undersized brain lobes, juvenile at mid-third instar (jami) and reduced optic and imaginal expansion (roie) were selected for detailed molecular and genetic analysis and comparison. Both genes are required in differing region- and stage-specific manners throughout the CNS. jami positively regulates CNS growth by both non-cell autonomous and cell-autonomous mechanisms, according to the region and stage. In contrast roie promotes growth in a strictly cell-autonomous manner with a strong requirement in symmetrically dividing precursors. Using deficiencies, jami was fine-mapped to a region containing 5 genes and one strong candidate gene for roie, CGI3074, was identified by P-element mediated recombination mapping combined with genetic techniques and available Drosophila database resources

Energy Efficient Construction Methods in UK Dwellings

This paper examines the thermal performance of housing in the UK and the associated costs for different fabric construction methods of the envelope for a typical four bedroom detached house. The energy ratings were assessed using the UK Government’s Standard Assessment Procedure (SAP), which is based on the Building Research Establishment Domestic Energy Model. The capital costs were estimated from data published by the Building Cost Information Services applied to Leicester UK area in 2011. Through alterations to the dwelling fabric alone, a reduction of 30.1% in carbon emissions of the base property could be achieved. Standard methods proved to be as effective as alternative methods at reducing carbon emissions by 22.6% for an average capital cost increase of 9.1% against the base property. This was equivalent to an extra cost of £13.7 for each kg of CO2 emissions reduction. It was found that alternative methods could reduce carbon emissions by 20.5% for an extra cost of 18.4% over the base property. The optimum construction method that would help achieve the UK government’s carbon emissions target was also discussed. The paper also discusses the methods for improving energy efficiency in existing dwellings, using a typical solid-wall terraced house with a new single storey extension, as a case study. In this study, it was found that by increasing refurbishment costs by only 4.7% could result in carbon emissions reduction by 21.7%

Assessing the antimicrobial potential of aerosolised electrochemically activated solutions (ECAS) for reducing the microbial bio-burden on fresh food produce held under cooled or cold storage conditions

© 2017 The main aim of this study was to assess the antimicrobial efficacy of electrochemically activated fog (ECAF) for reducing the microbial bio-burden on artificially inoculated fresh produce held under cooled (cucumber and vine tomatoes) or cold (rocket and broccoli) storage conditions. The ECAF treatment (1100 ± 5 mV ORP; 50 ± 5 mg L−1 free chlorine; 2.7 ± 0.1 pH) resulted in a significant log reduction in the potential pathogen E. coli recovered from rocket (2.644 Log10 CFU g−1), broccoli (4.204 Log10 CFU g−1), cucumber (3.951 Log10 CFU g−1) and tomatoes (2.535 Log10 CFU g-1) after 5 days. ECAF treatment also resulted in a significant log reduction in potential spoilage organisms, whereby a 3.533 Log10 CFU g−1, 2.174 Log10 CFU g−1 and 1.430 Log10 CFU g−1 reduction in presumptive Pseudomonads was observed for rocket, broccoli and cucumber respectively, and a 3.527 Log10 CFU g−1 reduction in presumptive Penicillium spp. was observed for tomatoes (after 5 days). No adverse visual effects on produce were recorded. The results of this study will inform industrial scale-up trials within commercial facilities (assessing shelf-life, microbial quality and organoleptic assessment) to assess the developed ECAF technology platform within a real food processing environment

A Family of H723R Mutation for SLC26A4 Associated with Enlarged Vestibular Aqueduct Syndrome

Recessive mutations of the SLC26A4 (PDS) gene on chromosome 7q31 can cause sensorineural deafness with goiter (Pendred syndrome, OMIM 274600) or NSRD with goiter (at the DFNB4 locus, OMIM 600791). H723R (2168A>G) is the most commonly reported SLC26A4 mutations in Korean and Japanese and known as founder mutation. We recently experienced one patient with enlarged vestibular aqueduct syndrome. The genetic study showed H723R homozygous in the proband and H723R heterozygous mutation in his family members. The identification of a disease-causing mutation can be used to establish a genotypic diagnosis and provide important information to both families and their physicians

Purpose vs performance : what does marine protected area success look like?

Marine protected areas (MPAs) are an increasingly deployed spatial management tool. MPAs are primarily designed for biodiversity conservation, with their success commonly measured using a narrow suite of ecological indicators. However, for MPAs to achieve their biodiversity conservation goals they require community support, which is dependent on wider social, economic and political factors. Despite this, research into the human dimensions of MPAs continues to lag behind our understanding of ecological responses to MPA protection. Here, we explore stakeholders’ perceptions of what MPA success is. We conducted a series of semi-structured interviews and focus groups with a diverse group of stakeholders local to a South Australian MPA. What constitutes success varied by stakeholder group, and stakeholders’ stated understanding of the purpose of the MPA differed from how they would choose to measure the MPA’s success. Indeed, all interviewees stated that the primary purpose of the MPA was ecological, yet almost all (>90%) would measure the success of the MPA using social and economic measures, either exclusively or in conjunction with ecological ones. Many respondents also stated that social and economic factors were key to the MPA achieving ongoing/future success. Respondents generated a large range of novel socio-economic measures of MPA success, many of which could be incorporated into monitoring programs for relatively little additional cost. These findings also show that success is not straightforward and what constitutes success depends on who you ask. Even where an MPA’s primary ecological purpose is acknowledged by stakeholders, stakeholders are likely to only consider the MPA a success if its designation also demonstrates social and economic benefits to their communities. To achieve local stakeholder support MPAs and associated monitoring programs need to be designed for a variety of success criteria in mind, criteria which reflect the priorities and needs of the adjacent communities as well as national and international conservation objectives

Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model

BACKGROUND: Pendred syndrome, a common autosomal-recessive disorder characterized by congenital deafness and goiter, is caused by mutations of SLC26A4, which codes for pendrin. We investigated the relationship between pendrin and deafness using mice that have (Slc26a4(+/+)) or lack a complete Slc26a4 gene (Slc26a4(-/-)). METHODS: Expression of pendrin and other proteins was determined by confocal immunocytochemistry. Expression of mRNA was determined by quantitative RT-PCR. The endocochlear potential and the endolymphatic K(+ )concentration were measured with double-barreled microelectrodes. Currents generated by the stria marginal cells were recorded with a vibrating probe. Tissue masses were evaluated by morphometric distance measurements and pigmentation was quantified by densitometry. RESULTS: Pendrin was found in the cochlea in apical membranes of spiral prominence cells and spindle-shaped cells of stria vascularis, in outer sulcus and root cells. Endolymph volume in Slc26a4(-/- )mice was increased and tissue masses in areas normally occupied by type I and II fibrocytes were reduced. Slc26a4(-/- )mice lacked the endocochlear potential, which is generated across the basal cell barrier by the K(+ )channel KCNJ10 localized in intermediate cells. Stria vascularis was hyperpigmented, suggesting unalleviated free radical damage. The basal cell barrier appeared intact; intermediate cells and KCNJ10 mRNA were present but KCNJ10 protein was absent. Endolymphatic K(+ )concentrations were normal and membrane proteins necessary for K(+ )secretion were present, including the K(+ )channel KCNQ1 and KCNE1, Na(+)/2Cl(-)/K(+ )cotransporter SLC12A2 and the gap junction GJB2. CONCLUSIONS: These observations demonstrate that pendrin dysfunction leads to a loss of KCNJ10 protein expression and a loss of the endocochlear potential, which may be the direct cause of deafness in Pendred syndrome