1,154 research outputs found

    Factors influencing growth of the African penguin colony at Boulders, South Africa, 1985–1999

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    This paper reports on growth of the Boulders colony of African penguins Spheniscus demersus from inception in 1985 to the present. More than 900 pairs now breed there. Growth of the colony slowed in 1995 and 1996and reversed in 1998, coinciding with periods of low abundance of Cape anchovy Engraulis capensis off South Africa. In December 1996, penguins were excluded from a portion of land where they had formerly bred. Theyresponded by increasing the density of their nests in other areas and expanding their area of breeding longshore. These patterns indicate that food and not space are currently controlling colony growth rate. Much of the colonygrowth probably results from immigration of first-time breeders from other colonies. Of immigrants, 70–80% may be from Dyer Island to the south-east, where numbers of penguins have decreased. Boulders also is frequentlyvisited by penguins from other colonies, and by rehabilitated birds

    African penguins as predators and prey — coping (or not) with change

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    African penguins Spheniscus demersus live in the Benguela and western Agulhas ecosystems off southern Africa. Their numbers decreased throughout the 20th century from at least 1.5 million to about 0.18 million adults, although different regional trends were apparent. They feed to a large extent on shoaling epipelagic fish, notably anchovy Engraulis capensis and sardine Sardinops sagax, and regional trends in the abundance of penguins are associated with trends in the abundance and distribution of these prey fish. Many first-time breeders emigrate from colonies where feeding or other conditions at the time are unfavourable to more favourable breeding localities. This has led to both the extinction and formation of colonies. Food now may limit colonies at relatively small sizes, a fact attributable to industrial fisheries reducing the densities of forage fish. African penguins share their habitat with several other predators, with which they compete for food and breeding space. One of these, the Cape fur seal Arctocephalus p. pusillus, increased through the 20th century to 1.5–2 million animals at its close. Reported observations of predation by fur seals on seabirds have increased in recent decades and threaten the continued existence of small colonies of penguins. Stochastic modelling suggests that colonies of 10 000 pairs have a 9% probability of extinction in 100 years, so smaller populations should be regarded as “Vulnerable”. However, in a period of prolonged food scarcity off southern Namibia, the regional population decreased from more than 40 000 pairs in 1956 to about 1 000 pairs in 2000, and many colonies numbering less than 1 000 pairs became extinct. The minimum viable population for African penguins is currently considered to be >40 000 pairs, likely of the order of 50 000 pairs, a figure equivalent to its level in 2000. The chance of survival of the species through the 21st century is tenuous.African Journal of Marine Science 2001, 23: 435–44

    Knockout studies reveal an important role of <i>plasmodium</i> lipoic acid protein ligase a1 for asexual blood stage parasite survival

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    Lipoic acid (LA) is a dithiol-containing cofactor that is essential for the function of a-keto acid dehydrogenase complexes. LA acts as a reversible acyl group acceptor and 'swinging arm' during acyl-coenzyme A formation. The cofactor is post-translationally attached to the acyl-transferase subunits of the multienzyme complexes through the action of octanoyl (lipoyl): &lt;i&gt;N&lt;/i&gt;-octanoyl (lipoyl) transferase (LipB) or lipoic acid protein ligases (LplA). Remarkably, apicomplexan parasites possess LA biosynthesis as well as scavenging pathways and the two pathways are distributed between mitochondrion and a vestigial organelle, the apicoplast. The apicoplast-specific LipB is dispensable for parasite growth due to functional redundancy of the parasite's lipoic acid/octanoic acid ligases/transferases. In this study, we show that &lt;i&gt;LplA1&lt;/i&gt; plays a pivotal role during the development of the erythrocytic stages of the malaria parasite. Gene disruptions in the human malaria parasite &lt;i&gt;P.falciparum&lt;/i&gt; consistently were unsuccessful while in the rodent malaria model parasite &lt;i&gt;P. berghei&lt;/i&gt; the &lt;i&gt;LplA1&lt;/i&gt; gene locus was targeted by knock-in and knockout constructs. However, the &lt;i&gt;LplA1&lt;/i&gt; &lt;sup&gt;(-)&lt;/sup&gt; mutant could not be cloned suggesting a critical role of LplA1 for asexual parasite growth &lt;i&gt;in vitro&lt;/i&gt; and &lt;i&gt;in vivo&lt;/i&gt;. These experimental genetics data suggest that lipoylation during expansion in red blood cells largely occurs through salvage from the host erythrocytes and subsequent ligation of LA to the target proteins of the malaria parasite

    What’s a box of “Bakewell Tarts” got to do with it? Performing gender as a judicial virtue in the theatre of justice

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    On a July morning in 2013 a box of a popular English branded confection called“Cherry Bakewells’ appeared in the court of the Lord Chief Justice of England and Wales. It generated much laughter. The event was the swearing in ceremony for Dame Julia Wendy Macur as a judge of the Court of Appeal. If her appointment was a cause for celebration, the backdrop to the event was the serious business of judicial renewal and the gender composition of the judiciary. Neither topic is a laughing matter. Drawing upon data generated through the observation of 18 swearing in events this chapter uses the gender/humour interface to examine the gender dynamics of the social world of the judiciary as an institution. Keywords: ceremonial archive, gender, judicial diversity, wi

    Nucleoside diphosphate kinase A as a controller of AMP-kinase in airway epithelia

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    This review integrates recent understanding of a novel role for NDPK-A in two related directions: Firstly, its role in an airway epithelial cell when bound to the luminal (apical) membrane and secondly in the cytosol of many different cells (epithelial and non-epithelial) where an isoform-specific interaction occurs with a regulatory partner, AMPKα1. Thus NDPK-A is present in both a membrane and cytosolic environment but in the apical membrane, its roles are not understood in detail; preliminary data suggest that it co-localises with the cystic fibrosis protein (CFTR). In cytosol, we find that NDPK-A is coupled to the catalytic alpha1 isoform of the AMP-activated protein kinase (AMPKα subunit), which is part of a heterotrimeric protein complex that responds to cellular energy status by switching off ATP-consuming pathways and switching on ATP-generating pathways when ATP is limiting. We find that ATP is located within this complex and ‘fed’ from NDPK to AMPK without ever ‘seeing’ bulk solution. Importantly, the reverse can also happen such that AMPK activity can be made to decline when NDPK-A ‘steals’ ATP from AMPK. Thus we propose a novel paradigm in NDPK-A function by suggesting that AMP-kinase can be regulated by NDPK-A, independently of AMP

    Mechanism and timing of Mcm2–7 ring closure during DNA replication origin licensing

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    The opening and closing of two ring-shaped Mcm2-7 DNA helicases is necessary to license eukaryotic origins of replication, although the mechanisms controlling these events are unclear. The origin-recognition complex (ORC), Cdc6 and Cdt1 facilitate this process by establishing a topological link between each Mcm2-7 hexamer and origin DNA. Using colocalization single-molecule spectroscopy and single-molecule Förster resonance energy transfer (FRET), we monitored ring opening and closing of Saccharomyces cerevisiae Mcm2-7 during origin licensing. The two Mcm2-7 rings were open during initial DNA association and closed sequentially, concomitant with the release of their associated Cdt1. We observed that ATP hydrolysis by Mcm2-7 was coupled to ring closure and Cdt1 release, and failure to load the first Mcm2-7 prevented recruitment of the second Mcm2-7. Our findings identify key mechanisms controlling the Mcm2-7 DNA-entry gate during origin licensing, and reveal that the two Mcm2-7 complexes are loaded via a coordinated series of events with implications for bidirectional replication initiation and quality control.National Institutes of Health (U.S.) (Grant R01 GM52339)National Institutes of Health (U.S.) (Pre-Doctoral Training Grant GM007287)National Cancer Institute (U.S.) (Koch Institute Support Grant P30-CA14051

    Tumour necrosis factor gene polymorphism: a predictive factor for the development of post-transplant lymphoproliferative disease

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    Epstein–Barr virus-positive post-transplant lymphoproliferative disease (PTLD) is a potentially lethal complication of iatrogenic immunosupression after transplantation. Predicting the development of PTLD allowing early and effective intervention is therefore of importance. Polymorphisms within cytokine genes are implicated in susceptibility to, and progression of, disease however the published data are often conflicting. We undertook investigation of polymorphic alleles within cytokine genes in PTLD and non-PTLD transplant cohorts to determine risk factors for disease. &lt;br/&gt; Methods: SSP-PCR was used to analyse single nucleotide polymorphism within tumour necrosis factor (TNF)-α, interleukin- 1, -6, -10 and lymphotoxin-α genes. The TNF-α levels were measured by standard enzyme-linked immuno-absorbant assay. &lt;br/&gt; Results: We show an association between variant alleles within the TNF-α promoter (−1031C (&lt;i&gt;P&lt;/i&gt;=0.005)); −863A (&lt;i&gt;P&lt;/i&gt;=0.0001) and TNF receptor I promoter regions (−201T (&lt;i&gt;P&lt;/i&gt;=0.02)); −1135C (&lt;i&gt;P&lt;/i&gt;=0.03) with the development of PTLD. We also show an association with TNF-α promoter haplotypes with haplotype-3 significantly increased (&lt;i&gt;P&lt;/i&gt;=0.0001) and haplotype-1 decreased (P=0.02) in PTLD patients compared to transplant controls. Furthermore, we show a significant increase (&lt;i&gt;P&lt;/i&gt;=0.02) in the level of TNF-α in PTLD patient plasma (range 0–97.97 pg ml&lt;sup&gt;−1&lt;/sup&gt;) compared to transplant controls (0–8.147 pg ml&lt;sup&gt;−1&lt;/sup&gt;), with the highest levels found in individuals carrying the variant alleles. &lt;br/&gt; Conclusion: We suggest that genetic variation within TNF-α loci and the level of plasma cytokine could be used as a predictive risk factor for the development of PTLD

    Estimated pre-morbid IQ effects on cognitive and functional outcomes in Alzheimer disease: a longitudinal study in a treated cohort

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    Abstract Background Cognitive reserve is thought to influence the degree of neuropathology needed for diagnosis of Alzheimer disease (AD). Cognitive reserve can be operationally defined as the hypothesized capacity of the mature adult brain to sustain the effects of disease or injury without manifesting clinical symptoms of AD, but sufficient to cause clinical dementia in an individual possessing less cognitive reserve. Its effect on the subsequent course of AD is less clear. Pre-morbid IQ is a useful measure of cognitive reserve. Methods We studied 659 consecutive patients with AD at a tertiary referral memory clinic. Patients were assessed on six cognitive tests at baseline. Activities of Daily Living (ADL) were measured on the Instrumental Activities of Daily Living (IADL) scale and Physical Self-Maintenance Scale (PSMS). The National Adult Reading Test (NART) was used to estimate pre-morbid IQ. Patients were followed up after starting a cholinesterase inhibitor over 78 weeks. Mixed general linear models estimated the effects of NART on cognition and ADL. Results Three hundred and fifty-five patients had NART scored with a mean estimated pre-morbid IQ of 104.7 (standard deviation 18.5). NART increased overall cognitive ability by 2.7% for every 10 IQ points (p Conclusion Our data support the hypothesis that cognitive reserve continues to have a limited influence on cognition after AD has been diagnosed and thus, indirectly, has an impact on ADL.</p

    Framework, principles and recommendations for utilising participatory methodologies in the co-creation and evaluation of public health interventions

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    Background: Due to the chronic disease burden on society, there is a need for preventive public health interventions to stimulate society towards a healthier lifestyle. To deal with the complex variability between individual lifestyles and settings, collaborating with end-users to develop interventions tailored to their unique circumstances has been suggested as a potential way to improve effectiveness and adherence. Co-creation of public health interventions using participatory methodologies has shown promise but lacks a framework to make this process systematic. The aim of this paper was to identify and set key principles and recommendations for systematically applying participatory methodologies to co-create and evaluate public health interventions. Methods: These principles and recommendations were derived using an iterative reflection process, combining key learning from published literature in addition to critical reflection on three case studies conducted by research groups in three European institutions, all of whom have expertise in co-creating public health interventions using different participatory methodologies. Results: Key principles and recommendations for using participatory methodologies in public health intervention co-creation are presented for the stages of: Planning (framing the aim of the study and identifying the appropriate sampling strategy); Conducting (defining the procedure, in addition to manifesting ownership); Evaluating (the process and the effectiveness) and Reporting (providing guidelines to report the findings). Three scaling models are proposed to demonstrate how to scale locally developed interventions to a population level. Conclusions: These recommendations aim to facilitate public health intervention co-creation and evaluation utilising participatory methodologies by ensuring the process is systematic and reproducible
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