Investigation of free-living honey bee colonies in Ireland

Apis mellifera mellifera (Linnaeus), the Western European honey bee, is considered extinct in the wild over most of its range due largely to hybridisation and replacement by other subspecies, parasitism by Varroa destructor, habitat loss, and effects from agricultural pesticides. The purity of the subspecies within the managed cohort is also at risk over much of its range. Here, we investigated if honey bee colonies inhabited locations outside of the apiaries. In those we located, we explored how long the colony persisted and we investigated the genotypes of the bees using multiple markers. We show here that unmanaged free-living honey bee colonies are present and widespread in Ireland, inhabiting a mixture of nesting habitats with some colonies persisting naturally and unaided over multiple years. Molecular data including mitochondrial, microsatellite, and SNPs evidence indicate that the free-living population sampled is largely comprised of pure A. m. mellifera. Finally, we discuss the implications of conserving free-living A. m. mellifera in Ireland and its possible role in improving the fitness of the managed population both in Ireland and the rest of its European range.We particularly thank the custodians of the free-living honey bee colonies and the Native Irish Honey Bee Society (NIHBS) for their assistance. KAB is a recipient of an Irish Research Council postgraduate fellowship (GOIPG/2015/2767) and a Tony Ryan Postgraduate fellowship. Additional funding was gratefully received from the Department of Agriculture, Food and the Marine [grant number GRGAS 16/GR/09], the Federation of Irish Beekeeping Associations, the Eva Crane Trust [grant number ECTA20160303] and The Native Irish Honey Bee Society. Financial support for DH was provided through the program COMPETE 2020 – POCI (Programa Operacional para a Competividade e Internacionalizac¸~ao) and by Portuguese funds through FCT (Fundac¸~ao para a Ci^encia e a Tecnologia) in the framework of the project BeeHappy (POCI-01-0145-FEDER-029871).info:eu-repo/semantics/publishedVersio

Assessing computer skills in Tanzanian medical students: an elective experience.

BACKGROUND: One estimate suggests that by 2010 more than 30% of a physician's time will be spent using information technology tools. The aim of this study is to assess the information and communication technologies (ICT) skills of medical students in Tanzania. We also report a pilot intervention of peer mentoring training in ICT by medical students from the UK tutoring students in Tanzania. DESIGN: Cross sectional study and pilot intervention study. PARTICIPANTS: Fourth year medical students (n = 92) attending Muhimbili University College of Health Sciences, Dar es Salaam, Tanzania. MAIN OUTCOME MEASURES: Self-reported assessment of competence on ICT-related topics and ability to perform specific ICT tasks. Further information related to frequency of computer use (hours per week), years of computer use, reasons for use and access to computers. Skills at specific tasks were reassessed for 12 students following 4 to 6 hours of peer mentoring training. RESULTS: The highest levels of competence in generic ICT areas were for email, Internet and file management. For other skills such as word processing most respondents reported low levels of competence. The abilities to perform specific ICT skills were low - less than 60% of the participants were able to perform the core specific skills assessed. A period of approximately 5 hours of peer mentoring training produced an approximate doubling of competence scores for these skills. CONCLUSION: Our study has found a low level of ability to use ICT facilities among medical students in a leading university in sub-Saharan Africa. A pilot scheme utilising UK elective students to tutor basic skills showed potential. Attention is required to develop interventions that can improve ICT skills, as well as computer access, in order to bridge the digital divide

Fermionic T-duality in the pp-wave limit

AdS5 X S5 and its pp-wave limit are self-dual under transformations involving eight fermionic T-dualities, a property which accounts for symmetries seen in scattering amplitudes in N=4 super-Yang-Mills. Despite strong evidence for similar symmetries in the amplitudes of three-dimensional N=6 ABJM theory, a corresponding self-duality in the dual geometry AdS4 X CP3 currently eludes us. Here, working with the type IIA pp-wave limit of AdS4 X CP3 preserving twenty four supercharges, we show that the pp-wave is self-dual with respect to eight commuting fermionic T-dualities and not the six expected. In addition, we show the same symmetry can be found in a superposition pp-wave and a generic pp-wave with twenty and sixteen unbroken supersymmetries respectively, strongly suggesting that self-duality under fermionic T-duality may be a symmetry of all pp-waves.Comment: 21 pages, typos fixe

Self-duality of the D1-D5 near-horizon

We explore fermionic T-duality and self-duality in the geometry AdS3 x S3 x T4 in type IIB supergravity. We explicitly construct the Killing spinors and the fermionic T-duality isometries and show that the geometry is self-dual under a combination of two bosonic AdS3 T-dualities, four fermionic T-dualities and either two additional T-dualities along T4 or two T-dualities along S3. In addition, we show that the presence of a B-field acts as an obstacle to self-duality, a property attributable to S- duality and fermionic T-duality not commuting. Finally, we argue that fermionic T-duality may be extended to CY2 = K3, a setting where we cannot explicitly construct the Killing spinors.Comment: 24 pages, references added, changes made to reinforce the point that S-duality and fermionic T-duality generically do not commute, version accepted to JHE

Longitudinal Synaptic Loss in Primary Tauopathies: An In Vivo [11 C]UCB-J Positron Emission Tomography Study

BACKGROUND: Synaptic loss is characteristic of many neurodegenerative diseases; it occurs early and is strongly related to functional deficits. OBJECTIVE: In this longitudinal observational study, we determine the rate at which synaptic density is reduced in the primary tauopathies of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), and we test the relationship with disease progression. METHODS: Our cross-sectional cohort included 32 participants with probable PSP and 16 with probable CBD (all amyloid-negative corticobasal syndrome), recruited from tertiary care centers in the United Kingdom, and 33 sex- and age-matched healthy control subjects. Synaptic density was estimated by positron emission tomography imaging with the radioligand [11 C]UCB-J that binds synaptic vesicle 2A. Clinical severity and cognition were assessed by the PSP Rating Scale and the Addenbrooke's cognitive examination. Regional [11 C]UCB-J nondisplaceable binding potential was estimated in Hammersmith Atlas regions of interest. Twenty-two participants with PSP/CBD had a follow-up [11 C]UCB-J positron emission tomography scan after 1 year. We calculated the annualized change in [11 C]UCB-J nondisplaceable binding potential and correlated this with the change in clinical severity. RESULTS: We found significant annual synaptic loss within the frontal lobe (-3.5%, P = 0.03) and the right caudate (-3.9%, P = 0.046). The degree of longitudinal synaptic loss within the frontal lobe correlated with the rate of change in the PSP Rating Scale (R = 0.47, P = 0.03) and cognition (Addenbrooke's Cognitive Examination-Revised, R = -0.62, P = 0.003). CONCLUSIONS: We provide in vivo evidence for rapid progressive synaptic loss, correlating with clinical progression in primary tauopathies. Synaptic loss may be an important therapeutic target and outcome variable for early-phase clinical trials of disease-modifying treatments. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Using internet enabled mobile devices and social networking technologies to promote exercise as an intervention for young first episode psychosis patients

<p>Abstract</p> <p>Background</p> <p>Young people with first episode psychosis are at an increased risk for a range of poor health outcomes. In contrast to the growing body of evidence that suggests that exercise therapy may benefit the physical and mental health of people diagnosed with schizophrenia, there are no studies to date that have sought to extend the use of exercise therapy among patients with first episode psychosis. The aim of the study is to test the feasibility and acceptability of an exercise program that will be delivered via internet enabled mobile devices and social networking technologies among young people with first episode psychosis.</p> <p>Methods/Design</p> <p>This study is a qualitative pilot study being conducted at Orygen Youth Health Research Centre in Melbourne, Australia. Participants are young people aged 15-24 who are receiving clinical care at a specialist first episode psychosis treatment centre. Participants will also comprise young people from the general population. The exercise intervention is a 9-week running program, designed to gradually build a person's level of fitness to be able to run 5 kilometres (3 miles) towards the end of the program. The program will be delivered via an internet enabled mobile device. Participants will be asked to post messages about their running experiences on the social networking website, and will also be asked to attend three face-to-face interviews.</p> <p>Discussion</p> <p>This paper describes the development of a qualitative study to pilot a running program coupled with the use of internet enabled mobile devices among young people with first episode psychosis. If the program is found to be feasible and acceptable to patients, it is hoped that further rigorous evaluations will ultimately lead to the introduction of exercise therapy as part of an evidence-based, multidisciplinary approach in routine clinical care.</p

Discovering and linking public omics data sets using the Omics Discovery Index.

Biomedical data are being produced at an unprecedented rate owing to the falling cost of experiments and wider access to genomics, transcriptomics, proteomics and metabolomics platforms1, 2. As a result, public deposition of omics data is on the increase. This presents new challenges, including finding ways to store, organize and access different types of biomedical data stored on different platforms. Here, we present the Omics Discovery Index (OmicsDI; http://www.omicsdi.org), an open-source platform that enables access, discovery and dissemination of omics data sets

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production

Prominent skin involvement is a defining characteristic of autoinflammatory disorders caused by abnormal IL-1 signaling. However, the pathways and cell types that drive cutaneous autoinflammatory features remain poorly understood. We sought to address this issue by investigating the pathogenesis of pustular psoriasis, a model of autoinflammatory disorders with predominant cutaneous manifestations. We specifically characterized the impact of mutations affecting AP1S3, a disease gene previously identified by our group and validated here in a newly ascertained patient resource. We first showed that AP1S3 expression is distinctively elevated in keratinocytes. Because AP1S3 encodes a protein implicated in autophagosome formation, we next investigated the effects of gene silencing on this pathway. We found that AP1S3 knockout disrupts keratinocyte autophagy, causing abnormal accumulation of p62, an adaptor protein mediating NF-kappa B activation. We showed that as a consequence, AP1S3-deficient cells up-regulate IL-1 signaling and overexpress IL-36 alpha, a cytokine that is emerging as an important mediator of skin inflammation. These abnormal immune profiles were recapitulated by pharmacological inhibition of autophagy and verified in patient keratinocytes, where they were reversed by IL-36 blockade. These findings show that keratinocytes play a key role in skin autoinflammation and identify autophagy modulation of IL-36 signaling as a therapeutic target.Peer reviewe

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms