1,183 research outputs found

    UK Breastfeeding Helpline support: An investigation of influences upon satisfaction

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    Background Incentive or reward schemes are becoming increasingly popular to motivate healthy lifestyle behaviours. In this paper, insights from a qualitative and descriptive study to investigate the uptake, impact and meanings of a breastfeeding incentive intervention integrated into an existing peer support programme (Star Buddies) are reported. The Star Buddies service employs breastfeeding peer supporters to support women across the ante-natal, intra-partum and post-partum period. Methods In a disadvantaged area of North West England, women initiating breastfeeding were recruited by peer supporters on the postnatal ward or soon after hospital discharge to participate in an 8 week incentive (gifts and vouchers) and breastfeeding peer supporter intervention. In-depth interviews were conducted with 26 women participants who engaged with the incentive intervention, and a focus group was held with the 4 community peer supporters who delivered the intervention. Descriptive analysis of routinely collected data for peer supporter contacts and breastfeeding outcomes before and after the incentive intervention triangulated and retrospectively provided the context for the qualitative thematic analysis. Results A global theme emerged of 'incentives as connectors', with two sub-themes of 'facilitating connections' and 'facilitating relationships and wellbeing'. The incentives were linked to discussion themes and gift giving facilitated peer supporter access for proactive weekly home visits to support women. Regular face to face contacts enabled meaningful relationships and new connections within and between the women, families, peer supporters and care providers to be formed and sustained. Participants in the incentive scheme received more home visits and total contact time with peer supporters compared to women before the incentive intervention. Full participation levels and breastfeeding rates at 6-8 weeks were similar for women before and after the incentive intervention. Conclusion The findings suggest that whilst the provision of incentives might not influence women's intentions or motivations to breastfeed, the connections forged provided psycho-social benefits for both programme users and peer supporters

    Molecular and Cellular Basis of Microvascular Perfusion Deficits Induced by Clostridium perfringens and Clostridium septicum

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    Reduced tissue perfusion leading to tissue ischemia is a central component of the pathogenesis of myonecrosis caused by Clostridium perfringens. The C. perfringens α-toxin has been shown capable of inducing these changes, but its potential synergy with perfringolysin O (θ-toxin) is less well understood. Similarly, Clostridium septicum is a highly virulent causative agent of spontaneous gas gangrene, but its effect on the microcirculation has not been examined. Therefore, the aim of this study was to use intravital microscopy to examine the effects of C. perfringens and C. septicum on the functional microcirculation, coupled with the use of isogenic toxin mutants to elucidate the role of particular toxins in the resultant microvascular perfusion deficits. This study represents the first time this integrated approach has been used in the analysis of the pathological response to clostridial toxins. Culture supernatants from wild-type C. perfringens induced extensive cell death within 30 min, as assessed by in vivo uptake of propidium iodide. Furthermore, significant reductions in capillary perfusion were observed within 60 min. Depletion of either platelets or neutrophils reduced the alteration in perfusion, consistent with a role for these blood-borne cells in obstructing perfusion. In addition, mutation of either the α-toxin or perfringolysin O structural genes attenuated the reduction in perfusion, a process that was reversed by genetic complementation. C. septicum also induced a marked reduction in perfusion, with the degree of microvascular compromise correlating with the level of the C. septicum α-toxin. Together, these data indicate that as a result of its ability to produce α-toxin and perfringolysin O, C. perfringens rapidly induces irreversible cellular injury and a marked reduction in microvascular perfusion. Since C. septicum induces a similar reduction in microvascular perfusion, it is postulated that this function is central to the pathogenesis of clostridial myonecrosis, irrespective of the causative bacterium

    Maternal psychological distress in primary care and association with child behavioural outcomes at age three

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    Observational studies indicate children whose mothers have poor mental health are at increased risk of socio-emotional behavioural difficulties, but it is unknown whether these outcomes vary by the mothers’ mental health recognition and treatment status. To examine this question, we analysed linked longitudinal primary care and research data from 1078 women enrolled in the Born in Bradford cohort. A latent class analysis of treatment status and self-reported distress broadly categorised women as (a) not having a common mental disorder (CMD) that persisted through pregnancy and the first 2 years after delivery (N = 756, 70.1 %), (b) treated for CMD (N = 67, 6.2 %), or (c) untreated (N = 255, 23.7 %). Compared to children of mothers without CMD, 3-year-old children with mothers classified as having untreated CMD had higher standardised factor scores on the Strengths and Difficulties Questionnaire (d = 0.32), as did children with mothers classified as having treated CMD (d = 0.27). Results were only slightly attenuated in adjusted analyses. Children of mothers with CMD may be at risk for socio-emotional and behavioural difficulties. The development of effective treatments for CMD needs to be balanced by greater attempts to identify and treat women. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00787-015-0777-2) contains supplementary material, which is available to authorized users

    The Cysteine Protease α-Clostripain is Not Essential for the Pathogenesis of Clostridium perfringens-Mediated Myonecrosis

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    Clostridium perfringens is the causative agent of clostridial myonecrosis or gas gangrene and produces many different extracellular toxins and enzymes, including the cysteine protease α-clostripain. Mutation of the α-clostripain structural gene, ccp, alters the turnover of secreted extracellular proteins in C. perfringens, but the role of α-clostripain in disease pathogenesis is not known. We insertionally inactivated the ccp gene C. perfringens strain 13 using TargeTron technology, constructing a strain that was no longer proteolytic on skim milk agar. Quantitative protease assays confirmed the absence of extracellular protease activity, which was restored by complementation with the wild-type ccp gene. The role of α-clostripain in virulence was assessed by analysing the isogenic wild-type, mutant and complemented strains in a mouse myonecrosis model. The results showed that although α-clostripain was the major extracellular protease, mutation of the ccp gene did not alter either the progression or the development of disease. These results do not rule out the possibility that this extracellular enzyme may still have a role in the early stages of the disease process

    Extensive Copy-Number Variation of Young Genes across Stickleback Populations

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    MM received funding from the Max Planck innovation funds for this project. PGDF was supported by a Marie Curie European Reintegration Grant (proposal nr 270891). CE was supported by German Science Foundation grants (DFG, EI 841/4-1 and EI 841/6-1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

    The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

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    The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex might be connected on a unique pathway essential for the safe expansion of neuronal cells. Here, we show that MYCN transcriptionally controls the expression of each component of the MRN complex. By genetic and pharmacological inhibition of the MRN complex in a MYCN overexpression model and in the more physiological context of the Hedgehog-dependent expansion of primary cerebellar granule progenitor cells, we also show that the MRN complex is required for MYCN-dependent proliferation. Indeed, its inhibition resulted in DNA damage, activation of a DNA damage response, and cell death in a MYCN- and replication-dependent manner. Our data indicate the MRN complex is essential to restrain MYCN-induced replication stress during neural cell proliferation and support the hypothesis that replication-born DNA damage is responsible for the neuronal defects associated with MRN dysfunctions.Cell Death and Differentiation advance online publication, 12 June 2015; doi:10.1038/cdd.2015.81

    Neurospora from natural populations: Population genomics insights into the Life history of a model microbial Eukaryote

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    The ascomycete filamentous fungus Neurospora crassa played a historic role in experimental biology and became a model system for genetic research. Stimulated by a systematic effort to collect wild strains initiated by Stanford geneticist David Perkins, the genus Neurospora has also become a basic model for the study of evolutionary processes, speciation, and population biology. In this chapter, we will first trace the history that brought Neurospora into the era of population genomics. We will then cover the major contributions of population genomic investigations using Neurospora to our understanding of microbial biogeography and speciation, and review recent work using population genomics and genome-wide association mapping that illustrates the unique potential of Neurospora as a model for identifying the genetic basis of (potentially adaptive) phenotypes in filamentous fungi. The advent of population genomics has contributed to firmly establish Neurospora as a complete model system and we hope our review will entice biologists to include Neurospora in their research

    Coalition Culls and Zoonotic Ontologies

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    Diseases which can pass between animals and humans (zoonoses) have been headline news several times in the last ten years. This paper looks at bovine tuberculosis (bTB) in the United Kingdom, which, although not a major health hazard for humans, has been problematic for farmers and the veterinary health institutions. At its current rate of spread, the disease will cost the authorities £1 billion in compensation to farmers for slaughtered animals and in administrative expenses over the next decade. The present Coalition government is planning to cull badgers in England because they are the principal wildlife reservoir of bTB and are said to pass infection to cattle. We argue in five stories that the heterogeneities of bTB help explain the difficulties in dealing with it. In our opinion, the present reductive set of policies would be improved by taking this ontological multiplicity into account

    Interaction of hope and optimism with anxiety and depression in a specific group of cancer survivors: a preliminary study

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    <p>Abstract</p> <p>Background</p> <p>Anxiety and depression have been identified as a common psychological distress faced by the majority of cancer patients. With the increasing number of cancer cases, increasing demands will be placed on health systems to address effective psychosocial care and therapy. The objective of this study was to assess the possible role of hope and optimism on anxiety and depression. We also wanted to investigate if there is a specific component of hope that could play a role in buffering anxiety and depression amongst cancer patients.</p> <p>Methods</p> <p>A retrospective cross sectional study was conducted in the outpatient station of the Oral and Maxillofacial Surgery at the University of Hong Kong, Hong Kong SAR, PR-China. Fifty patients successfully treated for OC cancer were recruited after their informed consents had been obtained during the review clinic. During their regular follow-up controls in the outpatient clinic the patients compiled the hospital anxiety and depression scale (HADS), hope scale (HS) and the life orientation scale-revised (LOT-R).</p> <p>Results</p> <p>Hope was negatively correlated with depression (<it>r </it>= -.55, <it>p </it>< .001) and anxiety (r = -.38, <it>p </it>< .05). Similar pattern was found between optimism and the latter adjustment outcomes (depression: <it>r </it>= -.55, <it>p </it>< .001; anxiety: <it>r </it>= -.35, <it>p </it>< .05). Regression analyses indentified that both hope and optimism were significant predictors of depression. Hope and optimism had equal association with depression (hope: <it>β </it>= .40 versus optimism: <it>β </it>= .38). Hope and optimism together were significantly predictive of anxiety, whereas neither hope nor optimism alone was significant individual predictors of anxiety.</p> <p>Conclusions</p> <p>Hope and optimism both negatively correlated with patients' level of anxiety and depression. Besides theoretical implications, this study brings forward relevant findings related to developing specific clinical psychological care in the field of oncology that to date has not been researched specifically in the field of oncology. The results of this study will help guide the direction of future prospective studies in the field of oncology. This will contribute significantly to increasing patients quality of life as well enabling health care facilities to provide all cancer patients a more holistic cancer care.</p

    Association of food security status with overweight and dietary intake: exploration of White British and Pakistani-origin families in the Born in Bradford cohort.

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    BACKGROUND: Food insecurity has been associated with dietary intake and weight status in UK adults and children although results have been mixed and ethnicity has not been explored. We aimed to compare prevalence and trajectories of weight and dietary intakes among food secure and insecure White British and Pakistani-origin families. METHODS: At 12 months postpartum, mothers in the Born in Bradford cohort completed a questionnaire on food security status and a food frequency questionnaire (FFQ) assessing their child's intake in the previous month; at 18 months postpartum, mothers completed a short-form FFQ assessing dietary intake in the previous 12 months. Weights and heights of mothers and infants were assessed at 12-, 24-, and 36-months postpartum, with an additional measurement of children taken at 4-5 years. Associations between food security status and dietary intakes were assessed using Wilcoxon-Mann-Whitney for continuous variables and χ2 or Fisher's exact tests for categorical variables. Quantile and logistic regression were used to determine dietary intakes adjusting for mother's age. Linear mixed effects models were used to assess longitudinal changes in body mass index (BMI) in mothers and BMI z-scores in children. RESULTS: At 12 months postpartum, White British mothers reported more food insecurity than Pakistani-origin mothers (11% vs 7%; p < 0.01) and more food insecure mothers were overweight. Between 12 and 36 months postpartum, BMI increased more among food insecure Pakistani-origin mothers (β = 0.77 units, [95% Confidence Interval [CI]: 0.40, 1.10]) than food secure (β = 0.44 units, 95% CI: 0.33, 0.55). This was also found in Pakistani-origin children (BMI z-score: food insecure β = 0.40 units, 95% CI: 0.22, 0.59; food secure β = 0.25 units, 95% CI: 0.20, 0.29). No significant increases in BMI were observed for food secure or insecure White British mothers while BMI z-score increased by 0.17 (95% CI: 0.13, 0.21) for food secure White British children. Food insecure mothers and children had dietary intakes of poorer quality, with fewer vegetables and higher consumption of sugar-sweetened drinks. CONCLUSIONS: Food security status is associated with body weight and dietary intakes differentially by ethnicity. These are important considerations for developing targeted interventions
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