200 research outputs found

    Reflections on #SocMedHE20

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    A reflection on the #SocMedHE20 Tweetposium

    Phytochrome A mediates blue-light enhancement of second-positive phototropism in Arabidopsis

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    Hypocotyl phototropism of etiolated Arabidopsis seedlings is primarily mediated by the blue-light receptor kinase phototropin 1 (phot1). Phot1-mediated curvature to continuous unilateral blue light irradiation (0.5 µmol m-2 s-1) is enhanced by overhead pre-treatment with red light (20 µmol m-2 s-1 for 15 min) through the action of phytochrome (phyA). Here, we show that pre-treatment with blue light is equally as effective in eliciting phototropic enhancement and is dependent on phyA. Although blue pre-treatment was sufficient to activate early phot1 signalling events, phot1 autophosphorylation in vivo was not found to be saturated, as assessed by subsequently measuring phot1 kinase activity in vitro. However, enhancement effects to red and blue pre-treatment were not observed at higher intensities of phototropic stimulation (10 µmol m-2 s-1). Phototropic enhancement to red and blue pre-treatments to 0.5 µmol m-2 s-1 unilateral blue light irradiation was also lacking in transgenic Arabidopsis where PHOT1 expression was restricted to the epidermis. Together, these findings indicate that phyA-mediated effects on phot1 signalling are restricted to low intensities of phototropic stimulation and originate from tissues other than the epidermis

    The roles of phytohormones in floral arrest and carpic dominance

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    The number of reproductive organs, and their positioning in both space and time (‘reproductive architecture’) are vital factors for the production of offspring in plants. We do not yet fully understand the mechanisms by which plants ‘decide’ how many reproductive organs to make, and where to make them, although elements are known to be controlled by long-distance hormonal signalling. Here, we have examined the control of reproductive architecture in Arabidopsis and the wider Brassicaceae; focusing on the control of inflorescence production, the quantity and positioning of fruits, and the mechanisms underlying floral arrest. We have shown that early signals control the number of inflorescences produced, and that these strongly predict the number of fruits that the plant will make. Fruit are distributed across these inflorescences in a highly predictable manner, with ~50% being supported by the secondary inflorescences, likely as a consequence of the timing of inflorescence arrest. Our examination of inflorescence arrest shows that arrest is a two-stage process, beginning with inflorescence meristem arrest, and followed by floral arrest. We clarify previous misconceptions around floral arrest, showing that it is in fact a local process, and is not regulated globally. Our data highlight the importance of both cytokinin and auxin in inflorescence arrest, with auxin export from developing fruits being required for normal arrest. In support of recent work, we have shown that cytokinin is a key promoter of inflorescence meristem activity, and that increasing cytokinin signalling can delay both inflorescence meristem and floral arrest. Development of this work highlights how the cytokinin signalling receptors ARABIDOPSIS HISTIDINE KINASE2 (AHK2) and AHK3 are differentially involved in the regulation of meristem activity in the inflorescence meristem and flowers respectively. Overall, this work provides a basis on which to develop future crop research; manipulation of cytokinin signalling and/or sensitivity shows excellent promise for yield increases without the need for increased inputs

    Increased risk of type 3c diabetes mellitus after acute pancreatitis warrants a personalised approach including diabetes screening

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    BACKGROUND: Acute pancreatitis (AP) is a frequent cause of hospitalization with long-term health consequences, including type 3c diabetes mellitus (DM). The incidence and risk factors for new-onset morbidities after AP need to be clarified to inform a personalized medicine approach. METHODS: Using a longitudinal electronic healthcare record-linkage analysis, all patients admitted to hospital in Scotland with a first episode of AP between 1 April 2009 and 31 March 2012 and followed for a minimum of 5 years after their index AP admission were identified. All new-onset morbidity with specific focus on type 3c DM were analysed and, using time-split multiple regression. RESULTS: A total of 2047 patients were included. AP requiring critical care was followed by 2 years of heightened risk (HR 5.24) of developing type 3c DM, increased risk of new-onset cardiac disease (HR 1.61), and renal disease (HR 2.96). The additional risk conferred by critical care AP had a negative interaction with time, whereas additional risk associated with male sex and a non-gallstone aetiology was long lasting. CONCLUSION: Based on these findings, a personalized approach to include type 3c DM screening for a minimum of 2 years for individuals who required critical care when hospitalized with AP is recommended

    Hydrogen bonding and the design of twist-bend nematogens

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    Acknowledgements The work was supported by the National Science Centre (Poland) under the grant no. 2016/22/A/ST5/00319. RW gratefully thanks the Carnegie Trust for the Universities of Scotland for the award of a PhD Scholarship (2015-2018). The Erasmus programme is thanked for supporting a study visit for CAC to Warsaw. Declaration of competing interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Author statement Rebecca Walker: Investigation, Formal analysis, Validation, Visualisation, Writing – Original Draft, Writing – Reviewing and Editing Damian Pociecha: Visualisation, Investigation, Formal analysis Catriona Crawford: Investigation, Formal analysis John MD Storey: Resources, Supervision Ewa Gorecka: Investigation, Formal analysis, Resources, Supervision Corrie T Imrie: Conceptualization, Supervision, Resources, Writing – Reviewing and EditingPeer reviewedPostprin

    'The difference in determinants of Chlamydia trachomatis and Mycoplasma genitalium in a sample of young Australian women.'

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    BACKGROUND Differences in the determinants of Chlamydia trachomatis ('chlamydia') and Mycoplasma genitalium (MG) genital infection in women are not well understood. METHODS A cohort study of 16 to 25 year old Australian women recruited from primary health care clinics, aimed to determine chlamydia and MG prevalence and incidence. Vaginal swabs collected at recruitment were used to measure chlamydia and MG prevalence, organism-load and chlamydia-serovar a cross-sectional analysis undertaken on the baseline results is presented here. RESULTS Of 1116 participants, chlamydia prevalence was 4.9% (95% CI: 2.9, 7.0) (n = 55) and MG prevalence was 2.4% (95% CI: 1.5, 3.3) (n = 27). Differences in the determinants were found - chlamydia not MG, was associated with younger age [AOR:0.9 (95% CI: 0.8, 1.0)] and recent antibiotic use [AOR:0.4 (95% CI: 0.2, 1.0)], and MG not chlamydia was associated with symptoms [AOR:2.1 (95% CI: 1.1, 4.0)]. Having two or more partners in last 12 months was more strongly associated with chlamydia [AOR:6.4 (95% CI: 3.6, 11.3)] than MG [AOR:2.2 (95% CI: 1.0, 4.6)] but unprotected sex with three or more partners was less strongly associated with chlamydia [AOR:3.1 (95%CI: 1.0, 9.5)] than MG [AOR:16.6 (95%CI: 2.0, 138.0)]. Median organism load for MG was 100 times lower (5.7 × 104/swab) than chlamydia (5.6 × 10⁶/swab) (p < 0.01) and not associated with age or symptoms for chlamydia or MG. CONCLUSIONS These results demonstrate significant chlamydia and MG prevalence in Australian women, and suggest that the differences in strengths of association between numbers of sexual partners and unprotected sex and chlamydia and MG might be due to differences in the transmission dynamics between these infections.This project was funded by the Commonwealth of Australia, as part of a National Chlamydia Pilot program that is currently running to test the effectiveness of a number of models for chlamydia testing in Australia. This project will assist in developing possible recommendations for a National Chlamydia Program. The analysis of MG was funded by the National Health and Research Council (research grant number 509144)

    Candida albicans Hypha Formation and Mannan Masking of β-Glucan Inhibit Macrophage Phagosome Maturation

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    Received 28 August 2014 Accepted 28 October 2014 Published 2 December 2014 This is an open-access article distributed under the terms of the Creative Commons Attribution 3.0 Unported license. ACKNOWLEDGMENTS We thank Janet Willment, Aberdeen Fungal Group, University of Aberdeen, for kindly providing the soluble Dectin-1-Fc reporter. All microscopy was performed with the assistance of the University of Aberdeen Core Microscopy & Histology Facility, and we thank the IFCC for their assistance with flow cytometry. We thank the Wellcome Trust for funding (080088, 086827, 075470, 099215, 097377, and 101873). E.R.B. and A.J.P.B. are funded by the European Research Council (ERC-2009-AdG-249793), and J.L. is funded by a Medical Research Council Clinical Training Fellowship.Peer reviewedPublisher PD

    ABCC1 modulates negative feedback control of the hypothalamic-pituitary-adrenal axis in vivo in humans

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    BACKGROUND: Cortisol and corticosterone both circulate in human plasma and, due to differing export by ATP-binding cassette (ABC) transporters, may exert differential cellular effects. ABCB1 (expressed in brain) exports cortisol not corticosterone while ABCC1 (expressed in adipose and skeletal muscle) exports corticosterone not cortisol. We hypothesised that ABCC1 inhibition increases corticosteroid receptor occupancy by corticosterone but not cortisol in humans. METHODS: A randomised double-blind crossover study was conducted in 14 healthy men comparing placebo and ABCC1 inhibitor probenecid. Blood sampling, including from veins draining adipose and muscle, was undertaken before and after administration of mineralocorticoid receptor antagonist potassium canrenoate and glucocorticoid receptor antagonist mifepristone (RU486). RESULTS: During placebo, systemic plasma cortisol and corticosterone concentrations increased promptly after canrenoate. Cortisol uptake was detected from adipose but not muscle following canrenoate + RU486. Probenecid significantly increased systemic cortisol concentrations, and tended to increase corticosterone and ACTH concentrations, after combined receptor antagonism but had no effects on net glucocorticoid balance in either adipose or muscle. Using quantitative PCR in brain bank tissue, ABCC1 expression was 5-fold higher in human pituitary than hypothalamus and hippocampus. ABCB1 was more highly expressed in hypothalamus compared to pituitary. CONCLUSIONS: Although displacement of corticosterone and/or cortisol from receptors in adipose and skeletal muscle could not be measured with sufficient precision to detect effects of probenecid, ABCC1 inhibition induced a greater incremental activation of the hypothalamic-pituitary-adrenal axis after combined receptor blockade, consistent with ABCC1 exporting corticosterone from the pituitary and adding to the evidence that ABC transporters modulate tissue glucocorticoid sensitivity
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