42 research outputs found

    Phenotypic response to different predator strategies can be mediated by temperature

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    Abstract Temperature change affects biological systems in multifaceted ways, including the alteration of species interaction strengths, with implications for the stability of populations and communities. Temperature‐dependent changes to antipredatory responses are an emerging mechanism of destabilization and thus there is a need to understand how prey species respond to predation pressures in the face of changing temperatures. Here, using ciliate protozoans, we assess whether temperature can alter the strength of phenotypic antipredator responses in a prey species and whether this relationship depends on the predator's hunting behavior. We exposed populations of the ciliate Paramecium caudatum to either (i) a sit‐and‐wait generalist predator (Homalozoon vermiculare) or (ii) a specialized active swimmer predator (Didinium nasutum) across two different temperature regimes (15 and 25°C) to quantify the temperature dependence of antipredator responses over a 24‐h period. We utilized a novel high‐throughput automated robotic monitoring system to track changes in the behavior (swimming speed) and morphology (cell size) of P. caudatum at frequencies and resolutions previously unachievable by manual sampling. The change in swimming speed through the 24 h differed between the two temperatures but was not altered by the presence of the predators. In contrast, P. caudatum showed a substantial temperature‐dependent morphological response to the presence of D. nasutum (but not H. vermiculare), changing cell shape toward a more elongated morph at 15°C (but not at 25°C). Our findings suggest that temperature can have strong effects on prey morphological responses to predator presence, but that this response is potentially dependent on the predator's feeding strategy. This suggests that greater consideration of synergistic antipredator behavioral and physiological responses is required in species and communities subject to environmental changes

    Why do plasmids manipulate the expression of bacterial phenotypes?

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    From The Royal Society via Jisc Publications RouterHistory: received 2021-03-17, accepted 2021-07-09, pub-electronic 2021-11-29, pub-print 2022-01-17Article version: VoRPublication status: PublishedFunder: Natural Environment Research Council; Id: http://dx.doi.org/10.13039/501100000270; Grant(s): NE/R008825/1Funder: Biotechnology and Biological Sciences Research Council; Id: http://dx.doi.org/10.13039/501100000268; Grant(s): BB/R014884/1Conjugative plasmids play an important role in bacterial evolution by transferring niche-adaptive traits between lineages, thus driving adaptation and genome diversification. It is increasingly clear, however, that in addition to this evolutionary role, plasmids also manipulate the expression of a broad range of bacterial phenotypes. In this review, we argue that the effects that plasmids have on the expression of bacterial phenotypes may often represent plasmid adaptations, rather than mere deleterious side effects. We begin by summarizing findings from untargeted omics analyses, which give a picture of the global effects of plasmid acquisition on host cells. Thereafter, because many plasmids are capable of both vertical and horizontal transmission, we distinguish plasmid-mediated phenotypic effects into two main classes based upon their potential fitness benefit to plasmids: (i) those that promote the competitiveness of the host cell in a given niche and thereby increase plasmid vertical transmission, and (ii) those that promote plasmid conjugation and thereby increase plasmid horizontal transmission. Far from being mere vehicles for gene exchange, we propose that plasmids often act as sophisticated genetic parasites capable of manipulating their bacterial hosts for their own benefit. This article is part of the theme issue ‘The secret lives of microbial mobile genetic elements’

    Trial of Dexamethasone for Chronic Subdural Hematoma

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    BACKGROUND: Chronic subdural hematoma is a common neurologic disorder that is especially prevalent among older people. The effect of dexamethasone on outcomes in patients with chronic subdural hematoma has not been well studied. METHODS: We conducted a multicenter, randomized trial in the United Kingdom that enrolled adult patients with symptomatic chronic subdural hematoma. The patients were assigned in a 1:1 ratio to receive a 2-week tapering course of oral dexamethasone, starting at 8 mg twice daily, or placebo. The decision to surgically evacuate the hematoma was made by the treating clinician. The primary outcome was a score of 0 to 3, representing a favorable outcome, on the modified Rankin scale at 6 months after randomization; scores range from 0 (no symptoms) to 6 (death). RESULTS: From August 2015 through November 2019, a total of 748 patients were included in the trial after randomization - 375 were assigned to the dexamethasone group and 373 to the placebo group. The mean age of the patients was 74 years, and 94% underwent surgery to evacuate their hematomas during the index admission; 60% in both groups had a score of 1 to 3 on the modified Rankin scale at admission. In a modified intention-to-treat analysis that excluded the patients who withdrew consent for participation in the trial or who were lost to follow-up, leaving a total of 680 patients, a favorable outcome was reported in 286 of 341 patients (83.9%) in the dexamethasone group and in 306 of 339 patients (90.3%) in the placebo group (difference, -6.4 percentage points [95% confidence interval, -11.4 to -1.4] in favor of the placebo group; P = 0.01). Among the patients with available data, repeat surgery for recurrence of the hematoma was performed in 6 of 349 patients (1.7%) in the dexamethasone group and in 25 of 350 patients (7.1%) in the placebo group. More adverse events occurred in the dexamethasone group than in the placebo group. CONCLUSIONS: Among adults with symptomatic chronic subdural hematoma, most of whom had undergone surgery to remove their hematomas during the index admission, treatment with dexamethasone resulted in fewer favorable outcomes and more adverse events than placebo at 6 months, but fewer repeat operations were performed in the dexamethasone group. (Funded by the National Institute for Health Research Health Technology Assessment Programme; Dex-CSDH ISRCTN number, ISRCTN80782810.)

    Trial of Dexamethasone for Chronic Subdural Hematoma

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    (Trial funded by NIHR, Dex-CSDH Current Controlled Trials number ISRCTN80782810). ACKNOWLEDGEMENTS In memory of Mrs. Kate Massey, who was the patient representative involved in study design. Peter Hutchinson is supported by a Research Professorship and Senior Investigator Award from the NIHR, the NIHR Cambridge Biomedical Research Centre, and the Royal College of Surgeons of England. Ellie Edlmann is supported by the Royal College of Surgeons of England. Angelos Kolias is supported by a Lectureship, School of Clinical Medicine, University of Cambridge and the Royal College of Surgeons of England. SUPPORT This paper presents independent research funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care.Peer reviewedPublisher PD

    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

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    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

    Influence of iodide ingestion on nitrate metabolism and blood pressure following short-term dietary nitrate supplementation in healthy normotensive adults

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    This paper was accepted for publication in the journal Nitric Oxide and the definitive published version is available at http://dx.doi.org/10.1016/j.niox.2016.12.008Uptake of inorganic nitrate (NO3−) into the salivary circulation is a rate-limiting step for dietary NO3− metabolism in mammals. It has been suggested that salivary NO3− uptake occurs in competition with inorganic iodide (I−). Therefore, this study tested the hypothesis that I− supplementation would interfere with NO3− metabolism and blunt blood pressure reductions after dietary NO3− supplementation. Nine healthy adults (4 male, mean ± SD, age 20 ± 1 yr) reported to the laboratory for initial baseline assessment (control) and following six day supplementation periods with 140 mL·day−1 NO3−-rich beetroot juice (8.4 mmol NO3−·day−1) and 198 mg potassium gluconate·day−1 (nitrate), and 140 mL·day−1 NO3−-rich beetroot juice and 450 μg potassium iodide·day−1 (nitrate + iodide) in a randomized, cross-over experiment. Salivary [I−] was higher in the nitrate + iodide compared to the control and NIT trials (P < 0.05). Salivary and plasma [NO3−] and [NO2−] were higher in the nitrate and nitrate + iodide trials compared to the control trial (P < 0.05). Plasma [NO3−] was higher (474 ± 127 vs. 438 ± 117 μM) and the salivary-plasma [NO3−] ratio was lower (14 ± 6 vs. 20 ± 6 μM), indicative of a lower salivary NO3− uptake, in the nitrate + iodide trial compared to the nitrate trial (P < 0.05). Plasma and salivary [NO2−] were not different between the nitrate and nitrate + iodide trials (P > 0.05). Systolic blood pressure was lower than control (112 ± 13 mmHg) in the nitrate (106 ± 13 mmHg) and nitrate + iodide (106 ± 11 mmHg) trials (P < 0.05), with no differences between the nitrate and nitrate + iodide trials (P > 0.05). In conclusion, co-ingesting NO3− and I− perturbed salivary NO3− uptake, but the increase in salivary and plasma [NO2−] and the lowering of blood pressure were similar compared to NO3− ingestion alone. Therefore, increased dietary I− intake, which is recommended in several countries worldwide as an initiative to offset hypothyroidism, does not appear to compromise the blood pressure reduction afforded by increased dietary NO3− intake
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