2,212 research outputs found

    The effects of catchment and riparian forest quality on stream environmental conditions across a tropical rainforest and oil palm landscape in Malaysian Borneo

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    Freshwaters provide valuable habitat and important ecosystem services, but are threatened worldwide by habitat loss and degradation. In Southeast Asia, rainforest streams are particularly threatened by logging and conversion to oil palm, but we lack information on the impacts of this on freshwater environmental conditions, and the relative importance of catchment versus riparian-scale disturbance. We studied sixteen streams in Sabah, Borneo, including old growth forest, logged forest, and oil palm sites. We assessed forest quality in riparian zones and across the whole catchment, and compared it with stream environmental conditions including water quality, structural complexity and organic inputs. We found that streams with the highest riparian forest quality were nearly 4 °C cooler, over 20 cm deeper, had over 40% less sand, greater canopy cover, more stored leaf litter and wider channels than oil palm streams with the lowest riparian forest quality. Other variables were significantly related to catchment-scale forest quality, with streams in the highest quality forest catchments having 40% more bedrock and 20 times more dead wood, along with higher phosphorus, and lower nitrate-N levels compared to streams with the lowest catchment-scale forest quality. Although riparian buffer strips went some way to protecting waterways, they did not maintain fully forest-like stream conditions. In addition, logged forest streams still showed signs of disturbance 10-15 years after selective logging. Our results suggest that maintenance and restoration of buffer strips can help to protect healthy freshwater ecosystems, but logging practices and catchment-scale forest management also need to be considered.During this work SHL was funded by a Natural Environment Research Council (NERC) studentship (number 1122589), Proforest, the Varley Gradwell Travelling Fellowship, Tim Whitmore Fund, Panton Trust and the Cambridge University Commonwealth Fund. MP and RME were supported by European Research Council Project number 281986. HB was funded by the S.T. Lee Fund

    Wind from the black-hole accretion disk driving a molecular outflow in an active galaxy

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    Powerful winds driven by active galactic nuclei (AGN) are often invoked to play a fundamental role in the evolution of both supermassive black holes (SMBHs) and their host galaxies, quenching star formation and explaining the tight SMBH-galaxy relations. Recent observations of large-scale molecular outflows in ultra-luminous infrared galaxies (ULIRGs) have provided the evidence to support these studies, as they directly trace the gas out of which stars form. Theoretical models suggest an origin of these outflows as energy-conserving flows driven by fast AGN accretion disk winds. Previous claims of a connection between large-scale molecular outflows and AGN activity in ULIRGs were incomplete because they were lacking the detection of the putative inner wind. Conversely, studies of powerful AGN accretion disk winds to date have focused only on X-ray observations of local Seyferts and a few higher redshift quasars. Here we show the clear detection of a powerful AGN accretion disk wind with a mildly relativistic velocity of 0.25c in the X-ray spectrum of IRAS F11119+3257, a nearby (z = 0.189) optically classified type 1 ULIRG hosting a powerful molecular outflow. The AGN is responsible for ~80% of the emission, with a quasar-like luminosity of L_AGN = 1.5x10^46 erg/s. The energetics of these winds are consistent with the energy-conserving mechanism, which is the basis of the quasar mode feedback in AGN lacking powerful radio jets.Comment: Revised file including the letter, methods and supplementary information. Published in the March 26th 2015 issue of Natur

    Getting into hot water:sick guppies frequent warmer thermal conditions

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    Ectotherms depend on the environmental temperature for thermoregulation and exploit thermal regimes that optimise physiological functioning. They may also frequent warmer conditions to up-regulate their immune response against parasite infection and/or impede parasite development. This adaptive response, known as ‘behavioural fever’, has been documented in various taxa including insects, reptiles and fish, but only in response to endoparasite infections. Here, a choice chamber experiment was used to investigate the thermal preferences of a tropical freshwater fish, the Trinidadian guppy (Poecilia reticulata), when infected with a common helminth ectoparasite Gyrodactylus turnbulli, in female-only and mixed-sex shoals. The temperature tolerance of G. turnbulli was also investigated by monitoring parasite population trajectories on guppies maintained at a continuous 18, 24 or 32 °C. Regardless of shoal composition, infected fish frequented the 32 °C choice chamber more often than when uninfected, significantly increasing their mean temperature preference. Parasites maintained continuously at 32 °C decreased to extinction within 3 days, whereas mean parasite abundance increased on hosts incubated at 18 and 24 °C. We show for the first time that gyrodactylid-infected fish have a preference for warmer waters and speculate that sick fish exploit the upper thermal tolerances of their parasites to self medicate

    Immunohistochemical detection and regulation of α5 nicotinic acetylcholine receptor (nAChR) subunits by FoxA2 during mouse lung organogenesis

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    <p>Abstract</p> <p>Background</p> <p>α<sub>5 </sub>nicotinic acetylcholine receptor (nAChR) subunits structurally stabilize functional nAChRs in many non-neuronal tissue types. The expression of α<sub>5 </sub>nAChR subunits and cell-specific markers were assessed during lung morphogenesis by co-localizing immunohistochemistry from embryonic day (E) 13.5 to post natal day (PN) 20. Transcriptional control of α<sub>5 </sub>nAChR expression by FoxA2 and GATA-6 was determined by reporter gene assays.</p> <p>Results</p> <p>Steady expression of α<sub>5 </sub>nAChR subunits was observed in distal lung epithelial cells during development while proximal lung expression significantly alternates between abundant prenatal expression, absence at PN4 and PN10, and a return to intense expression at PN20. α<sub>5 </sub>expression was most abundant on luminal edges of alveolar type (AT) I and ATII cells, non-ciliated Clara cells, and ciliated cells in the proximal lung at various periods of lung formation. Expression of α<sub>5 </sub>nAChR subunits correlated with cell differentiation and reporter gene assays suggest expression of α<sub>5 </sub>is regulated in part by FoxA2, with possible cooperation by GATA-6.</p> <p>Conclusions</p> <p>Our data reveal a highly regulated temporal-spatial pattern of α<sub>5 </sub>nAChR subunit expression during important periods of lung morphogenesis. Due to specific regulation by FoxA2 and distinct identification of α<sub>5 </sub>in alveolar epithelium and Clara cells, future studies may identify possible mechanisms of cell differentiation and lung homeostasis mediated at least in part by α<sub>5</sub>-containing nAChRs.</p

    The 'Switch' study protocol: a randomised-controlled trial of switching to an alternative tumour-necrosis factor (TNF)-inhibitor drug or abatacept or rituximab in patients with rheumatoid arthritis who have failed an initial TNF-inhibitor drug

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    Background: Rheumatoid Arthritis (RA) is one of the most common autoimmune diseases, affecting approximately 1% of the UK adult population. Patients suffer considerable pain, stiffness and swelling and can sustain various degrees of joint destruction, deformity, and significant functional decline. In addition, the economic burden due to hospitalisation and loss of employment is considerable, with over 50% of patients being work-disabled within 10 years of diagnosis. Despite several biologic disease modifying anti-rheumatic drugs (bDMARD) now available, there is a lack of data to guide biologic sequencing. In the UK, second-line biologic treatment is restricted to a single option, rituximab. The aim of the SWITCH trial is to establish whether an alternative-mechanism-TNF-inhibitor (TNFi) or abatacept are as effective as rituximab in patients with RA who have failed an initial TNFi drug. Methods/Design: SWITCH is a pragmatic, phase IV, multi-centre, parallel-group design, open-label, randomised, controlled trial (RCT) comparing alternative-mechanism-TNFi and abatacept with rituximab in patients with RA who have failed an initial TNFi drug. Participants are randomised in a 1:1:1 ratio to receive alternative mechanism TNFi, (monoclonal antibodies: infliximab, adalimumab, certolizumab or golimumab or the receptor fusion protein, etanercept), abatacept or rituximab during the interventional phase (from randomisation up to week 48). Participants are subsequently followed up to a maximum of 96 weeks, which constitutes the observational phase. The primary objective is to establish whether an alternative-mechanism-TNFi or abatacept are non-inferior to rituximab in terms of disease response at 24 weeks post randomisation. The secondary objectives include the comparison of alternative-mechanism-TNFi and abatacept to rituximab in terms of disease response, quality of life, toxicity, safety and structural and bone density outcomes over a 12-month period (48 weeks) and to evaluate the cost-effectiveness of switching patients to alternative active therapies compared to current practice. Discussion: SWITCH is a well-designed trial in this therapeutic area that aims to develop a rational treatment algorithm to potentially inform personalised treatment regimens (as opposed to switching all patients to only one available (and possibly unsuccessful) therapy), which may lead to long-term improved patient outcomes and gains in population health

    Does publication bias inflate the apparent efficacy of psychological treatment for major depressive disorder? A systematic review and meta-analysis of US national institutes of health-funded trials

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    Background The efficacy of antidepressant medication has been shown empirically to be overestimated due to publication bias, but this has only been inferred statistically with regard to psychological treatment for depression. We assessed directly the extent of study publication bias in trials examining the efficacy of psychological treatment for depression. Methods and Findings We identified US National Institutes of Health grants awarded to fund randomized clinical trials comparing psychological treatment to control conditions or other treatments in patients diagnosed with major depressive disorder for the period 1972–2008, and we determined whether those grants led to publications. For studies that were not published, data were requested from investigators and included in the meta-analyses. Thirteen (23.6%) of the 55 funded grants that began trials did not result in publications, and two others never started. Among comparisons to control conditions, adding unpublished studies (Hedges’ g = 0.20; CI95% -0.11~0.51; k = 6) to published studies (g = 0.52; 0.37~0.68; k = 20) reduced the psychotherapy effect size point estimate (g = 0.39; 0.08~0.70) by 25%. Moreover, these findings may overestimate the "true" effect of psychological treatment for depression as outcome reporting bias could not be examined quantitatively. Conclusion The efficacy of psychological interventions for depression has been overestimated in the published literature, just as it has been for pharmacotherapy. Both are efficacious but not to the extent that the published literature would suggest. Funding agencies and journals should archive both original protocols and raw data from treatment trials to allow the detection and correction of outcome reporting bias. Clinicians, guidelines developers, and decision makers should be aware that the published literature overestimates the effects of the predominant treatments for depression

    Deletion of the GABAA α2-subunit does not alter self dministration of cocaine or reinstatement of cocaine seeking

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    Rationale GABAA receptors containing α2-subunits are highly represented in brain areas that are involved in motivation and reward, and have been associated with addiction to several drugs, including cocaine. We have shown previously that a deletion of the α2-subunit results in an absence of sensitisation to cocaine. Objective We investigated the reinforcing properties of cocaine in GABAA α2-subunit knockout (KO) mice using an intravenous self-administration procedure. Methods α2-subunit wildtype (WT), heterozygous (HT) and KO mice were trained to lever press for a 30 % condensed milk solution. After implantation with a jugular catheter, mice were trained to lever press for cocaine (0.5 mg/kg/infusion) during ten daily sessions. Responding was extinguished and the mice tested for cue- and cocaine-primed reinstatement. Separate groups of mice were trained to respond for decreasing doses of cocaine (0.25, 0.125, 0.06 and 0.03 mg/kg). Results No differences were found in acquisition of lever pressing for milk. All genotypes acquired self-administration of cocaine and did not differ in rates of self-administration, dose dependency or reinstatement. However, whilst WT and HT mice showed a dose-dependent increase in lever pressing during the cue presentation, KO mice did not. Conclusions Despite a reported absence of sensitisation, motivation to obtain cocaine remains unchanged in KO and HT mice. Reinstatement of cocaine seeking by cocaine and cocaine-paired cues is also unaffected. We postulate that whilst not directly involved in reward perception, the α2-subunit may be involved in modulating the “energising” aspect of cocaine’s effects on reward-seeking

    Serologic evidence of human orthopoxvirus infections in Sierra Leone

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    <p>Abstract</p> <p>Background</p> <p>Orthopoxviruses, including variola virus, vaccinia virus, and monkeypox virus, have previously been documented in humans in West Africa, however, no cases of human orthopoxvirus infection have been reported in the region since 1986. We conducted a serosurvey to determine whether human exposure to orthopoxviruses continues to occur in eastern Sierra Leone.</p> <p>Findings</p> <p>To examine evidence of exposure to orthopoxviruses in the Kenema District of Sierra Leone, we collected and tested sera from 1596 persons by IgG ELISA and a subset of 313 by IgM capture ELISA. Eleven persons born after the cessation of smallpox vaccination had high orthopoxvirus-specific IgG values, and an additional 6 persons had positive IgM responses. No geographic clustering was noted.</p> <p>Conclusions</p> <p>These data suggest that orthopoxviruses continue to circulate in Sierra Leone. Studies aimed at obtaining orthopoxvirus isolates and/or genetic sequences from rodents and symptomatic humans in the area are indicated.</p
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