Acidification in the Cairngorms and Lochnagar: a palaeoecological assessment

Sensitive lakes in areas of the United Kingdom with moderate to high sulphur deposition have been acidified since the middle of the nineteenth century- (Battarbee et al. 1988). Regions such as Galloway, south west Scotland (eg. Flower and Battarbee 1983, Flower et al. 1987), Wales (eg. Battarbee et al. 1988, Fritz et aL 1990), Cumbria (eg. Battarbee et al 1988, Atkinson and Haworth 1990), and Rannoch Moor in the central Scottish Highlands (eg. Flower et al 1988) have been affected. This study extends the geographical survey of lake acidification to the Caimgorm and Lochnagar regions of north east Scotland (Figure 1). The Caimgorms and Lochnagar are areas of considerable conservation value, forming the largest single area of land over 1000 m in the UK. The Caimgorm mountain plateau is a National Nature Reserve, noted for its alpine flora and fauna, whilst the Lochnagar range is a Scottish Wildlife Trust reserve. A secondary- aim of the study was to evaluate the 11land-use 11 hypothesis (eg. Rosenqvist 1977, 1978, 1981) as a mechanism for lake acidification by examining high altitude sites with no active land-management. Sites selected are all remote, lie above the tree line and have undisturbed catchments. Lochnagar and the Caimgorms are situated on sensitive granite geology (Kinniburgh and Edmunds 1986, Wells et al. 1986) in an area of moderate acid deposition (c. 0.95 g S yr-1 ). It can be predicted that sensitive lakes in this area (those having Ca2 + values of <60 μeq i-1 ) will have acidified (Battarbee 1989)

G protein-coupled receptor kinase 2 moderates recruitment of THP-1 cells to the endothelium by limiting histamine-invoked Weibel-Palade body exocytosis.

G protein-coupled receptors (GP-CRs) are a major family of signaling molecules, central to the regulation of inflammatory responses. Their activation upon agonist binding is attenuated by GPCR kinases (GRKs), which desensitize the receptors through phosphorylation. G protein-coupled receptor kinase 2(GRK2) down-regulation in leukocytes has been closely linked to the progression of chronic inflammatory disorders such as rheumatoid arthritis and multiple sclerosis. Because leukocytes must interact with the endothelium to infiltrate inflamed tissues, we hypothesized that GRK2 down-regulation in endothelial cells would also be pro-inflammatory

Lake Acidification in the United Kingdom II. A preliminary report to the Department of the Environment under Contract PECD 7/10/167

This report summarises progress made in Department of the Environment project PECD 7/10/167 - "causes and extent of lake acidification in the United Kingdom". It includes data and results available at the present time and indicates where work is still in progress. We expect that all work will be completed on schedule and that a final report will be issued shortly after completion of the contract (March 31st 1990)

The Epstein-Barr Virus G-Protein-Coupled Receptor Contributes to Immune Evasion by Targeting MHC Class I Molecules for Degradation

Epstein-Barr virus (EBV) is a human herpesvirus that persists as a largely subclinical infection in the vast majority of adults worldwide. Recent evidence indicates that an important component of the persistence strategy involves active interference with the MHC class I antigen processing pathway during the lytic replication cycle. We have now identified a novel role for the lytic cycle gene, BILF1, which encodes a glycoprotein with the properties of a constitutive signaling G-protein-coupled receptor (GPCR). BILF1 reduced the levels of MHC class I at the cell surface and inhibited CD8+ T cell recognition of endogenous target antigens. The underlying mechanism involves physical association of BILF1 with MHC class I molecules, an increased turnover from the cell surface, and enhanced degradation via lysosomal proteases. The BILF1 protein of the closely related CeHV15 c1-herpesvirus of the Rhesus Old World primate (80% amino acid sequence identity) downregulated surface MHC class I similarly to EBV BILF1. Amongst the human herpesviruses, the GPCR encoded by the ORF74 of the KSHV c2-herpesvirus is most closely related to EBV BILF1 (15% amino acid sequence identity) but did not affect levels of surface MHC class I. An engineered mutant of BILF1 that was unable to activate G protein signaling pathways retained the ability to downregulate MHC class I, indicating that the immune-modulating and GPCR-signaling properties are two distinct functions of BILF1. These findings extend our understanding of the normal biology of an important human pathogen. The discovery of a third EBV lytic cycle gene that cooperates to interfere with MHC class I antigen processing underscores the importance of the need for EBV to be able to evade CD8+ T cell responses during the lytic replication cycle, at a time when such a large number of potential viral targets are expressed

The therapeutic potential of attentional bias modification training for insomnia: study protocol for a randomised controlled trial.

The efficacy of attentional bias modification (ABM) as a treatment for anxiety and depression has been extensively studied with promising results. Despite some evidence of sleep-related attentional biases in insomnia, only a small number of studies, yielding mixed results, have examined the application of ABM in insomnia. This study specifically aims to determine whether ABM can reduce (i) the presence of an attentional bias for sleep-related threatening words; (ii) insomnia symptom severity; (iii) sleep onset latency; and (iv) pre-sleep cognitive arousal amongst individuals with insomnia compared to a non-treatment control group of individuals with insomnia. We propose a randomised controlled trial of 90 individuals from the general population who meet the criteria for Insomnia Disorder. Following an initial examination for the presence of a sleep-related attentional bias using the dot-probe paradigm, participants will be randomised to an online attentional bias modification training condition, or to a standard attentional bias task (non-treatment) control condition. Both conditions will be delivered online by a web platform. All participants allocated to the non-treatment control group will be offered ABM training once the study is complete. The primary outcome will be the attentional bias indices of vigilance and disengagement and self-reported insomnia symptoms, sleep onset latency and pre-sleep cognitive arousal. Attentional bias and insomnia symptoms will be assessed at baseline (day 1) and post-treatment (2 days after the final training session: day 9). Insomnia symptoms will be again assessed at follow-up (day 16). Secondary outcomes include examining whether sleep associated monitoring and worry are related to a sleep-related attentional bias in insomnia, and whether such reports reduce following ABM. All main analyses will be carried out on completion of follow-up assessments. The trial is supported by the Department of Psychology, Sociology and Politics at Sheffield Hallam University. This study will extend the research base examining the efficacy of attentional bias modification for insomnia. ISRCTN ( ISRCTN11643569 , registered on 5 June 2018)

Patient Care Teams in treatment of diabetes and chronic heart failure in primary care: an observational networks study

Contains fulltext : 97203.pdf (publisher's version ) (Open Access)ABSTRACT: BACKGROUND: Patient care teams have an important role in providing medical care to patients with chronic disease, but insight into how to improve their performance is limited. Two potentially relevant determinants are the presence of a central care provider with a coordinating role and an active role of the patient in the network of care providers. In this study, we aimed to develop and test measures of these factors related to the network of care providers of an individual patient. METHODS: We performed an observational study in patients with type 2 diabetes or chronic heart failure, who were recruited from three primary care practices in The Netherlands. The study focused on medical treatment, advice on physical activity, and disease monitoring. We used patient questionnaires and chart review to measure connections between the patient and care providers, and a written survey among care providers to measure their connections. Data on clinical performance were extracted from the medical records. We used network analysis to compute degree centrality coefficients for the patient and to identify the most central health professional in each network. A range of other network characteristics were computed including network centralization, density, size, diversity of disciplines, and overlap among activity-specific networks. Differences across the two chronic conditions and associations with disease monitoring were explored. RESULTS: Approximately 50% of the invited patients participated. Participation rates of health professionals were close to 100%. We identified 63 networks of 25 patients: 22 for medical treatment, 16 for physical exercise advice, and 25 for disease monitoring. General practitioners (GPs) were the most central care providers for the three clinical activities in both chronic conditions. The GP's degree centrality coefficient varied substantially, and higher scores seemed to be associated with receiving more comprehensive disease monitoring. The degree centrality coefficient of patients also varied substantially but did not seem to be associated with disease monitoring. CONCLUSIONS: Our method can be used to measure connections between care providers of an individual patient, and to examine the association between specific network parameters and healthcare received. Further research is needed to refine the measurement method and to test the association of specific network parameters with quality and outcomes of healthcare

Search for new phenomena in final states with an energetic jet and large missing transverse momentum in pp collisions at √ s = 8 TeV with the ATLAS detector

Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses 20.3 fb−1 of √ s = 8 TeV data collected in 2012 with the ATLAS detector at the LHC. Events are required to have at least one jet with pT > 120 GeV and no leptons. Nine signal regions are considered with increasing missing transverse momentum requirements between Emiss T > 150 GeV and Emiss T > 700 GeV. Good agreement is observed between the number of events in data and Standard Model expectations. The results are translated into exclusion limits on models with either large extra spatial dimensions, pair production of weakly interacting dark matter candidates, or production of very light gravitinos in a gauge-mediated supersymmetric model. In addition, limits on the production of an invisibly decaying Higgs-like boson leading to similar topologies in the final state are presente

Deletion of a Malaria Invasion Gene Reduces Death and Anemia, in Model Hosts

Malaria parasites induce complex cellular and clinical phenotypes, including anemia, cerebral malaria and death in a wide range of mammalian hosts. Host genes and parasite ‘toxins’ have been implicated in malarial disease, but the contribution of parasite genes remains to be fully defined. Here we assess disease in BALB/c mice and Wistar rats infected by the rodent malaria parasite Plasmodium berghei with a gene knock out for merozoite surface protein (MSP) 7. MSP7 is not essential for infection but in P. falciparum, it enhances erythrocyte invasion by 20%. In vivo, as compared to wild type, the P. berghei Δmsp7 mutant is associated with an abrogation of death and a decrease from 3% to 2% in peak, circulating parasitemia. The Δmsp7 mutant is also associated with less anemia and modest increase in the size of follicles in the spleen. Together these data show that deletion of a single parasite invasion ligand modulates blood stage disease, as measured by death and anemia. This work is the first to assess the contribution of a gene present in all plasmodial species in severe disease