Managing pressure: patterns of appraisals and coping strategies of non-elite and elite athletes during competition

The purpose of this study was to compare moment-to-moment appraisals and coping strategies of 4 non-elite and 2 elite male trap shooters during competitions and in particular during periods of competition perceived as critical to performance. Appraisals and coping patterns of trap shooters were captured via verbal reports of thinking provided between sets of shots during major competitions. Verbal reports were coded according to an appraisal and coping typology. Coded data as well as shooting performance data were subjected to a sequential analysis of probabilities of pairs of events. Fewer reports of negative appraisals (NEGAs) and more frequent reports of problem-focused coping (PFC) were observed among both elite athletes compared to non-elite athletes. After making a NEGA, non-elite shooters often progressed to the next target without attempting to cope, whereas elite shooters used both PFC and emotion-focused coping (EFC) before proceeding to the next target. After missing a target, the non-elite athletes used more EFC than expected. These results indicate that elite athletes are more likely to cope with NEGAs than non-elite athletes using a wider variety of coping strategies. Athletes might benefit from increased awareness of the potentially detrimental impact of NEGAs on performance and by integrating coping strategies within preparatory routines.

Covert dose reduction is a distinct type of medication non-adherence observed across all care settings in inflammatory bowel disease.

BACKGROUND: Non-adherence by dose omission is common and deleterious to outcomes in Inflammatory Bowel Disease (IBD), but covert dose reduction (CDR) remains unexplored. AIMS: To determine frequency and attitudinal predictors of overall medication non-adherence and of covert dose reduction as separate entities. METHODS: A cross sectional questionnaire was undertaken involving IBD patients in three different geographical regions and care settings. Demographics, medication adherence by dose omission, and rate of patient initiated dose reduction of conventional meds without practitioner knowledge (CDR) were assessed, along with attitudes toward IBD medication. RESULTS: Of 473 respondents (mean age 50.3 years, 60.2% female) frequency of non-adherence was 21.9%, and CDR 26.9% (p<0.001). By logistic regression, significant independent predictors of non-adherence were dissatisfaction with the patient-doctor relationship (p<0.001), depression (p=0.001), anxiety (p=0.047), and negative views regarding medication efficacy (p<0.001) or safety (p=0.017). Independent predictors of covert dose reduction included regular complementary medicine (CAM) use (p<0.001), experiencing more informative (p<0.001) and comfortable (p=0.006) consultations with alternative practitioners, disbelieving doctor delivered information (p=0.021) and safety concerns regarding conventional medication (p<0.001). Neither the frequency of non-adherence (p=0.569) nor CDR (p=0.914) differed between cohorts by different treatment settings. CONCLUSIONS: Covert dose reduction of IBD medication is more common than omission of medication doses, predicted by different factors to usual non-adherence, and has not been previously reported in IBD. The strongest predictor of CDR is regular CAM use.

Quand les interactions avec les professionnels orientent le choix des sources de soutien des proches aidants accompagnant à domicile une personne âgée atteinte d’un trouble de l’humeur

Méthodologie: Théorisation ancrée, Interactionnisme symbolique

Non-indigenous Japanese oyster drill Pteropurpura (Ocinebrellus) inornata (Récluz, 1851) (Gastropoda: Muricidae) on the south-west coast of Portugal

The Japanese oyster drill or rock snail Pteropurpura (Ocinebrellus) inornata (Récluz, 1851), a marine mollusc, belonging to the family Muricidae, is reported from Portugal for the first time. This non-indigenous species, most likely introduced accidentally from French oyster rearing areas into mainland Portugal, has been regularly sampled in shellfish-culture and nearby environments in Sagres, Algarve, Southwest Portugal since 2005–2008. Detailed studies are urgently needed in order to assess whether or not it has become an invasive species due to a range expansion beyond its point of initial introduction. Outputs should provide information to decision-makers to predict and limit further spread which might result in biodiversity loss and negative economical consequences in locally species-rich areas.

The role of non-coding RNA in the development of pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a progressive disease of the small pulmonary arteries, characterised by pulmonary vascular remodelling due to excessive proliferation and resistance to apoptosis of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). The increased pulmonary vascular resistance and elevated pulmonary artery pressures result in right heart failure and premature death. Germline mutations of the bone morphogenetic protein receptor-2 (bmpr2) gene, a receptor of the transforming growth factor beta (TGF-β) superfamily, account for approximately 75%-80% of the cases of heritable form of PAH (HPAH) and 20% of sporadic cases or idiopathic PAH (IPAH). IPAH patients without known bmpr2 mutations show reduced expression of BMPR2. However only ~ 20% of bmpr2-mutation carriers will develop the disease, due to an incomplete penetrance, thus the need for a ‘second hit’ including other genetic and/or environmental factors is accepted. Diagnosis of PAH occurs most frequently when patients have reached an advanced stage of disease. Although modern PAH therapies can markedly improve a patient’s symptoms and slow the rate of clinical deterioration, the mortality rate from PAH remains unacceptably high. Therefore, the development of novel therapeutic approaches is required for the treatment of this multifaceted disease. Noncoding RNAs (ncRNAs) include microRNAs (miRNAs) and long noncoding RNAs (lncRNAs). MiRNAs are ~ 22 nucleotide long and act as negative regulators of gene ex-pression via degradation or translational inhibition of their target mRNAs. Previous studies showed extensive evidence for the role of miRNAs in the development of PAH. LncRNAs are transcribed RNA molecules greater than 200 nucleotides in length. Similar to classical mRNA, lncRNAs are translated by RNA polymerase II and are generally alternatively spliced and polyadenylated. LncRNAs are highly versatile and function to regulate gene expression by diverse mechanisms. Unlike miRNAs, which exhibit well-defined actions in negatively regulating gene expression via the 3’-UTR of mRNAs, lncRNAs play more diverse and unpredictable regulatory roles. Although a number of lncRNAs have been intensively investigated in the cancer field, studies of the role of lncRNAs in vascular diseases such as PAH are still at a very early stage. The aim of this study was to investigate the involvement of specific ncRNAs in the development of PAH using experimental animal models and cell culture. The first ncRNA we focused on was miR-143, which is up-regulated in the lung and right ventricle tissues of various animal models of PH, as well as in the lungs and PASMCs of PAH patients. We show that genetic ablation of miR-143 is protective against the development of chronic hypoxia induced PH in mice, assessed via measurement of right ventricular systolic pressure (RVSP), right ventricular hypertrophy (RVH) and pulmonary vascular remodelling. We further report that knockdown of miR-143-3p in WT mice via anti-miR-143-3p administration prior to exposure of mice to chronic hypoxia significantly decreases certain indices of PH (RVSP) although no significant changes in RVH and pulmo-nary vascular remodelling were observed. However, a reversal study using antimiR-143-3p treatment to modulate miR-143-3p demonstrated a protective effect on RVSP, RVH, and muscularisation of pulmonary arteries in the mouse chronic hypoxia induced PH model. In vitro experiments showed that miR-143-3p overexpression promotes PASMC migration and inhibits PASMC apoptosis, while knockdown miR-143-3p elicits the opposite effect, with no effects observed on cellular proliferation. Interestingly, miR-143-3p-enriched exosomes derived from PASMCs mediated cell-to-cell communication between PASMCs and PAECs, contributing to the pro-migratory and pro-angiogenic phenotype of PAECs that underlies the pathogenesis of PAH. Previous work has shown that miR-145-5p expression is upregulated in the chronic hypoxia induced mouse model of PH, as well as in PAH patients. Genetic ablation and pharmacological inhibition (subcutaneous injection) of miR-145-5p exert a protective against the de-velopment of PAH. In order to explore the potential for alternative, more lung targeted delivery strategies, miR-145-5p expression was inhibited in WT mice using intranasal-delivered antimiR-145-5p both prior to and post exposure to chronic hypoxia. The decreased expression of miR-145-5p in lung showed no beneficial effect on the development of PH compared with control antimiRNA treated mice exposed to chronic hypoxia. Thus, miR-143-3p modulated both cellular and exosome-mediated responses in pulmonary vascular cells, while the inhibition of miR-143-3p prevented the development of experimental pulmonary hypertension. We focused on two lncRNAs in this project: Myocardin-induced Smooth Muscle Long noncoding RNA, Inducer of Differentiation (MYOSLID) and non-annotated Myolnc16, which were identified from RNA sequencing studies in human coronary artery smooth muscle cells (HCASMCs) that overexpress myocardin. MYOSLID was significantly in-creased in PASMCs from patients with IPAH compared to healthy controls and increased in circulating endothelial progenitor cells (EPCs) from bmpr2 mutant PAH patients. Exposure of PASMCs to hypoxia in vitro led to a significant upregulation in MYOSLID expres-sion. MYOSLID expression was also induced by treatment of PASMC with BMP4, TGF-β and PDGF, which are known to be triggers of PAH in vitro. Small interfering RNA (siR-NA)-mediated knockdown MYOSLID inhibited migration and induced cell apoptosis without affecting cell proliferation and upregulated several genes in the BMP pathway in-cluding bmpr1α, bmpr2, id1, and id3. Modulation of MYOSLID also affected expression of BMPR2 at the protein level. In addition, MYOSLID knockdown affected the BMP-Smad and BMP-non-Smad signalling pathways in PASMCs assessed by phosphorylation of Smad1/5/9 and ERK1/2, respectively. In PAECs, MYOSLID expression was also induced by hypoxia exposure, VEGF and FGF2 treatment. In addition, MYOSLID knockdown sig-nificantly decreased the proliferation of PAECs. Thus, MYOSLID may be a novel modulator in pulmonary vascular cell functions, likely through the BMP-Smad and –non-Smad pathways. Treatment of PASMCs with inflammatory cytokines (IL-1 and TNF-α) significantly in-duced the expression of Myolnc16 at a very early time point. Knockdown of Myolnc16 in vitro decreased the expression of il-6, and upregulated the expression of il-1 and il-8 in PASMCs. Moreover, the expression levels of chemokines (cxcl1, cxcl6 and cxcl8) were sig-nificantly decreased with Myolnc16 knockdown. In addition, Myolnc16 knockdown decreased the MAP kinase signalling pathway assessed by phosphorylation of ERK1/2 and p38 MAPK and inhibited cell migration and proliferation in PASMCs. Thus, Myolnc16 may a novel modulator of PASMCs functions through anti-inflammatory signalling pathways. In summary, in this thesis we have demonstrated how miR-143-3p plays a protective role in the development of PH both in vivo animal models and patients, as well as in vitro cell cul-ture. Moreover, we have showed the role of two novel lncRNAs in pulmonary vascular cells. These ncRNAs represent potential novel therapeutic targets for the treatment of PAH with further work addressing to investigate the target genes, and the pathways modulated by these ncRNAs during the development of PAH.

Barn owl feathers as biomonitors of mercury: sources of variation

Given their central role in mercury (Hg) excretion and suitability as reservoirs, bird feathers are useful Hg biomonitors. Nevertheless, the interpretation of Hg concentrations is still questioned as a result of a poor knowledge of feather physiology and mechanisms affecting Hg deposition. Given the constraints of feather availability to ecotoxicological studies, we tested the effect of intraindividual differences in Hg concentrations according to feather type (body vs. flight feathers), position in the wing and size (mass and length) in order to understand how these factors could affect Hg estimates. We measured Hg concentration of 154 feathers from 28 un-moulted barn owls (Tyto alba), collected dead on roadsides. Median Hg concentration was 0.45 (0.076–4.5) mg kg-1 in body feathers, 0.44 (0.040–4.9) mg kg-1 in primary and 0.60 (0.042–4.7) mg kg-1 in secondary feathers, and we found a poor effect of feather type on intra-individual Hg levels. We also found a negative effect of wing feather mass on Hg concentration but not of feather length and of its position in the wing. We hypothesize that differences in feather growth rate may be the main driver of between-feather differences in Hg concentrations, which can have implications in the interpretation of Hg concentrations in feathers. Finally, we recommend that, whenever possible, several feathers from the same individual should be analysed. The five innermost primaries have lowest mean deviations to both betweenfeather and intra-individual mean Hg concentration and thus should be selected under restrictive sampling scenarios.