20 research outputs found

    A serial mediation model of approaches to learning and course complaints

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    Social-psychological dimensions of learning are under-researched, but they affect student achievement. Within a marketized higher education context in England, United Kingdom, this study examined whether the relation between students’ social identities as members of their discipline and academic achievement could be further understood by considering the mediating roles of approaches to learning and frequency of making course complaints. Undergraduates (N = 679) completed a questionnaire to assess these constructs. As expected, approaches to learning and course complaining both acted as serial mediators of the link between discipline identification and academic achievement: stronger discipline identification was related to more deep approaches to learning, less complaining, and higher achievement, whereas weaker discipline identification was related to more surface approaches to learning, more complaining, and lower achievement. The findings suggest that addressing these social-psychological aspects of learning could improve students’ academic achievement

    The Relation Between Discipline Identity and Academic Achievement Within a Marketized Higher Education Context: A Serial Mediation Model of Approaches to Learning and Course Complaints

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    From Frontiers via Jisc Publications RouterHistory: received 2021-07-29, collection 2022, accepted 2022-02-09, epub 2022-09-27Peer reviewed: TruePublication status: PublishedSocial-psychological dimensions of learning are under-researched, but they affect student achievement. Within a marketized higher education context in England, United Kingdom, this study examined whether the relation between students’ social identities as members of their discipline and academic achievement could be further understood by considering the mediating roles of approaches to learning and frequency of making course complaints. Undergraduates (N = 679) completed a questionnaire to assess these constructs. As expected, approaches to learning and course complaining both acted as serial mediators of the link between discipline identification and academic achievement: stronger discipline identification was related to more deep approaches to learning, less complaining, and higher achievement, whereas weaker discipline identification was related to more surface approaches to learning, more complaining, and lower achievement. The findings suggest that addressing these social-psychological aspects of learning could improve students’ academic achievement

    Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue

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    Susceptibility to prostate or endometrial cancer is linked with obesity, a state of oestrogen excess. Oestrogen receptor (ER) splice variants may be responsible for the tissue-level of ER activity. Such micro-environmental regulation may modulate cancer initiation and/or progression mechanisms. Real-time reverse transcriptase (RT) polymerase chain reaction (PCR) was used to quantitatively assess the levels of four ER splice variants (ERαΔ3, ERαΔ5, ERβ2 and ERβ5), plus the full-length parent isoforms ERα and ERβ1, in high-risk [tumour-adjacent prostate (n = 10) or endometrial cancer (n = 9)] vs. low-risk [benign prostate (n = 12) or endometrium (n = 9)], as well as a comparison of UK (n = 12) vs. Indian (n = 15) benign prostate. All three tissue groups expressed the ER splice variants at similar levels, apart from ERαΔ5. This splice variant was markedly raised in all of the tumour-adjacent prostate samples compared to benign tissues. Immunofluorescence analysis for ERβ2 in prostate tissue demonstrated that such splice variants are present in comparable, if not greater, amounts as the parent full-length isoform. This small pilot study demonstrates the ubiquitous nature of ER splice variants in these tissue sites and suggests that ERαΔ5 may be involved in progression of prostate adenocarcinoma

    Antidepressants for the prevention of depression following first-episode psychosis (ADEPP): study protocol for a multi-centre, double-blind, randomised controlled trial

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    Background: Depressive episodes are common after first-episode psychosis (FEP), affecting more than 40% of people, adding to individual burden, poor outcomes, and healthcare costs. If the risks of developing depression were lower, this could have a beneficial effect on morbidity and mortality, as well as improving outcomes. Sertraline is a selective serotonin reuptake inhibitor and a common first-line medication for the treatment of depression in adults. It has been shown to be safe when co-prescribed with antipsychotic medication, and there is evidence that it is an effective treatment for depression in established schizophrenia. We present a protocol for a multi-centre, double-blind, randomised, placebo-controlled clinical trial called ADEPP that aims to investigate the efficacy and cost-effectiveness of sertraline in preventing depression after FEP. Methods: The recruitment target is 452 participants between the ages of 18 and 65 years who are within 12 months of treatment initiation for FEP. Having provided informed consent, participants will be randomised to receive either 50 mg of sertraline daily or matched placebo for 6 months, in addition to treatment as usual. The primary outcome measure will be a comparison of the number of new cases of depression between the treatment and placebo arms over the 6-month intervention phase. Secondary outcomes include suicidal behaviour, anxiety, rates of relapse, functional outcome, quality of life, and resource use. Discussion: The ADEPP trial will test whether the addition of sertraline following FEP is a clinically useful, acceptable, and cost-effective way of improving outcomes following FEP. Trial registration: ISRCTN12682719 registration date 24/11/2020

    Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

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    Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

    Expression of ERAlfa, its ERAlfaTrangle3 Splice Variant and Gama-SYNUCLEIN in Ovarian Cancer: A Pilot Study

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    Aims: Ovarian cancer has the highest mortality of any gynaecological malignancy; this is due to rapid peritoneal spread of tumour cells and neovascularization. Understanding the mechanisms underlying this is critical to developing early diagnostic or treatment strategies. We devised a pilot study to examine the role of g-SYNUCLEIN (g-SYN), oestrogen receptor (ER)a, and the splice variant ERaΔ3. Methodology: With ethical approval, ovarian tissue was collected from patients (n=24) undergoing oopherectomy for non-ovarian pathology or primary surgery for suspected ovarian cancer. Quantitative gene expression analysis was employed for g-SYN, ERa, and ERaΔ3. To identify the in situ localization, immunofluorescence for g-syn was carried out. Results: Ovarian tumour tissue exhibited an elevated expression of g-SYN and high-grade tumours had an elevated ERaΔ3:ERa ratio compared with benign tissue. The majority of previous studies point to the g-syn protein being present in epithelial cells of high-grade disease. Our study supports this, but additionally we conclusively identify its presence in the endothelial cells of vasculature surrounding low-grade disease; immunofluorescence was strongest in the apical cells surrounding the lumen. Conclusion: Our results demonstrate for the first time that there are readily-expressed levels of g-SYN and ERaΔ3 in normal ovarian tissue and ovarian tumours. In high-grade disease, g-syn and an elevated ERaΔ3:ERa ratio might confer metastatic potential to the tumourigenic cells and promote neoangiogenesis. Future in vitro studies might be necessary to delineate such a mechanism, which could potentially be the basis of early intervention
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