710 research outputs found

    The spiritual revolution and suicidal ideation: an empirical enquiry among 13- to 15-year-old adolescents in England and Wales

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    The association between conventional religiosity and suicide inhibition has been well explored and documented since the pioneering work of Durkheim. Commentators like Heelas and Woodhead point to ways in which conventional religiosity is giving way in England and Wales to a range of alternative spiritualities, including renewed interest in paranormal phenomena. Taking a sample of 3095 13- to 15-year-old adolescents, the present study examines the association between suicidal ideation and both conventional religiosity and paranormal beliefs, after controlling for individual differences in sex, age and personality (extraversion, neuroticism and psychoticism). The data demonstrate that, while conventional religiosity is slightly associated with lower levels of suicidal ideation, paranormal beliefs are strongly associated with higher levels of suicidal ideation

    Barriers to equality, diversity and inclusion in research and academia stubbornly persist. So, what are we doing about it?

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    Despite an appetite for change, equality, diversity and inclusivity (EDI)-related issues continue to ripple through the world of research and academia, from inequity at the point of entry into education, through to lack of diversity and equality in senior roles. Many academic institutes and governments are taking action to solve these issues, and we welcome the growing number of inclusive practices in the science communication arena. Building from this, we – at the University of Sheffield, UK – have assessed our own situation, responded to pressures applied by research councils, and listened to our staff and student voice. Our new ‘One University’ initiative puts EDI on a par with research, innovation and education as a core university priority, and our Gender, Disability and Race Action Plans allow us to make measurable and impactful changes. Tackling EDI issues needs a collaborative approach, action at an institutional- or sector-wide level and clear commitment from senior leaders

    Enhanced cerebral blood volume under normobaric hyperoxia in the J20-hAPP mouse model of Alzheimer’s disease

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    Early impairments to neurovascular coupling have been proposed to be a key pathogenic factor in the onset and progression of Alzheimer’s disease (AD). Studies have shown impaired neurovascular function in several mouse models of AD, including the J20-hAPP mouse. In this study, we aimed to investigate early neurovascular changes using wild-type (WT) controls and J20-hAPP mice at 6 months of age, by measuring cerebral haemodynamics and neural activity to physiological sensory stimulations. A thinned cranial window was prepared to allow access to cortical vasculature and imaged using 2D-optical imaging spectroscopy (2D-OIS). After chronic imaging sessions where the skull was intact, a terminal acute imaging session was performed where an electrode was inserted into the brain to record simultaneous neural activity. We found that cerebral haemodynamic changes were significantly enhanced in J20-hAPP mice compared with controls in response to physiological stimulations, potentially due to the significantly higher neural activity (hyperexcitability) seen in the J20-hAPP mice. Thus, neurovascular coupling remained preserved under a chronic imaging preparation. Further, under hyperoxia, the baseline blood volume and saturation of all vascular compartments in the brains of J20-hAPP mice were substantially enhanced compared to WT controls, but this effect disappeared under normoxic conditions. This study highlights novel findings not previously seen in the J20-hAPP mouse model, and may point towards a potential therapeutic strategy

    The IL-1RI co-receptor TILRR (FREM1 isoform 2) controls aberrant inflammatory responses and development of vascular disease

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    Summary Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and interleukin-1 receptor regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction and in the atherosclerotic plaque, whereas levels in healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation of inflammatory genes, which underlie progression of cardiovascular disease. The authors show that genetic deletion of TILRR or antibody blocking of TILRR function reduces development of atherosclerotic plaques. Lesions exhibit decreased levels of monocytes, with increases in collagen and smooth muscle cells, characteristic features of stable plaques. The results suggest that TILRR may constitute a rational target for site- and signal-specific inhibition of vascular disease

    PENGEMBANGAN SISTEM INFORMASI AKUNTANSI PENJUALAN PADA PT. TEKNOLABINDO PENTA PERKASA

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    PENGEMBANGAN SISTEM INFORMASI AKUNTANSI PENJUALAN PADA PT. TEKNOLABINDO PENTA PERKASA
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