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Office workers spend most of their working day sitting, and prolonged sitting has been associated with increased risk of poor health. Standing in meetings has been proposed as a strategy by which to reduce workplace sitting but little is known about the standing experience. This study documented workers’ experiences of standing in normally seated meetings. Twenty-five participants (18+ years), recruited from three UK universities, volunteered to stand in 3 separate, seated meetings that they were already scheduled to attend. They were instructed to stand when and for however long they deemed appropriate, and gave semi-structured interviews after each meeting. Verbatim transcripts were analysed using Framework Analysis. Four themes, central to the experience of standing in meetings, were extracted: physical challenges to standing; implications of standing for meeting engagement; standing as norm violation; and standing as appropriation of power. Participants typically experienced some physical discomfort from prolonged standing, apparently due to choosing to stand for as long as possible, and noted practical difficulties of fully engaging in meetings while standing. Many participants experienced marked psychological discomfort due to concern at being seen to be violating a strong perceived sitting norm. While standing when leading the meeting was felt to confer a sense of power and control, when not leading the meeting participants felt uncomfortable at being misperceived to be challenging the authority of other attendees. These findings reveal important barriers to standing in normally-seated meetings, and suggest strategies for acclimatising to standing during meetings. Physical discomfort might be offset by building standing time slowly and incorporating more sit-stand transitions. Psychological discomfort may be lessened by notifying other attendees about intentions to stand. Organisational buy-in to promotional strategies for standing may be required to dispel perceptions of sitting norms, and to progress a wider workplace health and wellbeing agenda. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to investigate the role of PINK1 in Parkinson's disease, we studied PINK1 loss of function in human and primary mouse neurons. Using RNAi, we created stable PINK1 knockdown in human dopaminergic neurons differentiated from foetal ventral mesencephalon stem cells, as well as in an immortalised human neuroblastoma cell line. We sought to validate our findings in primary neurons derived from a transgenic PINK1 knockout mouse. For the first time we demonstrate an age dependent neurodegenerative phenotype in human and mouse neurons. PINK1 deficiency leads to reduced long-term viability in human neurons, which die via the mitochondrial apoptosis pathway. Human neurons lacking PINK1 demonstrate features of marked oxidative stress with widespread mitochondrial dysfunction and abnormal mitochondrial morphology. We report that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine. In addition we provide evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in PINK1 deficiency. The phenotypic effects of PINK1 loss-offunction described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD. [ABSTRACT FROM AUTHOR]