The Effect of Organisational Factors in Motivating Healthcare Employees: A Systematic Review

Healthcare employee motivation is a key concept in the achievement of efficient,effective and good quality healthcare delivery. In this paper a systematic review of primary data from the UK, Europe, Africa and Asia was conducted to consolidate the available evidence on the effect of organisational factors on healthcare employee motivation. Because healthcare delivery is highly labour intensive, it must be acknowledged that human resources are extremely critical in the drive for healthcare organisations to deliver on their organisational goals. The organisational factors which were identified as having a great effect on healthcare employee motivation can be divided into financial and non-financial factors. Remuneration was identified as a strong extrinsic factor, while conducive working conditions, increased responsibilities and appreciation from the communities in which they serve were identified as strong intrinsic factors. Even though there is a cultural aspect to motivation, remuneration, managerial support and career advancement are core factors that affect all healthcare professionals irrespective of country. Many of the factors that were observed in the literature as affecting motivation can be addressed by an overhaul of the reward strategy of healthcare organisations

PD-L1 up-regulation restrains Th17 cell differentiation in STAT3 loss- and STAT1 gain-of-function patients

Patients with hypomorphic mutations in STAT3 and patients with hypermorphic mutations in STAT1 share several clinical and cellular phenotypes suggesting overlapping pathophysiologic mechanisms. We, therefore, examined cytokine signaling and CD4+ T cell differentiation in these cohorts to characterize common pathways. As expected, differentiation of Th17 cells was impaired in both cohorts. We found that STAT1 was hyperphosphorylated in response to cytokine stimulation in both cohorts and that STAT1-dependent PD-L1 up-regulation—known to inhibit Th17 differentiation in mouse models—was markedly enhanced as well. Overexpression of SOCS3 strongly inhibited phosphorylation of STAT1 and PD-L1 up-regulation, suggesting that diminished SOCS3 expression may lead to the observed effects. Defects in Th17 differentiation could be partially overcome in vitro via PD-L1 inhibition and in a mouse model of STAT3 loss-of-function by crossing them with PD-1 knockout mice. PD-L1 may be a potential therapeutic target in several genetic diseases of immune deficiency affecting cytokine signaling