Mixed shift rotations, sleep, burnout and well-being in professions similar to radiographers: A systematic review.

INTRODUCTION: Delivering 24 h healthcare requires rotational shift work from doctors and the medical imaging team, while contributing to safe and timely care of patients. Additional service pressure and staff shortfall leads to workload pressures, adjusted shift patterns and risk of burnout. Evidence should be sought to the effects of this work on staff. METHODS: This systematic review followed PRISMA reporting guidelines, using a convergent mixed methods approach according to Guidance from Joanna Briggs International. Quantitative trends and results were qualified in order to thematically analyse in conjunction with qualitative data and discussed together in context. Following initial searching, returned articles were screened by title and abstract. A team of 3 reviewers undertook blinded critical appraisal of those suitable, with quality assurance from a 4th team member. Papers passing a threshold of 75% on JBI appraisal tools were accepted for synthesis. Data extraction of appropriate articles retrieved was undertaken in parallel. RESULTS: Following screening and critical appraisal, 13 studies were returned focusing exclusively on Non Consultant Doctors. No studies investigated diagnostic radiographers. 85% (n = 11) reported negative association between shift work and the three themes of sleep/fatigue, burnout and wellbeing: including after the introduction of shift pattern control or adjusted shift patterns. The remainder showed no change, or any improvement nullified by countermeasures to maintain service delivery. CONCLUSION: Current working practices and shift plans in the target population showed detrimental effects on the participants - this can be suggested that Diagnostic Radiographers may suffer fatigue, burnout and poor mental health from stretched shift working patterns. IMPLICATIONS FOR PRACTICE: Further study into the effects of shift work on Diagnostic Radiographers and other allied health professionals is indicated - relating to the above themes in the context of errors and patient safety. Additional research into Non Consultant Doctors, shift work effects and the context of wider service delivery required; with suitable interventions and education to maximise understanding of legal working practices, monitoring and self-management of symptoms.

Differential distribution of Fos expression within the male rat preoptic area and hypothalamus in response to physical vs. psychological stress.

Recent studies on stress-induced adrenal glucocorticoid secretion have demonstrated quantitatively different effects of individual stress stimuli on hormone release, suggesting that the hypothalamic-pituitary-adrenal axis exhibits discriminative, rather than ubiquitous responses to such challenges, particularly psychological vs. physical stressors. The immediate-early gene, cfos, is expressed by central nervous system neurons in response to numerous physiological stimuli, including stress. The following study investigated whether the distribution and/or intensity of immunolabeling for Fos in the preoptic area and hypothalamus differ after imposition of stressors of variable intensity. Groups of male rats were sacrificed by transcardial perfusion 2 h after (1) transfer to a novel environment (NE stress), (2) confinement within a restraint tube (REST stress), or (3) immobilization (IM) stress. Nonstressed controls remained undisturbed in their home cages. Whereas the NE-stress group exhibited Fos immunoreactivity (ir) only within anterior and lateroanterior hypothalamus, both physical stressors induced immunostaining for Fos in the lateral preoptic area, median preoptic, paraventricular, arcuate, dorsomedial hypothalamic nuclei, and lateral hypothalamus, while numbers of Fos-ir-positive neurons were generally greater in the IM vs. REST stress group. In the IM-stressed rats, additional Fos-ir was observed in the supraoptic and suprachiasmatic nuclei. These studies show that neurons expressing Fos-ir in response to the relatively mild stress of novel environment are distributed differently than those that are transcriptionally activated by more aversive stressors. Findings that Fos-ir occurs in several common sites following exposure to REST or IM stress suggest that local neuron populations may comprise a common neural pathway(s) that is activated by intense forms of stress.

Induction of immediate-early gene expression in preoptic and hypothalamic neurons by the glucocorticoid receptor agonist, dexamethasone.

Glucocorticoid receptors (GR) exist in several preoptic and hypothalamic nuclei that participate in neuroendocrine control of anterior pituitary function. GR may mediate effects of endogenous steroids on hormone secretion, since intracerebral administration of exogenous ligands alters plasma levels of several pituitary hormones. The following studies utilized selective antisera for the transcriptional proteins, Fos and Jun, to examine whether these immediate-early gene products are upregulated in response to the GR agonist, dexamethasone (DEX). DEX was administered to groups of male rats by either a subcutaneous (s.c., 5.0 mg/kg) or intracerebroventricular route (i.c.v., 10.0 microg/rat); matched controls received vehicle only. Two hours later, the rats were sacrificed by transcardial perfusion, and serial 25 microm sections through the preoptic area and hypothalamus were processed by avidin-biotin immunocytochemistry for Fos- and Jun-like proteins. Animals treated with DEX i.c.v. exhibited Fos-like immunoreactivity (-li) in several sites in close proximity to the third ventricle, including the preoptic and anterior hypothalamic nuclei, and the periventricular zone of the paraventricular nucleus. In the same group, Jun-li was detected only in the arcuate and suprachiasmatic nuclei. Subcutaneous injection of DEX resulted in more widespread immunostaining for Fos, which occurred in lateral, as well as medial, loci in the preoptic area and hypothalamus, whereas Jun-li was restricted to only medial sites. These data show that discrete populations of preoptic/hypothalamic neurons express c fos and/or jun in response to GR activation. The differential distribution of Fos-li following s.c. vs. i.c.v. administration of DEX suggests that steroid induction and/or amplification of this cellular signaling cascade may depend upon resultant hormone concentrations in neural tissue. In addition, the wide pattern of immunolabeling for Fos in the systematically treated group may reflect both central and peripheral (indirect) steroid effects. Additional studies are in progress to characterize those neurons within sites of neuroendocrine significance that exhibit possible upregulation of these regulatory gene products in response to GR stimulation.

Expression of Fos-like proteins in the preoptic area and hypothalamus of the rat brain following intracerebral or peripheral administration of colchicine.

Colchicine is frequently employed as a pharmacologic tool to enhance perikaryal neuropeptide concentrations, in order to facilitate mapping of functional neuron populations in the brain. However, it is not clear if effects of colchicine on central neurons include transcriptional activation. The following studies utilized immunocytochemical techniques to evaluate the effects of intracerebroventricular (i.c.v.) drug treatment on Fos-like immunoreactivity (Fos-li) in preoptic and hypothalamic neurons. Since colchicine is administered orally in the treatment of gout-associated arthritis, additional experiments examined whether intragastric delivery of colchicine elicits protooncogene expression by neurons in the brain. Groups of adult male rats were treated with colchicine by i.c.v. injection (150 micrograms/3.0 microliters 0.9% saline) or by gavage (4.0 mg/1.0 ml 0.9% saline); vehicle-treated controls received saline alone. All animals were sacrificed 24 hr after drug or vehicle treatment. Serial 25 microns brain sections were processed for Fos-like immunoreactivity using anti-human Fos4-17 antibodies (Ab-2, Oncogene Sciences) in conjunction with avidin-biotin immunoperoxidase cytochemistry. These studies revealed negligible immunolabeling for Fos 24 hr after vehicle treatment, 24 hr after intracerebral delivery of colchicine, Fos-li was observed within the medial preoptic area, the arcuate nucleus, the supraoptic nucleus, and parvocellular neurons in the paraventricular nucleus. Animals treated with colchicine by gavage exhibited Fos-immunopositive neurons in the same sites, but additional immunolabeling for Fos was also observed within the median preoptic nucleus, suprachiasmatic nucleus, dorsomedial nucleus, and magnocellular neurons in the paraventricular nucleus. These results suggest, first of all, that neuronal responses to colchicine exposure include the synthesis of Fos-like proteins in a number of brain sites, at least over the time frame examined here. The present findings that protooncogene expression occurs within central neurons in response to intragastric drug administration suggest that neuronal activation may in response to drug-induced neural afferent and/or endocrine stimuli of peripheral origin.