Covid-19 shelter-at-home and work, lifestyle and well-being in desk workers.

BACKGROUND: Emerging cross-sectional reports find that the COVID-19 pandemic and related social restrictions negatively affect lifestyle behaviours and mental health in general populations. AIMS: To study the longitudinal impact of COVID-19 on work practices, lifestyle and well-being among desk workers during shelter-at-home restrictions. METHODS: We added follow-up after completion of a clinical trial among desk workers to longitudinally measure sedentary behaviour, physical activity, sleep, diet, mood, quality of life and work-related health using validated questionnaires and surveys. We compared outcomes assessed before and during COVID-19 shelter-at-home restrictions. We assessed whether changes in outcomes differed by remote working status (always, changed to or never remote) using analysis of covariance (ANCOVA). RESULTS: Participants (N = 112; 69% female; mean (SD) age = 45.4 (12.3) years; follow-up = 13.5 (6.8) months) had substantial changes to work practices, including 72% changing to remote work. Deleterious changes from before to during shelter-at-home included: 1.3 (3.5)-h increase in non-workday sedentary behaviour; 0.7 (2.8)-point worsening of sleep quality; 8.5 (21.2)-point increase in mood disturbance; reductions in five of eight quality of life subscales; 0.5 (1.1)-point decrease in work-related health (P < 0.05). Other outcomes, including diet, physical activity and workday sedentary behaviour, remained stable (P ≥ 0.05). Workers who were remote before and during the pandemic had greater increases in non-workday sedentary behaviour and stress, with greater declines in physical functioning. Wake time was delayed overall by 41 (61) min, and more so in workers who changed to remote. CONCLUSIONS: Employers should consider supporting healthy lifestyle and well-being among desk workers during pandemic-related social restrictions, regardless of remote working status.

A chromaffin cell-derived protein induces the NADPH-diaphorase phenotype in cultured rat spinal cord neurons.

We have recently demonstrated that neurotrophins induce reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity in cultured spinal cord neurons. One prominent neuron population of the spinal cord expressing NADPH-diaphorase activity in vivo are preganglionic sympathetic neurons, including those innervating the adrenal medulla. These neurons receive trophic support from their target. We have shown previously that chromaffin cells contain as yet unidentified neurotrophic molecules, which may include releasable factors relevant for the survival and differentiation of developing preganglionic sympathetic neurons. We have studied the influence of proteins derived from bovine chromaffin cells and released by nicotine on NADPH-diaphorase expression in spinal cord cultures established from 16-day-old rat embryos. At this embryonic age, NADPH-diaphorase activity becomes apparent in the spinal cord and predominantly expressed in sympathetic nuclei. Similar to brain-derived neurotrophic factor and neurotrophin-4, a heat- and trypsin-sensitive component from chromaffin cells contained in granule preparations up-regulated the number of NADPH-diaphorase-positive neurons in spinal cord cultures. Combined application of this activity and neurotrophin-4 resulted in an additive effect, indicating that the effect of the chromaffin cell-derived active component is not mediated by one of the trk B ligands. This was confirmed by co-treatment studies with the trk-signalling pathway inhibitor K252b, which did not inhibit the effect of the chromaffin cell-derived protein(s). Further studies revealed that NADPH-diaphorase reactivity is inducible in spinal cord neurons at any time point throughout the entire culture period of six days, suggesting de novo induction of the enzyme rather than a survival-promoting effect of the activity from chromaffin cells. Culture supernatants from nicotine-stimulated bovine chromaffin cells induced NADPH-diaphorase-positive neurons at the same magnitude as the material obtained from chromaffin granule preparations. Our data suggest that chromaffin cell-derived proteins are capable of up-regulating NADPH-diaphorase activity or to induce de novo this transmitter phenotype in neuron populations of the spinal cord, which may include preganglionic sympathetic neurons.

The neurotrophins BDNF, NT-3 and -4, but not NGF, TGF-beta 1 and GDNF, increase the number of NADPH-diaphorase-reactive neurons in rat spinal cord cultures.

Neurotrophins have multiple functions for the development of the nervous system. They can promote survival and differentiation of select neuronal populations, but have also been shown to play instructive roles in the determination of the transmitter phenotype of neurons. We have investigated the influence of neurotrophins on the expression of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), a histochemical marker for nitric oxide synthase, in spinal cord cultures established from 16-day-old rat embryos. At this embryonic age we found NADPH-d reactivity becoming apparent in the spinal cord and predominantly expressed in preganglionic autonomic nuclei. Numbers of NADPH-d-positive neurons in spinal cord cultures were very low 24 h after plating. They did not change significantly until day 4 in vitro. However, treatment with the neurotrophins BDNF, NT-3 or NT-4 significantly increased their numbers. The effect became apparent after just 24 h, and was significant with concentrations as low as 1 ng/ml. Treatment with BDNF, NT-3 and NT-4 also augmented numbers of NADPH-d-positive neurons when initiated after three or five days in culture, and became consistently apparent within 24 h. This suggests that the neurotrophin-mediated increase in NADPH-d-positive neurons is unlikely to be due to promotion of neuron survival. NGF and two members of the transforming growth factor-beta superfamily, which have pronounced trophic effects on select neuron populations in vitro, TGF-beta 1 and GDNF, were not effective. Combined application of NT-4 and NT-3 had no additive effect. Our data therefore suggest that neurotrophins are involved in the developmental regulation of NADPH-d activity in neuron populations of the spinal cord. Neuron populations affected may include preganglionic autonomic neurons. NADPH-d activity may be induced in neurons expressing the enzyme constitutively, yet at undetectable levels, or may be induced de novo.