ORCID Profile
0000-0001-5777-4232
Current Organisations
Chalmers tekniska hogskola
,
Karolinska Institutet
,
Healthcare Provision, Stockholm County
,
KTH Royal Institute of Technology
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Publisher: Scandinavian Journal of Work, Environment and Health
Date: 27-07-2022
DOI: 10.5271/SJWEH.4047
Abstract: Forward bending of the back is common in many jobs and a risk factor for sickness absence. However, this knowledge is based on self-reported forward bending that is generally imprecise. Thus, we aimed to investigate the dose-response relation between device-measured forward bending at work and prospective register-based risk of long-term sickness absence (LTSA). At baseline, 944 workers (93% from blue-collar jobs) wore accelerometers on their upper back and thigh over 1-6 workdays to measure worktime with forward bending (>30˚ and >60˚) and body positions. The first event of LTSA (≥6 consecutive weeks) over a 4-year follow-up were retrieved from a national register. Compositional Cox proportional hazard analyses were used to model the association between worktime with forward bending of the back in an upright body position and LTSA adjusted for age, sex, body mass index (BMI), occupational lifting/carrying, type of work, and, in an additional step, for leisure time physical activity (PA) on workdays. During a mean worktime of 457 minutes/day, the workers on average spent 40 and 10 minutes on forward bending >30˚ and >60˚ in the upright position, respectively. Five more minutes forward bending >30˚ and >60˚ at work were associated with a 4% [95% confidence interval (CI) 1.01-1.07] and 8% (95% CI 1.01-1.16) higher LTSA risk, respectively. Adjustment for leisure-time PA did not influence the results. We found a dose-response association between device-measured forward bending of the back and prospective LTSA risk. This knowledge can be integrated into available feasible methods to measure forward bending of the back for improved workplace risk assessment and prevention.
Publisher: American Physiological Society
Date: 05-2006
Abstract: Cholera toxin (CT) may induce uncontrolled firing in recurrent networks of secretomotor neurons in the submucous plexus. This hypothesis was tested in chloralose-anesthetized rats in vivo. The secretory reflex response to graded intestinal distension was measured with or without prior exposure to luminal CT. The transmural potential difference (PD) was used as a marker for electrogenic chloride secretion. In controls, distension increased PD, and this response was reduced by the neural blocker tetrodotoxin given serosally and the vasoactive intestinal peptide (VIP) receptor antagonist [4Cl-d-Phe 6 ,Leu 17 ]VIP (2 μg·min −1 ·kg −1 iv) but unaffected by the serotonin 5-HT 3 receptor antagonist granisetron, by the nicotinic receptor antagonist hexamethonium, by the muscarinic receptor antagonist atropine, or by the cyclooxygenase inhibitor indomethacin. Basal PD increased significantly with time in CT-exposed segments, an effect blocked by granisetron, by indomethacin, and by [4Cl-d-Phe 6 ,Leu 17 ]VIP but not by hexamethonium or atropine. In contrast, once the increased basal PD produced by CT was established, [4Cl-d-Phe 6 ,Leu 17 ]VIP and indomethacin had no significant effect, whereas granisetron and hexamethonium markedly depressed basal PD. CT significantly reduced the increase in PD produced by distension, an effect reversed by granisetron, indomethacin, and atropine. CT also activated a specific motility response to distension, repeated cluster contractions, but only in animals pretreated with granisetron, indomethacin, or atropine. These data are compatible with the hypothesis that CT induces uncontrolled activity in submucous secretory networks. Development of this state depends on 5-HT 3 receptors, VIP receptors, and prostaglandin synthesis, whereas its maintenance depends on 5-HT 3 and nicotinic receptors but not VIP receptors. The motility effects of CT (probably reflecting myenteric activity) are partially suppressed via a mechanism involving 5-HT 3 and muscarinic receptors and prostaglandin synthesis.
Publisher: Scandinavian Journal of Work, Environment and Health
Date: 28-11-2021
DOI: 10.5271/SJWEH.4000
Publisher: Springer Science and Business Media LLC
Date: 28-08-2010
No related grants have been discovered for Mikael Forsman.