| 41. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Acute mental stress but not enforced muscle activity transiently increases natural cytotoxicity in spontaneously hypertensive rats.
- 1996
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 157:4, s. 443-9
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Tidskriftsartikel (refereegranskat)abstract
- The influence of acute mental stress and the effect of electrically induced skeletal muscle contractions on natural cytotoxicity in vivo was investigated in spontaneously hypertensive rats Natural cytotoxicity in vivo was measured as the clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs, which are specifically lysed by natural killer cells. The mental stress consisted of an air jet directed towards the animals in their cage for 25 min. During the mental stress there was a significant increase in natural cytotoxicity. Thus, retained radioactivity in the lungs was decreased to 74 +/- 6% of the control levels which was set to 100% (P < 0.01). This augmentation of YAC-1-cell clearance could be blocked with the beta-adrenergic receptor antagonist Timolol. Two hours after termination of the air stress, in vivo cytotoxicity had returned to control levels. In contrast, acute physical stress, consisting of electrically induced muscle contractions for 60 min, had no significant effects on in vivo cytotoxicity, either during the stimulation or 1, 2 or 24 h after the stimulation. Further, significantly increased plasma levels of adrenaline were seen after the air jet stress, but not after muscle stimulation. There were no significant changes in plasma noradrenaline levels either after air stress or muscle stimulation. These results indicate that changes in in vivo cytotoxicity after mild mental stress are dependent on increased plasma catecholamine levels while acute physical stress without changes in catecholamine levels, does not influence in vivo cytotoxicity.
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| 42. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
-
Chronic intracerebroventricular administration of beta-endorphin augments natural killer cell cytotoxicity in rats.
- 1996
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Ingår i: Regulatory peptides. - 0167-0115. ; 62:2-3, s. 113-8
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Tidskriftsartikel (refereegranskat)abstract
- We have studied the effect of chronic intracerebroventricular (i.c.v.) infusion of different opioid peptides on natural killer (NK) cell mediated cytotoxicity in vivo in the spontaneously hypertensive rat (SHR). The in vivo NK cell activity was measured as the clearance of 51Cr-labelled YAC-l lymphoma cells from the lung tissues. Further, the phenotype of lymphocytes in spleen and peripheral blood was analysed by flow cytometry (FACS). All opioid drugs were administered i.c.v. for 6 days with osmotic minipumps releasing 1.0 microliter/h. beta-Endorphin (10 or 20 micrograms/rat per day) significantly increased NK cell cytotoxicity in vivo. The opioid receptor antagonist naloxone (10 mg/kg, i.p.) given immediately before the injection of YAC-lymphoma cells, completely abolished the effects of i.c.v. administered beta-endorphin. Corresponding doses of beta-endorphin administered subcutaneously (s.c.) with minipumps for 6 days did not significantly affect NK cell cytotoxicity. Neither Leu- or Met-enkephalin (20 micrograms/rat per day) nor dynorphin (20 micrograms/rat per day) administered i.c.v. had any significant effects on NK cell activity. In beta-endorphin treated SHR, the percentage of cells with NK cell phenotype (OX52+/CD5-) in peripheral blood was not significantly different from that of controls, while the percentage of cells with T cell phenotype (CD5+/OX52-) was significantly decreased. The percentage of splenic NK cells (OX52+/CD5-) and T cells (CD5+/OX52-) was also unchanged by beta-endorphin treatment i.c.v. These results suggest that of the opioid peptides administered i.c.v., only beta-endorphin augments in vivo NK cell mediated cytotoxicity. We thus conclude that these effects most probably are centrally and opioid receptor mediated effects, since beta-endorphin in the same dose administered peripherally does not influence in vivo NK cell cytotoxicity.
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| 43. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Cognitive impairment in patients with stress-related exhaustion
- 2013
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Ingår i: Stress-the International Journal on the Biology of Stress. - : Informa UK Limited. - 1025-3890 .- 1607-8888. ; 16:2, s. 181-190
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Tidskriftsartikel (refereegranskat)abstract
- Patients who seek medical care for stress-related mental health problems frequently report cognitive impairments as the most pronounced symptom. The purpose of the present study was to compare cognitive function in patients with stress-related exhaustion with that in healthy controls, using a comprehensive battery of cognitive tests. We also explored whether neuropsychological findings were related to severity of illness measured using the Shirom–Melamed burnout questionnaire and hospital anxiety and depression scale. Thirty-three patients (15 males) and 37 healthy controls (11 males), mean age 46 years [standard deviation (SD) 3.9] and 47 years (SD 4.3), respectively, were included in the final analysis. Five cognitive domains were assessed: (1) speed, attention and working memory, (2) learning and episodic memory, (3) executive functions, (4) visuospatial functions and (5) language. The most pronounced difference between patients and controls was seen on executive function, when tested with a multidimensional test, including aspects of speed, control and working memory. The patients also performed poorer on Digit span, measuring attention span and working memory as well as on learning and episodic memory, when measured as delayed recall and the difference between immediate and delayed recall. Delayed recall was the only test that was significantly related to severity of burnout symptoms among the patients. This could reflect poor cognitive sustainability in the patients with the highest burnout scores, as this particular test was the last one performed during the test session. This study clearly shows that cognitive impairment should be considered when evaluating and treating patients who seek medical care for stress-related exhaustion.
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| 44. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
-
Duration and mechanisms of the increased natural cytotoxicity seen after chronic voluntary exercise in rats.
- 1997
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 160:4, s. 333-9
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Tidskriftsartikel (refereegranskat)abstract
- We have recently shown that in vivo natural cytotoxicity is enhanced after chronic exercise in spontaneously hypertensive rats (SHRs). In the present report, we have studied the duration of this augmentation and some possible mechanisms involved. Exercise consisted of voluntary running for 4-5 weeks, with the running distance ranging from 2.7-15.6 km day(-1) during the last week of running. In vivo cytotoxicity was measured as clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs. The in vivo natural cytotoxicity was increased in running SHRs, and also in SHRs that had their running wheel locked for 24 and 48 h prior to the experiment, and was still present after 96 h. The enhancement of in vivo cytotoxicity after 5 weeks of exercise was abolished after an acute injection of the beta-adrenergic receptor antagonist timolol (0.5 mg kg(-1) i.v.), indicating that catecholamines are involved in this augmentation. Interestingly, 24 h after the last exercise bout, the increased natural cytotoxicity could be blocked by timolol. The opioid receptor antagonist naloxone given subcutaneously for 7 days by osmotic pumps (6 mg kg(-1) h(-1)) could not reverse the increased in vivo cytotoxicity seen in the running SHRs, suggesting that opioid receptor mechanisms are not involved, or at least not the naloxone-sensitive mu-receptor. Natural immunity was not influenced by the histamine H2 receptor antagonist ranitidine, either in controls or in runners, indicating that the natural killer cell-regulatory effect of histamine is not present in SHRs and does not seem to be involved in the exercise-induced changes in natural immune function. We conclude that the augmentation of in vivo natural cytotoxicity after voluntary chronic exercise in rats is long-lasting and that the augmentation is partly mediated by beta-adrenergic receptors.
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| 45. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Endocrine and immunological aspects of burnout: a narrative review
- 2019
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Ingår i: European Journal of Endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 180:3, s. R147-R158
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Forskningsöversikt (refereegranskat)abstract
- Burnout has several different definitions, and attempts have been made to discriminate between burnout as a psychological construct and burnout as a clinical entity. A large body of research has focused on elucidating the biological link between stress exposure and burnout and/or finding a clinically usable biomarker for burnout. The objective of this narrative review is to summarize the main end ocrine and immune findings in relation to burnout. The literature has primarily focused on dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis. However, albeit the large body of studies, it cannot be concluded that clear effects are seen on HPA axis function in people with burnout. The HPA axis and anabolic acute reactivity to stress might be affected in clinical burnout. Plausible, effects of chronic stress might rather be seen when measuring responses to acute stress rather than resting state hormonal levels. Studies on other hormones, including thyroid hormones, prolactin and growth hormone in burnout subjects are inconclusive. It is important to note that this field is faced with many methodological challenges, one being the diurnal and pulsatile nature of many of the hormones of interest, including cortisol, which is not always considered. Another challenge is the heterogeneity regarding definitions and measurements of stress and burnout. Existing studies on burnout and immune function are heterogeneous regarding the results and no firm conclusion can be made if clinically relevant immune changes are present in burnout subjects. An overall conclusion is that existing research cannot confirm any homogenous reliable endocrinological or immunological changes related to burnout.
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| 46. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Enhancement of natural immunity seen after voluntary exercise in rats. Role of central opioid receptors.
- 2000
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Ingår i: Life sciences. - 0024-3205. ; 66:13, s. 1231-9
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Tidskriftsartikel (refereegranskat)abstract
- Chronic voluntary exercise in wheels for 5 weeks in spontaneously hypertensive rats (SHR) augments in vivo natural killer (NK) cell cytotoxicity. Endogenous beta-endorphin is increased in cerebrospinal fluid after voluntary exercise in rats and we have recently shown that beta-endorphin administered i.c.v. augments NK cell mediated cytotoxicity in vivo in a similar way as chronic voluntary exercise. We have now further investigated the involvement of central opioid systems in the exercise-induced augmentation in natural immunity. Exercise consisted of voluntary running in wheels for 5 weeks. In vivo cytotoxicity was measured as clearance of injected 51Cr-labeled YAC-1 lymphoma cells from the lungs. The clearance of YAC-1 cells in vivo was significantly increased in runners as compared to sedentary controls. Selective delta, kappa, or mu-opioid receptor antagonists were administered i.c.v. with osmotic minipumps during the last 6 days of the 5 weeks of running. The delta-receptor antagonist naltrindole (40-50 microg/day) significantly but not completely inhibited the enhanced NK-cell cytotoxicity seen after 5 weeks of exercise. Neither the kappa-receptor antagonist nor-BNI or the mu-receptor antagonist beta-FNA influenced the augmentation in NK cell cytotoxicity. Nor-BNI per se significantly augments in vivo cytotoxicity, indicating some inhibiting effect on natural immunity that could be mediated through the kappa-opioid receptor. Our data suggest the involvement of central delta-opioid receptors in the enhancement of natural cytotoxicity seen after chronic voluntary exercise.
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| 47. |
- Jonsdottir, Ingibjörg H, 1966
(författare)
-
Exercise immunology: neuroendocrine regulation of NK-cells.
- 2000
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Ingår i: International journal of sports medicine. - 0172-4622. ; 21 Suppl 1, s. S20-3
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Forskningsöversikt (refereegranskat)abstract
- Natural immunity, including that of the natural killer (NK) cells, is strongly influenced by physical exercise, but the physiological significance of the reported changes in NK cells after exercise training is as yet unclear. The exercise effect is likely mediated by interactions between the central nervous and endocrine systems. Chronic activation of endogenous opioid systems augments natural cytotoxicity. We have investigated the possible involvement of opioids in the exercise-induced enhancement of NK cell function. The pathways by which the central nervous system may communicate with the periphery include neuroendocrine outflow via the hypothalamic-pituitary-adrenal axis and the autonomic nervous system (ANS) through direct nerve fiber connections with cells or the organs of the immune system. This review will discuss the role of various neuroendocrine factors such as growth hormone, catecholamines and glucocorticoids and the role of the ANS, in particular the sympathetic division, in modulating NK cell function in response to exercise.
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| 48. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Healthcare workers' participation in a healthy-lifestyle-promotion project in western Sweden.
- 2011
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Ingår i: BMC public health. - : Springer Science and Business Media LLC. - 1471-2458. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: Background: Healthcare professionals play a central role in health promotion and lifestyle information towards patients as well as towards the general population, and it has been shown that own lifestyle habits can influence attitudes and counselling practice towards patients. The purpose of this study was to explore the participation of healthcare workers (HCWs) in a worksite health promotion (WHP) programme. We also aimed to find out whether HCWs with poorer lifestyle-related health engage in health-promotion activities to a larger extent than employees reporting healthier lifestyles. Method: A biennial questionnaire survey was used in this study, and it was originally posted to employees in the public healthcare sector in western Sweden, one year before the onset of the WHP programme. The response rate was 61% (n = 3207). In the four-year follow-up, a question regarding participation in a three-year-long WHP programme was included, and those responding to this question were included in the final analysis (n = 1859). The WHP programme used a broad all-inclusive approach, relying on the individual’s decision to participate in activities related to four different themes: physical activity, nutrition, sleep, and happiness/enjoyment. Results: The participation rate was around 21%, the most popular theme being physical activity. Indicators of lifestyle-related health/behaviour for each theme were used, and regression analysis showed that individuals who were sedentary prior to the programme were less likely to participate in the programme’s physical activities than the more active individuals. Participation in the other three themes was not significantly predicted by the indicators of the lifestyle-related health, (body mass index, sleep disturbances, or depressive mood). Conclusion: Our results indicate that HCWs are not more prone to participate in WHP programmes compared to what has been reported for other working populations, and despite a supposedly good knowledge of healthrelated issues, HCWs reporting relatively unfavourable lifestyles are not more motivated to participate. As HCWs are key actors in promoting healthy lifestyles to other groups (such as patients), it is of utmost importance to find strategies to engage this professional group in activities that promote their own health.
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| 49. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
-
Increase in nitric oxide formation after chronic voluntary exercise in spontaneously hypertensive rats.
- 1998
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 162:2, s. 149-53
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Tidskriftsartikel (refereegranskat)abstract
- The effect of chronic voluntary exercise on the plasma level of nitrate, a major stable metabolite of nitric oxide (NO) was studied in spontaneously hypertensive rats (SHR). Exercise consisted of spontaneous running in wheels for 3-35 days. Blood samples were collected after 3, 7, 14, 21 and 35 days of exercise and all samples were drawn after the running wheel had been locked during the preceding 12 h. The plasma nitrate level was significantly (P < 0.05) elevated in SHR after 35 days of exercise. Surprisingly after 7 days of exercise a significant (P < 0.001) decrease in the nitrate level in plasma was noted. Further research is needed to elucidate this biphasic change in nitrate seen in this study. The elevated level of plasma nitrate seen after 35 days of voluntary exercise was still present up to 36 h after termination of exercise. We conclude that exercise training in SHR elicits an enhanced formation of NO.
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| 50. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
-
Monocyte chemotactic protein-1 (MCP-1) and growth factors called into question as markers of prolonged psychosocial stress.
- 2009
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Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 4:11
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Psychosocial stress is becoming a major contributor to increased mental ill-health and sick leave in many countries. Valid markers of chronic stress would be valuable for diagnostic and prognostic purposes. A recent study suggested monocyte chemotactic protein-1 (MCP-1), epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) as markers of chronic stress. We aimed to confirm these potential biomarkers of prolonged psychosocial stress in female patients. METHODOLOGY/PRINCIPAL FINDINGS: Circulating levels of MCP-1, EGF and VEGF, along with several other cytokines, were measured in plasma from 42 female patients suffering from exhaustion due to prolonged psychosocial stress and 42 control subjects, using a protein biochip immunoassay. There were no significant differences between patients and controls in any of the cytokines or growth factors analyzed. Furthermore, when using a different protein bioassay and reanalyzing MCP-1 and VEGF in the same samples, markedly different levels were obtained. To further explore if inflammation is present in patients with exhaustion, the classical inflammatory marker C-reactive protein (CRP) was measured in another group of patients (n=89) and controls (n=88) showing a small but significant increase of CRP levels in the patients. CONCLUSIONS/SIGNIFICANCE: MCP-1, EGF and VEGF may not be suitable markers of prolonged psychosocial stress as previously suggested. Furthermore, significant differences were obtained when using two different protein assays measuring the same samples, indicating that comparing studies where different analytic techniques have been used might be difficult. Increased levels of CRP indicate that low-grade inflammation might be present in patients with exhaustion due to prolonged stress exposure but this inflammation does not seem to be reflected by increase in circulating MCP-1 or other cytokines measured.
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