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Stress-Related Diseases
(36 References)
Williams, T. D., K. Gensberg, et al. (2003). "A DNA expression array to detect toxic stress response in European flounder (Platichthys flesus)." Aquat Toxicol 65(2): 141-57.
As a first stage in developing a DNA array-based approach to investigating the effects of pollutants on an environmentally relevant European fish species, we have constructed a 160-gene custom microarray for European flounder. Degenerate primers were used to amplify 110 different fragments of stress-related and other genes from European flounder cDNA and genomic DNA. Additionally, 22 fragments were obtained by suppressive subtractive hybridisation (SSH). These fragments were cloned and sequenced, then, with additional control genes, used to create a cDNA microarray for flounder. After optimisation of the arraying process, hepatic mRNA was isolated from flounder caught in the polluted Tyne and relatively unpolluted Alde estuaries. Fluorescent cDNA probes were synthesised from the mRNA and used in dual-colour hybridisations to the microarray. A number of transcripts were differentially expressed between Tyne and Alde female flounder but these changes were not significant, due to high inter-individual variation. However, in comparisons between Tyne and Alde male flounder, 11 transcripts were found to significantly differ in expression (P<0.05). Seven transcripts were more highly expressed in the Tyne male fish (CYP1A, UDPGT, alpha-2HS-glycoprotein, dihydropyrimidine dehydrogenase, Cu/Zn SOD, aldehyde dehydrogenase and paraoxonase). Four transcripts (Elongation factor 1 (EF1), EF2, Int-6 and complement component C3) were found to be significantly less abundant in the Tyne male fish. Selected genes were assayed by real-time PCR, then normalised to alpha-tubulin. These assays confirmed the significance of the array results for CYP1A, UDPGT and EF1, but not for Cu/Zn SOD. This study provides a link between traditional single-gene biomarker studies and the emerging field of eco-toxicogenomics, demonstrating the utility of microarray studies on environmentally sampled, non-model organisms.
Wijnberger, L. D., T. G. Krediet, et al. (2003). "Early neonatal antioxidant capacity after preexisting impaired placental function." Early Hum Dev 71(2): 111-6.
Plasma antioxidant capacity in very preterm infants (n=17), measured as the ferric-reducing ability of plasma (FRAP), increased significantly until day 2 postpartum and decreased thereafter until day 7. Within this period, the FRAP values in matched infants, born after impaired placental function (IPF, n=17), did not change. Their FRAP values were lower and the incidence of oxidative stress-related diseases was significantly higher in these infants.
Visser, M. R., E. M. Smets, et al. (2003). "Stress, satisfaction and burnout among Dutch medical specialists." Cmaj 168(3): 271-5.
BACKGROUND: Stress and stress-related illnesses are increasing among medical specialists. This threatens the quality of patient care. In this study we investigated (a) levels of job stress and job satisfaction among medical specialists, (b) factors contributing to stress and satisfaction and (c) the effect of stress and satisfaction on burnout. METHODS: A questionnaire was mailed to a random sample of 2400 Dutch medical specialists. Measures included job stress, job satisfaction, burnout, personal characteristics, job characteristics and perceived working conditions. RESULTS: The final response rate was 63%. Of the respondents, 55% acknowledged high levels of stress, and 81% reported high job satisfaction. Personal and job characteristics explained 2%-6% of the variance in job stress and satisfaction. Perceived working conditions were more important, explaining 24% of the variance in job stress and 34% of the variance in job satisfaction. Among perceived working conditions, the interference of work on home life (odds ratio [OR] 1.54, 95% confidence interval [CI] 1.35-1.76) and not being able to live up to one's professional standards (OR 1.57, 95% CI 1.37-1.80) were most related to stress. Feeling poorly managed and resourced (OR 2.07, 95% CI 1.76-2.43) diminished job satisfaction. Burnout was explained by both high stress and low satisfaction (41% of variance explained) rather than by stress alone. INTERPRETATION: Our study showed a protective effect of job satisfaction against the negative consequences of work stress as well as the importance of organizational rather than personal factors in managing both stress and satisfaction.
Stunkard, A. J. and K. C. Allison (2003). "Two forms of disordered eating in obesity: binge eating and night eating." Int J Obes Relat Metab Disord 27(1): 1-12.
OBJECTIVE: Binge eating disorder (BED) and the night eating syndrome (NES) have been linked to obesity. This review summarizes their characteristics, implications of their diagnoses and treatment outcomes. METHOD: Selective review of the literature on BED and NES. RESULTS: BED was proposed as a distinctive disorder on the basis of two large multisite studies in the early 1990s. It is associated with more severe and earlier onset of obesity, earlier onset of dieting and greater psychopathology. It shows large placebo responses and reduction of bingeing in patients on waiting-list controls. Traditional weight reduction programs reduce bingeing at least as well as psychological treatments designed for this purpose. NES is a stress-related eating, sleeping and mood disorder that is associated with disordered neuroendocrine function. It follows a characteristic circadian pattern and has responded to an agent that enhances serotonin function. CONCLUSIONS: BED responds well to weight reduction programs. It is proposed that this diagnosis be used as a marker for psychological problems that deserve treatment in their own right. NES is an eating, sleep, and mood disorder with distinctive behavioral and neuroendocrine characteristics. Studies of treatment for NES are in their infancy but selective serotonin reuptake inhibitors (SSRI) show promise.
Sandman, C. A., L. Glynn, et al. (2003). "Maternal hypothalamic-pituitary-adrenal disregulation during the third trimester influences human fetal responses." Dev Neurosci 25(1): 41-9.
Maternal peptides from the hypothalamic-pituitary-adrenal (HPA) axis rise during human pregnancy. The effects of circulating maternal adrenocorticotropin (ACTH) and beta-endorphin (BE) on human fetal behavior was determined in 135 women during their 32nd week of gestation. Fetal behavior was measured by assessing heart rate habituation to a series of repeated vibroacoustic stimuli. Individual differences in habituation were determined by computing the number of consecutive responses above the standard deviation during a control period. There was no significant relation between levels of ACTH, BE and the rate of fetal heart rate habituation. However, an index of HPA disregulation (uncoupling of ACTH and BE) was related significantly to fetal behavior. Fetal exposure to high levels of maternal BE relative to ACTH was associated with significantly lower rates of habituation. Results indicate that maternal stress and stress-related peptides influence fetal response patterns. It is possible that this influence persists over the life span.
Sahin, K., M. Onderci, et al. (2003). "Dietary vitamin C and folic acid supplementation ameliorates the detrimental effects of heat stress in Japanese quail." J Nutr 133(6): 1882-6.
We evaluated the effects of vitamin C (L-ascorbic acid) and folic acid supplementation on performance, carcass characteristics and concentrations of the oxidative stress markers [malondialdehyde (MDA), homocysteine], adrenocorticotropic hormone (ACTH), vitamins C, E, A, B-12 and folic acid, and mineral status in broiler Japanese quail (Coturnix coturnix japonica) exposed to high ambient temperature (34 degrees C, 8 h/d, 0900-1700 h). The birds (n = 150; 10-d-old) kept at 34 degrees C were fed a basal diet (HS group) or the basal diet supplemented with 250 mg of L-ascorbic acid/kg of diet (Vit C group), 1 mg of folic acid/kg of diet (FA group) or both (Vit C + FA group), whereas birds kept at 22 degrees C were fed the basal diet (TN group). Supplementing heat-stressed quail with vitamin C and folic acid improved performance compared to the HS group. Effects generally were greatest in quail supplemented with both. Although supplementation did not consistently restore concentrations to those of the TN group, it increased serum concentrations of the vitamins under study. Furthermore, serum and tissue MDA, homocysteine and ACTH concentrations were lower in the supplemented groups than in the heat-stressed controls. Retention of N, ash, Ca, P, Zn, Fe, Cu and Cr were highest in the Vit C + FA group and lowest in the HS group (P < 0.05). The results of the study indicate that vitamin C and folic acid supplementation attenuates the decline in performance and antioxidant status caused by heat stress. Such supplementation may offer protection against heat stress-related depression in performance of Japanese quail.
Roitsch, T., M. E. Balibrea, et al. (2003). "Extracellular invertase: key metabolic enzyme and PR protein." J Exp Bot 54(382): 513-24.
Extracellular invertase is the key enzyme of an apoplasmic phloem unloading pathway and catalyses the hydrolytic cleavage of the transport sugar sucrose released into the apoplast. This mechanism contributes to long-distance assimilate transport, provides the substrate to sustain heterotrophic growth and generates metabolic signals known to effect various processes of primary metabolism and defence responses. The essential function of extracellular invertase for supplying carbohydrates to sink organs was demonstrated by the finding that antisense repression of an anther-specific isoenzyme provides an efficient method for metabolic engineering of male sterility. The regulation of extracellular invertase by all classes of phytohormones indicates an essential link between the molecular mechanism of phytohormone action and primary metabolism. The up-regulation of extracellular invertase appears to be a common response to various biotic and abiotic stress-related stimuli such as pathogen infection and salt stress, in addition to specific stress-related reactions. Based on the observed co-ordinated regulation of source/sink relations and defence responses by sugars and stress-related stimuli, the identified activation of distinct subsets of MAP kinases provides a mechanism for signal integration and distribution within such complex networks. Sucrose derivatives not synthesized by higher plants, such as turanose, were shown to elicit responses distinctly different from metabolizable sugars and are rather perceived as stress-related stimuli.
Post, J., J. M. Rebel, et al. (2003). "Automated blood cell count: a sensitive and reliable method to study corticosterone-related stress in broilers." Poult Sci 82(4): 591-5.
In chickens the heterophil/lymphocyte ratio (H/L) has proved to be a valuable tool in stress related research. In general, H/L is determined with the microscopic differential count on a blood film. We evaluated automated analysis for measuring blood cell parameters in relation to corticosterone in a recently introduced corticosterone model. Discrepancies between microscopic and automated counts were found for the percentage of monocytes and basophils. The relative H/L ratio appeared to be sensitive for increased plasma corticosterone levels. However, the increase in heterophil frequencies measured with the hematology analyzer proved to be the most sensitive method for the measurement of changes in plasma corticosterone concentrations. We therefore propose automated hematological analysis as a simple and sensitive tool to study the effects of physiological corticosterone concentrations on blood cell parameters in relation to stress in broiler chickens.
Post, J., J. M. Rebel, et al. (2003). "Physiological effects of elevated plasma corticosterone concentrations in broiler chickens. An alternative means by which to assess the physiological effects of stress." Poult Sci 82(8): 1313-8.
Research on physical or psychological stress, in order to monitor objective parameters for animal welfare, is usually performed during experimental stress induction. To avoid treatment of animals with physical or physiological stress, addition of the stress-related hormone corticosterone to the drinking water, may serve as a practical alternative to reproducibly investigate hormone-related stress in broiler chickens. Rapid uptake of the hormone and distribution in the bloodstream were affirmed by elevated plasma corticosterone concentrations immediately after start of the treatment. The effect of hormone administration was evaluated by examination of corticosterone-sensitive organs. Comparable to the observations during physiological stress, we found in our model that uptake of endogenous corticosterone reduced body and spleen growth, increased heterophil counts, and decreased formation of antibodies against sheep red blood cells. Furthermore, corticosterone decreased adrenal gland responsiveness, measured by corticosterone production, after a challenge with adrenocorticotropic hormone. The simple performance, and the close relation between circulating corticosterone levels and heterophil counts, makes this an easy and quick method that is sensitive to increased levels of circulating corticosterone from base levels. The changed responsiveness of the adrenal glands to adrenocorticotropic hormone after increased circulating corticosterone levels may be an indication of the coping strategies during stress. Therefore, this test may be a promising tool in the research of adaptation to stress by broiler chickens.
Olofsson, B., C. Bengtsson, et al. (2003). "Absence of response: a study of nurses' experience of stress in the workplace." J Nurs Manag 11(5): 351-8.
It has become clear that nursing is a high-risk occupation with regards to stress-related diseases. In this study, we were interested in nurses' experiences of stress and the emotions arising from stress at work. Results showed that nurses experienced negative stress which was apparently related to the social environment in which they worked. Four nurses were interviewed. The method used was grounded theory. Analysis of the interviews singled out absence of response as the core category. Recurring stressful situations obviously caused problems for the nurses in their daily work. Not only did they lack responses from their supervisors, they also experienced emotions of frustration, powerlessness, hopelessness and inadequacy, which increased the general stress experienced at work. Our conclusion is that the experience of absence of response leads to negative stress in nurses.
Oben, J. A., T. Roskams, et al. (2003). "Sympathetic nervous system inhibition increases hepatic progenitors and reduces liver injury." Hepatology 38(3): 664-73.
Recovery from liver damage might be enhanced by encouraging repopulation of the liver by endogenous hepatic progenitor cells. Oval cells are resident hepatic stem cells that promote liver regeneration and repair. Little is known about the mediators that regulate the accumulation of these cells in the liver. Parasympathetic nervous system inhibition reduces the number of oval cells in injured livers. The effect of sympathetic nervous system (SNS) inhibition on oval cell number is not known. Adrenergic inhibition mobilizes hematopoietic precursors into the circulation and has also been shown to promote liver regeneration. Thus, we hypothesized that SNS inhibition would promote hepatic accumulation of oval cells and reduce liver damage in mice fed antioxidant-depleted diets to induce liver injury. Our results confirm this hypothesis. Compared with control mice that were fed only the antioxidant-depleted diets, mice fed the same diets with prazosin (PRZ, an alpha-1 adrenoceptor antagonist) or 6-hydroxydopamine (6-OHDA, an agent that induces chemical sympathectomy) had significantly increased numbers of oval cells. Increased oval cell accumulation was accompanied by less hepatic necrosis and steatosis, lower serum aminotransferases, and greater liver and whole body weights. Neither PRZ nor 6-OHDA affected the expression of cytokines, growth factors, or growth factor receptors that are known to regulate progenitor cells. In conclusion, stress-related sympathetic activity modulates progenitor cell accumulation in damaged livers and SNS blockade with alpha-adrenoceptor antagonists enhances hepatic progenitor cell accumulation.
Mayr, A. (2003). "Development of a non-immunising, paraspecific vaccine from attenuated pox viruses: a new type of vaccine." New Microbiol 26(1): 7-12.
The various research periods leading to the development of paraspecific vaccines are described. Paraspecific vaccines are new, pyrogen-free, non-toxic preparations that contain non-immunising antigens and can be used to generate endogenic protective, non-antigen specific mechanisms in the sense of paramunization in humans and animals. They consist of highly attenuated and inactivated (0.05% Betapropiolactone) virus strains of various poxvirus genera. They activate the T helper cells and cellular elements of the paraspecific (innate) immune system and initiate the associated production and release of cytokines (cytokine cascade) with the goal of eliminating dysfunctions of the immune systems, rapidly enhancing the individual's non-pathogen- and non-antigen-specific defences and exerting a regulatory effect on the interplay between the immune, hormone, nervous and vascular systems (signal-transduction mediators). They can be used systemically (intramuscularly) and locally (mucous membranes, skin). Immunization with paraspecific vaccines does not lead to postvaccinal complications and can be carried out as often as necessary, even for a number of years. They are compatible with conventional medicines and conventional specific vaccines. Closely linked protein complexes in the envelopes of the virus particles are responsible for their efficacy, some of those envelope protein complexes possess the properties of weak super antigens. Paraspecific vaccines have proved effective in combating viral infections, in particular herpes and hepatitis B and C infections, and chronic inflammatory diseases, and also as adjuvant therapy for tumours, for curing stress-related disturbances and dysfunctions of the immune system.
Marana, E., G. Scambia, et al. (2003). "Neuroendocrine stress response in patients undergoing benign ovarian cyst surgery by laparoscopy, minilaparotomy, and laparotomy." J Am Assoc Gynecol Laparosc 10(2): 159-65.
STUDY OBJECTIVE: To quantify and compare neuroendocrine stress responses during and immediately after surgery by laparoscopy, minilaparotomy, and laparotomy for benign ovarian cysts. DESIGN: Prospective study (Canadian Task Force classification II-1). SETTING: Tertiary care university hospital. PATIENTS: Thirty healthy women with no major diseases and without endocrine disorders. INTERVENTIONS: Surgery for benign ovarian cysts performed by laparoscopy (10), minilaparotomy (10), or laparotomy (10). MEASUREMENTS AND MAIN RESULTS: Venous blood samples were collected at fixed times as follows: at 8 A.M. in the ward before transferring the patient to the operating room (time 0), 30 minutes after the beginning of surgery (time 1), at the end of surgery after extubation with the patient awake (time 2), and 2 and 4 hours after the end of surgery (times 3 and 4). We evaluated intraoperative and postoperative variations of the following stress-related markers: norepinephrine (NE), epinephrine (E), adrenocorticotropic hormone (ACTH), human growth hormone (hGH), prolactin (PRL), and cortisol, and postoperative pain. No differences were present in demographic characteristics and operating times in the three groups. No anesthesiologic or surgical complications occurred. Postoperative pain was similar in the laparoscopy and minilaparotomy group but significantly higher in the laparotomy group (p <0.001). Serum levels of markers were not significantly different among the groups at baseline. In the laparoscopy group the increase of hGH was limited to intraoperative time (p <0.05); increases in NE, E, ACTH, and PRL were limited to intraoperative and early postoperative time after extubation (p <0.01), with only PRL persisting with significantly higher levels after the end of surgery (p <0.05). In the minilaparotomy group no increase was detected for hGH, a significant intraoperative increase in cortisol was present (p <0.05), and NE, E, ACTH, and PRL were significantly higher even after the end of surgery (p <0.01). In this group levels of NE, E, and hGH were significantly higher than in the laparoscopy group 2 and 4 hours after the end of surgery (p <0.05). In the laparotomy group significant intraoperative increases were present for all stress markers and persisted until after extubation for ACTH (p <0.01) and to the postoperative period for NE (p <0.01), E (p <0.01), cortisol (p <0.01), PRL (p <0.05), and hGH (p <0.01). In this group levels of NE, E, ACTH, and hGH were significantly higher than those in the laparoscopy group from the beginning (NE p <0.05, E p <0.01, ACTH p <0.05, hGH p <0.01) until after the end of surgery. Comparison of laparotomy and minilaparotomy groups showed the former to have significantly higher plasma levels of E, cortisol, and hGH in intraoperative and postoperative times (p <0.001); significantly higher NE at sampling times 1 and 2 (p <0.001) and time 4 (p <0.01), and no difference at sampling time 3; and ACTH significantly higher only during surgery (p <0.01). CONCLUSION: Laparoscopic surgery causes minimal activation of stress hormones, which in some instances is confined to the intraoperative period. Minilaparotomy may be a valid alternative to laparoscopy in high-risk patients who cannot tolerate abdominal distention.
Lee, Y. C., H. P. Wang, et al. (2003). "Urgent bedside endoscopy for clinically significant upper gastrointestinal hemorrhage after admission to the intensive care unit." Intensive Care Med 29(10): 1723-8.
OBJECTIVE: To investigate the sources of hemorrhage and use of endoscopic hemostasis in patients with clinically significant upper gastrointestinal (UGI) hemorrhage after admission to the intensive care unit (ICU). DESIGN AND SETTING: Prospective study, 123 beds of ICU in a 1,629-bed medical center. MEASUREMENTS AND RESULTS: Of the 9,512 consecutive admissions over a 2-year period 105 UGI hemorrhage patients underwent urgent bedside UGI endoscopy. We compared two groups of these patients, one receiving and the other not receiving endoscopic hemostasis. Ulcers with profusely bleeding stigmata occurred in 31 patients (29.5%), ulcers with clean bases or firmly adherent blood clots in 27 (25.7%), stress-related mucosal diseases in 23 (21.9%), esophageal varices in 5 (4.8%), malignancy in 4 (3.8%), and no detectable bleeding site in 15 (14.3%). Endoscopic hemostasis was attempted in 34 patients (32.4%). Primary hemostasis for them was achieved in 67.6% and the rebleeding rate was 30.4%. In-hospital mortality rate was 77.1% and death related to hemorrhage 6.2%. Length of ICU stay before endoscopic diagnosis was significantly shorter in those who underwent endoscopic hemostasis than those who did not (28.2+/-26.3 vs. 41.2+/-57.5 days). CONCLUSIONS: Endoscopic hemostasis may be more beneficial when the period between ICU admission and development of hemorrhage is shorter. Bleeders can be more readily identified and controlled endoscopically in such patients. A significant proportion of bleeding sites cannot be identified by UGI endoscopy. It may indicate higher risk of small bowel hemorrhage in these critically ill patients.
Landsbergis, P. A. (2003). "The changing organization of work and the safety and health of working people: a commentary." J Occup Environ Med 45(1): 61-72.
Recent trends in the organization of work may affect worker health through a variety of pathways--by increasing the risk of stress-related illnesses, such as cardiovascular disease, musculoskeletal disorders, and psychological disorders, by increasing exposure to hazardous substances and violence on the job, or by affecting occupational health services and training programs. Much remains to be learned about the nature of changes in work organization, and how they affect worker health and safety. While available evidence is limited, such evidence suggests that recent trends in work organization may be increasing the risk of occupational illnesses. In a groundbreaking publication, the National Institute for Occupational Safety and Health has provided a concise summary of available knowledge and a detailed agenda for research and development.
Kruidenier, L., I. Kuiper, et al. (2003). "Intestinal oxidative damage in inflammatory bowel disease: semi-quantification, localization, and association with mucosal antioxidants." J Pathol 201(1): 28-36.
Intestinal inflammation is accompanied by excessive production of reactive oxygen and nitrogen metabolites. In order to counteract their harmful effects, the intestinal mucosa contains an extensive system of antioxidants. It has previously been shown that the levels of and the balance between the most important antioxidants are seriously impaired within the intestinal mucosa from inflammatory bowel disease (IBD) patients compared with normal mucosa. The present study investigated the consequences of this antioxidative imbalance by evaluating parameters of oxidative stress-related mucosal damage in the same tissue samples. The extent of apoptosis, peroxynitrite-mediated protein nitration (3-NT), and lipid peroxidation were assessed in relation to the expression of nitric oxide synthase (NOS) and the superoxide-producing enzyme xanthine oxidase (XO). In addition, bi- and multi-variate regression analyses were performed to associate these parameters with the levels of the antioxidants assessed previously. Apoptotic cell death was visualized by TUNEL staining in luminal epithelium of normal controls, and in IBD additionally in the inflammatory infiltrate and in deeper parts of the crypts, but its frequency was unrelated to the severity of inflammation. In Crohn's disease (CD), epithelial apoptosis levels were strongly associated with the expression of XO, implying a role for this enzyme in the regulation of epithelial cell homeostasis, although its levels were unaffected by intestinal inflammation and were comparable to those in normal control mucosa. 3-NT immunoreactivity was substantially increased in luminal crypt cells, neutrophils, and mononuclear cells in the inflamed mucosa of ulcerative colitis (UC) patients. The inflamed IBD luminal epithelium, but not the inflammatory cells, also contained increased amounts of NOS. The immunoreactivity of both 3-NT and NOS was significantly higher in UC than in CD. Unexpectedly, the increased 3-NT expression in UC was associated with neutrophilic myeloperoxidase and not with NOS, which suggests that 3-NT is formed in areas with a dense neutrophilic infiltrate via a peroxynitrite-independent oxidation pathway. Lipid peroxidation, as estimated by the malondialdehyde (MDA) concentration, was elevated in both the inflamed CD and the inflamed UC mucosa, and was identified in the luminal epithelium using a histochemical technique. In CD, lipid peroxidation was independently associated with the concentration of metallothionein and with Mn-superoxide dismutase activity, suggesting the involvement of hydroxyl radicals and superoxide anions. In UC, however, the amount of MDA was associated with epithelial catalase expression and neutrophilic myeloperoxidase activity, suggesting a hydrogen peroxide- and/or hypochlorous acid-mediated mechanism. The present study underlines the importance of oxidative stress in the pathogenesis of IBD and provides clues regarding the (anti)oxidants involved which indicate that this process evolves through diverging pathways in CD and UC.
Knowlton, N. and F. Rohwer (2003). "Multispecies microbial mutualisms on coral reefs: the host as a habitat." Am Nat 162(4 Suppl): S51-62.
Reef-building corals associate with a diverse array of eukaryotic and noneukaryotic microbes. Best known are dinoflagellates in the genus Symbiodinium ("zooxanthellae"), which are photosynthetic symbionts found in all reef-building corals. Once considered a single species, they are now recognized as several large, genetically diverse groups that often co-occur within a single host species or colony. Variation among Symbiodinium in host identities, tolerance to stress, and ability to colonize hosts has been documented, but there is little information on the ecology of zooxanthellar free-living stages and how different zooxanthellae perform as partners. Other microbial associates of reef corals are much less well known, but studies indicate that individual coral colonies host diverse assemblages of bacteria, some of which seem to have species-specific associations. This diversity of microbial associates has important evolutionary and ecological implications. Most mutualisms evolve as balanced reciprocations that allow partners to detect cheaters, particularly when partners are potentially diverse and can be transmitted horizontally. Thus, environmental stresses that incapacitate the ability of partners to reciprocate can destabilize associations by eliciting rejection by their hosts. Coral bleaching (the loss of zooxanthellae) and coral diseases, both increasing over the last several decades, may be examples of stress-related mutualistic instability.
Kiuru, M. J., M. J. Mantysaari, et al. (2003). "Evaluation of stress-related anterior lower leg pain with magnetic resonance imaging and intracompartmental pressure measurement." Mil Med 168(1): 48-52.
The purpose of this work was to evaluate stress-related anterior lower leg pain with clinical examination, magnetic resonance imaging, and measurement of anterior tibial compartment pressure findings. All medical data were gathered from 24 conscripts with stress-related anterior lower leg pain. Twenty exhibited bilateral symptoms. In 22 of the 44 cases, the intracompartmental pressure was pathological. Symptoms were exhibited for longer periods by patients with chronic exertional compartment syndrome (CECS) than by other patients (p < 0.01). At rest, magnetic resonance imaging revealed no abnormal findings in the soft tissues of the legs but showed bone abnormalities in 35 symptomatic legs. Thirty-three exhibited bone stress injuries, and two exhibited leg traction periostitis. On magnetic resonance imaging, there was no difference in bone findings between patients with and without CECS (p > 0.05). Stress-related anterior lower leg pain can be related to CECS, bone stress injury, and traction periostitis. Clinical diagnosis is unreliable. CECS and bone stress injury or traction periostitis can occur separately or together.
Jezova, D., V. Kristova, et al. (2003). "Stress-induced rise in endothelaemia, von Willebrand factor and hypothalamic-pituitary-adrenocortical axis activation is reduced by pretreatment with pentoxifylline." J Physiol Pharmacol 54(3): 329-38.
Stress is considered to be a risk factor of several diseases. The following hypotheses were tested: (1) single exposure to an intensive stressor is followed by endothelial stimulation and/or damage to endothelial cells, (2) potential stress-induced endothelial cell damage is reduced by repeated pretreatment with pentoxifylline and (3) pentoxifylline treatment modifies neuroendocrine activation during stress reflected by changes in hypothalamic-pituitary-adrenocortical (HPA) axis function. Rats were treated with saline or pentoxifylline (20 mg/kg, s.c.) once daily for 7 days and then exposed to single immobilization stress for 20 or 120 min. In saline pretreated rats, stress exposure was followed by a rise in endothelaemia, von Willebrand factor concentrations, adrenocorticotropic hormone (ACTH) and corticosterone release, as well as by enhanced gene expression of hypothalamic corticotropin releasing factor (CRH). Stress-induced changes were reduced by pretreatment with pentoxifylline. Significant inhibition was observed in endothelaemia, plasma ACTH and corticosterone concentration in the adrenals. Thus, signs of endothelial injury as well as stress-induced hormone levels were reduced by pretreatment with pentoxifylline, although there is no evidence for a causal relationship. This protective action of pentoxifylline might be of benefit in the prevention and therapy of some stress-related disorders.
Jagoda, E., C. Contoreggi, et al. (2003). "Autoradiographic visualization of corticotropin releasing hormone type 1 receptors with a nonpeptide ligand: synthesis of [(76)Br]MJL-1-109-2." J Med Chem 46(17): 3559-62.
A high-affinity, nonpeptide radioligand for the CRHR1 was synthesized and showed distribution in rat brain consistent with CRHR1 using in vitro autoradiography. This is the first nonpeptide radiotracer combining high affinity and appropriate lipophilicity that penetrates the blood-brain barrier and hence has the potential to be used for PET imaging studies. In vivo visualization of changes in the CRH1 receptor or its occupancy would further the understanding of the pathophysiology of stress related diseases.
Holmes, A., M. Heilig, et al. (2003). "Neuropeptide systems as novel therapeutic targets for depression and anxiety disorders." Trends Pharmacol Sci 24(11): 580-8.
The health burden of stress-related diseases, including depression and anxiety disorders, is rapidly increasing, whereas the range of available pharmacotherapies to treat these disorders is limited and suboptimal with regard to efficacy and tolerability. Recent findings support a major role for neuropeptides in mediating the response to stress and thereby identify neuropeptide systems as potential novel therapeutic targets for the treatment of depression and anxiety disorders. In preclinical models, pharmacological and/or genetic manipulation of substance P, corticotropin-releasing factor (CRF), vasopressin, neuropeptide Y and galanin function alters anxiety- and depression-related responses. Recently, specific and highly potent small-molecule neuropeptide receptor agonists and antagonists have been developed that can readily cross the blood-brain barrier. Clinical assessment of several compounds is currently underway, with antidepressant efficacy confirmed in double-blind, placebo-controlled trials of tachykinin NK(1) (substance P) receptor antagonists, and preliminary evidence of antidepressant activity in an open-label trial of a CRF(1) receptor antagonist.
Hielm-Bjorkman, A. K., E. Kuusela, et al. (2003). "Evaluation of methods for assessment of pain associated with chronic osteoarthritis in dogs." J Am Vet Med Assoc 222(11): 1552-8.
OBJECTIVE: To identify variables and evaluate methods for assessing chronic pain in dogs. DESIGN: Prospective study. ANIMALS: 41 dogs with canine hip dysplasia (CHD), and 24 apparently healthy dogs with no history of pain. PROCEDURE: 2 veterinarians evaluated the dogs' locomotion and signs of pain. Owners of dogs with CHD and control dogs answered a questionnaire regarding their dogs' demeanor, behavior, and locomotion (descriptive scales) and assessed pain and locomotion (visual analog scales). Plasma concentrations of several stress-related hormones were determined, and 13 radiologic variables were assessed in affected hip joints. RESULTS: For many of the questions, answers provided by owners of dogs with CHD differed significantly from those of owners of control dogs. Stress hormone concentrations differed significantly between dogs with CHD and controls, but individual variation was too great for them to be of value in pain assessment. None of the radiologic variables examined correlated well with owner or veterinarian pain scores. CONCLUSIONS AND CLINICAL RELEVANCE: Chronic pain could be assessed in dogs with CHD through completion of the study questionnaire by a person familiar with the pet (eg, owner) after receiving appropriate education in its use. Eleven variables were identified as being potentially useful in assessment of chronic pain in dogs.
Hermann, J., R. Gulati, et al. (2003). "Oxidative stress-related increase in ubiquitination in early coronary atherogenesis." Faseb J 17(12): 1730-2.
The ubiquitin-proteasome system (UPS) is involved in the removal of damaged proteins and the activation of transcription factors, such as nuclear-factor-kappaB. Recent reports, however, questioned the functional activity of the UPS under conditions of increased oxidative stress, such as experimental hypercholesterolemia, which was the objective of our study. Pigs were placed on a normal chow diet (N) or on a hypercholesterolemic diet without (HC) or with vitamin C and E supplementation (HC+VIT) for 12 weeks. Compared with N, plasma concentration of total cholesterol increased in both HC and HC+VIT [76 +/- 21 vs. 400 +/- 148 (P<0.05) and 329 +/- 102 (P<0.05) mg/dL], whereas increase in lipid peroxidation, as assessed by LDL-malondialdehyde plasma concentration, was found in HC but not in HC+VIT [6.6 +/- 0.7 vs. 8.5 +/- 0.3 (P<0.05) and 6.8 +/- 0.7 nmol/mg protein]. In comparison with N, the level of ubiquitin conjugates in the coronary artery, as assessed by immunoblotting, increased by 42% in HC but not in HC+VIT and was localized predominantly to media vascular smooth muscle cells by immunostaining. There was no difference in proteasome proteolytic activity among the study groups. These results demonstrate that the UPS is functionally active in early atherogenesis despite increase in oxidative stress with important repercussions in the pathophysiology and therapy of cardiovascular diseases.
Grasso, S., C. Scifo, et al. (2003). "Adaptive responses to the stress induced by hyperthermia or hydrogen peroxide in human fibroblasts." Exp Biol Med (Maywood) 228(5): 491-8.
Perturbation of oxidant/antioxidant cellular balance, induced by cellular metabolism and by exogenous sources, causes deleterious effects to proteins, lipids, and nucleic acids, leading to a condition named "oxidative stress" that is involved in several diseases, such as cancer, ischemia-reperfusion injury, and neurodegenerative disorders. Among the exogenous agents, both H(2)O(2) and hyperthermia have been implicated in oxidative stress promotion linked with the activation of apoptotic or necrotic mechanisms of cell death. The goal of this work was to better understand the involvement of some stress-related proteins in adaptive responses mounted by human fibroblasts versus the oxidative stress differently induced by 42 degrees C hyperthermia or H(2)O(2.) The research was developed, switching off inducible nitric oxide synthase (iNOS) expression through antisense oligonucleotide transfection by studying the possible coregulation in the expression of HSP32 (also named HO-1), HSP70, and iNOS and their involvement in the induction of DNA damage. Several biochemical parameters, such as cell viability (MTT assay), cell membrane integrity (lactate dehydrogenase release), reactive oxygen species formation, glutathione levels, immunocytochemistry analysis of iNOS, HSP70, and HO-1 levels, genomic DNA fragmentation (HALO/COMET assay), and transmembrane mitochondrial potential (deltaPsi) were examined. Cells were collected immediately at the end of the stress-inducing treatment. The results, confirming the pleiotropic function of i-NOS, indicate that: (i). HO-1/HSP32, HSP70, and iNOS are finely tuned in their expression to contribute all together, in human fibroblasts, in ameliorating the resistance to oxidative stress damage; (ii). ROS exposure, at least in hyperthermia, in human fibroblasts contributes to growth arrest more than to apoptosis activation; and (iii). mitochondrial dysfunction, in presence of iNOS inhibition seems to be clearly involved in apoptotic cell death of human fibroblasts after H(2)O(2) treatment, but not after hyperthermia.
Giles, N. M., G. I. Giles, et al. (2003). "Targeting oxidative stress-related diseases: organochalcogen catalysts as redox sensitizers." Biochem Pharmacol 66(10): 2021-8.
Tumor cells proliferate under conditions of oxidative stress. A novel therapeutic approach would be to enhance the cellular effects of the reactive oxygen species formed under these conditions by supplementation with a redox catalyst. This provides a means to target and specifically destroy cancer cells via oxidation of redox-sensitive proteins, such as transcription factors, while leaving cells with a normal redox balance largely unaffected. We have previously reported a preliminary observation on the effects of pro-oxidant catalysts that enhance cancer cell death. This paper presents a detailed in vitro investigation into the mechanism of action of synthetic glutathione peroxidase mimics on a model Sp1 transcription factor peptide. The structure and redox potential of these mimics correlate with their ability to catalyze the oxidation of this zinc-binding motif by H(2)O(2) and these compounds promise therapeutic potential by promoting H(2)O(2)-induced PC12 cell death.
Frieri, M. (2003). "Neuroimmunology and inflammation: implications for therapy of allergic and autoimmune diseases." Ann Allergy Asthma Immunol 90(6 Suppl 3): 34-40.
OBJECTIVES: To review concepts of neuroendocrinoimmunology and provide an overview of the role of immune dysregulation, stress, and the understanding of the pathogenesis and treatment of allergic and autoimmune diseases. DATA SOURCES: Articles include original research papers, review articles, and references identified from the bibliographies of pertinent articles. RESULTS: Neuroendocrine hormones triggered during stress may lead to immune dysregulation or altered or amplified cytokine production, resulting in atopic, autoimmune diseases or decreased host defense. Various types of transmitter substances of the neuroendocrine-immune (NEI) network include epinephrine, norepinephrine, acetylcholine, substance P, vasoactive intestinal peptide, glucagon, insulin, cytokines, growth factors, and numerous other mediators. The stress response and induction of a dysregulation of cytokine balance can trigger the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Disorders in which abnormalities in immune function are mediated by the NEI network include allergic diseases: allergic rhinitis, atopic dermatitis, and gastro-intestinal allergies and asthma through overproduction of neuropeptides and cytokines. The multiple roles of Th2 cells in maintaining allergic inflammation and altering the balance between Th1 and Th2 responses are important mechanisms for allergic inflammation and tissue damage. In addition, several autoimmune diseases mediated by NEI network such as rheumatoid arthritis, systemic lupus erythematosus, and diabetes mellitus can be attributable to immune dysregulation. CONCLUSIONS: Understanding the NEI network will contribute to novel treatments for immediate and late allergic reactions. Chronic stress or depression could lead to decreased host defenses, decreased response to vaccines, viral susceptibility, or malignancy. Treatment of allergic, autoimmune diseases and asthma should include stress management and behavioral intervention to prevent stress-related immune imbalances.
Feldker, D. E., N. A. Datson, et al. (2003). "Serial analysis of gene expression predicts structural differences in hippocampus of long attack latency and short attack latency mice." Eur J Neurosci 17(2): 379-87.
The genetically selected long attack latency (LAL) and short attack latency (SAL) mice differ in a wide variety of behavioural traits and display differences in the serotonergic system and the hypothalamus-pituitary-adrenocortical (HPA)-axis. Serial analysis of gene expression (SAGE) was used to generate a hippocampal expression profile of almost 30 000 genes in LAL and SAL mice. Using SAGE, we found differential expression of 191 genes. Among these were genes involved in growth, signal transduction, and cell metabolism. The SAGE study was supported by GeneChip analysis (Affymetrix). Strikingly, both SAGE and GeneChips showed a higher expression of numerous cytoskeleton genes, such as cofilin and several tubulin isotypes in LAL mice. LAL mice also showed a higher expression of several calmodulin-related genes and genes encoding components of a MAPK cascade, namely raf-related oncogene and ERK2. The findings were confirmed by in situ hybridization. Our results of differential expression of cytoskeleton and signal transduction genes therefore suggest differential regulation of the raf/ERK pathway that may be related to structural differences in the hippocampus of LAL and SAL mice. As stress-related disorders, such as depression, are also linked to differential regulation of the HPA-axis and the serotonergic system and are associated with altered hippocampal morphology, differential regulation of these genes may be involved in the pathogenesis of these diseases.
Esch, T., G. L. Fricchione, et al. (2003). "The therapeutic use of the relaxation response in stress-related diseases." Med Sci Monit 9(2): RA23-34.
The objective of this work was to investigate a possible (therapeutic) connection between the relaxation response (RR) and stress-related diseases. Further, common underlying molecular mechanisms and autoregulatory pathways were examined. For the question of (patho)physiology and significance of RR techniques in the treatment of stress-related diseases, we analyzed peer-reviewed references only. The RR has been shown to be an appropriate and relevant therapeutic tool to counteract several stress-related disease processes and certain health-restrictions, particularly in certain immunological, cardiovascular, and neurodegenerative diseases/mental disorders. Further, common underlying molecular mechanisms may exist that represent a connection between the stress response, pathophysiological findings in stress-related diseases, and physiological changes/autoregulatory pathways described in the RR. Here, constitutive or low-output nitric oxide (NO) production may be involved in a protective or ameliorating context, whereas inducible, high-output NO release may facilitate detrimental disease processes. In mild or early disease states, a high degree of biological and physiological flexibility may still be possible (dynamic balance). Here, the therapeutic use of RR techniques may be considered particularly relevant, and the observable (beneficial) effects may be exerted via activation of constitutive NO pathways. RR techniques, regularly part of professional stress management or mind/body medical settings, represent an important tool to be added to therapeutic strategies dealing with stress-related diseases. Moreover, as part of 'healthy' life-style modifications, they may serve primary (or secondary) prevention. Further studies are necessary to elucidate the complex physiology underlying the RR and its impact upon stress-related disease states.
Duerksen, D. R. (2003). "Stress-related mucosal disease in critically ill patients." Best Pract Res Clin Gastroenterol 17(3): 327-44.
Stress-related mucosal disease is common in critically ill patients and can result in significant morbidity. The pathophysiology of this condition is multifactorial but mucosal ischaemia and gastric acid have pivotal roles. The major risk factors for developing stress-related mucosal bleeding are prolonged mechanical ventilation and coagulopathy. The mainstay of clinical management is prevention with acid-suppressing medications and cytoprotective agents. This chapter discusses medications used to prevent this condition and suggests an approach for management. Recent developments in gastroenterology include the development and use of proton pump inhibitors and the discovery of the association Helicobacter pylori with gastritis. The role of each of these in stress-related mucosal disease is discussed. Finally, an approach to the bleeding critically ill patient is presented.
de Kloet, E. R. (2003). "Hormones, brain and stress." Endocr Regul 37(2): 51-68.
The stress system orchestrates body and brain responses to the environment. This action exerted by the mediators of the stress system has two modes of operation. The immediate response mode driven by corticotropin-releasing hormone (CRH) organises via CRH-1 receptors the behavioural, sympathetic and hypothalamic-pituitary-adrenal (HPA) responses to a stressor. In the other - slower - mode, which facilitates behavioural adaptation, the urocortins acting through CRH-2 receptors seem prominent. Corticosteroid hormones secreted by the adrenal cortex are implicated in both modes through their high affinity type 1 (mineralocorticoid receptors - MR) and lower affinity type 2 (glucocorticoid receptors - GR) receptors that are co-localised in limbic neural circuitry. Current data suggest that MR controls in specific afferents the threshold or sensitivity of the fast CRH-1 driven stress system mode and thus prevents disturbance of homeostasis, while GR facilitates its recovery by restraining in these very same circuits stress responses and by mobilising energy resources. In preparation for future events GR facilitates behavioural adaptation and promotes storage of energy. The balance in the two stress system modes is thought to be essential for cell homeostasis, mental performance and health. Imbalance induced by genetic modification or chronic stressors changes specific neural signalling pathways underlying psychic domains of cognition and emotion, anxiety and aggression. This Yin-Yang stress concept is fundamental for genomic strategies to understand the mechanistic underpinning of cortisol-induced stress-related disorders such as i.e. severe forms of depression and co-morbid diseases.
Caine, R. M. and L. Ter-Bagdasarian (2003). "Early identification and management of critical incident stress." Crit Care Nurse 23(1): 59-65.
Everyone experiences stress. That stress may be related to work (internal), community (external), or family; it may be cumulative or related to a particular critical incident. The cost related to treating acute stress is staggering, both to individuals and to organizations. Critical care nurses are well educated in the physiological responses to the stress of acute illness. Recognizing the emotional impact of stress and the techniques to manage it in themselves and in those with whom they work is equally as important. CISD is widely advocated as an intervention after critical incidents. Although debriefing in and of itself is effective, a single-session semistructured crisis intervention will not prevent posttraumatic stress; thus, the use of CISD as part of a comprehensive multifaceted approach to the management of acute stress related to a critical incident is recommended.
C, P. D. and S. W. Bagley (2003). "Health-related challenges in United States Peace Corps Volunteers serving for two years in Madagascar." J Travel Med 10(5): 263-7.
BACKGROUND: The United States Peace Corps has nearly 8000 Volunteers (PCVs) working in more than 70 countries, predominantly in the developing part of the world. The volunteers are challenged by many new and unfamiliar health problems, as a result of change in living conditions during their service. The goal of this study was to assess the health problems of PCVs in Madagascar, and to use this information to evaluate the effectiveness of the current PCV health support program. METHODS: PCVs, finalizing their 2 years of service, were enrolled in the study. Data were retrieved from individual Peace Corps service medical records, the close of service (COS) physical evaluation, and a PCV questionnaire, which elicited additional self-reported health problems and concerns. RESULTS: Sixty-nine PCVs took part in the study. Median age at COS was 24 years (95% CI 23-26 years), and the male/female ratio was 1 : 3.6 (15 males and 54 females). Skin, gastrointestinal and respiratory infections constituted the three most common reported health problems. Among the registered parasitic infections were ova and parasites in the stool (42.0%), confirmed and presumptive malaria (15.9%) and schistosomiasis (11.6%). Female PCVs more frequently reported dermatologic manifestations than male PCVs: postadolescent acne (48.2% vs. 13.3%) and telogen hair loss (33.3% vs. 6.7%). Amenorrhea, as the most commonly reported menstrual alteration during service, was reported by 15 (27.7%) female PCVs. CONCLUSIONS: The PCVs in Madagascar encounter a broad range of health-related problems, most of which are preventable infectious diseases. Reinforcement of the preservice personal health-training curriculum later during service is needed. Reported dermatologic and menstrual disturbances in female subjects may be associated with stress-related estrogen imbalance. More studies are warranted to assess the stress impact of long-term travel on the female physiology.
Brosschot, J. F. and J. F. Thayer (2003). "Heart rate response is longer after negative emotions than after positive emotions." Int J Psychophysiol 50(3): 181-7.
Summary. Recent ambulatory findings showing comparable cardiovascular effects of positive and negative emotions are not consistent with the assumed etiological role of negative affect in stress-related diseases. We tested the hypothesis that regardless of initial reactivity, responses associated with negative emotions would be prolonged compared to responses associated with positive emotions. During 8 h, 33 healthy subjects from a general population reported their emotional arousal, emotional valence and physical activity and recorded their heart rates (HR) after a beep at each 60th min ('initial HR'; T0), followed by two 'prolonged activation' recordings, respectively 5 min later (T1) and 10 min later (T2). While emotional arousal and activity predicted initial HR, prolonged activation at T1 was solely predicted by emotional valence (negative affect) at T0, independent of emotional recovery. The results lend support to the hypothesis that cardiovascular activation after negative emotions last longer than after positive emotions. This finding is consistent with the view that prolonged activation, and not so much reactivity, might be a mechanism underlying the etiological role of negative emotions ('stress') in somatic disease. Perseverative cognition (worry, rumination) might be responsible for this prolonged activation.
Black, P. H. (2003). "The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X." Brain Behav Immun 17(5): 350-64.
In previous publications, we presented the hypothesis that repeated episodes of acute or chronic psychological stress could induce an acute phase response (APR) and subsequently a chronic inflammatory process such as atherosclerosis. In this paper, that hypothesis, namely that such stress can induce an APR and inflammation, has been extended to include a chronic inflammatory process(s), characterized by the presence of certain cytokines and acute phase reactants (APR), which is associated with certain metabolic diseases. The loci of origin of these cytokines, particularly interleukin 6 (IL-6), and their induction, has been considered. Evidence is presented that the liver, the endothelium, and fat cell depots are the primary sources of cytokines, particularly IL-6, and that IL-6 and the acute phase protein (APP), C-reactive protein (CRP), are strongly associated with, and likely play a dominant role in, the development of this inflammatory process which leads to insulin resistance, non-insulin dependent diabetes mellitus type II, and Metabolic syndrome X. The possible role of psychological stress and the major stress-related hormones as etiologic factors in the pathogenesis of these metabolic diseases, as well as atherosclerosis, is discussed. The fact that stress can activate an APR, which is part of the innate immune inflammatory response, is evidence that the inflammatory response is contained within the stress response or that stress can induce an inflammatory response. The evidence that the stress, inflammatory, and immune systems all evolved from a single cell, the phagocyte, is further evidence for their intimate relationship which almost certainly was maintained throughout evolution.
Baldaro, B., G. Gentile, et al. (2003). "Psychological distress of conservative and nonconservative uterine surgery: a prospective study." J Psychosom Res 54(4): 357-60.
OBJECTIVE: The aim of the present study is to evaluate the psychological reaction to conization before and after the operation compared to hysterectomy. To study the incidence of psychological stress related to conization, 60 women undergoing conization were compared to 40 women who had undergone hysterectomy. METHOD: Psychological disease was rated in the pre- and postoperative periods using the Symptom Questionnaire (SQ). Each patient was evaluated 2 weeks before the operation, and 3, 6 and 12 months after it. RESULTS: Both the conization and hysterectomy groups showed a significant reduction in anxiety and depression at the 3-, 6- and 12-month follow-ups compared to the preoperative period. Two weeks before surgery, 8 conization patients (19.5%) showed an anxious status, while 10 (24.3%) presented high levels of anxiety and depression. Within hysterectomy patients, the occurrence was respectively of 4 (12.9%) and 10 women (32.2%). Twelve months after surgery, of the women with preoperative depression, only four (9.7%) conization and four (12.9%) hysterectomy patients presented a negative mood status. A similar trend was present for somatic symptoms but only in the conization group, because the hysterectomy patients did not show a reduction in these symptoms from the preoperative to the postoperative period. This result could be related to the surgical menopause due to the bilateral oophoriectomy executed in more than half of the hysterectomy group. CONCLUSION: In general, the results of the present study show that the conservative and nonconservative uterine surgery determines a good psychological prognosis in the short- and long-term postoperative periods.
Ahlberg, J., M. Kononen, et al. (2003). "Self-reported stress among multiprofessional media personnel." Occup Med (Lond) 53(6): 403-5.
BACKGROUND: Recent research shows increasing rates of occupational stress and stress-related disorders. OBJECTIVE: To study self-reported stress and its association with work (work duty, working hours and shift work), sick leave and gender among multiprofessional media personnel. METHODS: We used a questionnaire study among 30- to 55-year-old radio and TV broadcasting employees (n = 1339). RESULTS: Stress was felt 'rather much' by 18% and 'very much' by 6%. Females reported stress (P < 0.05) and absence from work (P < 0.05) more often than males. The probability of having 'rather much' or 'very much' stress was significantly associated with self-reported overtime (P < 0.01) and the amount of reported sick leave (P < 0.05) CONCLUSION: Self-reported overtime and sick leave appear to be associated with higher level of self-reported stress, regardless of age, gender or work duty.