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At least 973 records · Page 54Linked to original sources
PubMed2002

Occupational stress in consultants in accident and emergency medicine: a national survey of levels of stress at work.

OBJECTIVE: To assess levels of occupational stress in UK accident and emergency (A&E) consultants. METHOD: Postal survey of complete enumeration of UK consultants. MAIN OUTCOME MEASURES: GHQ-12 and SCL-D, and respondents' reported perceptions of stressors. RESULTS: Of 371 valid respondents (78%), 21 declined to participate. Of the remaining 350, 154 (44.4%) had GHQ-12 scores over the threshold for distress, which is much higher than found in other studies of doctors. Levels of depression as measured by the SCL-D at 18% (n=63) were slightly higher than other groups. Thirty four (10%) reported suicidal ideation. Women had significantly higher SCL-D scores than men (U=6604, p<0.01). Respondents were highly satisfied with A&E as a specialty. Protective factors found in other occupational groups did not apply. Only one demographic or work related factor; number of hours reportedly worked during previous week by respondents in full time posts (median=57, interquartile range=57), significantly correlated with either stress outcome measure (GHQ-12 scores) (rho=0.126, p<0.03). Logistic regression modelling revealed "being overstretched" (OR=1.18), "effect of hours (OR=0.82) and stress (OR=1.58) on family life", and "lack of recognition" (OR=1.32) were significant predictors of GHQ identified caseness, while "the effect of stress on family life" (OR=1.53), low prestige of specialty (OR=1.20), and "dealing with management" (OR=1.28) predicted SCL-D scores. CONCLUSION: There are high levels of psychological distress among doctors working in A&E compared with other groups of doctors. There is likely to be an effect on staff morale and career longevity. Interventions to improve the working lives of A&E consultants are required, in particular a reduction in hours worked.

Adult↗
PubMed1989

Stress resistant and stress susceptible landrace pigs: comparison of blood variables after exposure to halothane or exercise on a treadmill.

Stress susceptible pigs develop pale, soft, exudative pork as a consequence of exposure to natural stress or exposure to halothane. Hyperstimulation of glycolysis is a major component of the stress reaction. Whether natural and artificial stress have other similarities was investigated by exposing pigs to halothane or to physical exercise, and measuring their blood composition. There were many similarities between the two groups but the significant differences suggest that although both halothane and exercise induce glycolysis, the mechanisms involved are different.

Animals↗
PubMed2005

Norepinephrine-induced oxidative stress causes PC-12 cell apoptosis by both endoplasmic reticulum stress and mitochondrial intrinsic pathway: inhibition of phosphatidylinositol 3-kinase survival pathway.

Norepinephrine (NE) induces endoplasmic reticulum (ER) unfolded protein response and reduces maturation and translocation of NE transporter to cell membrane via enhanced formation of reactive oxygen species in PC-12 cells. In the present study, we investigated whether ER stress is also implicated in the proapoptotic effect of NE. We found that the apoptotic effect of NE was associated with increased processing of ER-resident pro-caspase-12, cleavage of caspase-9 and -3, and mitochondrial release of cytochrome c. ER stress was evidenced by upregulation of ER chaperone GRP78 and transcription factor CHOP and the translocation of XBP-1 from the ER to the nucleus by NE. NE also reduced phospho-Akt (Ser473), indicating suppression of the phosphatidylinositol 3-kinase (PI3-kinase)/Akt survival pathway. Similar results were produced by thapsigargin. NGF, which promotes the PI3-kinase/Akt activity, reduced the effects of NE and thapsigargin on apoptosis and activation of caspase-12 and -3. However, the effects of NE, but not of thapsigargin, were abolished by pretreatment with SOD and catalase. In contrast, the PI3-kinase inhibitors LY-294002 and wortmannin abolished the protective effects of both SOD/catalase and NGF on NE-induced apoptosis. The functional importance of caspase-12 activation was supported by the use of Z-ATAD-FMK, which reduced the NE-induced processing of caspase-12 and cell apoptosis, but the caspase-12, -9, and -3 inhibitors had no effects on the increase in cytosolic cytochrome c produced by NE. In contrast, the release of mitochondrial cytochrome c was abolished by SOD/catalase and NGF. These results indicate that NE induced cell apoptosis by both ER stress and a mitochondrial death pathway and that the effects of NE were mediated via oxidative stress and inhibition of the PI3-kinase/Akt survival pathway.

Animals↗
PubMed2001

Stress and gastrointestinal tract. II. Stress and intestinal barrier function.

The influence of stress on the clinical course of a number of intestinal diseases is increasingly being recognized, but the underlying mechanisms are largely unknown. This themes article focuses on recent findings related to the effects of stress on mucosal barrier function in the small intestine and colon. Experiments using animal models demonstrate that various types of psychological and physical stress induce dysfunction of the intestinal barrier, resulting in enhanced uptake of potentially noxious material (e.g., antigens, toxins, and other proinflammatory molecules) from the gut lumen. Evidence from several studies indicates that in this process, mucosal mast cells play an important role, possibly activated via neurons releasing corticotropin-releasing hormone and/or acetylcholine. Defining the role of specific cells and mediator molecules in stress-induced barrier dysfunction may provide clues to novel treatments for intestinal disorders.

Animals↗
PubMed2004

Norepinephrine induces endoplasmic reticulum stress and downregulation of norepinephrine transporter density in PC12 cells via oxidative stress.

Cardiac norepinephrine (NE) uptake is reduced in cardiomyopathy. This change is associated with a decrease of NE transporter (NET) receptor and can be reproduced in PC12 cells by extracellular NE. To study whether this effect of NE is mediated via impaired glycosylation and trafficking of NET in the endoplasmic reticulum (ER), we measured the distribution of glycosylated 80-kDa NET and unglycosylated 46-kDa NET in the membrane and cytosolic fractions of PC12 cells. We found that NE decreased glycosylated NET in both membrane and cytosolic fractions and increased cytosolic unglycosylated NET protein. Similar results were produced by tunicamycin and thapsigargin, two agents that induce ER stress by inhibiting N-glycosylation of membrane proteins and disrupting calcium homeostasis, respectively. Also, like the ER stressors, NE not only increased phosphorylation of both the alpha-subunit of eukaryotic initiation factor-2 and its upstream RNA-dependent protein kinase-like ER kinase over 12 h of treatment but also increased ER chaperone molecule glucose-regulated protein 78 and the nuclear transcription factor C/EBP homologous protein. Antioxidants superoxide dismutase and catalase prevented the downregulation of NET proteins and induction of ER stress signals produced by NE but not by tunicamycin or thapsigargin. The results indicate that the downregulation of membrane NET by NE is mediated by decreased N-glycosylation of NET proteins secondary to induction of ER stress pathways by NE-derived oxidative metabolites. Interventions involving the ER stress pathways may provide novel therapeutic strategies for the treatment of sympathetic dysfunction in heart failure.

Animals↗
PubMed1999

Defective ACTH response to stress in previously stressed rats: dependence on glucocorticoid status.

The effect of previous exposure to stress on the pituitary-adrenal response to a further stress was characterized in rats with different glucocorticoid status: sham-operated rats (Sham), adrenalectomized (ADX) rats, and ADX rats supplemented with a low corticosterone (B) dose in the drinking saline (ADX + B). Previous exposure of Sham rats to 1 h of immobilization (Imo) reduced, 2 h later, the ACTH response to a second severe stressor (Imo) but not to a less severe stressor (tail shock). In ADX rats, previous Imo totally suppressed the ACTH response to Imo or to shock. In ADX + B rats the response to shock was blocked and that to Imo tended to be lower. These changes were not explained by depletion of adenohypophysial ACTH stores. After previous Imo, reduced response to corticotropin-releasing factor was observed in Sham and ADX + B, but not in ADX, rats. Taken together, the present results suggest that the reduced ACTH response of previously stressed rats to a second severe stress is observed in the presence and absence of glucocorticoids, but the main site at which such inhibition occurs might be critically dependent on the glucocorticoid status.

Adrenalectomy↗
PubMed1997

Egr-1 is activated in endothelial cells exposed to fluid shear stress and interacts with a novel shear-stress-response element in the PDGF A-chain promoter.

Exposure of vascular endothelial cells to fluid mechanical forces can modulate the expression of many genes involved in vascular physiology and pathophysiology. Here, we report that platelet-derived growth factor (PDGF) A-chain gene expression is induced at the level of transcription in cultured bovine aortic endothelial cells exposed to a physiologic level of steady laminar shear stress (10 dyn/cm2). 5' Deletion analysis of the human PDGF-A promoter revealed that a GC-rich region near the TATA box was required for shear-inducible reporter gene expression. This element conferred shear inducibility onto a heterologous promoter-reporter construct that was otherwise unresponsive to shear stress. The induction of PDGF-A expression by shear was preceded by rapid and transient induction in the expression of the immediate-early gene, egr-1, which binds to GC-rich sequences. Gel shift studies indicated that shear-induced Egr-1 bound to the proximal PDGF-A promoter in a specific and time-dependent manner, displacing Sp1 from their overlapping recognition elements. Overlapping consensus binding sites for Egr-1 and Sp1 also appear in the proximal promoters of several other endothelial genes, including transforming growth factor-beta 1 and tissue factor, whose expression is modulated by shear stress. These findings define the Egr-1 binding site in the proximal PDGF-A promoter as a shear-stress-responsive element and suggest that shear-stimulated Egr-1 gene expression may be a unifying theme in the induction of various other endothelial genes exposed to biomechanical forces.

Animals↗
PubMedDate not supplied

Cardiovascular response to mental stress in normal adolescents with hypertensive parents. Hemodynamics and mental stress in adolescents.

The hemodynamic response to mental stress (mental arithmetic) was studied in adolscents with varying risk factors for essential hypertension (EH), One group (genetic) consisted of normotensive well adolescents who had at least one parentnt with EH. Another group (labile) consisted of adolescents with labile hypertension each of whom also had at least one pare with EH. The control population consisted of normotensive adolescents with a negative family history of EH. Subjects with labile hypertension demonstrated a sustained increase in systolic and diastolic pressure and heart rate during stress. This response was significantly different than the control population (P less than THE CONTROL POPULATION (P LESS THAN 0.001). The stress response of the normotensive genetic population was qualitatively similar to the group with labile hypertension and significantly different than the controls in diastolic pressure and heart rate (p less than 0.001, less than 0.02). Post-stress plasma catecholamines were higher in the labile hypertensive and genetic groups than in the control group. These findings demonstrate increased central nervous system mediated adrenergic activity and cardiovascular response in labile hypertension and also in some normotensive subjects with a genetic risk for hypertension.

Adolescent↗
PubMed2004

Assessing stress in cancer patients: a second-order factor analysis model for the Perceived Stress Scale.

Using the Perceived Stress Scale (PSS), perceptions of global stress were assessed in 111 women following breast cancer surgery and at 12 and 24 months later This is the first study to factor analyze the PSS. The PSS data were factor analyzed each time using exploratory factor analysis with oblique direct quartimin rotation. Goodness-of-fit indices (root mean square error of approximation [RMSEA]), magnitude and pattern of factor loadings, and confidence interval data revealed a two-factor solution of positive versus negative stress items. The findings, replicated across time, also indicate factor stability. Hierarchical factor analyses supported a second-order factor of "perceived stress." This alternative factor model of the PSS is presented along with observations regarding the measure's use in cancer research.

Adult↗
PubMed2006

A randomized clinical trial of group-based cognitive-behavioral stress management in localized prostate cancer: development of stress management skills improves quality of life and benefit finding.

BACKGROUND: Recent literature has indicated that a significant percentage of oncology patients describe finding some benefit (e.g., improved personal growth, sense of meaning, and enhanced interpersonal relationships) in the cancer experience. However, few studies have investigated the role of group-based psychosocial interventions in improving benefit finding (BF), and virtually none have investigated these constructs in men. PURPOSE: This study examined whether a cognitive-behavioral stress management (CBSM) intervention improves BF and quality of life (QoL) in men recovering from treatment for localized prostate cancer. METHODS: Participants in this study were 191 men (M age = 65.1) treated with radiation or radical prostatectomy for clinically localized (i.e., Stage I or II) prostate cancer. Participants were primarily non-Hispanic White (40%) or Hispanic (41%), followed by Black (18%) and other ethnicity (1%), were an average of 65.1 years old (SD = 7.7), and earned an average of 47,800 US dollars annually (SD = 41,000 US dollars). Participants were randomized to either a 10-week group-based cognitive-behavioral stress management intervention or a half-day educational seminar as a control condition. All participants provided demographic information and completed the Positive Contributions Scale-Cancer to assess BF, the Functional Assessment of Cancer Therapy to measure quality of life, and a measure of perceived stress management skills. Structural equation modeling was utilized for all analyses. RESULTS: Results indicated that the CBSM condition led to increases in BF and QoL and that these changes were mediated by the development of stress management skills. CONCLUSIONS: Results support the use of group-based cognitive-behavioral interventions in promoting QoL and BF in this population.

Aged↗
PubMed2002

Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes.

In both type 1 and type 2 diabetes, the late diabetic complications in nerve, vascular endothelium, and kidney arise from chronic elevations of glucose and possibly other metabolites including free fatty acids (FFA). Recent evidence suggests that common stress-activated signaling pathways such as nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases underlie the development of these late diabetic complications. In addition, in type 2 diabetes, there is evidence that the activation of these same stress pathways by glucose and possibly FFA leads to both insulin resistance and impaired insulin secretion. Thus, we propose a unifying hypothesis whereby hyperglycemia and FFA-induced activation of the nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases stress pathways, along with the activation of the advanced glycosylation end-products/receptor for advanced glycosylation end-products, protein kinase C, and sorbitol stress pathways, plays a key role in causing late complications in type 1 and type 2 diabetes, along with insulin resistance and impaired insulin secretion in type 2 diabetes. Studies with antioxidants such as vitamin E, alpha-lipoic acid, and N-acetylcysteine suggest that new strategies may become available to treat these conditions.

Animals↗
PubMed1986

Stress and immune responses. I. Suppression of T cell function in restraint-stressed mice.

Effects of restraint stress on humoral immune responses were investigated in mice. Mice were restrained for 12 hours per day at nighttime and released at daytime for 2 consecutive days, either before or after sheep red blood cell (SRBC) immunization. The antibody response to SRBC was markedly suppressed in mice that were restrained before antigen injection. In contrast, the response was not significantly affected when the stress was loaded after immunization. Oral administration of 10 mg/kg diazepam prevented the stress-induced suppression of anti-SRBC antibody response. On the other hand, antibody responses to T cell-independent antigens such as trinitrophenylated (TNP)-Ficoll and TNP-lipopolysaccharide were not suppressed. These results suggest that the restraint stress causes dysfunction of T cell populations in mice.

Animals↗
PubMed1986

Stress and immune responses. II. Identification of stress-sensitive cells in murine spleen cells.

The influences of restraint stress on the functions of T cells, B cells and adherent cells in antibody responses were investigated. Antibody response against sheep red blood cells (SRBC), a T cell-dependent antigen, in cultured splenocytes from restrained mice was reduced to about 40-50% of that from the control mice. Addition of normal T cells to these cultures, however, restored the suppressed response. Moreover, helper T cell activities were lowered in restrained mice. On the other hand, suppressor T cell activities induced by both concanavalin A (Con A) and SRBC were significantly decreased in restrained mice. However, the antibody responses to T cell-independent antigens in stressed mice were approximately 40% higher than the control response. These enhancement were also observed in T cell-depleted splenocytes. Polyclonal antibody response induced by lipopolysaccharide (LPS) was increased in stressed mice. Antigen presenting cell activities were little influenced by restraint stress. Proliferative response to Con A, but not that to LPS, was suppressed in splenocytes from restrained mice. These results suggest that both helper and suppressor activities of T cells are suppressed, but B cell activity is rather enhanced in splenocytes from restrained mice.

Animals↗
PubMed1991

Changes in CNS levels of serotonin and its metabolite in SART-stressed (repeatedly cold-stressed) rats.

Central nervous system levels of serotonin (5-HT) and 5-hydroxy-indoleacetic acid (5-HIAA) in SART (specific alternation of rhythm in temperature)-stressed (repeatedly cold-stressed) rats were examined by HPLC-ECD. In SART-stressed rats, the levels of both 5-HT and 5-HIAA decreased in many brain areas. In the spinal cord, only the 5-HT level decreased. Therefore, the ratio of 5-HIAA to 5-HT increased only in the spinal cord. These results suggest that SART-stressed rats have some form of abnormality in the synthetic system of 5-HT.

Animals↗
PubMed2004

The chemistry of nitrosative stress induced by nitric oxide and reactive nitrogen oxide species. Putting perspective on stressful biological situations.

This review addresses many of the chemical aspects of nitrosative stress mediated by N2O3. From a cellular perspective, N2O3 and the resulting reactive nitrogen oxide species target specific motifs such as thiols, lysine active sites, and zinc fingers and is dependant upon both the rates of production as well as consumption of NO and must be taken into account in order to access the nitrosative environment. Since production and consumption are integral parts of N2O3 generation, we predict that nitrosative stress occurs under specific conditions, such as chronic inflammation. In contrast to conditions of stress, nitrosative chemistry may also provide cellular protection through the regulation of critical signaling pathways. Therefore, a careful evaluation of the chemistry of nitrosation based upon specific experimental conditions may provide a better understanding of how the subtle balance between oxidative and nitrosative stress may be involved in the etiology and control of various disease processes.

Amines↗
PubMed2005

Bidirectional modulation of hippocampal long-term potentiation under stress and no-stress conditions in basolateral amygdala-lesioned and intact rats.

Hippocampal long-term potentiation (LTP) is widely considered as a cellular model for learning and memory formation. We have shown previously that protein synthesis-independent, early dentate gyrus (DG) LTP, lasting approximately 4-5 h, can be transformed into a late-LTP with a duration of > or = 24 h by a brief acute swim stress experience (high-stress condition). This reinforcement requires the activation of mineralocorticoid receptors and protein synthesis. The basolateral amygdala (BLA) is known to modulate glucocorticoid effects on the consolidation of spatial/contextual memory via a beta-adrenergic mechanism. Interestingly, hippocampal DG-LTP can also be indirectly modulated by beta-adrenergic and cholinergic/muscarinergic processes. Here, we show that the reinforcement of early-DG-LTP under high-stress conditions depends on the processing of novel spatial/contextual information. Furthermore, this reinforcement was blocked in BLA-lesioned animals compared with sham-operated and intact controls; however, it was not dependent on beta-adrenergic or cholinergic/muscarinergic receptor activation. In contrast, under low-stress conditions, the induction of late-LTP in BLA-lesioned animals is facilitated, and this facilitation, again, was dependent on beta-adrenergic activation. The data suggest that DG-LTP maintenance can be influenced by the BLA through different mechanisms: a short-lasting corticosterone-dependent and beta-adrenergic-independent mechanism and a long-lasting mechanism that facilitated hippocampal beta-adrenergic mechanisms.

Amygdala↗
PubMed2006

Previous experience with behavioral control over stress blocks the behavioral and dorsal raphe nucleus activating effects of later uncontrollable stress: role of the ventral medial prefrontal cortex.

Previous experience with stressors over which the subject has behavioral control blocks the typical behavioral consequences of subsequent exposure to stressors over which the organism has no behavioral control. The present experiments explored the involvement of the ventral medial prefrontal cortex (mPFCv) in mediating this "immunizing" or resilience producing effect of an initial experience with control. Behavioral immunization was blocked by inactivation of the mPFCv with muscimol at the time of the initial experience with control, as well as at the time of the later exposure to uncontrollable stress. Inhibition of protein synthesis within the mPFCv by anisomycin also blocked immunization when administered at the time of the initial controllable stress but had no effect when administered at the time of the later uncontrollable stress. Additional experiments found that the initial experience with control blocks the intense activation of serotonergic cells in the dorsal raphe nucleus that would normally be produced by uncontrollable stress, providing a mechanism for behavioral immunization. Furthermore, mPFCv activity during the initial controllable stressor was required for this effect to occur. These results suggest that the mPFCv is needed both to process information about the controllability of stressors and to utilize such information to regulate responses to subsequent stressors. Moreover, the mPFCv may be a site of storage or plasticity concerning controllability information. These results are consistent with recent research in other domains that explore the functions of the mPFCv.

Animals↗
PubMed2006

Fragile X mental retardation protein shifts between polyribosomes and stress granules after neuronal injury by arsenite stress or in vivo hippocampal electrode insertion.

Fragile X mental retardation protein (FMRP), the lack of which causes fragile X syndrome, is an RNA-binding protein encoded by the FMR1 gene. FMRP accompanies mRNAs from the nucleus to dendritic regions and is thought to regulate their translation at synapses. It has been shown that FMRP moves into nontranslating stress granules (SGs) during heat stress of cultured fibroblasts (Mazroui et al., 2002). We used a novel method to isolate SGs from neurons by virtue of their TIA-1 (T-cell intracellular antigen 1) protein component, and found that FMRP moved out of polyribosomes and into SGs subsequent to oxidative stress. We then examined FMRP changes in subcellular localization resulting from mechanically induced neuronal injury by placement of electrodes into the dentate gyrus and the perforant path of the hippocampus in vivo. During the first 10 min after electrode insertion into one hippocampus, FMRP shifted into SGs and away from polyribosomes, in both hippocampi. Although the injury discharge subsided beyond 10 s, FMRP levels in polyribosomes and stress granules did not return to basal levels until 30 min after electrode penetration. Our findings suggest that procedures for in vivo induction of long-term potentiation or long-term depression should incorporate a 30 min rest period after electrode insertion, and indicate that the contralateral hippocampus cannot be considered an unstimulated control tissue.

Animals↗