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Stress-induced hemoconcentration of blood cells and lipids in healthy women during acute psychological stress.

This study examined the effects of psychological stress on hemoconcentration in women. Hematologic and hemodynamic variables were assessed in 17 women before and after a 3-min speech task. Significant changes in hematocrit, hemoglobin levels, red and white blood cell (WBC) count, and calculated plasma volume occurred during psychological stress (all ps < .05). Significant increases were also observed for total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, and free fatty acid (FFA; all ps < .05) during stress. After statistically correcting for the hemoconcentration effects of decreased plasma volume during stress, only WBC count and FFA concentration remained significantly elevated during the stress task (p < .006 and p < .05, respectively). In sum, acute stress alters hemoconcentration in women, which in turn can account for most stress-induced changes in lipids.

Adult↗

Traumatic stress, perceived global stress, and life events: prospectively predicting quality of life in breast cancer patients.

The authors investigated the relationship between stress at initial cancer diagnosis and treatment and subsequent quality of life (QoL). Women (n = 112) randomized to the assessment-only arm of a clinical trial were initially assessed after breast cancer diagnosis and surgery and then reassessed at 4 months (during adjuvant treatment) and 12 months (postadjuvant treatment). There were 3 types of stress measured: number of stressful life events (K. A. Matthews et al., 1997), cancer-related traumatic stress symptoms (M. J. Horowitz, N. Wilner, & W. Alvarez, 1979), and perceived global stress (S. Cohen, T. Kamarck, & R. Mermelstein, 1983). Using hierarchical multiple regressions, the authors found that stress predicted both psychological and physical QoL (J. E. Ware, K. K. Snow, & M. Kosinski, 2000) at the follow-ups (all ps < .03). These findings substantiate the relationship between initial stress and later QoL and underscore the need for timely psychological intervention.

Adult↗

Differential activation of heat-shock and oxidation-specific stress genes in chemically induced oxidative stress.

Post-ischaemic reperfusion increases the level of the major heat-shock (stress) protein hsp 70 and of its mRNA by transcriptional mechanisms, and activates the binding of the heat-shock factor HSF to the consensus sequence HSE. In common with CoCl2 treatment, post-ischaemic reperfusion increases the level of haem oxygenase mRNA, an indicator of oxidative stress, but CoCl2 does not seem to induce the expression of the hsp 70 gene [Tacchini, Schiaffonati, Pappalardo, Gatti and Bernelli-Zazzera (1993) Lab. Invest. 68, 465-471]. Starting from these observations, we have now studied the expression of two genes of the hsp 70 family and of other possibly related genes under conditions of oxidative stress. Three different chemicals, which cause oxidative stress by various mechanisms and induce haem oxygenase, enhance the expression of the cognate hsc 73 gene, but do not activate the inducible hsp 70 gene. Expression of the other genes that have been studied seems to vary in intensity and/or time course, in relation to the particular mechanism of action of any single agent. The pattern of induction of the early-immediate response genes c-fos and c-jun observed during oxidative stress differs from that found in post-ischaemic reperfused livers. Oxidative-stress-inducing agents do not promote the binding of HSF to its consensus sequence HSE, such as occurs in heat-shock and post-ischaemic reperfusion, and fail to activate AP-1 (activator protein 1). With the possible exception of Phorone, the oxidative stress chemically induced in rat liver activates NFkB (nuclear factor kB) and AP-2 (activator protein 2) transcription factors.

Animals↗

Comparison of the cost-effectiveness of stress myocardial SPECT and stress echocardiography in suspected coronary artery disease considering the prognostic value of false-negative results.

BACKGROUND: The prognoses of patients with false-negative test results by myocardial single photon emission computed tomography (SPECT) and by stress echocardiography are known to be different; the prognosis with false-negative SPECT is better in suspected and proven coronary artery disease (CAD). METHODS AND RESULTS: Three strategies by which to diagnose CAD were compared for their cost-effectiveness when considering the prognostic value of false-negative results: (1) stress myocardial SPECT by dipyridamole or adenosine followed by coronary angiography (CAG), (2) exercise stress echocardiography followed by CAG, and (3) dobutamine stress echocardiography followed by CAG. Delta quality-adjusted life-year (QALY) was calculated for the three strategies separately when annual mortality and infarction rates were 0.5% and 0.5% for myocardial SPECT and 2% and 2% for stress echocardiography, respectively. Costs were estimated and costs per DeltaQALY were calculated according to the pretest likelihood of CAD (pCAD). The myocardial SPECT followed by CAG strategy was the most cost-effective in the patients with a pCAD of 0.3 or greater, and the dobutamine echocardiography followed by CAG strategy was the most cost-effective in patients with a pCAD of 0.2 or lower. This was the case when we assumed that the nondiagnostic test rate of dobutamine echocardiography was 9% (in contrast to 0% by myocardial SPECT and 18% by exercise echocardiography). Sensitivity analysis showed that the cost-effectiveness of dobutamine echocardiography followed by CAG was best only if the prognosis of false-negative results of dobutamine echocardiography was better. The cost-effectiveness of exercise echocardiography was dubious because of the high nondiagnostic rate with inadequate exercise. CONCLUSIONS: When the lower event rates of (false) negative SPECT were considered, the relatively expensive myocardial SPECT strategy was more cost-effective than the cheaper stress echocardiography strategy in patients with a pCAD of 0.3 or greater. According to sensitivity analysis, the prognostic value of false-negative results and the nondiagnostic test rate were important determinants of stress myocardial study cost-effectiveness.

Coronary Angiography↗

When stress happens matters: effects of earthquake timing on stress responsivity in pregnancy.

OBJECTIVE: The purpose of the study was to assess the effects of the timing of stress during pregnancy on emotional responses and birth outcome. We hypothesized that as pregnancy advanced women would become increasingly resistant to the adverse effects of stress, and so early stress would have more profound effects than later stress. STUDY DESIGN: Forty pregnant women who had experienced an earthquake during pregnancy or shortly afterward were identified. Using regression analyses we determined whether the timing of the earthquake was related to an affective response to this event and to length of gestation. RESULTS: The earthquake was rated as more stressful when it occurred early in pregnancy compared with late in pregnancy, and postpartum ratings were similar to first-trimester ratings (r (quad) =.39; P <.05). Stress experienced early in pregnancy was associated with shorter gestational length (r =.35; P <.05). CONCLUSIONS: As pregnancy advances, women become decreasingly sensitive to the effects of stress. This decrease in vulnerability may reflect increasing protection of the mother and fetus from adverse influences during pregnancy.

Corticotropin-Releasing Hormone↗

Up-expression of NapA and other oxidative stress proteins is a compensatory response to loss of major Helicobacter pylori stress resistance factors.

Twenty-six Helicobacter pylori targeted mutant strains with deficiencies in oxidative stress combating proteins, including 12 double mutant strains were analyzed via physiological and proteomic approaches to distinguish the major expression changes caused by the mutations. Mutations were introduced into both a Mtz(S) and a Mtz(R) strain background. Most of the mutations caused increased growth sensitivity of the strains to oxygen, and they all exhibited clear compensatory up-expression of oxidative stress resistance proteins enabling survival of the bacterium. The most frequent up-expressed oxidative stress resistance factor (observed in 16 of the mutants) was the iron-sequestering protein NapA, linking iron sequestration with oxidative stress resistance. The up-expression of individual proteins in mutants ranged from 2 to 10 fold that of the wild type strain, even when incubated in a low O(2) environment. For example, a considerably higher level of catalase expression (4 fold of that in the wild-type strain) was observed in ahpC napA and ahpC sodB double mutants. A Fur mutant up-expressed ferritin (Pfr) protein 20-fold. In some mutant strains the bacterial DNA is protected from oxidative stress damage apparently via overexpression of oxidative stress-combating proteins such as NapA, catalase or MdaB (an NADPH quinone reductase). Our results show that H. pylori has a variety of ways to compensate for loss of major oxidative stress combating factors.

Acid Phosphatase↗

Isolation of stress-related genes of rubber particles and latex in fig tree (Ficus carica) and their expressions by abiotic stress or plant hormone treatments.

Two rubber particle protein genes and one latex gene in fig tree (Ficus carica) have been isolated and their expression following various abiotic stress treatments have been investigated. The two major proteins that are tightly associated with the catalytically active rubber particles have been sequenced to be peroxidase (POX) and trypsin inhibitor (TRI). A cDNA encoding a basic class I chitinase (CHI) has also been isolated from the fig tree latex. Wounding treatment strongly induced the expression of the three stress-related genes. Among the abiotic stresses investigated, drought treatment greatly induced the expression of POX, whereas the expression of CHI and TRI decreased after the same treatment. Cold treatment reduced slightly the transcript levels of the thee genes, and NaCl reduced marginally the expression of CHI. The expression of POX, CHI, and TRI was induced by jasmonic acid and abscisic acid, by jasmonic acid, and by salicylic acid, respectively. Different expression of the stress-related genes following various abiotic stress or plant hormone treatments suggests that a crosstalk exists between the signal transduction pathways elicited by abiotic stresses and hormones in plants. Our present results showing the expression of stress-related proteins on the surface of rubber particles and latex in F. carica also imply the possible role of rubber particles and latex in defense in rubber-producing plant species.

Base Sequence↗

Effects of soybean oil emulsion and eicosapentaenoic acid on stress response and immune function after a severely stressful operation.

OBJECTIVE: To investigate the effects of soybean oil emulsion and oral or enteral administration of eicosapentaenoic acid (EPA) on stress response, cytokine production, protein metabolism, and immune function after surgery for esophageal cancer. SUMMARY BACKGROUND DATA: It has been reported that safflower oil, rich in n-6 polyunsaturated fatty acid (n-6 PUFA), affects the survival rate of septic animals and decreases the immune function. It has also been reported that the administration of fish oil, in contrast, reduces these stress responses and stress-induced immunosuppression. In humans, the effects of soybean oil emulsion and the administration of EPA on stress response and immune function after surgery have not been established. METHODS: Patients who underwent esophagectomy with thoracotomy were divided into three groups. Seven patients were fed by total parenteral nutrition (TPN) with soybean oil emulsion, which accounted for 20% of total calories. Seven patients were given oral or enteral administration of 1.8 g/day EPA, in addition to TPN with soybean oil emulsion. Nine patients served as the control group; these patients received fat-free TPN. Serum interleukin-6 (IL-6), C-reactive protein, concanavalin A (con A)- or phytohemagglutinin (PHA)-stimulated lymphocyte proliferation, natural killer cell activity, and stress hormones were measured. RESULTS: The postoperative level of serum IL-6 was significantly higher in the group receiving soybean oil emulsion than in the fat-free group. Oral or enteral supplementation of EPA with soybean oil emulsion significantly reduced the level of serum IL-6 compared with the patients receiving soybean oil emulsion. Con A- or PHA-stimulated lymphocyte proliferation decreased significantly on postoperative day 7 in all groups of patients. The supplementation of EPA with soybean oil emulsion significantly improved the lymphocyte proliferation and natural killer cell activity on postoperative day 21 compared with the group receiving soybean oil emulsion. CONCLUSIONS: Soybean oil emulsion amplifies, and the supplementation of EPA reduces, the stress response and stress-induced immunosuppression.

Eicosapentaenoic Acid↗

Does background stress heighten or dampen children's cardiovascular responses to acute stress?

OBJECTIVE: Does background stress heighten or dampen children's cardiovascular responses to acute stress? METHOD: To address this question, the cardiovascular responses to four acute laboratory stressors of 150 children and adolescents were evaluated according to their self-reported background stress level. Background stress was determined during a standardized interview and was a priori classified according to its importance, frequency, and whether it was ongoing or resolved. RESULTS: Results showed that children and adolescents who reported important stressors or stressors that were ongoing and frequent exhibited a larger increase in diastolic blood pressure and total peripheral resistance during all four laboratory stressors than their low stress counterparts. Additional analysis showed that the results could not be accounted for by sociodemographic variables or by the personality traits measured in this study. CONCLUSIONS: Results suggest the importance of measuring background stress in understanding an individual's acute stress response.

Adolescent↗

Roentgenologic diagnosis of stress fractures and stress reactions.

We examined 26 athletes with continued pain after strenuous exercise. We found stress fractures in 15 patients, all of whom had positive roentgenographic studies. Seven of these 15 also had bone scans, all of which were positive. Five patients had stress reactions, all of which showed positive results on bone scan and negative roentgenographic results. Five had occult stress reactions manifested by pain, with normal roentgenographic and scintigraphic results, and one had minor pain not requiring radiologic studies. Stress reaction is contrasted with stress fracture by demonstrating the role of bone imaging in the diagnostic continuum of stress reaction to stress fracture.

Adult↗

Stress and suicide in police officers: paradigm of occupational stress.

All occupations are associated with stress, but certain occupations are significantly more stressful than others. Stress is not always harmful. It is the individual's reaction to stress that determines the outcome, ie, whether the individual will adapt or become maladaptive. Individuals who feel they can control events or are in control of their lives are better able to handle stress than individuals who believe they are the victims of fate or chance and who feel powerless and helpless. For those individuals who feel powerless or helpless, suicide may be a means of taking control over their helplessness. Police officers, who are subject to extraordinary stress, present a paradigm for the study and treatment of stress in other occupations.

Adolescent↗

Techno-stress: a prospective psychophysiological study of the impact of a controlled stress-reduction program in advanced telecommunication systems design work.

There is a void of studies concerning occupational health aspects from working with the most advanced forms of information technologies techniques such as are found in some of the world-renowned telecommunication systems development laboratories. However, many of these techniques will later be applied in the regular office environment. We wanted to identify some of the major stressors perceived by advanced telecommunication systems design employees and develop a valid and reliable instrument by which to monitor such stressors. We were also interested in assessing the impact of a controlled prospective stress-reduction program on perceived mental stress and specific psychophysiological parameters. A total of 116 employees were recruited. Sixty-one were offered to participate in one of three stress-reduction training programs (intervention group). The additional 50 functioned as a reference group. After a detailed baseline assessment, including a comprehensive questionnaire and psychophysiological measurements, new assessments were made at the end of the formal training program (+ 3 months) and after an additional 5-month period. Results reveal a significant improvement in the intervention group with regard to circulating levels of the stress-sensitive hormone prolactin as well as an attenuation in mental strain. Cardiovascular risk indicators were also improved. Circulating thrombocytes decreased in the intervention group. Type of stress-reduction programs chosen and intensity of participation did not significantly impact results. Coping style was not affected and no beneficial effects were observed with regard to the psychological characteristics of the work, eg intellectual discretion and control over work processes. The survey instrument is now being used in the continuous improvement of work processes and strategic leadership of occupational health issues. The results suggest that prior psychophysiological stress research, based on low- and medium-skill, rather repetitive kinds of jobs, may not be completely applicable to that of skilled professionals. The results indicate that cutting-edge telecommunication systems design employees suffer from significant amounts of mental strain. In addition, there are limited but measurable benefits from a stress-reduction program. More attention should be directed as to how to design healthy and productive work environments in workplaces using advanced information technologies.

Hemodynamics↗

Melatonin attenuates stress-induced defecation: lesson from a rat model of stress-induced gut dysfunction.

Melatonin is known to alleviate stress and modulate gut motility. We investigated the modulating effects of melatonin on stress-induced gut dysfunction. One hundred Wistar rats were randomly assigned to five equal groups, receiving intraperitoneal injections of 0, 1, 10, 100 or 1000 microg kg(-1) melatonin, respectively. Fifteen minutes later, each group was divided again into four subgroups receiving no treatment, 0.25 mg luzindole (a non-selective melatonin receptor antagonist) intraperitoneally, wrap-restraint stress, and 10 mg kg(-1) serotonin intraperitoneally, respectively. Two hours later, serum serotonin, corticotropin-releasing factor (CRF) and melatonin levels, and faecal output were recorded. Results showed that intraperitoneal melatonin increased faecal output, but this effect was abolished by luzindole. In wrap-restraint group, prior intraperitoneal melatonin at doses of 100 or 1000 microg kg(-1) significantly inhibited stress-induced defecation. This effect was associated with corresponding reductions in serum serotonin and CRF concentrations. In serotonin-treated group, serotonin-induced defecation was also inhibited by melatonin. In conclusion, melatonin exhibited an excitatory effect on bowel output in rats placed under resting state, while attenuated defecation in those subjected to wrap-restraint stress or serotonin treatment. The inhibitory effects of melatonin on stress-induced defecation may stem from its antagonistic effect on stress-induced enhancement of serotonin and CRF secretion.

Animals↗

Distribution and morphology of skeletal muscle lesions after experimental restraint stress in normal and stress-susceptible pigs.

Six normal and 22 stress-susceptible (SS) pigs were subjected to experimental restraint stress to test the hypothesis that SS pigs are more affected by stress-induced skeletal muscle lesions than normal pigs. The stress was provoked by a 12 min intravenous infusion of the myorelaxant succinylcholine at a dose which induced leg paralysis. At necropsy 2-3 days after the stress, 24 muscles were examined macro- and microscopically. The plasma levels of noradrenaline and adrenaline increased significantly during the stress, especially in SS pigs. Significantly higher scores of acute muscle lesions (degeneration and phagocytosis) were recorded in the SS pigs than in the normal pigs. The antebrachial flexor muscles, m. gastrocnemius, crural flexor muscles, m. serratus and m. intercostalis were most affected, while m. semitendinosus, m. masseter, crural extensor muscles, m. quadriceps and antebrachial extensor muscles were the least affected. The muscle regeneration of SS pigs was greater than that of normal pigs indicating more active rhabdomyolysis in SS pigs than in normal pigs. The muscle lesions were also reflected in increased serum levels of creatine kinase (CK), aspartate aminotransferase (ASAT), potassium and creatinine in SS pigs. It is concluded that the restraint stress induced skeletal muscle lesions and increased sympathetic activity, predominantly in SS pigs. It was also shown that certain skeletal muscles are more affected by rhabdomyolysis than others.

Animals↗

Vaccination alone or in combination with pyridostigmine promotes and prolongs activation of stress-activated kinases induced by stress in the mouse brain.

Gulf war illnesses (GWI) are currently affecting thousands of veterans. To date, the molecular mechanisms underlying the pathogenesis of these illnesses remain unknown. During Gulf war I, military personnel were exposed to multiple stressors, one or more vaccines, pyridostigmine (PY), and other chemicals. In our previous studies, we found that stress induces activation of mitogen activated protein-kinase kinase 4 (MKK4) and c-Jun-N-terminal kinase (JNK) in the mouse brain (Liu et al. 2004). Our working hypothesis is that stress, vaccination, and PY may synergistically induce activation of MKK4 and JNK in the brain, leading to over-activation of these kinases and neurological injuries. To test our hypothesis, we examined the effect of keyhole limpet hemocyanin (KLH) immunization alone or in combination with PY on activation of MKK4 and JNK induced by stress. We found that KLH immunization alone had a small effect on MKK4 or JNK activity but it significantly enhanced and prolonged activation of these kinases induced by stress, from a few hours to several days. Additionally, KLH immunization caused activation of p38MAPK. PY treatment further enhanced and prolonged activation of these kinases induced by stress in combination with KLH immunization and triggered activation of caspase-3. Our current studies suggest that stress, vaccination, and PY may synergistically act on multiple stress-activated kinases in the brain to cause neurological impairments in GWI.

Animals↗

Mutations in amyloid precursor protein and presenilin-1 genes increase the basal oxidative stress in murine neuronal cells and lead to increased sensitivity to oxidative stress mediated by amyloid beta-peptide (1-42), HO and kainic acid: implications for Alzheimer's disease.

Oxidative stress is observed in Alzheimer's disease (AD) brain, including protein oxidation and lipid peroxidation. One of the major pathological hallmarks of AD is the brain deposition of amyloid beta-peptide (Abeta). This 42-mer peptide is derived from the beta-amyloid precursor protein (APP) and is associated with oxidative stress in vitro and in vivo. Mutations in the PS-1 and APP genes, which increase production of the highly amyloidogenic amyloid beta-peptide (Abeta42), are the major causes of early onset familial AD. Several lines of evidence suggest that enhanced oxidative stress, inflammation, and apoptosis play important roles in the pathogenesis of AD. In the present study, primary neuronal cultures from knock-in mice expressing mutant human PS-1 and APP were compared with those from wild-type mice, in the presence or absence of various oxidizing agents, viz, Abeta(1-42), H2O2 and kainic acid (KA). APP/PS-1 double mutant neurons displayed a significant basal increase in oxidative stress as measured by protein oxidation, lipid peroxidation, and 3-nitrotyrosine when compared with the wild-type neurons (p < 0.0005). Elevated levels of human APP, PS-1 and Abeta(1-42) were found in APP/PS-1 cultures compared with wild-type neurons. APP/PS-1 double mutant neuron cultures exhibited increased vulnerability to oxidative stress, mitochondrial dysfunction and apoptosis induced by Abeta(1-42), H2O2 and KA compared with wild-type neuronal cultures. The results are consonant with the hypothesis that Abeta(1-42)-associated oxidative stress and increased vulnerability to oxidative stress may contribute significantly to neuronal apoptosis and death in familial early onset AD.

Aldehydes↗

Sympathoadrenal activity and psychosocial stress. The significance of aging, long-term smoking, and stress models.

Recent studies have indicated that the increase in plasma norepinephrine and sympathetic activity with aging in healthy subjects is largely due to long-term cigarette smoking. In patients who have or have had duodenal ulcer the increase in plasma norepinephrine with age was markedly increased. These patients as a group perceive their lives somewhat more stressful than the general population and they tend to die prematurely due to smoking-associated diseases. These patients may select dysfunctional coping strategies like smoking, which may result in organ pathologies and a compensatory increase in plasma norepinephrine. No close correlation has been established between plasma epinephrine and "ill health." High plasma epinephrine levels may have a deleterious effect on the cardiovascular system in elderly subjects during certain conditions. In a population study, we found, however, that low resting plasma epinephrine levels were associated with an unfavorable survival rate. We speculate that an inadequate response to psychosocial stress and the choice of dysfunctional coping strategies may be more harmful and cause more "ill health" than hypersecretion of stress hormones like epinephrine and cortisol, which has been the traditional view. We suggest that there are different stress states. Stress hormones like epinephrine and cortisol may play a major role during situations like combat, illness, and strenuous exercise. In response to psychosocial stress, dysfunctional coping strategies are, however, largely responsible for harmful effects of stress.

Aging↗

Chronic stress induces sensitization in sympathoadrenal responses to stress in borderline hypertensive rats.

The effects of acute foot shock on cardiovascular and sympathoadrenal responses were investigated in chronically stressed borderline hypertensive rats (BHR) and Wistar-Kyoto (WKY) rats. Male BHRs were divided into two groups; the maturation group (Mat) was not stressed, whereas the chronic stress group (AJS) received 8 wk (5 days/wk, 30 min/day) of air-jet stress coupled with immobilization. After chronic stress, the rats were cannulated in the femoral artery and jugular vein. Resting mean arterial pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) levels were higher in the AJS group. In contrast, chronic stress failed to increase basal arterial pressure or HR in WKY rats. In response to acute foot shock, the Mat group had higher MAP increases, at which they plateaued, whereas the AJS rats displayed a progressive decline in MAP. This was associated with higher plasma NE and epinephrine levels but a smaller increase in adrenocorticotropic hormone in AJS versus Mat rats. This hyperactivity in the sympathoadrenal system of chronically stressed BHRs may, in part, account for their mild hypertension.

Adrenocorticotropic Hormone↗