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PubMed1978

Urethral closure pressure with stress--a comparison between stress-incontinent and continent women.

Stress incontinence has been said to occur as a consequence of a low urethral pressure and defective pressure transmission from the abdomen to the urethra due to descent of the bladder neck area. Equipment suitable for dynamic pressure measurements has been used to analyse the losses of urethral pressure that lead to incontinence. The pressure transmission from abdomen to urethra was found to be incomplete in both continent and stress-incontinent women. There was also significant loss of smooth muscle tone in the urethral wall after repeated straining, leading to a still narrower margin between the urethral pressure and the leakage treshold in both continent and stress-incontinent women. The main factor determining the degree of continence or incontinence seemed to be the urethral closure pressure at rest . As long as this pressure is sufficiently high, leakage during sudden stress will not occur.

Adult↗

PubMed1978

Beta-adrenergic blockade in stress protection. Limited effect of metoprolol in psychological stress reaction.

In a model system the influence of mental stress on blood pressure and heart rate was studied in normal persons and in patients with hypertension (WHO grade III). Metoprolol was employed to investigate the preventive effect of beta-adrenergic blockade on the response to stress. In all groups blood pressure increased significantly during mental stress. The effect was not inhibited by metoprolol. The rise in heart rate, however, was depressed by beta-blockade. Reaction time, opticomotor coordination and concentration ability were studied as parameters of vigilance, but no significant difference between the metoprolol and control groups were observed. Thus, metoprolol only influenced the heart rate in mental stress and it did not affect vigilance.

Adult↗

PubMed1992

Measuring life event stress in the lives of college students: the Undergraduate Stress Questionnaire (USQ).

We describe the development of the Undergraduate Stress Questionnaire (USQ), a life events checklist designed to measure stress among undergraduates. Several studies demonstrate the USQ's validity. The USQ correlates positively with physical symptoms and negatively with mood. Students rated the USQ as the most complete and accurate of four different life events questionnaires. In a panel study, the USQ closely tracked subjective reports of stress, both during the term and finals week. The USQ predicted symptoms more reliably than three other stress measures, controlling for negative affect. Students waiting in the college infirmary score higher on the USQ than students socializing on campus. Finally, we compare the checklist format to subjective scaling, and show the superiority of the checklist version. We discuss the usefulness of the USQ in terms of validity, representativeness, adaptability, brevity, and low confounding with negative affect.

Adult↗

PubMed2004

Exercise-induced oxidative stress and muscle stress protein responses in trotters.

Acute exercise induces oxidative stress and heat shock protein (HSP) expression. Information on the protection of stress proteins against oxidant insult and muscle damage during moderate exercise is scanty. We aimed to show how a single bout of moderate exercise affects the markers of oxidative stress and heat shock factor-1 (HSF1; the transcriptional regulator of HSP synthesis), and HSP70, HSP90 and glucose-regulated protein (GRP75) expression in horses. Eight clinically normal and regularly trained standardbred trotters were treadmill-exercised for 45 min at moderate intensity. Blood samples were collected prior to and immediately after exercise and at 4 and 24 h of recovery. Muscle biopsy samples from the middle gluteal muscle were taken before exercise and after 4 h of recovery. Acute exercise did not activate HSF1 or induce expression of HSP70, HSP90 or GRP75 in skeletal muscle. One bout of acute exercise increased protein oxidation, which was measured by protein carbonyls in plasma and muscle, but it did not effect 4-hydroxynonenal protein adducts, which are markers of lipid peroxidation. Furthermore, mild muscle damage was observed 4 h after exercise. Our results showed that horses are susceptible to oxidative stress. One bout of exercise at moderate intensity and duration did not induce HSP responses despite the increased protein oxidation and tissue inflammation in equine muscle.

Animals↗

PubMed1986

Opioid and non-opioid stress analgesia from cold water swim: importance of stress severity.

We have previously reported that stress severity plays an important role in determining the neurochemical basis of stress-induced analgesia from inescapable footshock. Increasing severity (duration or intensity of continuous footshock) causes a shift in mediation of the resultant analgesia from opioid to non-opioid. In this study, we find that stress severity plays a similar role in analgesia from cold water swim. More severe swims (longer duration or lower water temperature) produce stress analgesia insensitive to the opiate antagonist, naltrexone, whereas less severe swims produce analgesia significantly attenuated by this drug.

Analgesia↗

PubMed1988

Systemic naloxone administration potentiates locus coeruleus noradrenergic neuronal activity under stressful but not non-stressful conditions.

When administered during non-stressful, quiet-waking conditions, i.v. naloxone (1.0 mg/kg) had no effect on the activity of locus coeruleus (LC) noradrenergic neurons in behaving cats. In contrast, the activation of LC noradrenergic unit activity produced by restraint stress was greatly potentiated by the same dose of naloxone. Indices of behavioral distress, vocalization and struggling, were also found to be significantly increased in animals given naloxone during stress. These results suggest that endogenous opioids have a moderating influence upon the level of activity of the LC which operates only under specific conditions such as stress.

Animals↗

PubMed1995

Induction of the antioxidant stress proteins heme oxygenase-1 and MSP23 by stress agents and oxidised LDL in cultured vascular smooth muscle cells.

Enhanced expression of the antioxidant stress proteins heme oxygenase-1 (HO-1) and macrophage stress protein (MSP23) by oxidative stress agents and oxidatively modified low density lipoproteins (LDL) was investigated in cultured porcine aortic smooth muscle cells. Treatment of smooth muscle cells with glucose oxidase, CdCl2 or diethylmaleate resulted in a time-dependent (6-48 h) induction of HO-1 and MSP23 expression. Exposure of cells to 100 micrograms protein/ml highly oxidised LDL increased the expression of HO-1 and MSP23 within 24 h, and the induction was dependent on the degree of LDL oxidation. The induction of HO-1 and MSP23 may thus play an important cytoprotective role against oxidative stress in atherogenesis.

Animals↗

PubMed1988

Day-to-day variation in pineal serotonin N-acetyltransferase activity in stressed and non-stressed male Sprague-Dawley rats.

Previous studies involving physical-immobilization stress in laboratory rats have yielded inconsistent results with respect to melatonin synthesis in the pineal gland. As melatonin formation undergoes circadian and infradian rhythms, the aim of the present study was to examine whether stress experiments exhibit day-to-day variation. Toward this end, groups of male Sprague-Dawley rats were stressed by physical immobilization on eight consecutive days, respectively, or left relatively undisturbed, and killed. The pineal gland was rapidly dissected out and serotonin N-acetyltransferase (NAT) activity and melatonin levels were measured. NAT activity was significantly depressed on experimental days 1, 3 and 5, and slightly depressed on day 7. In addition, both in control and experimental animals NAT activity exhibited statistically significant differences between experimental days. Pineal melatonin levels were less variable. On experimental days 3 and 6 immobilization led to a significant increase of pineal melatonin levels. These results show that day-to-day variation is an important factor that influences the outcome of stress experiments and represent another example that NAT activity and pineal melatonin levels do not always show corresponding changes.

Acetyltransferases↗

PubMed1990

Maternal stress increases fetal brain and neonatal cerebral cortex 5-hydroxytryptamine synthesis in rats: a possible mechanism by which stress influences brain development.

Previous studies have shown that maternal stress modifies 5-hydroxytryptamine (5-HT) receptor binding in several brain regions of the adult offspring and alters the intensity of the behavioral responses to 5-HT receptor agonists. We now report that the same stress, crowding combined with daily saline injections during the final week of pregnancy, elevates maternal plasma free tryptophan level without significantly affecting total tryptophan. The increased maternal plasma tryptophan was associated with significantly increased fetal brain levels of tryptophan, 5-HT and 5-hydroxyindoleacetic acid. These increases were maintained after birth until at least postnatal day 10. Since 5-HT is recognised as having a role in the control of neuron development during the perinatal period, we suggest that the stress-induced increase in fetal brain 5-HT synthesis may play a part in the mechanisms by which prenatal stress alters adult behavior.

Animals↗

PubMed1985

Measurement of occupational stress in hospital settings: two validity studies of a measure of self-reported stress in medical emergency rooms.

The present study details the development of a stress scale for medical personnel. The Medical Personnel Stress Scale is a 48-item subjective stress measure capable of assessing both organizational and individual dimensions of stress. It demonstrated both the ability to discriminate between divergent medical emergency room organizations and to predict self reported on-the-job difficulties.

Emergency Service, Hospital↗

PubMed1995

Restraint-induced stress in pregnant mice--degree of immobilization affects maternal indices of stress and developmental outcome in offspring.

Maternal stress on gestational day 8 (GD8) in the CD-1 mouse can induce a syndrome of fetal anomalies, including encephalocele, supernumerary ribs, fused ribs and vertebral anomalies. Two forms of restraint were compared for their ability to induce these defects. The two types of restraint differed in the degree of mobility afforded the dam during confinement, either total restraint in a supine position or a less confining restraint in which restrained dams could move from a supine to a non-supine position, but could not turn from front to back. Dams were exposed to either form of restraint for 12 h on GD8 and their near-term fetuses examined for external and skeletal abnormalities. As both types of restraint precluded normal eating and drinking, an additional control group deprived of food/water was included for evaluation. Cohorts of dams were restrained for 3, 6 or 12 h on GD8 and end points commonly used to gauge the degree of stress evaluated. These included serum corticosterone level and the weight of body, spleen and thymus. Stress-induced analgesia, as measured by the tail-flick procedure, was monitored in these same dams as an additional non-invasive measure of stress. Both types of restraint induced greater and longer-lasting weight loss than food/water deprivation. Both also produced more fetal anomalies than observed in the offspring of caged controls or food/water deprived dams. Both forms of restraint equally elevated serum corticosterone levels above the increase exhibited by the food/water deprived dams. The most pronounced difference between the two types of restraint concerned the degree of analgesia. The type limiting mobility the most, caused much greater analgesia after 6 and 12 h of restraint although the dams subjected to the other form of restraint were significantly more analgesic than the food/water deprived dams by 12 h. Dams restrained in the supine position exhibited slightly greater weight loss, more analgesia and produced significantly more offspring with anomalies.

Analysis of Variance↗

PubMed2004

Fetal adaptation to stress: Part II. Evolutionary aspects; stress-induced hippocampal damage; long-term effects on behavior; consequences on adult health.

Humans share adaptative capacities to stress with other species, as demonstrated on amphibians: the physiological response to experimental water volume and food deprivation results in the activation of the endocrine axes that drive metamorphosis, in particular the neuroendocrine stress system. Unfavorable effects may, however, occur, probably due to inappropriate timing and/or duration of stress: recent experiments are converging to show a profound impairment of hippocampal functioning in the offspring of mothers exposed to prenatal stress. Moreover, fetal changes are likely one of the risk factors for a number of diseases in adulthood.

Adaptation, Physiological↗

PubMed2004

The effects of oxidative stress on telomerase activity and other stress-related proteins in lens epithelial cells.

Telomerase is a ribonucleoprotein complex responsible for maintaining the ends of chromosomes and for repair of DNA strand breaks. While telomerase activity is generally found in cells that have unlimited proliferative potential such as neoplastic cells, germline cells and some stem cells, lens epithelial cells (though not highly proliferative) have telomerase activity. Our previous studies indicated that lens epithelial cells express high levels of telomerase despite their low proliferative potential, thus we hypothesized that telomerase expression protects lens epithelial cells from oxidative stress. We also determined levels of the stress proteins gadd45 and p16 and the stress and proliferation-related protein, proliferating cell nuclear antigen (PCNA). In acute studies, lenses were exposed to TBHP for 0-120 min. In recovery studies, lenses were exposed to TBHP for 1 hr, then allowed to recover for up to 18 hr. In acute studies, telomerase activity was increased, p16 initially decreased then normalized, PCNA levels did not change significantly even in the overnight recovery groups, and gadd45 was decreased in some TBHP exposed groups. In recovery studies, telomerase activity was increased in all groups, gadd45 decreased then became elevated, and p16 levels were decreased at later recovery times. PCNA levels remained constant during the studies, indicating that there was no change in proliferation. These studies showed that elevated telomerase activity did not correlate with increased proliferation in lens epithelial cells; instead, increased telomerase activity was associated with increased levels of the stress-related protein gadd45 only in the later recovery times. These findings support the hypothesis that telomerase plays a protective rather than a proliferative role in lens epithelial cells.

Animals↗

PubMed2006

Acute psychological stress alerts the adaptive immune response: stress-induced mobilization of effector T cells.

Influences of psychological stress on the acquired immune system have not consequently been investigated. We found acute psychological stress to cause an increase in CD56+ and CCR5+ effector T cells in the peripheral blood of healthy human subjects (N=22), while skin-homing CLA+ T cells decreased. At the same time, we observed a stress-induced decrease in CD45RA+/CCR7+ naive and CD45RA-/CCR7+ central memory T cells, while CD45RA-/CCR7- effector memory and CD45RA+/CCR7- terminally differentiated T cells increased. This T cell redistribution translated into an increase in T cells expressing perforin/granzyme B and in Epstein-Barr virus-specific, cytomegalovirus-specific and influenza virus-specific CD8+ T cells. Thus, acute stress seems to promote the retention of less mature T cells within lymphoid tissue or skin while effector-type T cells are mobilized into the blood in order to be able to rapidly migrate into peripheral tissues.

Acute Disease↗

PubMed2005

In vivo protection of synaptosomes by ferulic acid ethyl ester (FAEE) from oxidative stress mediated by 2,2-azobis(2-amidino-propane)dihydrochloride (AAPH) or Fe(2+)/H(2)O(2): insight into mechanisms of neuroprotection and relevance to oxidative stress-related neurodegenerative disorders.

Ferulic acid ethyl ester (FAEE) is an ester derivative of ferulic acid, the latter known for its anti-inflammatory and antioxidant properties. Previous studies from our laboratory have shown that ferulic acid protects synaptosomal membrane system and neuronal cell culture systems against hydroxyl and peroxyl radical oxidation. FAEE is lipophilic and is able to penetrate lipid bilayer. Previous studies reported that FAEE reduces Alzheimer's amyloid beta peptide Abeta(1-42)-induced oxidative stress and cytotoxicity in neuronal cell culture by direct radical scavenging and by inducing certain antioxidant proteins. In the present study we tested the hypothesis that FAEE would provide neuroprotection against free radical oxidative stress in vivo. Synaptosomes were isolated from the gerbils that were previously injected intraperitoneally (i.p.) with FAEE or DMSO and were treated with oxidants, Fe(2+)/H(2)O(2) or 2,2-azobis(2-amidino-propane)dihydrochloride (AAPH). Synaptosomes isolated from the gerbil previously injected i.p. with FAEE and treated with Fe(2+)/H(2)O(2) and AAPH showed significant reduction in reactive oxygen species (ROS), levels of protein carbonyl, protein bound 4-hydroxynonenal (HNE, a lipid peroxidation product), and 3-nitrotyrosine (3-NT, another marker of protein oxidation formed by reaction of tyrosine residues with peroxynitrite) compared to Fe(2+)/H(2)O(2) or AAPH induced oxidative stress in synapotosomes isolated from the brain of gerbils that were previously injected with DMSO. The synaptosomes isolated from gerbil pre-injected with FAEE and subsequently treated with AAPH or Fe(2+)/H(2)O(2) showed induction of heme oxygenase (HO-1) and heat shock protein 70 (HSP-70) but reduced inducible nitric oxide synthase (iNOS) levels. These results are discussed with reference to potential use of this lipophilic antioxidant phenolic compound in the treatment of oxidative stress-related neurodegenerative disorders.

Aldehydes↗

PubMed2004

Role of oxidative stress in neurodegeneration: recent developments in assay methods for oxidative stress and nutraceutical antioxidants.

Reactive oxygen species (ROS) are produced in the course of normal metabolism and they serve important physiological functions. However, because of their high reactivity, accumulation of ROS beyond the immediate needs of the cell may affect cellular structure and functional integrity, by bringing about oxidative degradation of critical molecules, such as the DNA, proteins, and lipids. Although cells possess an intricate network of defense mechanisms to neutralize excess ROS and reduce oxidative stress, some tissues, especially the brain, are much more vulnerable to oxidative stress because of their elevated consumption of oxygen and the consequent generation of large amounts of ROS. For the same reason, the mitochondrial DNA (mtDNA) of brain cells is highly susceptible to structural alterations resulting in mitochondrial dysfunction. Several lines of evidence strongly suggest that these effects of ROS may be etiologically related to a number of neurodegenerative disorders. Nutraceutical antioxidants are dietary supplements that can exert positive pharmacological effects on specific human diseases by neutralizing the negative effects of ROS. The present communication concentrates on a review of recent concepts and methodological developments, some of them based on the results of work from our own laboratory, on the following aspects: (1) the complex interactions and complementary interrelationships between oxidative stress, mitochondrial dysfunction, and various forms of neural degeneration; (2) fractionation and isolation of substances with antioxidant properties from plant materials, which are extensively used in the human diet and, therefore, can be expected to be less toxic in any pharmacological intervention; (3) recent developments in methodologies that can be used for the assay of oxidative stress and determination of biological activities of exogenous and endogenous antioxidants; and (4) presentation of simple procedures based on polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) of the resulting amplicon for investigations of structural alterations in mtDNA.

Animals↗

PubMed2006

Early post-traumatic stress disorder in relation to acute stress reaction: an ICD-10 study among help seekers following an earthquake.

Disaster research related to earthquakes has almost exclusively dealt with their long-term psychosocial impact; besides, diagnoses were previously based only on DSM criteria. Therefore, it is pertinent to assess stress-related reactions of earthquake victims during the early post-disaster period through the application of ICD-10 criteria. For the first 3 weeks following an earthquake, 102 help-seekers were assessed based on a checklist of sociodemographic variables and a semi-structured interview for the detection of acute stress reaction (ASR) and posttraumatic stress disorder (PTSD) according to ICD-10. Forty-four subjects (43%) fulfilled the ICD-10 criteria for PTSD; all but one of them had suffered ASR. Moreover, among a series of potential predictors for PTSD, ASR was found to be the only significant one; this indicates a definite association between ASR and early development of PTSD. Logistic regression to predict group membership (PTSD/no PTSD) based on specific ASR symptoms showed that accelerated heart rate and feelings of derealization were the only significant predictors for early PTSD. Individuals who fulfill the ICD-10 diagnostic criteria for ASR following an earthquake are at high risk for subsequent occurrence of early PTSD. Increased heart rate and feelings of derealization within the first 48 h after the traumatic event appear to be the principal factors associated with the development of early PTSD. In addition to their potential value for timely prevention and treatment, these findings raise important nosological issues pertaining to the current diagnostic classification of stress-related disorders (ICD-10 versus DSM-IV).

Adolescent↗

PubMed2005

Hepatitis C virus, ER stress, and oxidative stress.

Hepatitis C virus (HCV) replication is associated with the endoplasmic reticulum (ER), where the virus causes stress. Cells cope with ER stress by activating an adaptive program called the unfolded protein response (UPR), which alleviates this stress by stimulating protein folding and degradation in the ER and down-regulating overall protein synthesis. Recent work suggests that HCV also alters ER calcium homeostasis, inducing oxidative stress. Future progress in understanding the control that HCV exerts over the ER will provide insight into viral strategies for pathogenesis and persistence in chronically infected patients.

Adaptation, Physiological↗