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At least 595 records · Page 33Linked to original sources
PubMed2004

Effects of age on the stress-strain and stress-relaxation properties of the rat molar periodontal ligament.

OBJECTIVE: We examined the stress-strain and stress-relaxation properties of the periodontal ligament (PDL) in the rat molar at 2, 6, 12, and 24 months of age to elucidate age-related changes in the tooth support function of the PDL. DESIGN: From the dissected left and right mandibles in each rat, a pair of transverse sections (ca. 0.45 mm in thickness) of the first molar was cut at the middle part of the mesial root. We then obtained a load-deformation curve for the PDL, using one of the paired sections. The other section was loaded to as much as 50% of the maximum load as determined from the contralateral section, and keeping the deformation constant for 10 min, a load-relaxation curve was obtained and analysed. RESULTS: The maximum shear stress and tangent modulus decreased between 2 and 24 months of age. As the maximum shear strain increased with age (P < 0.001), the failure strain energy density did not change between 2 and 24 months of age. The stress-relaxation during the 10 min period decreased from 2 to 24 months of age (P < 0.01). The relaxation process of the PDL in each age was well described by a sum of three exponential decay functions. The age-related decrease in the relaxation was found to be mainly due to the increase in the relaxation time for the long-term relaxation component. CONCLUSION: These results indicate that the maximum shear stress and stiffness of the rat molar PDL decrease between 2 and 24 months of age; but its toughness remains unchanged due to an increase in the extensibility. Our findings further indicate that the fluid flow and movements of macromolecules within the stretched PDL fibres during the stress-relaxation decrease with advancing age.

Aging↗
PubMed2004

Higher Beck depression scores predict delayed epinephrine recovery after acute psychological stress independent of baseline levels of stress and mood.

Depressive symptoms in the non-clinical range have been linked to increased health risks. Recent theorizing raises the possibility that heightened physiologic responses to acute stress and/or slowed stress recovery in individuals with depressive symptoms may contribute to increased risk. We investigated stress-induced catecholamine responses and recovery patterns using a modified version of the Trier Social Stress Test (15 min) with a sample of 52 healthy women and compared subgroups with high normal versus low scores on the Beck Depression Inventory (BDI, median split) to 29 women randomly assigned to a non-stressed control group. The BDI-high normal and BDI-low groups showed similar acute increases in epinephrine immediately post stressor, but only the BDI-high normal group remained significantly elevated above control group levels during the recovery period. No differences were found in norepinephrine responses. Elevations in BDI scores within the normal range may selectively predict slower physiological recovery following acute stress.

Adult↗
PubMed2006

Acute heat stress induces oxidative stress in broiler chickens.

The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.

Animals↗
PubMed2006

Oxidative stress in Perna perna and other bivalves as indicators of environmental stress in the Brazilian marine environment: antioxidants, lipid peroxidation and DNA damage.

Oxidative stress can take place in marine bivalves under a series of environmental adverse conditions. The study of different systems related to oxidative stress in these organisms can give important information about their physiological status and also about environmental health. Bivalves have been proposed as good sentinel organisms in pollution monitoring studies through the analysis of biochemical biomarkers, and most of the biomarkers analyzed are those related to oxidative stress. However, it is very important to know how other environmental factors not associated to the presence of pollutants might affect these parameters. We have studied a series of mechanisms related to oxidative stress in mussels which inhabit the Brazilian coast, especially in Perna perna species, subjected to different stress conditions, such as the exposure to different contaminants in the laboratory and in the field, the exposure of mussels to air and re-submersion, simulating the tidal oscillations, and in mussels collected at different seasons. Both oxidative damage levels and antioxidant defense systems were strongly affected by the different environmental stress. This review summarizes the data obtained in some studies carried out in bivalves from the Brazilian coast.

Animals↗
PubMed2003

Acute and chronic stress exert opposing effects on antibody responses associated with changes in stress hormone regulation of T-lymphocyte reactivity.

Here we show that stress exerts a differential effect on T-cell-dependent antibody production. IgG production is augmented after acute stress and impaired in a chronic situation. We found catecholamines and corticosterone levels were increased in acute situations although they were not modified after prolonged stress conditions. However, lymphocyte sensitivity to corticosterone and catecholamines was altered under stress conditions. These results point out the role of the adrenal's hormones as mediators of the differential effects of stress on the immune response providing the basis for a functional significance of stress hormone receptors on lymphocytes.

Acute Disease↗
PubMed2004

Perceived stress, stress attributions and psychological distress in psoriasis.

OBJECTIVE: The objective of this study was to measure causal beliefs in individuals with psoriasis and to explore their relationship with perceived stress, quality of life, psychological well-being and psoriasis severity. METHODS: This study was cross-sectional in design, and patients were required to complete validated questionnaires assessing perceptions of illness, quality of life, psoriasis severity, perceived stress and psychological mood. A total of 141 individuals were recruited from two settings: an outpatient skin clinic at King's College Hospital and the Psoriasis Association. RESULTS: A strong belief in stress/psychological attributes as a causal factor was found in 61% of the sample. This belief was significantly associated with higher levels of anxiety, depression and perceived stress (r > or = .38; P < or = .0001). Perceived stress in this sample was significantly associated with a poorer level of quality of life, higher levels of anxiety and depression (r > or = .27; P < or = .002) but not with psoriasis severity. CONCLUSIONS: The belief that stress is causal was associated with lower levels of psychological well-being. However, there was no association between perceived stress and more objective measures of psoriasis severity.

Adult↗
PubMed2005

Model of coupled transient changes of Rac, Rho, adhesions and stress fibers alignment in endothelial cells responding to shear stress.

Interactions of cell adhesions, Rho GTPases and actin in the endothelial cells' response to external forces are complex and not fully understood, but a qualitative understanding of the mechanosensory response begins to emerge. Here, we formulate a mathematical model of the coupled dynamics of cell adhesions, small GTPases Rac and Rho and actin stress fibers guiding a directional reorganization of the actin cytoskeleton. The model is based on the assumptions that the interconnected cytoskeleton transfers the shear force to the adhesion sites, which in turn transduce the force into a chemical signal that activates integrins at the basal surface of the cell. Subsequently, activated and ligated integrins signal and transiently de-activate Rho, causing the disassembly of actin stress fibers and inhibiting the maturation of focal complexes into focal contacts. Focal complexes and ligated integrins activate Rac, which in turn enhances focal complex assembly. When Rho activity recovers, stress fibers re-assemble and promote the maturation of focal complexes into focal contacts. Merging stress fibers self-align, while the elevated level of Rac activity at the downstream edge of the cell is translated into an alignment of the cells and the newly forming stress fibers in the flow direction. Numerical solutions of the model equations predict transient changes in Rac and Rho that compare well with published experimental results. We report quantitative data on early alignment of the stress fibers and its dependence on cell shape that agrees with the model.

Actin Cytoskeleton↗
PubMed2006

Role of the universal stress protein UspA of Salmonella in growth arrest, stress and virulence.

Pathogenic bacteria employ a variety of mechanisms to resist a barrage of stresses they encounter during active growth in or outside the host as well as during growth stasis. An in silico screen of the Salmonella genome sequence revealed that Salmonella typhimurium LT2 possesses a homologue belonging to the universal stress protein A (UspA) family. We assessed the transcriptional profile of uspA in S. typhimurium C5 by constructing a lacZ fusion revealing that uspA is induced by metabolic, oxidative, and temperature stresses. The highest transcriptional levels occurred in cells entering stationary phase, an observation consistent with expression patterns in Escherichia coli. The protein was purified as a fusion with GST (UspA(F)) and antibodies raised against UspA(F) revealed elevated protein levels in stressed and growth-arrested cells. Inactivation of uspA in S. typhimurium C5, lead to increased susceptibility to stress conditions. Furthermore, UspA makes an important contribution to the in vivo virulence of Salmonella in mice thus highlighting the importance of stress resistance regulation in pathogenicity and survival within the host.

Animals↗
PubMed2005

Chronic stress, as well as acute stress, reduces BDNF mRNA expression in the rat hippocampus but less robustly.

Daily restraint for 3 weeks was shown to atrophy dendrites of hippocampal pyramidal neurons in rats. Brain-derived neurotrophic factor (BDNF), which maintains neuronal survival and morphology, has been shown to decrease in response to acute stress. Plasma glucocorticoid (GC) and serotonergic projections from the raphe nuclei play major roles in reducing BDNF synthesis in the hippocampus. We investigated BDNF mRNA levels there, together with plasma GC levels, GC receptors in the hippocampus/hypothalamus and 5-HT synthesizing enzyme, tryptophan hydroxylase in the raphe nuclei, in animals chronically stressed for 1-3 weeks, using in situ hybridization and immunohistochemistry. In these animals, BDNF mRNA levels were significantly decreased in the hippocampus after 6 h of restraint, but the ability of restraint to reduce BDNF synthesis seemed less robust than that seen in acute stress models. HPA axis response to stress in these animals assessed by plasma GC levels was delayed and sustained, and the GC receptor in the paraventricular hypothalamic nucleus was increased at 1 week. Tryptophan hydroxylase immunoreactivity was increased in the median raphe nucleus at 2-3 weeks. Repetitive stress-induced reduction of BDNF may partly contribute to the neuronal atrophy/death and reduction of hippocampal volume observed both in animals and humans suffering chronic stress and/or depression.

Animals↗
PubMed2006

Chronic social stress in the visible burrow system modulates stress-related gene expression in the bed nucleus of the stria terminalis.

Prolonged social subjugation produces physiological indices of chronic stress in rats. In the current study, we examined the impact of social stress on glutamic acid decarboxylase (GAD) isoforms, corticotropin-releasing hormone (CRH) and vasopressin mRNA expression in forebrain stress circuitry, using the visible burrow system model of dominance-subordination. Subordinate male rats develop behavioral and neuroendocrine changes consistent with exposure to chronic stress, including marked loss of body weight and elevation of basal plasma corticosterone relative to dominant rats. Forebrain GAD65, GAD67, CRH and vasopressin mRNA expression in central stress-regulatory circuits were examined by in situ hybridization. Elevated CRH mRNA was observed in the oval nucleus of the bed nucleus of the stria terminalis (BST) of subordinate males. In contrast, GAD67 expression was decreased in the interfascicular nucleus of the BST in both the subordinate and dominant rats compared to non-burrow control rats. No changes in CRH, GAD or vasopressin were observed in amygdaloid nuclei, other BST nuclei or in the hypothalamic paraventricular nucleus. Collectively, these data suggest that exposure to the visible burrow system attenuates BST GAD expression regardless of social status, whereas the enhanced physiological responses to social stress seen in subordinates may be associated with enhanced CRH expression in the oval nucleus of the BST.

Adrenal Glands↗
PubMed2006

Prenatal stress alters Fos protein expression in hippocampus and locus coeruleus stress-related brain structures.

Prenatal stress (PS) durably influences responses of rats from birth throughout life by inducing deficits of the hypothalamo-pituitary-adrenal (HPA) axis feedback. The neuronal mechanisms sustaining such alterations are still unknown. The purpose of the present study was to determine whether in PS and control rats, the exposure to a mild stressor differentially induces Fos protein in hippocampus and locus coeruleus, brain areas involved in the feedback control of the HPA axis. Moreover, Fos protein expression was also evaluated in the hypothalamic paraventricular nucleus (PVN) that reflect the magnitude of the hormonal response to stress. Basal plasma corticosterone levels were not different between the groups, while, PS rats exhibited higher number of Fos-immunoreactive neurons than controls, in the hippocampus and locus coeruleus in basal condition. A higher basal expression of a marker of GABAergic synapses, the vGAT, was also observed in the hypothalamus of PS rats. Fifteen minutes after the end of the exposure to the open arm of the elevated plus-maze (mild stress) a similar increased plasma corticosterone levels was observed in both groups in parallel with an increased number of Fos-immunoreactive neurons in the PVN. Return to basal plasma corticosterone values was delayed only in the PS rats. On the contrary, after stress, no changes in Fos-immunoreactivity were observed in the hippocampus and locus coeruleus of PS rats compared to basal condition. After stress, only PS rats presented an elevation of the number of activated catecholaminergic neurons in the locus coeruleus. In conclusion, these results suggest for the first time that PS alters the neuronal activation of hippocampus and locus coeruleus implicated in the feedback mechanism of the HPA axis. These data give anatomical substrates to sustain the HPA axis hyperactivity classically described in PS rats after stress exposure.

Animals↗
PubMed2005

Gender-specific effects of prenatal stress on emotional reactivity and stress physiology of goat kids.

The aims of this study were to investigate the effects of maternal stress during pregnancy on the emotional reactivity, the hypothalamo-pituitary-adrenocortical (HPA) axis, and the sympatho-adrenomedullary (SAM) system of goat offspring according to their gender, and to investigate the role of maternal cortisol in prenatal stress effects. Goats were exposed to ten transports in isolation or ten ACTH injections (0.125 IU/kg body weight) during the last third of pregnancy. Control goats remained undisturbed. No effect of repeated transport during the last third of pregnancy was found on basal cortisol concentrations of the offspring. However, an increase in phenylethanolamine N-methyl transferase activity in the adrenals was observed in prenatally stressed kids compared to control kids (P = 0.031). In the presence of novelty, prenatally stressed female kids were more active (P = 0.049) than control females; they also showed more signs of arousal (P = 0.039) and tended to explore more of their environment (P = 0.053) in reaction to a startling stimulus. On the contrary, prenatally stressed male kids tended to be less active (P = 0.051) than control male kids but showed more signs of distress (P = 0.047) in the presence of novelty. Intermediate effects were found on the emotional reactivity to novelty of kids born from dams given injections of ACTH. In conclusion, transport stress in pregnant goats affects the sympatho-adrenomedullary system and the emotional reactivity of their offspring in a gender-specific manner. Moreover, the effects of prenatal transport and ACTH injections showed some similarities but differed in some critical details.

Adrenocorticotropic Hormone↗
PubMed2006

Chronic disruption of body weight but not of stress peptides or receptors in rats exposed to repeated restraint stress.

Rats exposed to restraint stress for 3 h on each of 3 days lose weight and do not return to the weight of their non-stressed controls for extended periods of time. Studies described here demonstrate that the initial weight loss is associated with increased energy expenditure and reduced food intake on the days of restraint but that there is no difference between stressed and control rats once stress ends. The failure to compensate for this energy deficit accounts for the sustained reduction in weight which lasts for up to 80 days after the end of restraint. In an additional experiment, in situ hybridization was used to measure mRNA expression of corticotrophin releasing factor (CRF) and CRF receptors in hypothalamic nuclei, of urocortin (UCN) in the Edinger Westphal nucleus and of UCN III in the rostral perifornical area and medial amygdaloidal nucleus. Immediately after the second 3 h bout of restraint stress, there was a significant increase in expression of UCN in the Edinger Westphal nucleus and of CRF-R1 in the paraventricular nucleus of the hypothalamus and a less pronounced decrease in CRF-R2 expression in the ventromedial nucleus of the hypothalamus. There were no differences in expression of stress-related peptides or their receptors 40 days after the end of repeated restraint. These results suggest that the sustained reduction in body weight and increased responsiveness to subsequent stressors in rats that have been exposed to repeated restraint are not associated with prolonged changes in mRNA expression of CRF receptors or their ligands.

Amygdala↗
PubMed1997

Prenatal stress induces a phase advance of circadian corticosterone rhythm in adult rats which is prevented by postnatal stress.

Prenatal and postnatal stressors can have different long-term neuroendocrine effects including modifications of stress-induced corticosterone secretion. However, very little is known about the possible long-term effects of prenatal or postnatal stress on the rhythmicity of basal corticosterone secretion in adult offspring. Corticosterone levels were thus determined at six different time points over 24 h in adult rats whose mothers had undergone restraint stress manipulations. The results demonstrate that prenatal stress induces a phase advance in the evening increase of corticosterone levels, and that this change is prevented by postnatal stress. It thus appears that the circadian system governing the HPA axis is modifiable by a prenatal stress, and remains susceptible to compensatory changes during the postnatal period.

Age Factors↗
PubMed1999

Variations in stress levels over the course of pregnancy: factors associated with elevated hassles, state anxiety and pregnancy-specific stress.

This prospective study tracked hassles, pregnancy-specific stress, and state anxiety during pregnancy. A second objective was to identify predictors of each stress dimension. Pregnant women (n=161) completed the Hassles Scale, the Pregnancy-Specific Stress Questionnaire (PEQ), and the state-anxiety scale (STAI-state) monthly, beginning in the third month of pregnancy. Hassles were found to be stable throughout the pregnancy. Women reported significantly higher pregnancy-specific stress in the first and third trimester of pregnancy, whereas state anxiety increased in the third trimester compared with the first and second trimesters. Poorer marital adjustment predicted higher Hassles during pregnancy and higher PEQ and STAI-state in the third trimester. Women who reported that the pregnancy would have a negative impact on their career scored higher on Hassles during pregnancy and higher on the PEQ in the third trimester. The occurrence of a gestational complication during pregnancy was related to higher pregnancy-specific stress in the third trimester. Younger women also reported higher PEQ results in the third trimester. The data provide support for a multidimensional conceptualization of stress during pregnancy.

Adaptation, Psychological↗
PubMed1998

Stress-dependent antinociceptive effects of carbamazepine: a study in stressed and nonstressed rats.

1. The present study examined the antinociceptive effects of carbamazepine on the tail flick test in stressed and nonstressed rats. 2. Carbamazepine produced a bimodal antinociceptive effect in stressed rats, the first peak appearing 30 min and the second 4 h after injection. Antinociceptive effect was not observed in nonstressed rats. 3. The secondary, but not the initial, carbamazepine antinociception in stressed rats was blocked by naloxone (0.2 mg/kg, i.p.), an opioid receptor antagonist. 4. Caffeine (5 mg/kg, i.p.), an adenosine A1/A2 receptor antagonist, inhibited the both initial and secondary antinociceptive effects of carbamazepine in stressed rats. 5. Carbamazepine increased the antinociceptive effect induced by either i.p. or i.c.v. administration of N6-cyclohexyl adenosine (CHA), an adenosine A1 receptor agonist, in stressed rats, but decreased it in nonstressed rats. 6. These results suggest that the initial antinociceptive effect of carbamazepine in stressed rats may be produced via an activation of the adenosine A1 receptors, such as was produced by CHA. The secondary long-lasting antinociceptive effects of carbamazepine may be mediated by an activation of opioid systems. 7. Furthermore, the initial activation of the adenosine A1 receptors by carbamazepine may be a triggering factor for the subsequent long-lasting activation of the opioid system, which results in the antinociception effects.

Adenosine↗
PubMed2000

Previous exposure to footshock stress attenuates nicotine-induced serotonin release in rat striatum during the subsequent stress.

We have analyzed the effects of chronic or repeated footshock stress on the release of serotonin (5-hydroxytryptamine: 5-HT) in the striatum of rats that received nicotine by using a microdialysis technique. Neither local infusion of nicotine alone nor stress application alone changed 5-HT release. Local infusion of 1 mM nicotine to the striatum, however, significantly increased 5-HT release in the striatum to 145.9 +/- 30.8 pg/dialysate during simultaneous stress application. These increases of extracellular 5-HT release induced by the combination of nicotine and stress application were also observed in rats that had received daily chronic footshock. However, the previously administered footshock induced the reduced release of 5-HT from the striatum to 33.5 +/- 8. 6 (repeated footshock) and 10.0 +/- 3.6 pg/dialysate (daily footshock) when footshock was given together with nicotine infusion. These results suggest that previous exposure to stress attenuated the nicotine-induced 5-HT release in the striatum during the subsequent stress.

Animals↗
PubMed2003

A stress-responsive glutathione S-transferase confers resistance to oxidative stress in Caenorhabditis elegans.

Previous studies demonstrated that the Caenorhabditis elegans GST-p24 is upregulated at the steady state mRNA level in response to oxidative stress. A transcriptional upregulation was confirmed in the current study by analyzing Ce-GST-p24 promoter-reporter constructs in transgenic C. elegans strains CL2166 and CL3166. The transgenic strain BL1, which overexpresses the Ce-GST-p24 enzyme (as a GFP fusion protein controlled by its own promoter), was generated to investigate the function of this enzyme in vivo. Stress experiments with BL1 demonstrated an increased resistance to intracellularly induced oxidative stress, as compared to wild type. The consequences of a decrease in the Ce-GST-p24 enzyme concentration were examined by RNAi-treatment of BL1 C. elegans to silence both the endogene and the transgene Ce-GST-p24 and by the analysis of the K08F4.7 homozygous deletion mutant. In both cases, the reduced Ce-GST-p24 enzyme level resulted in a significant decrease in the stress resistance of the nematodes. These results clearly demonstrate a direct correlation between the concentration of Ce-GST-p24 and the resistance to oxidative stress. We have demonstrated for the first time that manipulation of the expression of a single GST can modulate the organismal response to oxidative stress. The enzymatic activity of this detoxification enzyme was examined with various substrates, giving emphasis to lipid peroxidation products. The Ce-GST-p24 was also localized in BL1 C. elegans by confocal laser-scanning microscopy, revealing a wide-spread distribution profile.

Animals↗