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Acute stress disorder and posttraumatic stress disorder symptoms among patients severely injured in motor vehicle accidents in Japan.

OBJECTIVE: The prevalence of acute stress disorder (ASD) and posttraumatic stress disorder (PTSD) in seriously injured survivors of motor vehicle accidents (MVAs) in Japan was investigated. Furthermore, predictive factors in the early stage for development of PTSD were evaluated. METHOD: Subjects were consecutive samples (N=100) of patients hospitalized with severe MVA injuries surveyed at two time points: within 1 month after the MVA and then 6 months later. In the first survey, we conducted the Acute Stress Disorder Interview and compiled results of a self-rating questionnaire; in the second survey, we conducted a structured clinical interview via telephone. RESULTS: The prevalence of ASD and PTSD were 9.0% and 8.5%, respectively. The shift from ASD to PTSD was more pronounced when we included partial diagnoses of ASD and PTSD. Three predictive factors for PTSD were identified through multiple logistic analysis: ASD-positive, presence of persistent physical disability and physical injury severity. CONCLUSIONS: Even among severely injured MVA survivors, most acute stress symptoms subside over time. However, having ASD or partial ASD in the early stage, and the presence of physical disability as an aftereffect are strong predictive factors for PTSD. These findings validate the importance of evidence-based intervention for ASD to forestall PTSD.

Accidents, Traffic↗

The prediction of stress fractures using a 'stressed volume' concept.

This paper addresses an anomaly which exists in the current literature regarding stress fractures. Analysis of the data on fatigue strength of bone samples in vitro would conclude that these fractures should never occur at the strain levels known to occur in vivo. This anomaly can be resolved by including in the analysis the effect of stressed volume, whereby larger volumes of material are expected to have worse fatigue properties. A Weibull analysis was used to predict the probability of failure, Pf; this was an upper-bound prediction because it did not include the effects of remodelling and adaptation. Combining this analysis with a finite element model of the human tibia, we predicted a Pf value of 21% after five weeks of strenuous exercise, which is comparable with reported incidences in military personnel. The high incidence of stress fractures in the cannon bone of racehorses could also be predicted (Pf = 62%, compared to 70% experimentally). The approach can be used to investigate the effect of variables in the exercise regime such as the distance run per day and the use of improved footwear. It can also predict the increased risk of stress fractures in elderly people. The results suggest certain simple rules which may be of clinical value in designing exercise regimes and in understanding the risk factors for this type of injury.

Animals↗

Gender differences in oxidative stress in spinal cord of rats submitted to repeated restraint stress.

Behavioral and neurochemical gender-specific effects have been observed following repeated stress. The aim of this study is to verify the effects of repeated restraint stress on free radical production (evaluated by DCF test), lipoperoxidation (evaluated by TBARS levels), and total antioxidant reactivity (TAR) in the spinal cord of male and female rats. Results demonstrate no effect on lipoperoxidation; chronic stress decreased TAR both in male and female spinal cord. In addition, gender differences were observed both in TAR and in the production of free radicals, both being increased in females. These results may be relevant to the gender-specific differences observed after exposure to repeated stress.

Animals↗

Evaluation of stresses caused by dentin pin with finite elements stress analysis method.

The aim of the present study was to show the dimensions and the amount of stresses caused by pins on dentin. Mathematically modelled stainless steel and titanium pins were applied to mandibular first molar teeth with extensive crown destruction. The stress caused by the pins was examined with the finite elements method (FEM). In both types of pin, the maximum diffuse and the dense stress areas were located at the bottom of the pin channel. It is believed that these stresses should be taken into consideration when evaluating the advantages and disadvantages of pin application to teeth with destroyed crowns.

Alveolar Process↗

Annexin I is a stress protein induced by heat, oxidative stress and a sulfhydryl-reactive agent.

Annexin I (also called lipocortin 1) is a 37-kDa member of the annexin family of proteins. It has been proposed to be involved in the regulation of cell growth and differentiation, apoptosis, and inflammation. Previously, we have reported that annexin I displays a chaperone-like function (Kim, G.Y., Lee, H.B., Lee, S.O., Rhee, H.J. & Na, D.S. (1997) Biochem. Mol. Biol. Int. 43, 521-528). To determine the possibility that annexin I is a stress protein, we examined whether expression of annexin I and annexin I mRNA increases in response to stresses in A549 and HeLa cells. Treatments of cells with heat, hydrogen peroxide or sodium arsenite resulted in (a) an increase in annexin I and annexin I mRNA and (b) translocation of annexin I from the cytoplasm to the nucleus and perinuclear region. The annexin I gene promoter region, cloned upstream of a reporter gene, was inducible in response to heat, hydrogen peroxide, and sodium arsenite. These results indicate that annexin I serves as a stress protein and annexins may constitute a new class of stress proteins.

Adenocarcinoma↗

Gender differences in the relationship between acute stress disorder and posttraumatic stress disorder following motor vehicle accidents.

OBJECTIVE: Acute stress disorder (ASD) describes initial posttraumatic stress reactions that purportedly predict subsequent posttraumatic stress disorder (PTSD). This study aimed to index the influence of gender on the relationship between ASD and PTSD. METHOD: Motor vehicle accident survivors were assessed for ASD within 1-month posttrauma (n = 171) and were subsequently assessed for PTSD 6-months later (n = 134). RESULTS: Acute stress disorder was diagnosed in 8% of males and 23% of females, and PTSD was diagnosed in 15% of males and 38% of females. In terms of patients followed up at 6 months, 57% and 92% of males and females, respectively, who met criteria for ASD were diagnosed with PTSD. Females displayed significantly more peritraumatic dissociation than males. CONCLUSION: Peritraumatic dissociation and ASD is a more accurate predictor of PTSD in females than males. This gender difference may be explained in terms of response bias or biological differences in trauma response between males and females.

Accidents, Traffic↗

The influence of traumatic brain injury on acute stress disorder and post-traumatic stress disorder following motor vehicle accidents.

This study compared the acute stress disorder and post-traumatic stress disorder (PTSD) symptom profiles in motor vehicle accident survivors who sustained a mild traumatic brain injury (MTBI) or no TBI. Consecutive adult patients who sustained a MTBI (n = 79) and no TBI (n = 92) were assessed for acute stress disorder within 1 month of their trauma and reassessed for PTSD (MTBI: n = 63; non-TBI; n = 72) 6-months post-trauma. Comparable rates of acute stress disorder and PTSD were reported in MTBI and non-TBI patients. Intrusive memories and fear and helplessness in response to the trauma were reported less frequently by MTBI than non-TBI patients at the acute phase. Six-months post-trauma fewer MTBI patients than non-TBI reported fear and helplessness in response to the trauma. These findings suggest that, whereas impaired consciousness at the time of a trauma may reduce the frequency of traumatic memories in the initial month post-trauma, MTBI does not result in a different profile of longer-term PTSD.

Accidents, Traffic↗

Childhood stress disorder behaviors in veterans who do and do not develop posttraumatic stress disorder.

The purpose of this study was to test a variation of the stress-evaporation theory, which maintains that posttraumatic stress disorder (PTSD) symptoms are simply exacerbations of behaviors present before the trauma. Retrospective childhood self-ratings were made by 63 PTSD patients, 53 psychiatric controls, and 28 normals on 13 PTSD-like symptoms. The results did not support the hypothesis, and they give more support to the residual-stress model than to the stress-evaporation theory.

Adult↗

Repressive coping style, acute stress disorder, and posttraumatic stress disorder after myocardial infarction.

OBJECTIVE: The study examined the associations between repressive coping style, acute stress disorder (ASD) and subsequent posttraumatic stress disorder (PTSD) after myocardial infarction (MI) to ascertain the efficacy of repressive coping style in immediate and long-term adjustment to stress. METHODS: A total of 116 MI patients were examined twice: within a week of their MI (time 1) and 7 months later (time 2). At time 1, repressive coping style, perceived threat, and ASD were measured by self-report questionnaires. In addition, medical measures indicative of the severity of the MI were obtained from patients' hospital records. At time 2, PTSD was assessed. The distribution of the repressive coping style was compared with that of 72 matched control subjects. RESULTS: Findings revealed the adaptiveness of repressive coping style both in the immediate and longer-term aftermath of MI: repressors endorsed less ASD and PTSD than nonrepressors. In addition, the contribution of repressive coping style to PTSD was unique and beyond the implications of severity of MI, perceived threat, and immediate ASD. CONCLUSIONS: The findings support the role of repressive coping style as a stress-buffer; several mechanisms that explain this role are suggested.

Adaptation, Psychological↗

Dynamic responses to acute heat stress between 34 degrees C and 38.5 degrees C, and characteristics of heat stress response in mice.

We focused on dynamic responses to acute heat stress between 34 degrees C and 38.5 degrees C. Physiological and neuroendocrinological changes between 34 degrees C and 38.5 degrees C were studied in mice. The influence of humid conditions, 85% relative humidity (RH), on these changes was also investigated. Rectal temperatures increased above 34 degrees C and hematocrit levels increased at 38.5 degrees C 85% RH for 60 min. Food consumption and body weight gains decreased after a daily 60 min exposure to 34, 37 and 38.5 degrees C for 2 weeks. The corticosterone and vasopressin levels in the blood, and catecholamine and serotonin metabolite levels in the hypothalamus were not changed at 34 degrees C, but increased when above 37 degrees C for 60 min. Above 37 degrees C, these physiological and neuroendocrinological changes were accelerated by humid conditions. These results indicated that food consumption and body weight gains decreased above 34 degrees C, and the neuroendocrinological changes, which were accelerated by humid conditions, were induced above 37 degrees C. In comparison with restraint and water immersion stress, heat stress at 37 degrees C 85% RH showed a slower increase in serum corticosterone levels, smaller changes in plasma dopamine and dihydroxyphenylacetic acid levels, and, after repeated exposure, larger decreases in food consumption and body weight gains. This study clarified the relationships between temperature and humidity conditions and physiological and neuroendocrinological changes, along with the characteristics of responses in acute heat stress.

Animals↗

Pain and stress: correlation of stress hormone release to pain modulation in man.

The contribution of stress-induced and opioid-dependent mechanisms to the modulation of experimental pain was studied in man under different conditions. The contribution of these mechanisms to the possible attenuation of acute cardiac pain in human patients was also studied. According to the present series of investigations, stress-induced mechanisms might be involved in the modulation of pain caused by physical exercise but not by concurrent subacute pain or transcutaneous nerve stimulation. The lack of any negative correlation between the pain intensity and the release of stress hormones indicates that stress mechanisms do not attenuate acute ischaemic pain of the cardiac origin. The use of an opioid-antagonist, naloxone, and the measurement of plasma levels of beta-endorphin did not reveal any contribution of endogenous opinoids to pain modulation in the current study.

Coronary Disease↗

Pneumonia and stress ulceration in severely injured patients. A prospective evaluation of the effects of stress ulcer prophylaxis.

Stress ulcer prophylaxis is a routine aspect of the care of critically injured patients. Recent reports have suggested that patients undergoing prophylaxis with histamine antagonists are predisposed to nosocomial pneumonia, and that treatment with sucralfate can prevent this problem. An open, prospective randomized trial of three regimens was conducted with 278 evaluable patients. The patients were assigned to one of three group: the group receiving sucralfate, the group receiving a cimetidine hydrochloride bolus, and the group undergoing continuous infusion with cimetidine. Stress ulceration developed in 8% of patients in the sucralfate group, 13% of patients in the cimetidine bolus group, and 12% of patients in the cimetidine infusion group, while nosocomial pneumonia developed in 29% of patients in the sucralfate group, 32% of patients in the cimetidine bolus group, and 23% of patients in the cimetidine infusion group. Multivariate analysis of risk factors associated with pneumonia demonstrated independent significance for score on the Glasgow Coma Scale, Injury Severity Score, cord injury, shock, and head injury. Only spinal cord injury was associated with stress ulceration. We conclude that sucralfate and cimetidine are both effective for stress ulcer prophylaxis and that there is no association of cimetidine with nosocomial pneumonia.

Administration, Oral↗

Comparative efficacy of biofeedback and stress inoculation for stress reduction.

Evaluated the comparative effectiveness of frontalis electromyographic (EMG) biofeedback, a primarily somatic intervention, and stress inoculation, a self-instructional form of cognitive-behavior therapy. Both treatments were compared with a waiting list control group on systolic and diastolic blood pressure, the Taylor Manifest Anxiety Scale, and the Teaching Anxiety Scale (N = 24). Multivariate assessment on all four dependent measures indicated that both the frontalis feedback and stress inoculation groups improved significantly more than the no treatment control, but did not differ overall from one another. The stress inoculation group showed more improvement in self-reported anxiety than the EMG group, while the EMG group tended to do better than the stress inoculation group on blood pressure measures. The untreated control group regressed somewhat across all measures. It was proposed that each treatment may have specific effects that might suggest which treatment would be indicated for a particular client.

Adult↗

Cognitive-behavioral stress management improves stress-management skills and quality of life in men recovering from treatment of prostate carcinoma.

BACKGROUND: The current study evaluated the efficacy of a 10-week, group-based, cognitive-behavioral stress management (CBSM) intervention relative to a half-day seminar in improving quality of life (QoL) among men who were treated for localized prostate carcinoma (PC) with either radical prostatectomy (RP) or radiation therapy. METHODS: Ninety-two men were assigned randomly to either the 10-week CBSM group intervention or a 1-day seminar (control group). The intervention was designed to improve QoL by helping participants to identify and effectively manage stressful experiences and was focused on the treatment-related sequelae of PC. RESULTS: A hierarchical regression model was used to predict postintervention QoL. The final model, including all predictors and relevant covariates (i.e., income, baseline QoL, ethnicity, and group condition), explained 62.1% of the variance in QoL scores. Group assignment was a significant predictor (beta = - 0.14; P = 0.03) of QoL after the 10-week intervention period, even after controlling for ethnicity, income, and baseline QoL. Post-hoc analyses revealed that individuals in the CBSM intervention condition showed significant improvements in QoL relative to men in the 1-day control seminar. Improved QoL was mediated by greater perceived stress-management skill. CONCLUSIONS: A 10-week cognitive-behavioral group intervention was effective in improving the QoL in men treated for PC, and these changes were associated significantly with intervention-associated increases in perceived stress-management skills.

Aged↗

Reduced basal CaMKII levels in hippocampal CA1 region: possible cause of stress-induced impairment of LTP in chronically stressed rats.

Chronic psychosocial stress markedly reduces the expression of high-frequency stimulation (HFS)-evoked early long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. Immunoblotting was performed to determine changes in molecular levels of key signaling proteins that might be responsible for this inhibitory effect. Western blot analysis of the CA1 region demonstrates that chronic psychosocial stress decreases basal levels of calcium calmodulin kinase II (CaMKII), phosphorylated (P)-CaMKII, calmodulin, and protein kinase C (PKCgamma) while markedly increasing protein phosphatase 2B (calcineurin) levels. The decrease of basal levels of P-CaMKII may be triggered primarily by excessive dephosphorylation resulting from enhanced basal levels of calcineurin. The decline in the basal levels of the upstream molecules, PKCgamma and calmodulin may be a consequence of the diminished basal P-CaMKII levels. Analysis of signaling molecules in CA1 region of chronically stressed rat subjected to HFS in vivo showed only one difference compared to similarly stimulated control rats; no increase in P-CaMKII levels. Our results suggest that decreased P-CaMKII levels may be primarily responsible for the stress-induced reduction in LTP expression.

Animals↗

Prenatal stress causes gender-dependent neuronal loss and oxidative stress in rat hippocampus.

Our purpose was to investigate the effects of prenatal stress on neuronal changes in the hippocampus and the possible involvement of oxidative stress in female and male rats. Female and male offspring (1-month-old), whose dams were restrained in middle or later pregnant stage (MS or LS), were studied to observe changes in the number of hippocampal neurons and the expression of neuronal nitric oxide synthase (nNOS) in the hippocampus. Both MS and LS induced an increase in the number of nNOS-positive expression in female and male offspring in the hippocampus; however, both MS and LS caused a significant decrease in the number of hippocampal neurons in the female, but not in the male offspring. In addition, significant increases in calcium content and oxidant generation were induced by LS in the hippocampal CA3 region in female rats. These data suggest that prenatal stress can cause oxidative stress and consequent damage to neurons, leading to neuronal loss in the brain of offspring during development.

Animals↗

Cold stress does not induce stress proteins SP 25 and SP 72 in rat skeletal muscle.

Cryotherapy is a common treatment for musculoskeletal injuries, yet the mechanism(s) underlying its effects remain unclear. Since cryotherapeutic treatment often involves temperatures that are known to induce the protective stress proteins (SPs), we determined whether SP 25 and SP 72 expression was altered following a 20-min cold stress to the hindlimb muscles of Sprague-Dawley rats. The right hindlimb of anesthetized animals was placed in an ice bath until muscle temperature decreased to either 8.4 +/- 0.4 degrees C or 19.7 +/- 0.3 degrees C for 20 min. After a 24-h recovery, the white and red gastrocnemius, plantaris, soleus, extensor digitorum longus, and tibialis anterior muscles from both legs were removed and rapidly frozen in liquid nitrogen. Portions of the muscles were homogenized and SP 25 and SP 72 content was assessed by SDS-PAGE/Western blot analyses. Quantification of SP 25 and SP 72 by densitometric scanning of blots demonstrated no significant increases in SP 25 or SP 72 content in any of the muscles exposed to either the 8 or the 20 degrees C cold stress compared to muscles from the unstressed contralateral limbs. These results suggest that a 20-min cold stress of 8 degrees C or 20 degrees C does not increase muscle SP 25 or SP 72 content.

Animals↗

The neuronal stress response: nuclear translocation of heat shock proteins as an indicator of hyperthermic stress.

Two characteristic features of the heat shock response, (i) induction of hsp70 protein and (ii) nuclear translocation of constitutive hsc70 and stress-inducible hsp70 protein, were utilized as markers of cellular stress in the rabbit brain. Following a physiologically relevant increase in body temperature of 2.7 +/- .3 degrees C, nonneuronal cell types, such as ependymal cells and oligodendrocytes, undergo a stress response as assayed by the above criteria. In contrast, several neuronal cell populations required an increased degree of hyperthermic stress (3.4 +/- .2 degrees C) before exhibiting nuclear translocation of constitutive hsc70 protein. Induction of hsp70 protein was not observed in these neuronal cells at either temperature. The present results suggest that certain neurons in the rabbit brain are buffered against induction of the heat shock response, perhaps due to their high constitutive levels of hsc70 protein.

Animals↗