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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a component of the response to acute stress, p53 has a well established role in protecting against cancer development. However, it is now becoming clear that p53 can have a much broader role and can contribute to the development, life expectancy and overall fitness of an organism. Although the function of p53 as a tumour suppressor ensures that we can't live without it, an integrated view of p53 suggests that not all of its functions are conducive to a long and healthy life.
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PMID:p53 in health and disease. 1738 Jan 61

This study investigated the correlates of acute stress disorder (ASD) following a diagnosis of cancer. Adults diagnosed with first onset head, neck, or lung malignancy (N = 82) were assessed within one month of diagnosis using the ASD Interview, and the Structured Clinical Interview for DSM-IV to index the incidence of ASD and other affective disorders following their cancer diagnosis. Participants were also administered questionnaires that assessed dissociative symptoms, coping strategies, and quality of life. Acute stress disorder was diagnosed in 28% of participants. Acute stress disorder severity was associated with gender, elevated dissociative responses, trait anxiety, and preoccupation with one's diagnosis, and a decline in cognitive functioning. This study provides evidence for identifying recently diagnosed cancer patients who may benefit from psychological assistance.
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PMID:Correlates of acute stress disorder in cancer patients. 1759 36

Gender differences are related to the manner in which the heart responds to chronic and acute stress conditions of physiological and pathological nature. Depending on dose, sodium selenite acts as an antioxidant proven to have beneficial effects in several pathological conditions G. Drasch, J. Schopfer, and G. N. Schrauzer, Selenium/cadmium ratios in human prostates: indicators of prostate cancer risk of smokers and nonsmokers, and relevance to the cancer protective effects of selenium, Biol. Trace Element Res. 103(2), 103-107 (2005); R. G. Kasseroller and G. N. Schrauzer, Treatment of secondary lymphedema of the arm with physical decongestive therapy and sodium selenite: a review, Am. J. Ther. 7(4), 273-279 (2000); G. N. Schrauzer, Anticarcinogenic effects of selenium, Cell. Mol. Life Sci. 57(13-14), 1864-1873 (2000); I. S. Palmer and O. E. Olson, Relative toxicities of selenite and selenate in the drinking water of rats, J. Nutr. 104(3), 306-314 (1974). To date, little is known about the gender-dependent direct effects of toxic doses of selenite on electrophysiology of the cardiovascular system H. A. Schroeder and M. Mitchener, Selenium and tellurium in rats: effect on growth, survival and tumors, J. Nutr. 101(11), 1531-1540 (1971); G. N. Schrauzer, The nutritional significance, metabolism and toxicology of selenomethionine, Adv. Food Nutr. Res. 47, 73-112 (2003). In the present study, the effects of in vitro toxic concentrations of sodium selenite ranging from 10-6 M to 10-3 M were tested on both male and female rat heart preparations. The toxic effects seen in an electrocardiogram and left ventricular pressure were dose and sex dependent at most of the tested concentrations. The present study clearly shows that at toxic doses, stress conditions are induced by selenite, resulting in genderdependent modifications of the heart function. This modification is more pronounced in the contraction cascade of female rats. Males, on the other hand, had been much more affected in excitation-related parameters.
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PMID:Gender-dependent effects of selenite on the perfused rat heart: a toxicological study. 1770 10

The main aim of this study was to investigate the occurrence of cancer-related posttraumatic stress disorder (PTSD) among parents of children on cancer treatment. A longitudinal design with assessments at one week (T1), two (T2), and four (T3) months after the child's diagnosis was used. Two hundred and fourteen parents (107 mothers, 107 fathers) participated at T1-T3. The PTSD Checklist Civilian (PCL-C), a self-report screening instrument for PTSD, was answered by parents over the telephone. According to the PCL-C symptom criteria method 33%, more mothers than fathers, score as potential cases of acute stress disorder (ASD) at T1, whereas 28% as potential cases of PTSD at T2 and 22% at T3. The levels of acute- and posttraumatic stress symptoms show a linear, descending pattern, and mothers report higher levels than fathers. Half of the parents who score as potential cases of ASD a week after the child's diagnosis score as potential cases of PTSD four months later. The findings illustrate that a group of parents of children with cancer experience serious psychological distress related to their child's disease. A traumatic stress perspective on childhood cancer should be applied to paediatric oncology care and appropriate psychosocial interventions should be offered to parents when needed.
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PMID:Posttraumatic stress disorder among parents of children on cancer treatment: a longitudinal study. 1784 23

Stress is a powerful modulator of neuroendocrine, behavioral, and immunological functions. After 4.5-d repeated combined acoustic and restraint stress as a murine model of chronic psychological stress, severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with the severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turnover, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure, changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice. Thus, in our murine model, repeated stress caused severe metabolic dysregulations, leading to a drastic reduction of the individual's energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer.
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PMID:Hypermetabolic syndrome as a consequence of repeated psychological stress in mice. 1832 86

Thymopoiesis is essential for development and maintenance of a robust and healthy immune system. Acute thymic atrophy is a complication of many infections, environmental stressors, clinical preparative regimens, and cancer treatments used today. This undesirable sequela can decrease host ability to reconstitute the peripheral T cell repertoire and respond to new antigens. Currently, there are no treatments available to protect against acute thymic atrophy or accelerate recovery, thus leaving the immune system compromised during acute stress events. Several useful murine models are available for mechanistic studies of acute thymic atrophy, including a sepsis model of endotoxin-induced thymic involution. We have identified the IL-6 cytokine gene family members (i.e., leukemia inhibitory factor, IL-6, and oncostatin M) as thymosuppressive agents by the observation that they can acutely involute the thymus when injected into a young, healthy mouse. We have gone on to explore the role of thymosuppressive cytokines and specifically defined a corticosteroid-dependent mechanism of action for the leukemia inhibitory factor in acute thymic atrophy. We also have identified leptin as a novel, thymostimulatory agent that can protect against endotoxin-induced acute thymic atrophy. This review will highlight mechanisms of stress-induced thymic involution and focus on thymosuppressive agents involved in atrophy induction and thymostimulatory agents that may be exploited for therapeutic use.
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PMID:Cytokines, leptin, and stress-induced thymic atrophy. 1849 86

Risk of developing certain diseases correlates with human personality. Cardiologists have defined Type "A" personalities as coronary-prone. Associated psychological peculiarities are easily angered, competitive, impatient and hard-driving. Psychologically-opposite people who are prone to suppress emotions and avoid conflicts (Type "C"), have a high risk of infectious diseases and certain forms of cancer. The development of contemporary biology and medicine determined an important role of the neuroendocrine and immune systems in these correlations. The peculiarity of human personality, as much as of animal behavioral patterns, is strongly expressed under stress conditions. The strategies of stress coping display a normal distribution in the human and wild animal populations, with truly passive and active coping styles located at the outermost regions of the curve. However, there are a number of strategies to breed experimental animals with extreme coping styles; animals selected for a passive coping style to acute stress show marked activation of the hypothalamic-pituitary-adrenal (HPA) axis and low stimulation of the sympathetic-adrenal system; both are associated with immunosuppression. An opposite reaction of the neuroendocrine system has been shown in animals with an active coping style to stress; this was associated with the signs of immunostimulation. Similarly, people with passive coping style (type "C") might be at higher risk of infectious diseases and cancer, while people with active coping style (type "A") might be predisposed to coronary, allergic, and autoimmune diseases. Furthermore, pain, decreased productivity, and anxiety, all common in patients with different diseases, are additional stressful entities. Thus, an adequate coping with a disease is an important approach to improve life quality and disease prognosis. Therefore, psychological and psychopharmacotherapeutic interventions that enhance effective coping should have beneficial effects in patients with immune-mediated diseases.
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PMID:Personality, coping style, and constitutional neuroimmunology. 1856 93

Stress is known to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate asthma, and allergic, autoimmune and inflammatory diseases, although such diseases should be ameliorated by immunosuppression. Moreover, the short-term fight-or-flight stress response is one of nature's fundamental defense mechanisms that enables the cardiovascular and musculoskeletal systems to promote survival, and it is unlikely that this response would suppress immune function at a time when it is most required for survival (e.g. in response to wounding and infection by a predator or aggressor). These observations suggest that stress may suppress immune function under some conditions while enhancing it under others. The effects of stress are likely to be beneficial or harmful depending on the type (immunoprotective, immunoregulatory/inhibitory, or immunopathological) of immune response that is affected. Studies have shown that several critical factors influence the direction (enhancing vs. suppressive) of the effects of stress or stress hormones on immune function: (1) Duration (acute vs. chronic) of stress: Acute or short-term stress experienced at the time of immune activation can enhance innate and adaptive immune responses. Chronic or long-term stress can suppress immunity by decreasing immune cell numbers and function and/or increasing active immunosuppressive mechanisms (e.g. regulatory T cells). Chronic stress can also dysregulate immune function by promoting proinflammatory and type-2 cytokine-driven responses. (2) Effects of stress on leukocyte distribution: Compartments that are enriched with immune cells during acute stress show immunoenhancement, while those that are depleted of leukocytes, show immunosuppression. (3) The differential effects of physiologic versus pharmacologic concentrations of glucocorticoids, and the differential effects of endogenous versus synthetic glucocorticoids: Endogenous hormones in physiological concentrations can have immunoenhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immunosuppressive. (4) The timing of stressor or stress hormone exposure relative to the time of activation and time course of the immune response: Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response. We propose that it is important to study and, if possible, to clinically harness the immunoenhancing effects of the acute stress response, that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve. In view of the ubiquitous nature of stress and its significant effects on immunoprotection as well as immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.
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PMID:Enhancing versus suppressive effects of stress on immune function: implications for immunoprotection and immunopathology. 1957 91

Compared with young adults, older adults have significantly impaired capacities to resist oxidative damage when faced with acute stress such as ischemia/reperfusion. This impairment likely contributes to increased morbidity and mortality in older adults in response to acute trauma, infections, and the susceptibility to diseases such as atherosclerosis, cancer, diabetes, and Alzheimer's disease. Consumption of foods high in polyphenols, particularly anthocyanins, have been associated with improved health, but the mechanisms contributing to these salutary effects remain to be fully established. This study tested the hypothesis that consumption of tart cherry juice containing high levels of anthocyanins improves the capacity of older adults to resist oxidative damage during acute oxidative stress. In a double-blind, placebo-controlled, crossover design, 12 volunteers [6 men and 6 women; age 69 +/- 4 y (61-75 y)] consumed in random order either tart cherry juice or placebo (240 mL twice daily for 14 d) separated by a 4-wk washout period. The capacity to resist oxidative damage was measured as the changes in plasma F(2)-isoprostane levels in response to forearm ischemia-reperfusion (I/R) before and after each treatment. The tart cherry juice intervention reduced the I/R-induced F(2)-isoprostane response (P < 0.05), whereas placebo had no significant effect. The tart cherry juice intervention also reduced basal urinary excretion of oxidized nucleic acids (8-hydroxy-2'-deoxyguanosine, 8-hydroxyguanosine) (P < 0.05) but not urinary excretion of isoprostanes. These data suggest that consumption of tart cherry juice improves antioxidant defenses in vivo in older adults as shown by an increased capacity to constrain an oxidative challenge and reduced oxidative damage to nucleic acids.
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PMID:Tart cherry juice decreases oxidative stress in healthy older men and women. 1969 30

Long-term implications of the exposure to traumatizing experiences during childhood or adolescence, such as sexual abuse, or cancer, have been documented, namely the subjects' response to an acute stress in adulthood. Several indicators of the stress response have been considered (e.g. cortisol, heart rate). Oxytocin (OT) response to an acute stress of individuals exposed to trauma has not been documented. Eighty subjects (n=26 women who had experienced episodes of child abuse, n=25 men and women healthy survivors of cancer in childhood or adolescence, and 29 controls) have been submitted to a laboratory session involving an experimental stress challenge, the Trier social stress test. Overall, there was a clear OT response to the psychosocial challenge. Subjects having experienced a childhood/adolescence life-threatening illness had higher mean levels of OT than both abused and control subjects. There was a moderate negative relationship between OT and salivary cortisol. It is suggested that an acute stress stimulates OT secretion, and that the exposure to enduring life-threatening experiences in childhood/adolescence has long-lasting consequences regarding the stress system and connected functions, namely the activation of OT secretion. Better knowledge of such long-term implications is important so that to prevent dysregulations of the stress responses, which have been shown to be associated to the individual's mental health.
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PMID:Oxytocin response to an experimental psychosocial challenge in adults exposed to traumatic experiences during childhood or adolescence. 2001 29


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