Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test if a benzodiazepine would enhance or hinder the therapeutic effects of exposure, immediate and delayed effects of alprazolam on flight phobics were assessed by questionnaires and ambulatory physiological recording. Physiological measures included heart rate, skin conductance level and fluctuations, finger temperature, respiratory sinus arrhythmia, and various respiratory measures derived from two bands calibrated for each subject. Twenty-eight women with flying phobia flew twice at a 1-week interval. One and a half hours before flight 1, 14 randomly assigned phobics received double-blind 1 mg of alprazolam and 14 received placebo. On flight 1, alprazolam reduced self-reported anxiety (5.0 vs 7.4) and symptoms (5.3 vs 3.6) more than placebo, but induced an increase in heart rate (114 vs 105 bpm) and respiratory rate (22.7 vs 18.3 breaths/min). Before flight 2, the alprazolam group did not expect to be more anxious than the placebo group (6.7 vs 6.5), but in fact indicated more anxiety during flight (8.5 vs 5.6), and a substantial increase in panic attacks from flight 1 to flight 2 (7% vs 71%). Heart rates in the alprazolam group increased further (123 bpm). Results indicate that alprazolam increases physiological activation under acute stress conditions and hinders therapeutic effects of exposure in flying phobia.
Behav Res Ther 1997 Sep
PMID:Acute and delayed effects of alprazolam on flight phobics during exposure. 929 3

Adoptive immunotherapy represents a potentially effective approach by which to control the extent of viral infections in an immunocompromised host. However, the impact of psychological stress and its associated neuroendocrine components on the efficacy of such a treatment strategy has yet to be determined. In the studies described herein, we have developed and utilized a model of primary, local herpes simplex virus (HSV) infection in radiation-induced, immunosuppressed C57BL/6 mice to investigate the role of stress in altering the protective capacity of adoptively transferred lymphocytes that contribute to the resolution of primary HSV infection. The sublethal dose of irradiation chosen for this model was shown to abrogate the local, adaptive immune response to HSV infection as measured by the degree of in vivo lymphoproliferation, development of HSV-specific cytotoxic T lymphocytes (CTL), and production of gamma interferon (IFN-gamma). Both short- and long-term acute stress, applied in the form of physical restraint, diminished the effectiveness of adoptively transferred lymphocytes as was indicated by an enhancement of viral replication in the footpad tissue and an increased rate of mortality. A reduction in the levels of IFN-gamma at the site of primary HSV infection represented at least one mechanism underlying this suppression of anti-viral immunity. Furthermore, the time-dependent restoration of immune function following irradiation was shown to be compromised in mice subjected to the restraint stress procedure. Together, these findings emphasize the potential role of psychological stress in suppressing both the capability of adoptive immunotherapeutic procedures to combat viral infection and the reestablishment of immune function in individuals who have undergone immunosuppressive therapy.
J Neuroimmunol 1997 Sep
PMID:The impact of psychological stress on the efficacy of anti-viral adoptive immunotherapy in an immunocompromised host. 930 25

Plasma levels of the hypothalamo-pituitary-adrenal axis hormones beta-endorphin (BE), adrenocorticotropin hormone (ACTH), and cortisol were measured in autistic (N = 48), mentally retarded/cognitively impaired (MR/CI, N = 16), and normal control (N = 26) individuals. Comparison of log transformed data from the three groups revealed that levels of BE and ACTH were significantly higher (p < .05) in the autistic individuals than in normal controls. The higher means in the autistic group were due to significantly higher plasma levels of BE and ACTH, indices of acute stress response, in the more severely affected individuals. The data support the idea that individuals with severe autism have a heightened response to acute stressors rather than chronic hyperarousal or elevated basal stress response system functioning.
J Child Psychol Psychiatry 1997 Sep
PMID:Plasma beta-endorphin, adrenocorticotropin hormone, and cortisol in autism. 931 80

Neuroendocrine-immune interactions are profoundly regulated by corticotropin-releasing hormone (CRH) indirectly, through activation of a global stress response, and directly, through pro-inflammatory actions on peripheral immune functions. The indirect effects of stress on immune/inflammatory responses occur via the stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic/adrenomedullary system. We have demonstrated that glucocorticoids and catecholamines favor T helper 2 (TH2) over T helper 1 (TH1) immune cells and mediators, by controlling the production of specific key regulatory cytokines. This could explain the influences of chronic stress on the development, course, and pathology of certain allergic, autoimmune/inflammatory, infectious, and neoplastic diseases. We have also shown that 'immune CRH' is secreted peripherally and plays a direct immunomodulatory role as an autocrine or paracrine mediator of inflammation. Upon release from immune cells and peripheral sensory afferent and/or postganglionic sympathetic nerves, CRH acts locally to elicit pro-inflammatory responses. This would explain the triggering or exacerbation of certain allergic or vasokinetic states by acute stress.
Mol Psychiatry 1997 Sep
PMID:The role of corticotropin-releasing hormone in neuroendocrine-immune interactions. 932 25

The characteristics of short-term potentiation (STP) and long-term potentiation (LTP) in the CA1 region of hippocampal slices were determined at various times following exposure to acute stress produced by restraint and tail-shock in mice. In slices prepared from control animals, theta-burst stimulation resulted in a large increase in evoked field excitatory postsynaptic potentials (EPSPs) amplitude and slope that remained stable at least up to 30 min after stimulation. Slices prepared 1 h after stress exhibited a marked decrease in the extent of both STP and LTP. STP and LTP magnitude were still significantly decreased 24 h after stress exposure and were completely restored to control levels by 48 h. These results provide evidence for a reversible impairment of STP and LTP in CA1 following an acute episode of stress, and suggest that stress activates processes different from those activated by LTP-inducing stimuli.
Neurosci Lett 1997 Sep 12
PMID:Time-dependent blockade of STP and LTP in hippocampal slices following acute stress in mice. 932 35

The effect of EEG-driven photic stimulation on stress-related endocrine function was studied. Subjects were 16 healthy males divided into a photic stimulation group (n = 8) and a control group (n = 8). Electrodermal and emotional lability measures were assessed by nonspecific skin conductance response and the Maudsley Personality Inventory, respectively. Plasma cortisol and beta-endorphin concentrations were measured both before and after EEG-driven photic stimulation as well as the resting condition. Subjects with electrodermal, emotional, or both lability showed comparable decreases of plasma beta-endorphin on photic stimulation as did the stable subjects. Under resting control conditions, however, they showed significant increases of beta-endorphin compared to both stable subjects as well as the photic stimulation condition. In addition, labile subjects showed significant alpha enhancement on photic stimulation compared to stable subjects and to the resting control condition. The data suggest that increases of plasma beta-endorphin in labile control subjects may denote a stress response to the conditions of these experiments, and that any decrease by EEG-driven photic stimulation may indicate a reduction of responsiveness to an acute stress.
Appl Psychophysiol Biofeedback 1997 Sep
PMID:EEG-driven photic stimulation effect on plasma cortisol and beta-endorphin. 942 69

Cancer patients frequently have symptoms of anxiety and depression after diagnosis. Often these symptoms are apparent to the physician. We report the case of a cancer patient who appeared to her physician to be coping relatively well but was actually having psychologic symptoms that met criteria for acute stress disorder (ASD). Cancer patients who have psychologic trauma at diagnosis and meet criteria for ASD may appear to be coping better than they are. Mental health interventions for cancer patients are recommended.
South Med J 1998 Sep
PMID:Evidence of acute stress disorder after diagnosis of cancer. 974 61

Age-appropriate acute stress, such as cold exposure, provokes the secretion of corticotropin releasing factor (CRF) from the hypothalamus, leading to a robust increase of plasma corticosterone in the immature rat. This activation of the hypothalamic-pituitary-adrenal system is accompanied by a stress-induced increase of steady-state CRF-mRNA expression in the hypothalamic paraventricular nucleus (PVN). In the current study, we analysed changes in CRF-mRNA expression in the PVN and the central nucleus of the amygdala (ACe) in the immature rat in response to a single episode of cold stress and three repeated exposures to this same stressor. CRF-mRNA expression in the PVN increased after a single, but not repeated exposures to cold stress, while repeated acute stress increased the content of the CRF peptide in the anterior hypothalamus. In the ACe, repeated episodes of cold stress resulted in increased expression of CRF-mRNA. These findings indicate a differential regulation of CRF gene expression in the PVN and ACe of the immature rat by single and repeated acute stress.
J Neuroendocrinol 1998 Sep
PMID:Corticotropin releasing factor mRNA expression in the hypothalamic paraventricular nucleus and the central nucleus of the amygdala is modulated by repeated acute stress in the immature rat. 974 83

In this article we describe the development of a highly sensitive, accurate, and reproducible RIA for the measurement of 3,3'-diiodothyronine (3,3'-T2) in human serum and brain tissue. The detection limits were 1.8 fmol/g and 1.5 pmol/L in human brain tissue and serum, respectively. Serum concentrations of 3,3'-T2 were measured in 4 groups of patients with nonthyroidal illnesses (NTI), i.e. brain injuries (n = 15), sepsis (n = 24), liver disease (n = 22), and brain tumors (n = 23). The mean serum concentration of 3,3'-T2 in 62 healthy controls was 46.6 +/- 20.0 pmol/L. 3,3'-T2 levels declined significantly with increasing age. They were significantly lower in patients with brain injury (34.2 +/- 19.4 pmol/L; P = 0.006), were at the upper limit of normal in patients with sepsis (57.0 +/- 36.9 pmol/L; P = 0.06), and were elevated in patients with liver disease (72.6 +/- 56.7 pmol/L; P = 0.04) and brain tumors (89.0 +/- 40.9 pmol/L; P = 0.01). The serum levels of T3 were significantly lower than those in controls in all 4 patient groups. Serum concentrations of 3,3'-T2 were significantly enhanced in 9 patients with hyperthyroidism (85.4 +/- 43.0 pmol/L; P = 0.01) and were reduced in 12 patients with hypothyroidism (14.9 +/- 9.2 pmol/L; P = 0.001). In both normal brain tissue, obtained either intraoperatively or excised postmortem, and brain tumors, the concentrations of 3,3'-T2 ranged between 50-300 fmol/g. In healthy controls, 2 different forms of acute stress (sleep deprivation and delivering a lecture) significantly increased serum levels of T4 and T3, but did not affect those of 3,3'-T2 or 3,5-T2. In conclusion, our results show that, contrary to expectation, a low T3 syndrome in NTI is not always associated with low serum concentrations of 3,3'-T2. The production of 3,3'-T2 in NTI seems to be regulated in a disease-specific manner, resulting in unchanged, reduced, or elevated hormone concentrations.
J Clin Endocrinol Metab 1998 Sep
PMID:3,3'-Diiodothyronine concentrations in the sera of patients with nonthyroidal illnesses and brain tumors and of healthy subjects during acute stress. 974 5

Corticotropin releasing factor (CRF), a neuropeptide secreted by hypothalamic and extrahypothalamic neurons, is thought to mediate stress-related behaviors. The tension reduction hypothesis suggests that ethanol drinking reduces stress; that drinking is reinforced by this reduced stress; and that the probability of drinking therefore subsequently increases. CRF also decrease food intake, and might decrease ethanol drinking similarly. We addressed these hypotheses directly by assessing the effects of intracerebroventricular (i.c.v.) CRF upon ethanol drinking (1 h/day). Rats were provided drinking tubes containing ethanol solutions that were gradually incremented in concentration (from 2% to 8% w/v, over 38 days). Ethanol intakes remained stable, ranging from 0.4 to 0.5 g/kg per hour on average, and a two-bottle choice test revealed that ethanol was preferred reliably to water. Third-i.c.v. cannulae were surgically implanted and CRF or vehicle was acutely injected immediately prior to the sessions. CRF dose-dependently reduced ethanol intake by 31% (0.5 microg) and 64% (5.0 microg), and reduced 24-h food by 9% and 21%, respectively, but did not alter body weights. I.c.v. CRF reduced ethanol drinking despite any acute stress-like effects that may have been present. Hence, these data are inconsistent with the tension reduction hypothesis. On the other hand, our results support the concept that food intake and ethanol drinking may be mediated by similar mechanisms.
Psychopharmacology (Berl) 1998 Sep
PMID:Effects of third intracerebroventricular injections of corticotropin-releasing factor (CRF) on ethanol drinking and food intake. 976 50


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