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PubMed2004

Comparison of dobutamine stress magnetic resonance, adenosine stress magnetic resonance, and adenosine stress magnetic resonance perfusion.

BACKGROUND: Dobutamine stress MR (DSMR) is highly accurate for the detection of inducible wall motion abnormalities (IWMAs). Adenosine has a more favorable safety profile and is well established for the assessment of myocardial perfusion. We evaluated the diagnostic value of IWMAs during dobutamine and adenosine stress MR and adenosine MR perfusion compared with invasive coronary angiography. METHODS AND RESULTS: Seventy-nine consecutive patients (suspected or known coronary disease, no history of prior myocardial infarction) scheduled for cardiac catheterization underwent cardiac MR (1.5 T). After 4 minutes of adenosine infusion (140 microg x kg(-1) x min(-1) for 6 minutes), wall motion was assessed (steady-state free precession), and subsequently perfusion scans (3-slice turbo field echo-echo planar imaging; 0.05 mmol/kg Gd-BOPTA) were performed. After a 15-minute break, rest perfusion was imaged, followed by standard DSMR/atropine stress MR. Wall motion was classified as pathological if > or =1 segment showed IWMAs. The transmural extent of inducible perfusion deficits (<25%, 25% to 50%, 51% to 75%, and >75%) was used to grade segmental perfusion. Quantitative coronary angiography was performed with significant stenosis defined as >50% diameter stenosis. Fifty-three patients (67%) had coronary artery stenoses >50%; sensitivity and specificity for detection by dobutamine and adenosine stress and adenosine perfusion were 89% and 80%, 40% and 96%, and 91% and 62%, respectively. Adenosine IWMAs were seen only in segments with >75% transmural perfusion deficit. CONCLUSIONS: DSMR is superior to adenosine stress for the induction of IWMAs in patients with significant coronary artery disease. Visual assessment of adenosine stress perfusion is sensitive with a low specificity, whereas adenosine stress MR wall motion is highly specific because it identifies only patients with high-grade perfusion deficits. Thus, DSMR is the method of choice for current state-of-the-art treatment regimens to detect ischemia in patients with suspected or known coronary artery disease but no history of prior myocardial infarction.

Adenosine↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed2005

Combat stress reactions, posttraumatic stress disorder, cumulative life stress, and physical health among Israeli veterans twenty years after exposure to combat.

This study examined the association of initial combat stress reaction (CSR), chronic post-traumatic stress disorder (PTSD) and cumulative life stress on physical health 20 years after the 1982 war with Lebanon, in a sample of 504 Israeli veterans of the war. Two groups were assessed: male veterans who fought and suffered from CSR and a matched group of male veterans from the same units who did not exhibit such reactions. Twenty years following the war, participants were asked to rate their general physical health status, report health complaints and risk behaviors, and were screened for PTSD. CSR and, to a greater extent, PTSD, were found to be associated with general self-rated health, chronic diseases and physical symptoms, and greater engagement in risk behaviors. CSR and PTSD were also related to greater cumulative life stress since the war. Both negative and positive life events were independently related to most of the physical health measures but did not account for the associations of CSR and PTSD with poorer health. Tests of the interactions between CSR, PTSD and life stress in their association with physical health and risk behaviors showed that PTSD suppressed the effects of additional life stress (negative life events had a weaker effect on health among participants with PTSD).

Adult↗
PubMed2000

Stress-controlled transcription factors, stress-induced genes and stress tolerance in budding yeast.

The transcriptional response to environmental changes is a major topic in both basic and applied research. From a basic point of view, to understand this response includes unravelling how the stress signal is sensed and transduced to the nucleus, to identify which genes are induced under each stress condition and, finally, to establish the phenotypic consequences of this induction in stress tolerance. The possibility of using genetic approaches has made the yeast Saccharomyces cerevisiae a compelling model to study stress response at a molecular level. Moreover, this information can be used to isolate and characterise stress-related proteins in higher eukaryotes and to design strategies to increase stress resistance in organisms of industrial interest. In this review the progress made in recent years is discussed.

Genes, Fungal↗
PubMed2003

Stress integration after acute and chronic predator stress: differential activation of central stress circuitry and sensitization of the hypothalamo-pituitary-adrenocortical axis.

Predator exposure is a naturalistic stressor of high ethological relevance. In the current study, our group examined central and peripheral integration of stress responses in rats after acute or repeated exposure to a natural predator (cat). Acute cat exposure rapidly induced hypothalamo-pituitary-adrenocortical (HPA) axis activation and paraventricular nucleus (PVN) CRH mRNA production. Repeated daily cat exposure (7 and 14 d) also up-regulated PVN mRNA CRH expression, but did not result in frank adrenocortical hyperactivity. Unlike other chronic homotypic stress regimens, repeated cat exposure facilitated corticosterone secretion after the 6th or 13th day of exposure. Notably, ACTH secretion and central amygdaloid nucleus CRH mRNA expression were enhanced in animals that were preexposed to the holding chamber relative to chamber-naive rats, suggesting that contextual cues can sensitize subsequent responses to a fearful stimulus. Analysis of c-fos activation was then used to identify brain circuits activated by acute predator stress. Cat exposure elicited a pattern of central c-fos activation that differed substantially from that after either restraint or hypoxia. Predator-specific c-fos mRNA induction was observed in several brain regions comprising the hypothetical brain defense circuit (bed nucleus of the stria terminalis, medial region of the ventromedial nucleus, and dorsal premammillary nucleus). Surprisingly, acute cat exposure did not induce c-fos expression in the PVN. In summary, the data indicate that 1) predation stress invokes a unique stress circuitry that promotes homotypic sensitization of the HPA axis, and 2) familiarization of animals to testing environments can prime central stress pathways to respond robustly to novel threats.

Amygdala↗
PubMed1990

T lymphocyte stress response. II. Protection of translation and DNA replication against some forms of stress by prior hyperthermic stress.

We have compared the effects of a mild heat shock and febrile temperatures on heat-shock protein (hsp) synthesis and development of stress tolerance in T lymphocytes. Our previous studies demonstrated that febrile temperatures (less than or equal to 41 degrees C) induced the synthesis of hsp110, hsp90, and the constitutive or cognate form of hsp70 (hscp70; a weak induction of the strongly stress-induced hsp70 was also observed. In the studies reported herein, we demonstrate that a mild heat shock (42.5 degrees C) reverses this ratio; that is, hsp70 and not hscp70 is the predominate member of this family synthesized at this temperature. Modest heat shock also enhanced the synthesis of hsp110 and hsp90. In order to assess the relationship between hsp synthesis and the acquisition of thermotolerance, purified T cells were first incubated at 42.5 degrees C (induction temperature) and then subsequently subjected to a severe heat-shock challenge (45 degrees C, 30 min). T cells first incubated at a mild heat-shock temperature were capable of total protein synthesis at a more rapid rate following a severe heat shock than control cells (induction temperature 37 degrees C). This phenomenon, which has been previously termed translational tolerance, did not develop in cells incubated at the febrile temperature (induction temperature 41 degrees C). Protection of translation also extended to immunologically relevant proteins such as interleukin-2 and the interleukin-2 receptor. Because clonal expansion is a critical event during an immune response, the effects of hyperthermic stress on DNA replication (mitogen-induced T cell proliferation) was also evaluated in thermotolerant T cells. DNA synthesis in control cells (induction temperature 37 degrees C) was severely inhibited following heat-shock challenge at 44 degrees C or 45 degrees C; in contrast, T cells preincubated at 42.5 degrees C rapidly recovered their DNA synthetic capacity. T cells preincubated at a febrile temperature were moderately protected against hyperthermic stress. The acquisition of thermotolerance was also associated with enhanced resistance to chemical (ethanol)-induced stress but not to heavy metal toxicity (cadmium) or dexamethasone-induced immunosuppression. These studies suggest that prior hsp synthesis may protect immune function against some forms of stress (e.g., febrile episode) but would be ineffective against others such as elevated glucocorticoid levels which normally occur during an immune response.

Animals↗
PubMed2004

Stress-buffering or stress-exacerbation? Social support and social undermining as moderators of the relationship between perceived stress and depressive symptoms among married people.

This prospective panel study examined social support and social undermining from the spouse as moderators of the relationship between perceived stress and depressive symptoms. Participants were 181 married people who completed questionnaires at two points in time. The interval between time 1 (T1) and time 2 (T2) was approximately 6 weeks. Multiple regression analysis showed that T1 perceived stress and T1 spouse undermining, but not T1 spouse support, predicted increases in depressive symptoms from T1 to T2. T1 spouse undermining, but not T1 spouse support, moderated the association between T1 perceived stress and T2 depressive symptoms. These findings supported a stress-exacerbation hypothesis for the effect of spouse undermining on the stress process. Discussion focuses on possible mechanisms for the stress-exacerbation effect.

Journal Article↗
PubMed2003

Nicotine increases oxidative stress, activates NF-kappaB and GRP78, induces apoptosis and sensitizes cells to genotoxic/xenobiotic stresses by a multiple stress inducer, deoxycholate: relevance to colon carcinogenesis.

Epidemiologic studies indicate that environmental (smoking) and dietary factors (high fat) contribute to carcinogenesis in many organ systems. The aim of our study was to test the hypothesis that nicotine, a component of cigarette smoke, and sodium deoxycholate (NaDOC), a cytotoxic bile salt that increases in concentration in the gastrointestinal tract after a high fat meal, induce similar cellular stresses and that nicotine may enhance some of the NaDOC-induced stresses. We found that nicotine, at 0.8 microM, the very low sub-micromolar level occurring in the tissues of smokers: (1). increases oxidative stress; (2). activates NF-kappaB, a redox-sensitive transcription factor; (3). activates the 78 kD glucose regulated protein promoter, an indication of endoplasmic reticulum stress; (4). induces apoptosis; (5). enhances the ability of NaDOC to activate the 153 kD growth arrest and DNA damage promoter, an indication of increased genotoxic stress; and (6). enhances the ability of NaDOC to activate the xenobiotic response element. Our findings have applicability to G.I. cancer, in general, since smoking is a risk factor in the development of esophageal, pancreatic, gastric and colon cancer, and these cancers are also promoted by bile acids.

Apoptosis↗
PubMed2000

Stress induced spontaneous recurrence of methamphetamine psychosis: the relation between stressful experiences and sensitivity to stress.

We examined increased sensitivity to stress in relation to spontaneous recurrences of methamphetamine (MAP) psychosis (i.e., flashbacks). Plasma monoamine metabolite levels were assayed in: 26 flashbackers, of whom 11 were on neuroleptics before and during the study, and the other 15 received neuroleptics in the course of the study; 18 non-flashbackers with a history of MAP psychosis; eight subjects with persistent MAP psychosis; and 23 MAP user and 11 non-user controls. The 26 flashbackers had experienced stressful events and/or MAP-induced fear-related psychotic symptoms during previous MAP use. Mild psychosocial stressors then triggered flashbacks. During flashbacks plasma norepinephrine levels increased markedly; among the flashbackers, those with a history of stressful events, whether or not they had experienced fear-related symptoms, showed a further increase in 3-methoxytyramine levels. Stressful experiences, together with MAP use, may therefore induce sensitization to stress associated with noradrenergic hyperactivity, involving increased dopamine release, and so triggering flashbacks.

Adult↗
PubMed1995

Stress and alcohol: the moderating effect of chronic stress on the acute stress--intoxication relationship.

OBJECTIVE: The present study evaluated whether chronic stress levels moderated the impact of laboratory stressors on subjective and behavioral responses to alcohol. METHOD: Healthy volunteers (N = 60; 30 male) completed measures of background stress levels (e.g., major life events). In addition, subjects were exposed to two laboratory stressors (i.e., cold pressor or film stressor task) or a control condition after consuming a 0.7 g/kg dose of alcohol. RESULTS: Regression analyses showed that the combination of high background stress levels and exposure to a lab stressor reduced two measures of perceived intoxication (i.e., Sensation Scale, Visual Analog Intoxication Scale). CONCLUSIONS: These data are consistent with a biobehavioral model of alcohol use where acute and chronic stressors are associated with a diminished response to alcohol. The possible mechanisms that may underlie this sobering effect include stress-related cognitive deficits and situation specific tolerance associated with high chronic stress levels.

Adult↗
PubMed1999

[Mental health and stress coping among hospital nurses by stress & stress-coping questionnaire].

This study was aimed to evaluate the relationship between the mental health level and stress coping style in a group of female subjects in a public hospital. A self-administrated questionnaire including questions on nursing work, the General Health Questionnaire (GHQ) as well as the Stress and Stress Coping questionnaire (SSCQ) was used. The subjects of this study were 225 female nurses. The subjects' age and working experience (mean +/- SD) were 34.0 +/- 10.3 and 10.6 +/- 8.3 years, respectively. The results obtained were as follows: 1) Either of the following determinants was related to negative mental health: experience of 1-2 years; working in the operating room or in-patient department. 2) The subjects whose working experience was < 5 years or > or = 10 years had higher scores in the SSCQ. These subjects were among those who did not have higher scores in the GHQ. It was suggested that these subjects need to receive a guidance in stress coping. These findings suggest that because working conditions have a negative influence on mental health, educational system for both inexperienced and experienced nurses is needed to develop an effective stress-coping style in medical institutions.

Adaptation, Psychological↗
PubMed2002

Post-stress recovery of pituitary-adrenal hormones and glucose, but not the response during exposure to the stressor, is a marker of stress intensity in highly stressful situations.

Acute immobilization in male rats elicited the same ACTH, corticosterone and glucose response as foot shock when measured immediately after stress. However, post-stress recovery of plasma ACTH, corticosterone and glucose levels were delayed in immobilized versus shocked rats. Similarly, stress-induced anorexia was much greater in the former animals. All these data suggest that post-stress speed of recovery of some physiological variables is positively related to stressor intensity and could be used to evaluate it.

Adrenocorticotropic Hormone↗
PubMed2004

Chronic stress promotes palatable feeding, which reduces signs of stress: feedforward and feedback effects of chronic stress.

We suggested a new model of the effects of glucocorticoids (GCs) exerted during chronic stress, in which GCs directly stimulate activities in the brain while indirectly inhibiting activity in the hypothalamo-pituitary-adrenal (HPA) axis through their metabolic shifts in energy stores in the periphery. This study is an initial test of our model. In a 2 x 2 design, we provided ad lib access to calorically dense lard and sucrose (comfort food) + chow or chow alone, and repeatedly restrained half of the rats in each group for 5 d (3 h/d). We measured caloric intake, body weight, caloric efficiency, ACTH, corticosterone (B), and testosterone during the period of restraint and leptin, insulin, and fat depot weights, as well as hypothalamic corticotropin-releasing factor mRNA at the end of the period. We hypothesized that chronically restrained rats would exhibit a relative increase in comfort food ingestion and that these rats would have reduced HPA responses to repeated restraint. Although total caloric intake was reduced in both groups of restrained rats, compared with controls, the proportion of comfort food ingested increased in the restrained rats compared with their nonrestrained controls. Moreover, caloric efficiency was rescued in the stressed, comfort food group. Furthermore, ACTH and B responses to the repeated restraint bouts were reduced in the rats with access to comfort food. Corticotropin-releasing factor mRNA was reduced in control rats eating comfort food compared with those eating chow, but there were no differences between the stressed groups. The results of this experiment tend to support our model of chronic effects of stress and GCs, showing a stressor-induced preference for comfort food, and a comfort-food reduction in activity of the HPA axis.

Adrenalectomy↗
PubMed1985

[Stress and the endogenous opioid system. II. Stress, stress models and endogenous opioid peptides].

Biochemical and pharmacological findings indicate an activation of the opioid system under certain stress influences. In this paper findings are discussed, according to which the activation of the opioid system depends on the temporary distribution pattern and the kind of the stressor. In response to stress opioid peptides are involved in excitatory and inhibitory processes. The participation of different types of opioids in central and peripheral stress-induced effects is discussed. Some findings suggest that beta-endorphin acts mainly centrally rather than peripherally, whereas the enkephalins take part in peripheral regulatory processes (gastrointestinal system, adrenal glands). Now there is evidence that the endogenous opioids modulate stress-induced effects, but there has been much controversy on how this fact should be established. These controversies mainly resulted from the many factors that influence activation.

Animals↗
PubMed2000

A rapid stress-testing protocol for the detection of coronary artery disease: comparison of two-stage transesophageal atrial pacing stress echocardiography with dobutamine stress echocardiography.

OBJECTIVES: We compared a new two-stage transesophageal atrial pacing stress echocardiography (TAPSE) protocol with a standard dobutamine stress echocardiography (DSE) protocol. BACKGROUND: Transesophageal atrial pacing stress echocardiography has been proposed as an efficient alternative to DSE. METHODS: Two-stage TAPSE (85% and 100% of age-predicted maximum heart rate) and DSE (5 to 40 microg/kg/min at 3-min stages with or without atropine) were both performed, in random sequence, in each patient of a study group of 36 patients. Regional wall-motion analysis, patient acceptance (1 = low, 5 = high), hemodynamics and duration for performing and interpreting tests were compared. RESULTS: Transesophageal atrial pacing stress echocardiography was successful in 35 of the 36 patients (feasibility 97%). More TAPSE than DSE studies were called "ischemic" (37% vs. 14%; p = 0.005). Peak heart rate was higher with TAPSE (144 +/- 18 vs. 129 +/- 15 beats/min, p = 0.0001). Peak cardiac index (4.6 +/- 2.1 vs. 5.1 +/- 1.9 liters/min/m2, p = 0.14), patient acceptance score (4.2 +/- 0.7 vs. 3.8 +/- 1.3, p = 0.17) and study duration (14.2 +/- 9.3 vs. 13.3 +/- 3.3 min, p = 0.59) were similar. Recovery time (7.1 +/- 7.6 vs. 16.2 +/- 15.9 min, p = 0.0003) and interpretation time (9.1 +/- 2.8 vs. 13.5 +/- 4.4 min, p = 0.0001) were shorter for TAPSE than for DSE. CONCLUSIONS: Two-stage TAPSE permits rapid evaluation of cardiac patients. Peak cardiac index and patient acceptance scores were similar for TAPSE and DSE. Ischemia was detected more often with TAPSE; this result was attributed to the higher peak heart rate obtained with this protocol.

Aged↗
PubMed2001

Real-time three-dimensional dobutamine stress echocardiography in assessment stress echocardiography in assessment of ischemia: comparison with two-dimensional dobutamine stress echocardiography.

OBJECTIVES: This study was designed to test the feasibility and efficacy of using real-time three-dimensional echocardiography (RT-3D) to detect ischemia during dobutamine-induced stress (DSE) and compares the results with conventional two-dimensional echocardiography (2D). BACKGROUND: Real-time three-dimensional echocardiography, a novel imaging technique, offers rapid acquisition with multiple simultaneous views of the left ventricle (LV). These features make it attractive for application during stress. METHODS: Of 279 consecutive patients screened for image quality by 2D, 253 patients with adequate images underwent RT-3D and 2D within 30 s of each other at baseline and at peak DSE. RESULTS: Real-time three-dimensional echocardiography and 2D showed good concordance in detection of abnormal LV wall motion at baseline (84%: Kappa = 0.59) and at peak DSE (88.9%: Kappa = 0.72). Left ventricular wall motion scores were similar at baseline and peak DSE using both techniques. Interobserver agreements for detection of ischemia at peak DSE were superior for RT-3D, 92.7% compared with 84.6% for 2D (p < 0.05). Mean scanning time at peak stress by RT-3D in 50 randomly selected patients was shorter, 27.4 +/- 10.7 s compared with 62.4 +/- 20.1 s by 2D (p < 0.0001). In 90 patients with coronary angiograms, RT-3D had a sensitivity of 87.9% in the detection of coronary artery disease (CAD) compared with 79.3% by 2D. CONCLUSIONS: Real-time three-dimensional dobutamine stress echocardiography is feasible and sensitive in the detection of CAD. The procedure offers shorter scanning time, superior interobserver agreements and unique new views of the LV.

Coronary Disease↗
PubMed1998

Stress echocardiography: recommendations for performance and interpretation of stress echocardiography. Stress Echocardiography Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography.

Cardiovascular stress testing remains the mainstay of provocative evaluation for patients with known or suspected coronary artery disease. Stress echocardiography has become a valuable means of cardiovascular stress testing. It plays a crucial role in the initial detection of coronary disease, in determining prognosis, and in therapeutic decision making. The purpose of this document is to outline the recommended methodology for stress echocardiography with respect to personnel and equipment as well as the clinical use of this recently developed technique. Specific limitations will also be discussed.

Cardiovascular Agents↗
PubMed1998

Loss of cellular K+ mimics ribotoxic stress. Inhibition of protein synthesis and activation of the stress kinases SEK1/MKK4, stress-activated protein kinase/c-Jun NH2-terminal kinase 1, and p38/HOG1 by palytoxin.

The tumor promoter palytoxin has been found to activate the stress-activated protein kinase/c-Jun NH2-terminal kinase 1 (SAPK/JNK1), and it also potentiates, as demonstrated here, the p38/HOG1 mitogen-activated protein kinase and the upstream activator of SAPK/JNK1, SEK1/MKK4. In search of possible mechanisms for both the cytotoxicity and the activation of stress kinases by palytoxin, we found that palytoxin is a potent inhibitor of cellular protein synthesis. The inhibition of translation by palytoxin does not result from its direct binding to the translational apparatus. We have previously demonstrated that ribotoxic stressors (Iordanov, M. S., Pribnow, D., Magun, J. L., Dinh, T.-H., Pearson, J. A., Chen, S. L.-Y., and Magun, B. E. (1997) Mol. Cell. Biol. 17, 3373-3381) signal the activation of SAPK/JNK1 by binding to or covalently modifying 28 S rRNA in ribosomes that are active at the time of exposure to the stressor. Palytoxin acted as a ribotoxic stressor, inasmuch as it required actively translating ribosomes at the time of exposure to activate SAPK/JNK1. Palytoxin has been shown to augment ion fluxes by binding to the Na+/K+-ATPase in the plasma membrane of cells. To determine whether altered fluxes of either Na+ or K+ could be responsible for the effects of palytoxin on translation and on activation of SAPK/JNK1, cells were exposed to palytoxin in modified culture medium in which a major portion of the Na+ was replaced by either K+ or by choline+. The substitution of Na+ by K+ strongly inhibited the ability of palytoxin both to inhibit protein translation and to activate SAPK/JNK1, whereas the substitution of Na+ by choline+ did not. These results suggest that palytoxin-induced efflux of cellular K+ mimics ribotoxic stress by provoking both translational inhibition and activation of protein kinases associated with cellular defense against stress.

Acrylamides↗