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Potentiation of apoptosis by heat stress plus pesticide exposure in stress resistant human B-lymphoma cells and its attenuation through interaction with follicular dendritic cells: role for c-Jun N-terminal kinase signaling.

B lymphocytes (B cells) become increasingly resistant to apoptosis induction during their differentiation in the microenvironment of the germinal center of lymphoid follicles. This is due to increases in the levels of Bcl-2 protein as well as survival signals generated through B-cell binding to follicular dendritic cells (FDC). However, it is not known whether this cellular resistance may be bypassed as a result of exposure to multiple environmental stress factors resulting in excessive apoptosis induction in B cells. We examined this question of whether apoptosis may be induced, and possibly potentiated, as a result of exposure of the human EW36 B-lineage cell line, having elevated Bcl-2 protein, to heat stress and pesticide combination exposures in a co-culture system with a human FDC cell line. This co-culture system recapitulates essential features of a human germinal center including adherence of B cells to FDC generating survival signals. We found that heat stress plus pesticide exposures resulted in substantial potentiation of apoptosis in EW36 cells, effectively bypassing their stress resistance. Similar results were obtained when paraquat was substituted for heat stress. Furthermore, the JNK pathway was activated by some combination exposures, such as heat stress plus antimycin A, but this pathway was found to play a cytoprotective role in EW36 cells. Importantly, EW36 cell binding to FDC reduced the extent of apoptosis induction by most combination exposures. These results reveal cell stress scenarios that can greatly augment apoptosis in stress-resistant human B-cells and a germinal center interaction that selectively attenuates pesticide-induced apoptosis.

Apoptosis↗

The effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder and health-related quality of life in survivors.

OBJECTIVES: The exposure to intense physical and psychological stress during intensive care can result in posttraumatic stress disorder (PTSD) in survivors. Cortisol is a biological stress mediator that can have a protective effect during severe stress. The administration of stress doses of hydrocortisone during treatment in the intensive care unit could theoretically result in a lower incidence of PTSD. We tested this hypothesis in survivors of septic shock. DESIGN: A retrospective case-controlled analysis. SETTING: A 20-bed multidisciplinary intensive care unit of a tertiary-care university hospital. PATIENTS: We identified 27 patients who received standard therapy for septic shock. These patients served as controls and were compared with an equal number of patients who received hydrocortisone in addition to standard treatment. These patients were selected from our database with regard to age (+/-4 yrs), gender, and cause of septic shock to be as similar as possible with control patients. INTERVENTIONS: Patients from the hydrocortisone group had received stress doses of hydrocortisone (100 mg bolus, followed by 0.18 mg/kg/hr) in addition to standard treatment. Patients from the control group received standard protocol-driven treatment only. PTSD was diagnosed with the Posttraumatic Stress Syndrome-10 inventory, a self-report scale for diagnosis of PTSD. Health-related quality of life was measured using the Medical Outcomes Study Short-Form Survey (Medical Outcomes Trust, Boston, MA), which consists of 36 questions. MEASUREMENTS AND MAIN RESULTS: Patients who received hydrocortisone during septic shock had a significantly lower incidence of PTSD than patients who received standard treatment only (5 of 27 vs. 16 of 27; p = .01) and had significantly higher scores on the mental health index of the Medical Outcomes Study Short-Form health-related quality-of-life questionnaire (68 vs. 44 points; p = .009). CONCLUSIONS: Data from this study support the hypothesis that the administration of stress doses of hydrocortisone in doses equivalent to the maximal endocrine secretion rate during septic shock reduces the incidence of PTSD and improves emotional well-being in survivors. This hypothesis should be tested in a prospective randomized trial.

APACHE↗

A randomized, wait-list controlled clinical trial: the effect of a mindfulness meditation-based stress reduction program on mood and symptoms of stress in cancer outpatients.

OBJECTIVE: The objective of this study was to assess the effects of participation in a mindfulness meditation-based stress reduction program on mood disturbance and symptoms of stress in cancer outpatients. METHODS: A randomized, wait-list controlled design was used. A convenience sample of eligible cancer patients enrolled after giving informed consent and were randomly assigned to either an immediate treatment condition or a wait-list control condition. Patients completed the Profile of Mood States and the Symptoms of Stress Inventory both before and after the intervention. The intervention consisted of a weekly meditation group lasting 1.5 hours for 7 weeks plus home meditation practice. RESULTS: Ninety patients (mean age, 51 years) completed the study. The group was heterogeneous in type and stage of cancer. Patients' mean preintervention scores on dependent measures were equivalent between groups. After the intervention, patients in the treatment group had significantly lower scores on Total Mood Disturbance and subscales of Depression, Anxiety, Anger, and Confusion and more Vigor than control subjects. The treatment group also had fewer overall Symptoms of Stress; fewer Cardiopulmonary and Gastrointestinal symptoms; less Emotional Irritability, Depression, and Cognitive Disorganization; and fewer Habitual Patterns of stress. Overall reduction in Total Mood Disturbance was 65%, with a 31% reduction in Symptoms of Stress. CONCLUSIONS: This program was effective in decreasing mood disturbance and stress symptoms in both male and female patients with a wide variety of cancer diagnoses, stages of illness, and ages. cancer, stress, mood, intervention, mindfulness.

Ambulatory Care↗

Roles of stress, stress perception and trait-anxiety in the onset and course of alopecia areata.

Clinical observations suggest that the nervous system, including psychological factors, can influence the onset and course of alopecia areata (AA). The aim of this study was to determine whether stressful life events, stress perception, and trait-anxiety are risk factors in the onset and course of AA. A group of 45 patients diagnosed with AA and a group of 45 healthy controls were participants in the study. The patients with AA were divided into two subgroups: patients with a first episode of AA and patients with recidivism of the disease. All participants completed questionnaires addressing sociodemographic, clinical and psychological aspects of their disorder. The frequency and types of stressful life events experienced over the previous six months were recorded. Lemyre and Tessier's Mesure de Stress Psychologique was used to measure emotional, cognitive, behavioral, and physiological aspects of distress. Anxiety was evaluated by the Spielberg's Trait Anxiety Inventory. The subgroups of AA and the control group, using the same numbers of subjects matched for age and sex, education level, marital and employment status, were statistically compared. The number of patients with four stressful life events over the previous 6 months was significantly higher in the group of AA patients with recidivism of disease compared to the control group (P=0.004). There were no differences among the other groups with respect to the frequency of life events. Examination of the relationships between the two groups regarding anxiety, as well as perceived distress, revealed that the groups differed significantly with respect to psychosocial variables studied. A significantly higher degree of trait-anxiety and perceived distress were observed among patients in both AA subgroups (first onset and recidivism of AA) than in the healthy control group. The highest scores for anxiety and stress perception among examined groups were obtained in the group with recidivism of AA (33.42 +/- 12.71 and 90.32 +/- 50.74, respectively). Trait-anxiety and stress perception constitutes risk factors that may influence the onset and exacerbation of AA. The present study does not provide evidence of a significant role of stress in the onset of AA. Life events may play an important role in triggering of some episodes.

Adult↗

Effects of adrenal demedullation on stress-induced hypertension and cardiovascular responses to acute stress.

Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. In order to test the hypothesis that lowering A will attenuate stress-induced hypertension, rats who had their adrenal medullae removed (ADM) and sham-operated controls were subjected to chronic stress. All subjects were offspring of a cross between spontaneously hypertensive and Wistar-Kyoto rats. Prior to chronic stress, systolic pressures were the same in the two groups. The stress consisted of 60 2-h sessions of shock-shock conflict during 18 weeks. After conflict stress, the rats were implanted with arterial catheters and allowed two days to recover. The resting mean arterial pressure (MAP) was 141.2 mmHg in the ADM group and 142.3 mmHg in the Sham group. Cardiovascular responses to acute stress were then examined. The rats were transferred to a test-box and subjected to pulsed foot shocks (0.5-s duration, 5-s intervals) for 5 min. The MAP increase after transfer was 22.3% in the ADM and 4.2% in the Shams (P less than 0.001). After termination of the shocks, the MAP was elevated 22.2% above baseline in the ADM and 8.1% in the Shams (P less than 0.02). Five minutes after foot shocks the MAP increase was 21.6% in the ADM and 7.2% in the Shams (P less than 0.02). Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response. Therefore, the larger pressor responses of the ADM group seem to result from attenuation of beta-adrenoreceptor-mediated dilation of skeletal muscle vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

Stress-activated protein kinase pathway functions to support protein synthesis and translational adaptation in response to environmental stress in fission yeast.

The stress-activated protein kinase (SAPK) pathway plays a central role in coordinating gene expression in response to diverse environmental stress stimuli. We examined the role of this pathway in the translational response to stress in Schizosaccharomyces pombe. Exposing wild-type cells to osmotic stress (KCl) resulted in a rapid but transient reduction in protein synthesis. Protein synthesis was further reduced in mutants disrupting the SAPK pathway, including the mitogen-activated protein kinase Wis1 or the mitogen-activated protein kinase Spc1/Sty1, suggesting a role for these stress response factors in this translational control. Further polysome analyses revealed a role for Spc1 in supporting translation initiation during osmotic stress, and additionally in facilitating translational adaptation. Exposure to oxidative stress (H2O2) resulted in a striking reduction in translation initiation in wild-type cells, which was further reduced in spc1- cells. Reduced translation initiation correlated with phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF2alpha) in wild-type cells. Disruption of Wis1 or Spc1 kinase or the downstream bZip transcription factors Atf1 and Pap1 resulted in a marked increase in eIF2alpha phosphorylation which was dependent on the eIF2alpha kinases Hri2 and Gcn2. These findings suggest a role for the SAPK pathway in supporting translation initiation and facilitating adaptation to environmental stress in part through reducing eIF2alpha phosphorylation in fission yeast.

Cell Survival↗

Identification and characterization of the Yersinia enterocolitica gsrA gene, which protectively responds to intracellular stress induced by macrophage phagocytosis and to extracellular environmental stress.

Yersinia enterocolitica is able to resist the microbicidal mechanisms of macrophages and to grow within phagocytic cells. Some bacteria including Y. enterocolitica have been shown to respond to the hostile environment in macrophages by producing a set of stress proteins which are also induced by environmental stresses. To understand the role of stress proteins in intracellular survival of bacteria, we identified and cloned a Y. enterocolitica gene, called gsrA (global stress requirement). The gsrA gene was identified because its insertional inactivation by a transposon resulted in the inability of the organism to grow at an elevated temperature and to survive within macrophages after phagocytosis. The gsrA gene was sequenced and shown to encode a basic, 49,500-Da protein. The GsrA protein shows significant amino acid sequence homology to the HtrA stress protein which was originally identified in Escherichia coli. Furthermore, the genetically defined Y. enterocolitica gsrA mutant was constructed and characterized. The insertional mutation of gsrA resulted in inhibition of growth at temperatures above 39 degrees C and greatly increased susceptibility to oxidative and osmotic stresses. The mutant additionally lost the ability to survive and replicate within macrophages. These results, taken together, indicate that the gsrA gene is an essential component of the protection mechanism employed by Y. enterocolitica, allowing it to respond to the intracellular stress in macrophages as well as extracellular environmental stress.

Amino Acid Sequence↗

Stress symptoms induced by repeated morphine withdrawal in comparison to other chronic stress models in mice.

The present study was aimed at evaluating chronic stress models in mice with special attention to morphine treatment. We hypothesized that repeated periods of drug withdrawal induce chronic stress. To verify this hypothesis, mice were made dependent on morphine and then subjected to several types of repeated withdrawal. Body weight reduction, thymus involution, adrenal gland enlargement and activation of the hypothalamo-pituitary-adrenal axis were used as signs of chronic stress. The changes were compared to those induced by 'laboratory' models of chronic stress (2 weeks of repeated restraint or rat exposure) and to a disease model of streptozotocin-induced diabetes mellitus (STZ-DM). Mice were made dependent using increasing doses of morphine three times a day for 3 days (10-20-40 mg/kg s.c.). Thereafter, withdrawal was induced either spontaneously (morphine 40 mg/kg injected at 24- or 72-hour time intervals for 2 weeks) or repeatedly precipitated by naloxone (10 mg/kg s.c.) injected daily 3 h after morphine. The results show that repeated periods of spontaneous drug withdrawal (24 or 72 h) in morphine-dependent mice represent a mild stress load. Repeated withdrawal precipitated by naloxone induced clear chronic stress-like changes. Changes observed in the naloxone-precipitated withdrawal model were even more pronounced than those found in laboratory models, namely repeated restraint or exposure to the rat. The most severe chronic stress state developed in mice during untreated STZ-DM. Thus, naloxone-precipitated withdrawal in mice seems to be an appropriate model of chronic stress.

Animals↗

Low social support and poor emotional regulation are associated with increased stress hormone reactivity to mental stress in systemic hypertension.

CONTEXT: There is strong evidence for a physiological hyperreactivity to stress in systemic hypertension, but data on associated or potentially moderating psychological factors are scarce. OBJECTIVE: The objective of the study was to identify psychological correlates of physiological stress reactivity in systemic hypertension. DESIGN: This was a cross-sectional, quasi-experimentally controlled study. Study participants underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. SETTING: The study was conducted in the population in the state of Zurich, Switzerland. SUBJECTS: Subjects included 22 hypertensive and 26 normotensive men (mean +/- sem 44 +/- 2 yr). MAIN OUTCOME MEASURES: We assessed the psychological measures social support, emotional regulation, and cognitive appraisal of the stressful situation. Moreover, we measured salivary cortisol and plasma epinephrine and norepinephrine before and after stress and several times up to 60 min thereafter as well as blood pressure and heart rate. RESULTS: We found poorer hedonistic emotional regulation (HER) and lower perceived social support in hypertensives, compared with normotensives (P < 0.01). Compared with normotensives, hypertensives showed higher cortisol, epinephrine, and norepinephrine secretions after stress (P < 0.038) as well as higher systolic and diastolic blood pressure (P < 0.001). Cortisol reactivity and norepinephrine secretion were highest in hypertensive men with low HER (P < 0.05). In contrast, hypertensives with high HER did not significantly differ from normotensives in both cortisol and norepinephrine secretion after stress. Epinephrine secretion was highest in hypertensives with low social support but was not different between hypertensives with high social support and normotensives. CONCLUSIONS: The findings suggest that both low social support and low HER are associated with elevated stress hormone reactivity in systemic hypertension.

Adult↗

Myocardial perfusion imaging using adenosine triphosphate stress multi-slice spiral computed tomography: alternative to stress myocardial perfusion scintigraphy.

BACKGROUND: The present study was designed to: (i) detect myocardial ischemia in contrast enhanced multi-slice spiral computed tomography (CE-MSCT) using adenosine triphosphate (ATP) pharmacological stress test; and (ii) evaluate the potential of ATP stress CE-MSCT in a clinical setting. METHODS AND RESULTS: Twelve patients underwent ATP stress CE-MSCT and stress thallium-201 myocardial perfusion scintigraphy (MPS) and 9 of the patients received conventional coronary angiography (CAG). Dual CE-MSCT scans were performed for stress and rest images, with and without intravenous infusion of ATP (0.16 mg.kg-1.min-1) at intervals of 20 min. Myocardial perfusion and coronary artery were visually evaluated using MSCT and compared the results obtained from MPS and CAG. Of 36 territories, stress images of CE-MSCT described 26 hypo-perfusion areas and MPS described 22 redistributions. The agreement between MSCT and MPS was 83% (30/36, p<0.05). In 141 coronary artery segments of 9 patients undergoing CAG, rest images of CE-MSCT, which had significantly higher assessability than stress images (89% vs 48%, p<0.05), described 76% (13/17) of culprit coronary stenoses. CONCLUSIONS: Although CT-angiography should be currently assessed using rest images, ATP stress CE-MSCT can describe both ATP-induced myocardial ischemia and coronary artery stenoses in patients with coronary artery disease.

Adenosine Triphosphate↗

Stress and immune responses. III. Effect of restraint stress on delayed type hypersensitivity (DTH) response, natural killer (NK) activity and phagocytosis in mice.

Several experiments were conducted to evaluate the influences of restraint stress on cell-mediated immune events in mice. Delayed type hypersensitivity response to sheep red blood cells was inhibited by the stress, regardless of the timing of restraint stress loading. The activity of phagocytosis of macrophages in vitro and in vivo were measured by using the zymosan-particle uptake method and the carbon clearance test, respectively. Both activities were decreased in restraint-stressed mice. The suppressed carbon clearance rate in stressed mice, however, was recovered by the transfusion of serum from normal mice. Natural killer activity in spleen cells was decreased to 30-50% of the control in stressed mice. However, no suppressor cells which could inhibit NK activity existed in the spleen from stressed mice. These results show that the restraint stress suppresses various kinds of cell-mediated immune events, which might play an important role in anti-tumor immunity.

Animals↗

Blood coagulation and fibrinolysis in SART-stressed (repeated cold-stressed) rats and drug effects on the altered hemostatic parameters.

Blood coagulation and fibrinolytic activity was studied in SART (specific alternation of rhythm in temperature)-stressed animals found to exhibit thrombocytopenia and prolonged bleeding time, and drug effects on the abnormalities were evaluated. 1) SART-stressed rats revealed prolongation of activated partial thromboplastin and thrombin time, no change in prothrombin time, decreased plasma fibrinogen levels, and shortened euglobulin clot lysis time (ELT). Antithrombin III and alpha 2-plasmin inhibitor activity remained constant following stress exposure. 2) During stress, fibrinogen levels declined from day 5 and remained depressed up to day 14. Reduction in ELT developed in a similar manner to fibrinogen. 3) Decreased fibrinogen levels were prevented by consecutive doses of tranexamic acid, an antifibrinolytic, and Neurotropin, a sedative analgesic. Shortened ELT was counteracted by chronic treatment with Neurotropin and alprazolam, an anxiolytic. Single administrations of the above agents failed to affect either change. These results indicate that SART-stressed animals exhibit suppressed intrinsic coagulability and enhanced fibrinolytic activity, but normal extrinsic coagulability. Considering the previous report together with the above results, the hemostatic system under SART stress tends uniformly toward hemorrhage. Moreover, Neurotropin appears to improve and normalize hemostatic imbalance due to SART stress, a chronic form of stress.

Alprazolam↗

Anti-stress effect of ginseng on the inhibition of the development of morphine tolerance in stressed mice.

We examined how the ginseng extract (GE) acts on the antinociceptive effect induced by footshock (FS)-, psychological (PSY)- and forced swimming (SW)-stress (stress-induced analgesia, SIA), and also on the suppression by FS- and PSY-stress of the development of tolerance to morphine in mice. Neither an acute treatment nor 5 daily pretreatments with GE at 100 mg/kg, p.o. affected each SIA. Pretreatment with GE at 100 mg/kg, p.o. for 5 days followed by the treatment in combination with the exposure to stresses for another 5 days caused no appreciable changes in the development of tolerance to FS- and SW-SIA, but suppressed the development of tolerance to PSY-SIA. When mice were pretreated with GE for 5 days and given GE daily prior to morphine at 10 mg/kg/day, with stress exposure for another 5 days, the inhibitory effect of FS-stress on the development of tolerance to morphine was completely eliminated. The present results suggest that GE, by improving the general metabolism in the body, directs toward normalization of the adaptability which is impaired by stress exposure, while not compromising morphine antinociceptive activity or the SIA, another adaptability produced in confrontation to abnormal environmental stimuli. In addition, the differences in the mechanism underlying the FS- and PSY-stress effect which we have previously demonstrated are also reconfirmed.

Analgesics↗

Persistent hormonal effects of stress are not due to reduced food intake or exposure to stressed rats.

Exposure to inescapable stress elicits persistent effects on the physiology and behavior of rats. Elevated basal plasma corticosterone concentrations have been observed for several days after cessation of stress. In this study, we measured hormonal concentrations in multiple axes at multiple levels, 24 h after one or three consecutive exposures to the same stress paradigm. The data indicated persistent activation of plasma corticosterone and prolactin concentrations, whereas plasma triiodothyronine, thyroxine, luteinizing hormone, and growth hormone concentrations were inhibited after either one or three stress sessions. In addition, we isolated the effects of restraint/tail shock per se from the effects of being moved and exposed to other stressed rats, and from the effects of reduced feeding produced by our stress protocol. The data clearly indicated that the stress paradigm, rather than exposure to stressed rats or decreased nutrient intake, is necessary to induce the persistent physiologic changes we observe after stressor exposures.

Adrenal Cortex↗

Whole-blood concentrations of glutathione in cattle exposed to heat stress or a combination of heat stress and endophyte-infected tall fescue toxins in controlled environmental conditions.

OBJECTIVE: To determine whether cattle exposed to heat stress alone or heat stress while consuming endophyte-infected fescue (EIF) have lower whole-blood (WB) concentrations of glutathione (GSH). ANIMALS: 10 Simmental cows. PROCEDURE: Cows were sequentially exposed to thermoneutral (TN; 2 weeks; 18 C, 50% relative humidity [RH]), heat stress (HS; 2 weeks; alternating 4-hour intervals at 26 and 33 C; 50% RH), and heat stress while consuming EIF (10 microg of ergovaline/kg/d; 2 weeks, HS + EIF). Blood samples were collected after each period and tested for GSH and oxidized glutathione (GSSG) concentrations. RESULTS: Feed consumption was similar when data were analyzed for time points at which WB concentrations of GSH or GSSG were determined. However, significant effects of treatment, cow, days exposed to heat, cow-by-treatment interaction, and treatment-by-days exposed to heat interaction were detected when data were considered simultaneously. Mean +/- SD hematocrit for TN, HS, and HS + EIF were 35.3+/-3, 33.3+/-2, and 37.1+/-3%, respectively. Mean WBGSH concentrations for TN, HS, and HS + EIF were 3.2+/-0.65, 2.7+/-0.62, and 2.4+/-0.56 mmol/L of RBC, respectively. Reduced WBGSH concentrations were associated with reduced feed intake during the later part of each heat period. CONCLUSIONS AND CLINICAL RELEVANCE: Decreased GSH and increased GSSG concentrations were evident during heat stress, especially when cattle consumed EIF These were associated with reduced feed intake during heat stress. Heat stress, reductions in feed intake, and thermoregulatory effects of EIF may induce oxidative stress in cattle.

Animals↗

Selective in vivo stimulation of stress-activated protein kinase in different rat tissues by immobilization stress.

Stress activated protein kinases (SAPK) are key enzymes mediating the cellular response to stressful stimuli. While they are intensively studied in cultured cells, little is known about their physiological role in vivo, or relevance to pathological conditions. Therefore we examined the effect of various times of immobilization on c-Jun N-terminal protein kinase (JNK) activity in several rat stress responsive tissues and in a number of other locations. The abundance and relative distribution of JNK isoforms, the basal levels, time course and relative magnitude of stress induced JNK activity differed among tissues and regions of the brain of the same animal. JNK immunoreactive proteins were most abundant in the brain, especially in the hippocampus, hypothalamus and frontal cortex. Marked activation in response to immobilization stress was observed in adrenal medulla, adrenal cortex, aorta and hippocampus, less pronounced in locus coeruleus. JNK was not affected in superior cervical ganglia, pituitary, hypothalamus, frontal cortex and cerebellum. In adrenal medulla, the activation of JNK by single immobilization stress is correlated with increased transcription of stress-responsive genes, tyrosine hydroxylase and dopamine beta-hydroxylase. These data suggest a potential role of JNK signal transduction pathway in mediating the long term adaptation to stressful stimuli in vivo.

Animals↗

Does pulsed low intensity ultrasound allow early return to normal activities when treating stress fractures? A review of one tarsal navicular and eight tibial stress fractures.

We sought to evaluate the efficacy of daily pulsed low intensity ultrasound (LIUS) with early return to activities for the treatment of lower extremity stress fractures. Eight patients (2 males, 6 females) with radiographic and bone scan confirmed tibial stress fractures participated in this study. Additionally, a case report of a tarsal navicular stress fracture is described. All patients except one were involved in athletics. Prior to the study, subjects completed a 5 question, 10 cm visual analog scale (VAS) regarding pain level (10 = extreme pain, 1 = no pain) and were assessed for functional performance. Subjects received 20-minute LIUS treatments 5 times a week for 4 weeks. Subjects maintained all functional activities during the treatment period. Seven patients with posterior-medial stress fractures participated without a brace. Subjects were re-tested after 4 weeks of treatment. Mann-Whitney U tests (VAS data) and paired t-tests (functional tests) assessed statistical significance (p<0.05). Although the intensity of practice was diminished in some instances, no time off from competitive sports was prescribed for the patients with the tibial stress fractures. The patient with the anterior tibial stress fracture underwent tibial intramedullary nailing at the conclusion of a season of play. In this uncontrolled experience, treatment of tibial stress fractures with daily pulsed LIUS was effective in pain relief and early return to vigorous activity without bracing for the patients with posterior-medial stress fractures.

Basketball↗

Serum levels of interleukin 6 and stress related substances indicate mental stress condition in patients with rheumatoid arthritis.

OBJECTIVE: To evaluate the influence of mental stress on the neuroendocrine-immune system in patients with rheumatoid arthritis (RA). METHODS: Twenty-two patients with RA and 8 patients with osteoarthritis (OA) who underwent total knee or hip arthroplasties under general anesthesia were enrolled in the study. The blood levels of interleukin 6 (IL-6) and other substances related to stress were measured just before administering anesthesia on the day of the operation when the patients lay on the operating table and roughly 30 min later when the patients were under general anesthesia without mental stress. These values were compared with those at the same time on the day before the operation, which were considered the control levels. RESULTS: In patients with RA, the levels of IL-6, cortisol, and epinephrine in the peripheral blood were significantly increased under mental stress, before anesthesia (p < 0.01). However, under general anesthesia, the IL-6, cortisol, and epinephrine were significantly decreased, compared with the levels before anesthesia (p < 0.01). Such changes were not apparent in patients with OA. The levels of other substances in the peripheral blood known to be related to stress, such as corticotropin-releasing factor, dopamine, and norepinephrine, showed no changes in patients with RA or OA. CONCLUSION: In patients with RA, excessive mental stress should be eliminated to modify the interaction between the stress-immune system and stress-endocrine system as a method to better control disease activity.

Aged↗