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Unusual stress fracture of the femoral neck in a young adult not caused by excessive stress: a case report.

A 30-year-old man complained of a 10-day history of gradual onset of severe left leg pain. He did not have any history of trauma or excessive training. Routine laboratory data showed no abnormal findings. He was able to perform passive motions of the hip joint without pain, but active motion of the left hip joint was impossible due to anterolateral thigh pain. Plain radiographs of the hip showed no abnormal findings. However, bone scintigraphy indicated trace accumulation in the left femoral neck, and T(1)-weighted magnetic resonance imaging showed a linear low signal on the inferomedial aspect of the femoral neck. Bone mineral density of the lumbar spine was 1.053 g/cm(2), which ruled out osteoporosis. The thigh pain was resolved 2 months after onset with conservative treatment, when plain radiographs showed sclerotic change and a reduction in the intensity of the low signal of T(1)-weighted magnetic resonance imaging. Our diagnosis of unusual stress fracture indicates that the possibility of stress fractures without bone fragility should be kept in mind when young adults complain of atypical pain even without evidence of unusual activities.

Adult↗

A computational study of flow in a compliant carotid bifurcation-stress phase angle correlation with shear stress.

The present study presents a three-dimensional, unsteady supercomputer simulation of the coupled fluid-solid interaction problem associated with flow through a compliant model of the bifurcation of the common carotid artery into the internal and external carotid arteries. The fluid wall shear stress (WSS) and solid circumferential stress/strain (CS) are computed and analyzed for the first time using the complex ratio of CS to WSS (CS/WSS). This analysis reveals a large negative phase angle between CS and WSS (stress phase angle--SPA) on the outer wall of the carotid sinus where atherosclerotic plaques are localized. This finding is consistent with other measurements and computations of the SPA in coronary arteries and the aortic bifurcation that show large negative SPA correlating with sites of plaque location and in vitro studies of endothelial cells showing that large negative SPA induces pro-atherogenic gene expression and metabolite release profiles.

Animals↗

Autonomic responses to stress in Vietnam combat veterans with posttraumatic stress disorder.

This study tested the hypothesis that combat veterans with posttraumatic stress disorder (PTSD) experience sympathetic nervous system activation in response to war-related laboratory stimuli. Circulating plasma catecholamines, vital signs, and affect ratings were measured in 10 Vietnam combat veterans with PTSD and 11 control subjects, during and after viewing combat and noncombat stress films. PTSD subjects responded more strongly than controls to the combat film, with greater increases in plasma epinephrine, pulse, blood pressure, and subjective distress. The increases in autonomic activity of PTSD subjects was more pronounced and long lasting in response to the combat film than to the noncombat film, but type of film had no systematic effect on control subjects' responses. These findings are consistent with biological models that posit sympathoadrenal activation in response to memory-evoking cues of traumatic events in PTSD.

Adult↗

Repeated stressful experiences differently affect limbic dopamine release during and following stress.

The effects of repeated restraint stress exposures (daily 60 min, for 6 days) on extracellular dopamine in the nucleus accumbens, during and after the stress experience, have been investigated in rats by in vivo microdialysis. On the first day, restraint increased dopamine release during the first 40 min followed by a return to basal levels (50-60 min later). As soon as restraint ceased and the rats were set free, there was another increase in dopamine release lasting 40 min. On the second and third day, restraint produced only a slight increase in dopamine release, while no significant changes were evident from the fourth to the sixth day. By contrast, from the second to the sixth day the increase in dopamine release observed once rats were freed, was unchanged in comparison to the first day. The present results show that the activation of the mesolimbic dopaminergic system induced by aversive stimuli adapts to repeated experiences differently from that produced by pleasurable events, suggesting that aversive and rewarding experiences involve different neural systems.

3,4-Dihydroxyphenylacetic Acid↗

Chronic stress induced changes in LH secretion: the contribution of anorexia associated to stress.

The effects of chronic intermittent immobilization (IMO) on serum LH levels of adult male rats were studied. Chronic IMO (2 h daily for 13 days) did not alter basal LH levels, but abolished the LH response to acute stressors (IMO and tailshock). The inhibition of LH caused by acute exposure to IMO for 4 or 18 h was similar in control and chronic IMO rats. Also the LH response to exogenous LHRH administration was normal in chronically stressed rats. When a group of rats eating the same amount of food as that eaten by immobilized rats was introduced (pair-fed), an inhibition of LH response to acute stressors quite similar to that found in chronic IMO rats was observed. These data indicate that chronic stress-induced inhibition of LH release caused by short-term exposure to acute stressors was located above the pituitary and was mainly due to anorexia accompanying daily exposure to the stressor.

Analysis of Variance↗

Periodic maternal deprivation alters stress response in adult offspring: potentiates the negative feedback regulation of restraint stress-induced adrenocortical response and reduces the frequencies of open field-induced behaviors.

The effects of periodic maternal deprivation (PMD) treatment on the adrenocortical stress response and on open-field behavior in adult offspring were investigated. Sprague-Dawley rat pups were deprived of mothers daily for 4.5 h during the first 3 weeks of life. PMD treatment resulted in lower corticosterone levels during restraint stress later in life. The result of dexamethasone suppression test indicated that PMD treatment caused a potentiation of the negative feedback function of adrenocortical response. These effects of PMD were not accompanied by an increased density of the hippocampal glucocorticoid receptor which has been reported to be induced in neonatal handling treatment (brief 15-min maternal deprivation). Serotonin (5-HT)-2 and beta-adrenergic binding sites were also examined in cerebral cortex and no change of binding capacities were induced by PMD treatment. In the open-field test, PMD treatment decreased the number of ambulations and rearings but did not affect a frequency of defecation. From these results, it is suggested that PMD treatment leads rats to be insensitive to environmental stimuli in adulthood.

Adrenal Cortex↗

Life events, combat stress reaction and post-traumatic stress disorder.

The implication of life events just preceding a war in acute combat stress reaction and chronic PTSD were assessed in a sample of 716 Israeli combatants. Results show that life events were unrelated to combat stress reaction but were related to subsequent PTSD. Conceptual and methodological issues were discussed to explain the results.

Adaptation, Psychological↗

Effects of exercise stress and cold stress on glutathione and gamma-glutamyltransferase in rat liver.

Effects of acute and chronic stress (exercise and cold) on glutathione and gamma-glutamyltransferase (gamma GT) in the rat liver were investigated. Such stress, except for in the case of acute exercise, had no definite influence on the glutathione level. On the other hand, gamma GT activity in both the extramicrosomal and microsomal fractions varied substantially, suggesting that acute exercise increases the release ability of the microsomal membrane of the rat liver, and that swimming training and long-term cold exposure stabilize the membrane. Immunoreactive gamma GT, however, did not always correlate with the enzyme activity, especially in the extramicrosomal fraction. Cross-adaptation appeared to exist between swimming training and chronic cold exposure.

Animals↗

High glucose induced NF-kappaB DNA-binding activity in HAEC is maintained under low shear stress but inhibited under high shear stress: role of nitric oxide.

In the present study, we investigated whether low shear (LS, 2 dyn/cm2) favors high glucose (HG, 30 mM) induced nuclear factor kappa B (NF-kappaB) activity by regulating NO release in human aortic endothelial cells (HAEC). The results show that (i) under LS, the NF-kappaB activity of HAEC exposed to HG was significantly higher than HAEC in normal glucose (NG, 5.5mM) (P < 0.05). In contrast, under HS, the activation of NF-kappaB in HAEC exposed to HG showed no significant difference compared to that of NG. (ii) The NF-kappaB activity induced by HG is suppressed by high shear (HS) in the absence of a NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME) but restored in its presence, while LS + HG induced NF-kappaB activity remains the same in the presence or absence of L-NAME. (iii) Endothelial nitric oxide synthase (eNOS) protein expression and quantitative detection of NO indicated that high shear stress significantly induced higher eNOS expression and NO production compared to low shear stress condition. Collectively, these data suggest that HS exerts a protective effect on HG induced NF-kappaB activity through NO mediated signaling. LS, on the other hand, may down-regulate eNOS expression resulting in reduced NO release, and thereby maintain high glucose induced NF-kappaB DNA-binding activity. These observations explain, in part, the mechanism by means of which hyperglycemia accelerates the focal development of atherosclerotic lesions in low shear (lesion prone) areas of the arterial tree.

Analysis of Variance↗

Role of oxidative stress, endoplasmic reticulum stress, and c-Jun N-terminal kinase in pancreatic beta-cell dysfunction and insulin resistance.

Type 2 diabetes is the most prevalent and serious metabolic disease affecting people all over the world. Pancreatic beta-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Normal beta-cells can compensate for insulin resistance by increasing insulin secretion and/or beta-cell mass, but insufficient compensation leads to the onset of glucose intolerance. Once hyperglycemia becomes apparent, beta-cell function gradually deteriorates and insulin resistance aggravates. Under diabetic conditions, oxidative stress and endoplasmic reticulum stress are induced in various tissues, leading to activation of the c-Jun N-terminal kinase pathway. The activation of c-Jun N-terminal kinase suppresses insulin biosynthesis and interferes with insulin action. Indeed, suppression of c-Jun N-terminal kinase in diabetic mice improves insulin resistance and ameliorates glucose tolerance. Thus, the c-Jun N-terminal kinase pathway plays a central role in pathogenesis of type 2 diabetes and could be a potential target for diabetes therapy.

Animals↗

Role of oxidative stress, endoplasmic reticulum stress, and c-Jun N-terminal kinase in pancreatic beta-cell dysfunction and insulin resistance.

Type 2 diabetes is the most prevalent and serious metabolic disease affecting people all over the world. Pancreatic beta-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Normal beta-cells can compensate for insulin resistance by increasing insulin secretion and/or beta-cell mass, but insufficient compensation leads to the onset of glucose intolerance. Once hyperglycemia becomes apparent, beta-cell function gradually deteriorates and insulin resistance aggravates. Under diabetic conditions, oxidative stress and endoplasmic reticulum stress are induced in various tissues, leading to activation of the c-Jun N-terminal kinase pathway. The activation of c-Jun N-terminal kinase suppresses insulin biosynthesis and interferes with insulin action. Indeed, suppression of c-Jun N-terminal kinase in diabetic mice improves insulin resistance and ameliorates glucose tolerance. Thus, the c-Jun N-terminal kinase pathway plays a central role in pathogenesis of type 2 diabetes and could be a potential target for diabetes therapy.

Animals↗

Response of microcystis to copper stress: do phenotypes of microcystis make a difference in stress tolerance?

To elucidate the role of phenotype in stress-tolerant bloom-forming cyanobacterium Microcystis, two phenotypes of M. aeruginosa - unicellular and colonial strains were selected to investigate how they responded to copper stress. Flow cytometry (FCM) examination indicated that the percents of viable cells in unicellular and colonial Microcystis were 1.92-2.83% and 72.3-97.51%, respectively, under 0.25 mgl(-1) copper sulfate treatment for 24h. Upon exposure to 0.25 mgl(-1) copper sulfate, the activities of antioxidative enzyme, such as superoxide dismutase (SOD) and catalase (CAT), were significantly increased in colonial Microcystis compared to unicellular Microcystis. Meanwhile, the values of the photosynthetic parameters (F(v)/F(m), ETR(max), and oxygen evolution rate) decreased more rapidly in unicellular Microcystis than in colonial Microcystis. The results indicate that colonial Microcystis has a higher endurance to copper than unicellular Microcystis. This suggests that the efficient treatment concentration of copper sulfate as algaecides will be dependent on the phenotypes of Microcystis.

Antioxidants↗

Role of the stress sigma factor RpoS in GacA/RsmA-controlled secondary metabolism and resistance to oxidative stress in Pseudomonas fluorescens CHA0.

In Pseudomonas fluorescens biocontrol strain CHA0, the two-component system GacS/GacA positively controls the synthesis of extracellular products such as hydrogen cyanide, protease, and 2,4-diacetylphloroglucinol, by upregulating the transcription of small regulatory RNAs which relieve RsmA-mediated translational repression of target genes. The expression of the stress sigma factor sigmaS (RpoS) was controlled positively by GacA and negatively by RsmA. By comparison with the wild-type CHA0, both a gacS and an rpoS null mutant were more sensitive to H2O2 in stationary phase. Overexpression of rpoS or of rsmZ, encoding a small RNA antagonistic to RsmA, restored peroxide resistance to a gacS mutant. By contrast, the rpoS mutant showed a slight increase in the expression of the hcnA (HCN synthase subunit) gene and of the aprA (major exoprotease) gene, whereas overexpression of sigmaS strongly reduced the expression of these genes. These results suggest that in strain CHA0, regulation of exoproduct synthesis does not involve sigmaS as an intermediate in the Gac/Rsm signal transduction pathway whereas sigmaS participates in Gac/Rsm-mediated resistance to oxidative stress.

Bacterial Proteins↗

Effect of continuous application of shear stress on liver tissue: continuous application of appropriate shear stress has advantage in protection of liver tissue.

Rapid blood flow changes occur in the liver following a massive resection or in the grafted liver following transplantation, under which shear stress (SS) change induced by the flow change may determine the postoperative results. We observed changes in liver tissue structure and liver-specific function, and consequently assessed SS effect. The cultured liver tissue exposed to continuous application of moderate SS was shown to express and maintain a long-term liver-specific function. There was also evidence showing that destruction of the liver structure was inhibited. However, the cultured liver tissue not exposed to SS or exposed to high SS was shown to lose liver-specific function soon after expression. The liver structure was destroyed in the early stage of incubation. These results suggested that continuous application of appropriate SS has advantages over other types of stresses to protect liver tissue.

Animals↗

Multiple independent kinase cascades are targeted by hyperosmotic stress but only one activates stress kinase p38.

In this report, we analyse the effects of osmotic shock on signal transduction in CHO cells. We demonstrate that at least three different kinase cascades are switched on upon osmotic shock, namely PKA, AMPK, and MLTK. Whereas PKA from cells treated with forskolin activated stress kinase p38, PKA from cells treated with sorbitol did not activate p38, although the enzyme is activated in both cases as analysed in vitro using a specific peptide target. Further, osmolar shock activated AMPK but treatment of the cells with the AMPK activator 5-amino-4-imidazolecarboxamide (AICAr) did not result in p38 activation, strongly suggesting that AMPK is not involved in stress kinase activation. Transfection of CHO cells with dominant negative recombinants of MLTKalpha resulted in inhibition of sorbitol-mediated p38 activation, indicating that the mixed-lineage kinase is involved in the activation of p38 by sorbitol. Finally, in CHO cells overexpressing wild-type MLTKalpha, no activation of AMPK of PKA could be demonstrated, indicating that the activated kinase cascades are not involved in a cross-talk process.

AMP-Activated Protein Kinases↗

Expression of stress-response and cell proliferation genes in renal cell carcinoma induced by oxidative stress.

Ferric nitrilotriacetate induces oxidative damage in renal proximal tubules that ultimately leads to a high incidence of renal cell carcinoma (RCC) in rats. In search of genes specifically involved in oxystress-induced carcinogenesis, we have applied a modified fluorescent differential display technique to the tumors and an established cell line as well as their non-neoplastic counterparts. We screened approximately 84,000 products. Reverse Northern blotting confirmed differential expression of 20 transcripts, which showed either significant increase, decrease or lack of expression in the RCCs. Five cDNA clones encoded novel products of unknown function. Fifteen cDNA clones were identified by homology search, which included annexin II, Y-box binding protein, ribosomal proteins, heat shock proteins, DNA polymerase, nonmuscle caldesmon (increased); protein tyrosine phosphatase (decreased); selenoprotein P, stromal cell-derived factor 1, intestinal trefoil protein, nicotinamide adenine dinucleotide, reduced form (NADH) dehydrogenase, and insulin-like growth factor binding protein 7 (deleted). Most of the identified genes were associated with stress-response or cellular proliferation. These results suggest that multiple, interactive genetic pathways are involved in carcinogenesis induced by oxidative stress.

Animals↗

Maturation of the adrenocortical stress response: neuroendocrine control mechanisms and the stress hyporesponsive period.

During the first two weeks of life rat pups show a markedly reduced adrenocortical response to stress, and this period of adrenocortical quiescence has been termed the 'stress non-responsive period' (SNRP). The adaptive value of the SNRP can be understood in terms of the effects of glucocorticoids on CNS development: excessively high or low corticoid levels are associated with abnormal neural and behavioral development. We have attempted to explain adrenocortical activity during this period in terms of the unique pattern of glucocorticoid-receptor concentrations that exist in the brain and pituitary of the neonatal rat. This pattern of receptor concentrations results in a negative-feedback condition at the level of the brain and pituitary that ensures the low, stable corticoid levels that appear to be optimal for neuronal development in glucocorticoid-sensitive brain regions.

Adaptation, Physiological↗

Psychophysiologic assessment of mental imagery of stressful events in Israeli civilian posttraumatic stress disorder patients.

This study explored the physiological responses of posttraumatic stress disorder (PTSD) patients to reminders of a stressful event that had preceded the onset of their illness and was not related to its cause: the SCUD missile alarms of the Gulf War. A mental-imagery technique used in previous studies of PTSD was used. Three 30-second audiotapes were presented to each subject, including (1) the Gulf War's missile alarm, (2) a radio announcement of a terrorist attack, and (3) a standardized relaxing scene. Subjects were instructed to imagine each event as vividly as possible while heart rate (HR), skin conductance (SC), and left lateral frontalis electromyogram (EMG) responses were measured. The responses of 12 outpatients with PTSD were compared with those of panic disorder patients (n = 11), survivors of traumatic events who had not developed PTSD (n = 9), and mentally healthy subjects with no lifetime history of major trauma (n = 19). Multivariate analysis of variance (MANOVA) for the three physiological measures showed a significant group difference during imagery of the Gulf War alarm, with PTSD subjects showing higher SC and EMG responses than the others. The differences remained significant when age, level of distress during the war, and concurrent anxiety were controlled for. There were no group differences in responses to the other stimuli. We conclude that, PTSD patients may either acquire and maintain prolonged conditioned responses to various stressors during their life span or become sensitized to reminders of past traumata following the onset of their illness. Heightened conditionability may be expressed before the trauma in subjects who are liable to develop PTSD.

Adult↗