Home About us Contact | |||
Subjective Stress (subjective + stress)
Selected AbstractsStress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor , antagonistsARTHRITIS & RHEUMATISM, Issue 2 2008Sarosh J. Motivala Objective Psychological stress is thought to aggravate disease activity in rheumatoid arthritis (RA), although the physiologic mechanisms are unclear. Tumor necrosis factor , (TNF,) is an inflammatory cytokine involved in the exacerbation of RA, and TNF, antagonists have emerged as efficacious treatments. The purpose of this study was to determine whether RA patients show increased monocyte production of TNF, following acute psychological stress and whether such responses are abrogated in RA patients taking TNF, antagonists. Methods A standardized stress task was administered to 3 groups of subjects: RA patients taking TNF, antagonists, RA patients not taking such medications, and healthy controls. Lipopolysaccharide-stimulated monocyte production of inflammatory cytokines was repeatedly measured using intracellular staining and flow cytometry. Subjective stress, cardiovascular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured. Results The stress task induced increases in subjective stress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 groups. In addition, the stress task induced a significant increase (P < 0.001) in monocyte production of TNF, among RA patients who were not taking TNF, antagonists. However, monocyte production of TNF, did not change following psychological stress in RA patients taking TNF, antagonists or in healthy controls. Conclusion Brief psychological stress can trigger increased stimulated monocyte production of TNF, in RA patients. The use of TNF, antagonists protects against stress activation of cellular markers of inflammation in RA patients. [source] Psychotic reactivity in borderline personality disorderACTA PSYCHIATRICA SCANDINAVICA, Issue 2 2010J.-P. Glaser Glaser J-P, Van Os J, Thewissen V, Myin-Germeys I. Psychotic reactivity in borderline personality disorder. Objective:, To investigate the stress relatedness and paranoia specificity of psychosis in borderline personality disorder (BPD). Method:, Fifty-six borderline patients, 38 patients with cluster C personality disorder, 81 patients with psychotic disorder and 49 healthy controls were studied with the experience sampling method (a structured diary technique) to assess: i) appraised subjective stress and ii) intensity of psychotic experiences. Results:, All patient groups experienced significantly more increases in psychotic experiences in relation to daily life stress than healthy controls, borderline patients displaying the strongest reactivity. Borderline patients, moreover, reported significantly more hallucinatory reactivity than healthy controls and subjects with cluster C personality disorder. Paranoid reactivity to daily life stress did not differ between the patient groups. Conclusion:, These results are the first to ecologically validate stress-related psychosis in BPD. However, psychotic reactivity was not limited to expression of paranoia but involved a broader range of psychotic experiences including hallucinations. [source] Impact of exposure to war stress on exacerbations of multiple sclerosisANNALS OF NEUROLOGY, Issue 2 2008Daniel Golan MD Objective To assess the relation between stress caused by the perils of rocket attack on civilian centers in northern Israel during the 2006 war between Hezbollah and Israel and multiple sclerosis (MS) exacerbations. Methods Participants were 156 patients with relapsing-remitting MS. We compared the number of relapses during and after the war with similar time periods at the preceding year. Exposure to war events and resulting subjective stress were evaluated by means of structured interviews using questionnaires previously validated. Results During the 33 days of the war, there were 18 relapses among our patients, compared with 1 to 6 relapses in similar time periods over the 12 months before the war (p < 0.001,0.02). There was no increase in relapse rate during the 3 months that followed the war (p = 0.58). The percentage of patients reporting the experience of intense subjective stress during the hostilities was significantly greater among patients with wartime relapse compared with the rest of the patients (44 vs 20%). The proportion of patients reporting high levels of distress associated with exposure to rocket attacks, displacement from home, and perceived life threat was greater in relapsing patients compared with those in remission (67 vs 42%, p = 0.05; 33 vs 11%, p = 0.02; and 33 vs 15%, p = 0.08, respectively). Interpretation Our data suggest that civilian exposure to war stress is associated with increased risk for MS relapse. These findings provide insight to stress-related risk factors associated with relapses of MS. Ann Neurol 2008 [source] Stress activation of cellular markers of inflammation in rheumatoid arthritis: Protective effects of tumor necrosis factor , antagonistsARTHRITIS & RHEUMATISM, Issue 2 2008Sarosh J. Motivala Objective Psychological stress is thought to aggravate disease activity in rheumatoid arthritis (RA), although the physiologic mechanisms are unclear. Tumor necrosis factor , (TNF,) is an inflammatory cytokine involved in the exacerbation of RA, and TNF, antagonists have emerged as efficacious treatments. The purpose of this study was to determine whether RA patients show increased monocyte production of TNF, following acute psychological stress and whether such responses are abrogated in RA patients taking TNF, antagonists. Methods A standardized stress task was administered to 3 groups of subjects: RA patients taking TNF, antagonists, RA patients not taking such medications, and healthy controls. Lipopolysaccharide-stimulated monocyte production of inflammatory cytokines was repeatedly measured using intracellular staining and flow cytometry. Subjective stress, cardiovascular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured. Results The stress task induced increases in subjective stress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 groups. In addition, the stress task induced a significant increase (P < 0.001) in monocyte production of TNF, among RA patients who were not taking TNF, antagonists. However, monocyte production of TNF, did not change following psychological stress in RA patients taking TNF, antagonists or in healthy controls. Conclusion Brief psychological stress can trigger increased stimulated monocyte production of TNF, in RA patients. The use of TNF, antagonists protects against stress activation of cellular markers of inflammation in RA patients. [source] |