Stress in patients diagnosed with rheumatoid arthritis compared to chronic pain.

PURPOSE/OBJECTIVE: To examine potential differences in cognitions and traitlike factors that relate to stress among individuals diagnosed with rheumatoid arthritis (RA) compared to those with chronic pain (CP). Research Method/Design: A cross-sectional study was conducted with participants recruited from outpatient rheumatology and CP clinics. Participants completed self-report questionnaires of demographics, disease characteristics, cognitions, and traitlike constructs. Correlates of patient stress were considered using hierarchical multiple regression. RESULTS: Analyses included 445 participants: 226 patients diagnosed with RA and 229 patients diagnosed with CP. In participants with RA, excessive worrying and anxiety sensitivity were independently associated with feeling stressed (p < .001), and 29% of the variance in stress scores was explained after adjusting for age, gender, years of education, and average pain intensity. In participants with CP, fear of relaxation, anxiety sensitivity, and pain catastrophizing were independently associated with feeling stressed (p < .001), and 31% of variance in stress scores was explained after adjusting for age, gender, years of education, and average pain intensity. Comparison of the fit of the model in both groups of patients through use of Fisher's z test found that the set of variables did similarly well for both patients with RA and those with CP, with no significant difference between R2 values (z = .88, p = .388). CONCLUSIONS/IMPLICATIONS: This study establishes cognitions and traitlike factors that are related to reports of stress among patients with RA and CP. These factors should be considered when treating and developing interventions for patients who experience increased feelings of stress. (PsycINFO Database Record

Impact of Abuse on Adjustment and Chronic Pain Disability: A Structural Equation Model.

INTRODUCTION/AIM: Sexual abuse, state and trait psychosocial factors, pain intensity, and pain-related disability have been shown to be correlated among individuals with chronic pain. However, the interacting relationships among these factors are poorly understood. The current study aims to test model which examines the effect of abuse, state and trait psychosocial factors, and pain intensity on pain-related disability among individuals with chronic pain. METHODS: In total, 229 participants diagnosed with chronic pain were recruited from a specialist chronic pain hospital in London, Ontario. Participants completed self-report measures related to sexual abuse history, pain intensity, personality (anxiety sensitivity, experiential avoidance, perfectionism), and adjustment (depression, anxiety, disability, maladaptive worrying). A path analysis was used to test the relationship among these variables. RESULTS: The model provided a close fit to the data (χ21=17.02; P=0.71; root-mean-square error of approximation=0.00; normal fit index=0.97; comparative fit index=1.0). The model demonstrates the direct and indirect effects of childhood sexual abuse on state and trait psychosocial factors among individuals with chronic pain. Pain anxiety, maladaptive worrying, and pain intensity were the main determinants of pain-related disability. DISCUSSION/CONCLUSIONS: The current model has important implications in understanding the interplay of factors involved in adjustment of individuals with chronic pain. Sexual abuse did not have a direct effect on pain-related disability. However, indirect effects through other psychosocial factors were demonstrated.

Dispositional Affect in Unique Subgroups of Patients with Rheumatoid Arthritis.

Background. Patients with rheumatoid arthritis may experience increased negative outcomes if they exhibit specific patterns of dispositional affect. Objective. To identify subgroups of patients with rheumatoid arthritis based on dispositional affect. The secondary objective was to compare mood, pain catastrophizing, fear of pain, disability, and quality of life between subgroups. Methods. Outpatients from a rheumatology clinic were categorized into subgroups by a cluster analysis based on dispositional affect. Differences in outcomes were compared between clusters through multivariate analysis of covariance. Results. 227 patients were divided into two subgroups. Cluster 1 (n = 85) included patients reporting significantly higher scores on all dispositional variables (experiential avoidance, anxiety sensitivity, worry, fear of pain, and perfectionism; all p < 0.001) compared to patients in Cluster 2 (n = 142). Patients in Cluster 1 also reported significantly greater mood impairment, pain anxiety sensitivity, and pain catastrophizing (all p < 0.001). Clusters did not differ on quality of life or disability. Conclusions. The present study identifies a subgroup of rheumatoid arthritis patients who score significantly higher on dispositional affect and report increased mood impairment, pain anxiety sensitivity, and pain catastrophizing. Considering dispositional affect within subgroups of patients with RA may help health professionals tailor interventions for the specific stressors that these patients experience.

Nitric oxide signaling in plants.

Plants have four nitric oxide synthase (NOS) enzymes. NOS1 appears mitochondrial, and inducible nitric oxide synthase (iNOS) chloroplastic. Distinct peroxisomal and apoplastic NOS enzymes are predicted. Nitrite-dependent NO synthesis is catalyzed by cytoplasmic nitrate reductase or a root plasma membrane enzyme, or occurs nonenzymatically. Nitric oxide undergoes both catalyzed and uncatalyzed oxidation. However, there is no evidence of reaction with superoxide, and S-nitrosylation reactions are unlikely except during hypoxia. The only proven direct targets of NO in plants are metalloenzymes and one metal complex. Nitric oxide inhibits apoplastic catalases/ascorbate peroxidases in some species but may stimulate these enzymes in others. Plants also have the NO response pathway involving cGMP, cADPR, and release of calcium from internal stores. Other known targets include chloroplast and mitochondrial electron transport. Nitric oxide suppresses Fenton chemistry by interacting with ferryl ion, preventing generation of hydroxyl radicals. Functions of NO in plant development, response to biotic and abiotic stressors, iron homeostasis, and regulation of respiration and photosynthesis may all be ascribed to interaction with one of these targets. Nitric oxide function in drought/abscisic acid (ABA)-induction of stomatal closure requires nitrate reductase and NOS1. Nitric oxide synthasel likely functions to produce sufficient NO to inhibit photosynthetic electron transport, allowing nitrite accumulation. Nitric oxide is produced during the hypersensitive response outside cells undergoing programmed cell death immediately prior to loss of plasma membrane integrity. A plasma membrane lipid-derived signal likely activates apoplastic NOS. Nitric oxide diffuses within the apoplast and signals neighboring cells via hydrogen peroxide (H2O2)-dependent induction of salicylic acid biosynthesis. Response to wounding appears to involve the same NOS and direct targets.

Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders.

BACKGROUND: Repeated case series have documented the effectiveness of multidisciplinary in-patient behavioural treatment for conversion disorders. However, in the absence of controlled research, treatment success could be attributed to providing patients with a face-saving opportunity to get better. AIMS: The present study contrasts two behavioural treatments to elucidate the factors underlying successful in-patient rehabilitation of this population. METHOD: Thirty-nine patients underwent a standard behavioural programme. Using a crossover design, patients who did not improve underwent a strategic-behavioural treatment in which they and their families were told that full recovery constituted proof of an organic aetiology whereas failure to recover was definitive proof of a psychiatric aetiology. RESULTS: Chart review indicated that the standard behavioural treatment was effective for 8/9 'acute' patients but only for 1/28 'chronic' patients. Of the 21 patients with chronic motor disorder who then under went the strategic-behavioural intervention, 13 were symptom-free at discharge. CONCLUSIONS: The strategic intervention was superior to standard behavioural treatment for patients with chronic motor disorder. Treatment components previously deemed critical for the effectiveness of behavioural treatment may be unnecessary.

Feedback control of the Arabidopsis hypersensitive response.

The plant hypersensitive response (HR) to avirulent bacterial pathogens results from programmed cell death of plant cells in the infected region. Ion leakage and changes in signaling components associated with HR progression were measured. These studies compared Arabidopsis mutants affecting feedback loops with wild-type plants, with timepoints taken hourly. In response to Pseudomonas syringae pv. tomato DC3000 x avrB, npr1-2 mutant plants showed increased ion leakage relative to wild-type plants. Hydrogen peroxide accumulation was similar to that in wild type, but salicylic acid accumulation was reduced at some timepoints. With DC3000 x avrRpt2, similar trends were seen. In response to DC3000 x avrB, ndr1-1 mutant plants showed more ion leakage than wild-type or npr1-2 plants. Hydrogen peroxide accumulation was delayed by approximately 1 h and reached half the level seen with wild-type plants. Salicylic acid accumulation was similar to npr1-2 mutant plants. With DC3000 x avrRpt2, ndr1-1 mutant plants showed no ion leakage, no hydrogen peroxide accumulation, and minimal salicylic acid accumulation. Results with a ndr1-1 and npr1-2 double mutant were similar to ndr1-1. A model consistent with these data is presented, in which one positive and two negative regulatory circuits control HR progression. Understanding this circuitry will facilitate HR manipulation for enhanced disease resistance.

A dynamic mathematical model to clarify signaling circuitry underlying programmed cell death control in Arabidopsis disease resistance.

Plant cells undergo programmed cell death in response to invading pathogens. This cell death limits the spread of the infection and triggers whole plant antimicrobial and immune responses. The signaling network connecting molecular recognition of pathogens to these responses is a prime target for manipulation in genetic engineering strategies designed to improve crop plant disease resistance. Moreover, as alterations to metabolism can be misinterpreted as pathogen infection, successful plant metabolic engineering will ultimately depend on controlling these signaling pathways to avoid inadvertent activation of cell death. Programmed cell death resulting from infection of Arabidopsis thaliana with Pseudomonas syringae bacterial pathogens was chosen as a model system. Signaling circuitry hypotheses in this model system were tested by construction of a differential-equations-based mathematical model. Model-based simulations of time evolution of signaling components matched experimental measurements of programmed cell death and associated signaling components obtained in a companion study. Simulation of systems-level consequences of mutations used in laboratory studies led to two major improvements in understanding of signaling circuitry: (1) Simulations supported experimental evidence that a negative feedback loop in salicylic acid biosynthesis postulated by others does not exist. (2) Simulations showed that a second negative regulatory circuit for which there was strong experimental support did not affect one of two pathways leading to programmed cell death. Simulations also generated testable predictions to guide future experiments. Additional testable hypotheses were generated by results of individually varying each model parameter over 2 orders of magnitude that predicted biologically important changes to system dynamics. These predictions will be tested in future laboratory studies designed to further elucidate the signaling network control structure.

Nitric oxide does not trigger early programmed cell death events but may contribute to cell-to-cell signaling governing progression of the Arabidopsis hypersensitive response.

Nitric oxide (NO) has been suggested to play a role in the hypersensitive response (HR). Single- and double-label fluorescence microscopy experiments were conducted using Arabidopsis leaves infected with Pseudomonas syringae pv. tomato DC3000 carrying either avrB or avrRpt2. Kinetics of NO production were followed by measurement of green 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM) triazole fluorescence in leaves coinfiltrated with DAF-FM diacetate. Kinetics of hypersensitive cell death were followed by measurement of cytoplasmic red fluorescence following internalization of coinfiltrated propidium iodide through compromised plasma membranes. Neither NO accumulation nor cell death was seen until approximately 3 h postinoculation of Columbia leaves with DC3000.avrB or approximately 5.5 h post-inoculation with DC3000.avrRpt2. Subsequent NO accumulation kinetics closely paralleled HR progression in both Columbia and ndr1-1 mutant plants. These data established that NO accumulation does not happen sufficiently early for NO to be a signaling component controlling HR triggering. NO accumulation did contribute to the HR, as proven by an approximately 1-h delay in cell death kinetics caused by an NO scavenger or an NO synthase inhibitor. NO was first seen as punctate foci at the cell surface. Subsequent NO accumulation patterns were consistent with NO being an intercellular signal that functions in cell-to-cell spread of the HR.

Capillary electrophoresis-based profiling and quantitation of total salicylic acid and related phenolics for analysis of early signaling in Arabidopsis disease resistance.

A capillary electrophoresis-based method for quantitation of total salicylic acid levels in Arabidopsis leaves was developed. Direct comparison to previous high-performance liquid chromatography (HPLC)-based measurements showed similar levels of salicylic acid. Simultaneous quantitation of trans-cinnamic acid, benzoic acid, sinapic acid, and an internal recovery standard was achieved. A rapid, streamlined protocol with requirements for plant tissue reduced relative to those of HPLC-based protocols is presented. Complicated, multiparameter experiments were thus possible despite the labor-intensive nature of inoculating plants with bacterial pathogens. As an example of this sort of experiment, detailed time course studies of total salicylic acid accumulation by wild-type Arabidopsis and two lines with mutations affecting salicylic acid accumulation in response to either of two avirulent bacterial strains were performed. Accumulation in the first 12h was biphasic. The first phase was partially SID2 and NDR1 dependent with both bacterial strains. The second phase was largely independent of both genes with bacteria carrying avrB, but dependent upon both genes with bacteria carrying avrRpt2. Virulent bacteria did not elicit salicylic acid accumulation at these time points. Application of this method to various Arabidopsis pathosystems and the wealth of available disease resistance signaling mutants will refine knowledge of disease resistance and associated signal transduction.

Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression.

BACKGROUND: Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB. RESULTS: Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene. CONCLUSION: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.

Misdiagnosis of conversion disorders.

Five cases are presented describing the clinical features for which they were referred and admitted to a rehabilitation unit and later identified as having been misdiagnosed as having a conversion disorder. The diagnoses were sarcoma-induced osteomalacia, cerebellar medulloblastoma, Huntington's chorea, transverse myelitis, and lower extremity dystonia. A perceived history of psychological difficulties, an unusual neurologic presentation, and normal initial diagnostic testing in a female patient were associated with a misdiagnosis of conversion disorders; unfortunately, these factors also characterize actual conversion disorders.

The factor structure of the Coping Strategies Questionnaire.

The Coping Strategies Questionnaire (CSQ) (Rosenstiel and Keefe 1983) is the most widely used measure of pain coping strategies. To date, with one exception (Tuttle et al. 1991), studies examining the factor structure of the CSQ have used the composite scores of its 8 a-priori theoretically derived scales rather than the 48 individual items. An examination of the match between the 8 theoretically derived scales and scales empirically extracted from an item analysis is lacking. Accordingly, the CSQ was administered to 126 chronic pain (whiplash) patients. Factor analyses of the individual items revealed an 8-factor structure to be uninterpretable. Of the 2-9-factor solutions tested, the 5-factor structure was the most interpretable: Factor 1, Distraction; Factor 2, Ignoring Pain Sensations; Factor 3, Reinterpreting Pain Sensations; Factor 4, Catastrophizing; Factor 5, Praying and Hoping. Eighteen Ph.D. or M.D. level clinicians classified items into their corresponding category with a high degree of accuracy (on average, 90.2%), attesting to the face and construct validity of the subscales. Four subscales, Catastrophizing, Reinterpreting Pain Sensations, Praying and Hoping and (to a lesser degree) Ignoring Pain Sensations, correspond with parallel subscales proposed by Rosensteil and Keefe (1983). The fifth subscale, Distraction, is comprised of items from their Diverting Attention and Increasing Activity Level subscales, suggesting that cognitive and behavioural distraction comprise 1 rather than 2 coping strategies. That CSQ items on the original Coping Self-Statements and the Increasing Pain Behaviour subscales failed to load consistently on any factor suggests that they do not reliably measure distinct coping strategies.(ABSTRACT TRUNCATED AT 250 WORDS)