Styles of emotion regulation and their associations with perceived health in patients with rheumatoid arthritis

Background: Patients with rheumatoid arthritis face the challenge of adjusting to adverse health consequences and accompanying emotions. Styles of emotion regulation may affect health.Purpose: The objective is to examine associations between styles of emotion regulation and perceived health, consisting of psychological well-being, social functioning, physical functioning, and disease activity.Methods: Principal component analysis was used to summarize styles of emotion regulation of 335 patients with rheumatoid arthritis. Relationships between emotion regulation and perceived health were examined with structural equation modeling.Results: Four styles of emotion regulation were identified: ambiguity, control, orientation, and expression. Ambiguity and control were mutually correlated, as were orientation and expression. Styles of emotion regulation were not uniquely related to perceived physical functioning and disease activity. Emotional ambiguity and orientation were related to poorer, whereas expression and control were related to more favorable psychological well-being and social functioning.Conclusions: Our cross-sectional study suggests that emotion regulation is not of direct importance for perceived somatic health of patients with rheumatoid arthritis, but it may be of importance for psychological well-being and social functioning, and perhaps through this route for somatic health. The more conscious and controlled aspects of control and expression are positively related to psychosocial health, and the more unconscious automatic aspects of ambiguity and orientation are negatively related. Changing emotion regulation will potentially affect psychosocial health. It would be worthwhile to verify this possibility in prospective research. This study was financially supported by the Dutch Arthritis Association. We thank all rheumatologists and rheumatology nurses of the Arthritis Research Foundation Utrecht (SRU) for recruitment of participants. We also thank Bert Garssen and the reviewers and editor of this journal for their valuable comments and suggestions on previous drafts of the article.     

Short-term efficacy of a web-based computer-tailored nutrition intervention: Main Effects and Mediators

Background: This study evaluates the short-term efficacy and respondents’ evaluations of a Web-based computer-tailored nutrition intervention, aiming to decrease saturated fat intake and increase fruit and vegetable intake. Perceived personal relevance, individualization, and interestingness of the information were tested as mediators of the effects of the tailored intervention.Purpose: The objective was to study the short-term effects of a Web-based computer-tailored nutrition intervention.Methods: Respondents (N = 782) were randomly assigned to a tailored intervention group, a generic nutrition information control group, or a no-information control group. Fat, fruit, and vegetable intakes and behavioral determinants were measured at baseline and at 3 weeks postintervention. Posttest group differences were determined by multiple linear regression analyses.Results: The computer-tailored intervention produced significant effects for the determinants of fat, fruit, and vegetable intake and for vegetable and fruit intake. The tailored information was rated as more personally relevant, individualized, interesting, and new than the generic nutrition information. Perceived personal relevance, individualization, and interestingness were identified as mediators of some of the tailoring effects.Conclusions: The findings of this study indicate that Web-based, computer-tailored nutrition information can have a short-term effect on the determinants of fat, fruit, and vegetable intake. The effect of the tailored information may be partly explained by the perceived personal relevance and individualization of the information. The study was supported financially by ZonMw, the Netherlands Organisation for Health Research and Development. The research was conducted at the University of Maastricht, Maastricht, The Netherlands.     

Clinical and magnetic resonance imaging characteristics of sporadic cerebellar ataxia

BACKGROUND: It is unknown whether multiple system atrophy of the cerebellar type (MSA-C) and idiopathic cerebellar ataxia with extracerebellar presentation (IDCA-P) represent distinct entities. OBJECTIVE: To investigate the discriminative validity of magnetic resonance imaging in sporadic cerebellar ataxia. DESIGN: Basal ganglia and infratentorial structures were screened for signal abnormalities and atrophic changes. Magnetic resonance imaging raters were masked to the clinical diagnosis. SETTING: Outpatient clinic of a university hospital. PATIENTS: Forty-one individuals were diagnosed as having MSA-C (n = 30) or IDCA-P (n = 11) based on their clinical features. RESULTS: Shrinkage of the cerebellar vermis and hemispheres was found in both groups. Atrophy of the brainstem and middle cerebellar peduncles was significantly more frequent in patients with MSA-C (P<.001). Hyperintensities of infratentorial structures were common in patients with MSA-C (middle cerebellar peduncles: 87%; pons: 97%) but were absent in patients with IDCA-P. Hypointensities or hyperintensities of basal ganglia structures did not reliably differentiate the groups. CONCLUSIONS: Patients with MSA-C were characterized by a higher frequency and severity of magnetic resonance imaging abnormalities (atrophic changes and additional hyperintense signal changes) of the middle cerebellar peduncles and pons. The presence of these magnetic resonance imaging features points to the diagnosis of MSA-C and helps differentiate MSA-C from other types of sporadic cerebellar ataxia with extracerebellar features.     

Localization of breast cancer resistance protein (BCRP) in microvessel endothelium of human control and epileptic brain

PURPOSE: Breast cancer resistance protein (BCRP) is a half adenosine triphosphate (ATP)-binding cassette (ABC) transporter expressed on cellular membranes and included in the group of multidrug resistant (MDR)-related proteins. Recently, upregulation of different MDR proteins has been shown in human epilepsy-associated conditions. This study investigated the expression and cellular distribution of BCRP in human control and epileptic brain, including a large number of both neoplastic and nonneoplastic specimens from patients with chronic pharmacoresistant epilepsy. METHODS: Several epileptogenic pathologies, such as hippocampal sclerosis (HS), focal cortical dysplasia (FCD), dysembryoplastic neuroepithelial tumor, oligodendroglioma astrocytoma, and glioblastoma multiforme were studied by using Western blot and immunocytochemistry. RESULTS: With Western blot, we could demonstrate the presence of BCRP in both normal and epileptic human brain tissue. In contrast to P-glycoprotein (P-gp) and multidrug resistance-associated protein (MRP) 2, BCRP expression levels did not change in tissue from patients with HS, compared with control hippocampus. No BCRP immunoreactivity was observed in glial or neuronal cells, including reactive astrocytes and dysplastic neurons in FCD. BCRP expression was, however, increased in tumor brain tissue. Immunocytochemistry demonstrated that BCRP was exclusively located in blood vessels and was highly expressed at the luminal cell surface and in newly formed tumor capillaries. This localization closely resembles that of P-gp. The higher expression observed in astrocytomas by Western blot analysis was related to the higher vascular density within the tumor tissue. CONCLUSIONS: These results indicate a constitutive expression of BCRP in human endothelial cells, representing an important barrier against drug access to the brain. In particular, the strong BCRP expression in the microvasculature of epileptogenic brain tumors could critically influence the bioavailability of drugs within the tumor and contribute to pharmacoresistance.     

Memantine inhibits ethanol-induced NMDA receptor up-regulation in rat hippocampal neurons

The present study examined the effect of memantine, an uncompetitive NMDA receptor antagonist, on ethanol-induced NMDA receptor up-regulation. Primary glutamatergic rat hippocampal neurons were exposed to ethanol and memantine for 5 days. The ethanol-sensitive NMDA receptor subunits NR1, NR2A and NR2B were quantified by Western immunoblot analysis. Exposure to ethanol (50 mM) caused an increase in the levels of NR1 (137 +/- 11% of untreated control, P = 0.009), NR2A (128 +/- 14%, P = 0.022) and NR2B (136 +/- 19%, P = 0.012). Coincubation with memantine (10 microM) completely blocked the ethanol-induced up-regulation of NR1 (102 +/- 4%), NR2A (95 +/- 7%) and NR2B (105 +/- 13%). No effect of memantine on NR subunit expression was observable, except for NR2A, where a decrease (79 +/- 6%, P = 0.034) was noted. Neither ethanol nor memantine alone or in combination were toxic in the concentrations tested. These results may provide a molecular explanation for beneficial effects of memantine on ethanol-induced glutamatergic hyperexcitability reflected in the ethanol withdrawal syndrome and on the development of ethanol dependence.     

Epidemiology of staphylococcal scalded skin syndrome in Germany

Staphylococcal scalded skin syndrome (SSSS) is a blistering skin disorder caused by Staphylococcus aureus. The "Dokumentationszentrum schwerer Hautreaktionen", a unique population-based registry for severe skin reactions, included SSSS during a time period of 2 y in Germany. Statistical calculations indicated a low overall incidence between 0.09 and 0.13 cases per 1 million inhabitants per year with 95% confidence interval of [0-4]. The age distribution showed two clusters; one in young children and one in adults. The mortality rate was much lower in children than in adults. Young age was the main risk factor, whereas immunosuppression and consumptive infectious disease were the detected risk factors in adults.     

Electrophysiological signs of permanent axonal loss in a follow-up study of patients with Guillain-Barré syndrome

The neurophysiological mechanisms for persisting impairment of motor function after Guillain-Barre syndrome (GBS) were assessed in 37 unselected patients 1-13 years after diagnosis. For evaluation of reinnervation and axonal loss, macroelectromyography (macro-EMG) including measurement of fiber density (FD) was performed. Data from neuropathy symptom score, neuropathy disability score, nerve conduction studies, and quantitative sensory examination were ranked and summed to a neuropathy rank sum score (NRSS). The isokinetic muscle strength at the ankle was measured. Signs of axonal loss with increase of either macro motor unit potential (macro-MUP) amplitude or FD occurred in 76% of patients. The macro-MUP amplitude correlated with muscle strength and with NRSS. Patients with evidence of residual neuropathy had increased macro-MUP amplitude and FD as well as decreased muscle strength compared to patients without evidence of residual neuropathy. We conclude that axonal loss takes place in a substantial number of GBS patients and is associated with permanent muscle weakness caused by insufficient reinnervation. Possible patterns of pathology are discussed in relation to the macro-EMG findings.