Chronic stress experience and burnout syndrome have appreciable influence on health-related quality of life in patients with psoriasis.

BACKGROUND: Psoriasis has a negative impact on health-related quality of life (HRQoL) and may favour mental comorbidity. OBJECTIVE: To investigate the contribution of chronic stress and burnout experience to HRQoL and how mental health influences the efficacy of an inpatient rehabilitation measure in psoriasis patients. METHODS: Eighty-four psoriasis patients taking part in a 3-week inpatient rehabilitation measure participated in the study. Severity of psoriasis was assessed with the Psoriasis Area and Severity Index (PASI) and by patients' self-evaluation at the beginning and end of treatment. The following aspects of mental health were explored using validated questionnaires. Symptoms of chronic stress and burnout experience: Trier Inventory for the Assessment of Chronic Stress (TICS) and Shirom Melamed Burnout Measure (SMBM). Symptoms of depression: depression scale of the Patient Health Questionnaire in the German version (PHQ-D). HRQoL: Dermatology Life Quality Index (DLQI) and Short Form Health Survey-8 (SF-8). RESULTS: Linear regression analyses revealed that chronic stress, burnout experience and perceived symptom severity but not clinician-assessed severity of psoriasis had independent negative effects on HRQoL. Patients who achieved a PASI reduction of <75% at discharge from the rehabilitation measure had lower baseline QoL and showed more symptoms of depression, chronic stress and burnout than patients who achieved a PASI improvement of ≥75. CONCLUSION: Chronic stress and burnout have appreciable influence on HRQoL and may adversely affect treatment success in psoriasis patients. Our data underscore the importance of a multidimensional approach in the management of psoriasis.

Mice deficient in the alpha7 neuronal nicotinic acetylcholine receptor lack alpha-bungarotoxin binding sites and hippocampal fast nicotinic currents.

The alpha7 subunit of the neuronal nicotinic acetylcholine receptor (nAChR) is abundantly expressed in hippocampus and is implicated in modulating neurotransmitter release and in binding alpha-bungarotoxin (alpha-BGT). A null mutation for the alpha7 subunit was prepared by deleting the last three exons of the gene. Mice homozygous for the null mutation lack detectable mRNA, but the mice are viable and anatomically normal. Neuropathological examination of the brain revealed normal structure and cell layering, including normal cortical barrel fields; histochemical assessment of the hippocampus was also normal. Autoradiography with [3H]nicotine revealed no detectable abnormalities of high-affinity nicotine binding sites, but there was an absence of high-affinity [125I]alpha-BGT sites. Null mice also lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that are present in hippocampal neurons. The results of this study indicate that the alpha-BGT binding sites are equivalent to the alpha7-containing nAChRs that mediate fast, desensitizing nicotinic currents in the hippocampus. These mice demonstrate that the alpha7 subunit is not essential for normal development or for apparently normal neurological function, but the mice may prove to have subtle phenotypic abnormalities and will be valuable in defining the functional role of this gene product in vivo.

Immunohistochemical localization of the nicotinic acetylcholine receptor subunit alpha6 to dopaminergic neurons in the substantia nigra and ventral tegmental area.

Participation of the neuronal nicotinic receptor subunit alpha6 in a physiologically relevant receptor has yet to be demonstrated, but its high degree of expression in catecholaminergic nuclei has attracted considerable interest. To investigate the pattern of expression of the alpha6 protein, a subunit specific antibody against the alpha6 subunit was used to immunohistochemically label sections of the adult rat brain. Alpha6 immunoreactivity was found to be present in the substantia nigra, the ventral tegmental area, the locus coeruleus and the medial habenula, and double-labeling for tyrosine hydroxylase demonstrated that the alpha6 protein is present on dopaminergic neurons of the midbrain. A possible role for the alpha6 subunit in nicotinic modulation of dopaminergic transmission is therefore proposed.

Neuronal localization of the cyclophilin A protein in the adult rat brain.

Cyclophilin A is a small, soluble protein which binds the immunosuppressive drug cyclosporin A. Cyclophilin A is a peptidyl-prolyl isomerase and is widely expressed in a multitude of tissues, but is present in highest concentration in the brain. A role for this protein in the maturation and folding of neuron-specific membrane proteins has been hypothesized. Immunohistochemical staining for cyclophilin A was used to determine whether cyclophilin A is present in neurons, and whether there is variation in the level of expression with respect to brain regions and cell types. The specificity of the antibody used was demonstrated by Western blot analysis and cyclosporin affinity purification. Immunohistochemical staining of sections of adult rat brain showed labelled neurons throughout the neuraxis. The intensity of the immunostaining observed was roughly equivalent to neuronal cell density and was restricted to gray matter. On a cellular level, staining was present in cytosol and nuclei and extended into neuronal processes. Fluorescent double-labelling experiments on hippocampal cell cultures revealed that all cells labelled with the cyclophilin A antibody also showed staining for the neuron-specific marker for microtubule-associated protein (MAP)2, and could, therefore, be identified as neurons. Immunoreactivity in these neurons is present in punctate, spinelike structures along dendrites. Cyclophilin A immunoreactivity was undetectable in glial fibrillary acidic protein (GFAP)-positive cells. The pattern of cyclophilin. A expression is consistent with a role of cyclophilin A in neuronal protein maturation and folding in vivo.