Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

OBJECTIVES: This 6-week, open label randomized, multicenter study was conducted to evaluate the antidepressant effect and safety of milnacipran and fluoxetine in patients with major depression. METHODS: The study was done in patients with major depression diagnosed by DSM-IV who score > or =17 in 17 items Hamilton Rating Scale for Depression (17-item HAM-D) and score > or =25 in Montgomery and Asberg Depression Rating Scale (MADRS). A total of 87 patients were randomized to milnacipran group and fluoxetine group. In cases of the patients taking other antidepressants, 6 weeks of each medication was administered after 7 days of drug excretion period. The evaluation was done using 17 item HAM-D, MADRS, Clinical Global Impression Scale (CGI), and COVI scale after baseline, 1 week, 2 weeks, 4 weeks, and 6 weeks. The side effects that had occurred during the period of our study were put in records by developed/disappeared time, severities, incidences, managements and results. RESULTS: A total of 87 patients were enrolled. 70 (milnacipran group 39;fluoxetine group 31) of them were included for the 6 weeks of research and 17 of them dropped out within the first week, not due to adverse reactions or deficiency of effects. Total 17 item HAM-D scores, total points of MADRS, and CGI showed significant decrease after 1 week in each treatment group and continued decrease after 2 weeks and 4, 6 weeks. But there was no difference between milnacipran group and fluoxetine group in the antidepressant effect. There were no significant changes in vital sign, CBC, chemistry, and EKG in each treatment group. The commonly reported side effects of minlacipran were nausea (25.0%), headache (10.7%), vomiting (7.1%), constipation (7.1%), dizziness (7.1%) and those of fluoxetine were GI trouble (11.1%), diarrhea (11.1%), insomnia (11.1%), agitation (5.6%), and dizziness (5.6%). CONCLUSION: Milnacipran was effective for the improvement of depressive symptoms and was well tolerated and safe in patients with depression.
Antidepressive Agents ; Chemistry ; Constipation ; Depression* ; Diagnostic and Statistical Manual of Mental Disorders ; Diarrhea ; Dihydroergotamine ; Dizziness ; Electrocardiography ; Fluoxetine* ; Headache ; Humans ; Incidence ; Nausea ; Sleep Initiation and Maintenance Disorders ; Vital Signs ; Vomiting