Comparative analysis of the use of complementary and alternative medicine by Korean patients with androgenetic alopecia, atopic dermatitis and psoriasis.

BACKGROUND: Complementary and alternative medicine (CAM) is being increasingly used among Koreans with chronic dermatologic diseases, such as androgenetic alopecia (AGA), atopic dermatitis (AD) and psoriasis. OBJECTIVE: To quantify the usage of CAM in Korean patients with AGA, AD or psoriasis, and to offer valid information for the physicians frequently encountering such disorders. METHODS: Outpatients (n = 678) from three tertiary hospitals were investigated independently by constructed and self-directed questionnaire. RESULTS: Of the respondents, 62.1% (421/678) of the subjects reported current or previous use of CAM for their dermatologic conditions (AGA, 67.2%; AD, 68.9%; psoriasis, 46.6%). In AGA, topical applicants (50.2%) were most often used, followed by dietary therapy and health supplements. In AD, bath therapy (39.4%) was most often used, followed by oriental medicine and topical applicants. In psoriasis, oriental medicine (33.9%) was most frequently used, followed by bath therapy and health supplements. The proportion of patients who believed that CAM helped to improve their skin condition was relatively low (AGA, 16.1%; AD, 31.7%; psoriasis, 15.0%). LIMITATIONS: The results may not be applicable to other countries and generalized to general populations. CONCLUSION: These results indicate that CAM is widely used in Korean patients with chronic dermatological diseases despite their dissatisfactions. Thus, the advantages and disadvantages of CAM must be considered before its clinical practice.

Induction of striatal neurogenesis enhances functional recovery in an adult animal model of neonatal hypoxic-ischemic brain injury.

While intraventricular administration of epidermal growth factor (EGF) expands the proliferation of neural stem/progenitor cells in the subventricular zone (SVZ), overexpression of brain-derived neurotrophic factor (BDNF) is particularly effective in enhancing striatal neurogenesis. We assessed the induction of striatal neurogenesis and consequent functional recovery after chronic infusion of BDNF and EGF in an adult animal model of neonatal hypoxic-ischemic (HI) brain injury. Permanent brain damage was induced in CD-1 (ICR) mice (P7) by applying the ligation of unilateral carotid artery and hypoxic condition. At 6 weeks of age, the mice were randomly assigned to groups receiving a continuous 2-week infusion of one of the following treatments into the ventricle: BDNF, EGF, BDNF/EGF, or phosphate buffered saline (PBS). Two weeks after treatment, immunohistochemical analysis revealed an increase in the number of BrdU(+) cells in the SVZ and striata of BDNF/EGF-treated mice. The number of new neurons co-stained with BrdU and betaIII-tubulin was also significantly increased in the neostriata of BDNF/EGF-treated mice, compared with PBS group. In addition, the newly generated cells were expressed as migrating neuroblasts labeled with PSA-NCAM or doublecortin in the SVZ and the ventricular side of neostriata. The new striatal neurons were also differentiated as mature neurons co-labeled with BrdU(+)/NeuN(+). When evaluated post-surgical 8 weeks, BDNF/EGF-treated mice exhibited significantly longer rotarod latencies at constant speed (48 rpm) and under accelerating condition (4-80 rpm), relative to PBS and untreated controls. In the forelimb-use asymmetry test, BDNF/EGF-treated mice showed significant improvement in the use of the contralateral forelimb. In contrast, this BDNF/EGF-associated functional recovery was abolished in mice receiving a co-infusion of 2% cytosine-b-d-arabinofuranoside (Ara-C), a mitotic inhibitor. Induction of striatal neurogenesis by the intraventricular administration of BDNF and EGF promoted functional recovery in an adult animal model of neonatal HI brain injury. The effect of Ara-C to completely block functional recovery indicates that the effect may be the result of newly generated neurons. Therefore, this treatment may offer a promising strategy for the restoration of motor function for adults with cerebral palsy (CP).

Dopaminergic influences on the P300 abnormality in Parkinson's disease.

This study was designed to evaluate the contribution of central dopaminergic mechanisms to the P300 event-related potential (P300) abnormality in Parkinson's disease. We measured the P300 in 37 non-demented patients with Parkinson's disease (19 de novo and 18 levodopa-treated) and 15 age-matched healthy volunteers. The P300 measurement was repeated in 14 de novo patients, after 6-12 months levodopa therapy. The severity of parkinsonian symptom was assessed using the UPDRS-motor scale. De novo patients showed prolonged P300 latency compared with levodopa-treated patients, as well as healthy volunteers. The levodopa therapy for 6-12 months significantly shortened the P300 latency and reduced the UPDRS-motor examination score in de novo patients. However, the percent changes in the P300 latency were not correlated with those in the UPDRS-motor examination score. These results indicate that the central dopaminergic mechanisms apart from those responsible for motor symptoms, may contribute to the P300 abnormality in Parkinson's disease.