PURPOSE: Congenital pseudarthrosis of the tibia, which is recalcitrant to treatments and prone to recur, is frequently associated with neurofibromatosis. The causative gene for neurofibromatosis, NF1, has been identified, but the pathomechanism of congenital pseudarthrosis has not been elucidated. The purposes of this study were to establish primary cell culture from the fibrous hamartoma tissue of pseudoarthrosis, and to compare the gene expression patterns of the fibrous hamartoma and normal bone. MATERIALS AND METHODS: Incubation of the enzymatically treated fibrous hamartoma tissue resulted in growth of the adherent fibroblast-like spindle cells. Expression of hundreds of genes including bone morphogenetic protein-2 and -4, and NF1 were screened by reverse transcription-polymerase chain reaction and cDNA array hydridization methods. RESULTS: Bone morphogenetic protein-2 and -4, and, NF1 were found to express in normal bone, normal periosteum as well as fibrous hamartoma and adjacent hypotrophic bone. Twenty-four genes were found to express exclusively in the fibrous hamartoma, and fifty genes only in the normal bone. CONCLUSION: These findings suggest that the causative gene of neurofibromatosis, NF1, may be associated with pathogenesis of the congenital pseudoarthrosis of the tibia in neurofibromatosis patients.
Gene Expression ; Hamartoma ; Humans ; Neurofibromatoses* ; Oligonucleotide Array Sequence Analysis ; Periosteum ; Primary Cell Culture ; Pseudarthrosis* ; Tibia*

Olfactory receptors are chemosensory receptors that detect odorants and function in the initial perception of a smell. Intriguingly, olfactory receptors are also expressed in cells other than olfaction sensory cells, an expression pattern termed ectopic expression. Ectopically expressed olfactory receptors have a distinct role depending on the type of tissues or cells in which they are expressed. This review introduces current research on the ectopic expression and function of olfactory receptors in skin and provides insight into directions for future research.

OBJECTIVE: To investigate the clinical feasibility of a newly developed, portable, gait assistive robot (WA-H, ‘walking assist for hemiplegia’) for improving the balance function of patients with stroke-induced hemiplegia. METHODS: Thirteen patients underwent 12 weeks of gait training on the treadmill while wearing WA-H for 30 minutes per day, 4 days a week. Patients' balance function was evaluated by the Berg Balance Scale (BBS), Fugl-Meyer Assessment Scale (FMAS), Timed Up and Go Test (TUGT), and Short Physical Performance Battery (SPPB) before and after 6 and 12 weeks of training. RESULTS: There were no serious complications or clinical difficulties during gait training with WA-H. In three categories of BBS, TUGT, and the balance scale of SPPB, there was a statistically significant improvement at the 6th week and 12th week of gait training with WA-H. In the subscale of balance function of FMAS, there was statistically significant improvement only at the 12th week. CONCLUSION: Gait training using WA-H demonstrated a beneficial effect on balance function in patients with hemiplegia without a safety issue.
Gait* ; Hemiplegia ; Humans ; Rehabilitation* ; Robotics ; Stroke

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.