1. We studied the effects of extremely low frequency (ELF, 60 Hz) magnetic fields (MFs) on pain thresholds using the hot plate test. The implication of opioid and benzodiazepine system in the MFs-induced alteration of pain thresholds was also studied. 2. There was an increase at night time and a decrease at daytime of pain thresholds in normal mice. Exposure of MFs (24 h, 20 gauss (G)) inhibited the increase of pain thresholds at night time and even produced hyperalgesia at daytime. 3. The increase of pain thresholds induced by melatonin at daytime was inhibited by exposure to MFs (24 h, 20 G) or opioid antagonist naloxone. The MFs and naloxone synergically inhibited hypoalgesia produced by melatonin. The hyperalgesia at daytime after MFs exposure was potentiated by the benzodiazepine agonist, diazepam, and inhibited by the benzodiazepine antagonist, flumazenil. There was no significant difference in all rotarod performance we tested. 4. From these results, it is suggested that exposure to MFs inhibits the increase of pain thresholds at night time and produces hyperalgesia at daytime with the involvement of opioid and benzodiazepine systems.

Many reports demonstrate that extremely low frequency magnetic fields (ELF MFs, 60 Hz) may be involved in hyperalgesia. In a previous investigation, we suggested that MFs may produce hyperalgesia and such a response may be regulated by the benzodiazepine system. In order to further confirm this effect of MFs, we used diazepam and/or flumazenil with MFs exposure. When testing the pain threshold of rats using hot plate tests, MFs or diazepam (0.5 microg, i.c.v.; a benzodiazepine receptor agonist) induced hyperalgesic effects with the reduction of latency. These effects were blocked by a pretreatment of flumazenil (1.5 mg/kg, i.p.; a benzodiazepine receptor antagonist). When the rats were exposed simultaneously to MFs and diazepam, the latency tended to decrease without statistical significance. The induction of hyperalgesia by co-exposure to MFs and diazepam was also blocked by flumazenil. However, the pretreatment of GABA receptor antagonists such as bicuculline (0.1 microg, i.c.v.; a GABA(A) antagonist) or phaclofen (10 microg, i.c.v.; a GABA(B) antagonist) did not antagonize the hyperalgesic effect of MFs. These results suggest that the benzodiazepine system may be involved in MFs-induced hyperalgesia.

The effect of extremely low frequency (ELF, 60 Hz) magnetic fields (MFs) on convulsions was investigated in rats. We determined the onset and duration of convulsions induced by bicuculline alone or by co-exposure to MFs and bicuculline. In addition, we measured the GABA concentrations in the rat brains using HPLC-ECD. MFs strengthened the convulsion induced by bicuculline (0.3, 1, and 3 microg, i.c.v.), with a shortening of the onset time, but lengthening of the duration time. Co-exposure to MFs and bicuculline decreased the GABA levels in the cortex, hippocampus and hypothalamus, whereas MFs alone reduced the level of GABA only in the hippocampus. These results suggest that the exposure to MFs may modulate bicuculline-induced convulsions due to GABA neurotransmissions in rat brains.

left palate occurs because of failure of the palatal shelves to fuse. It is the most common congenital craniofacial deformity. 1 The management of cleft palate aims to address several issues, including oral feeding, speech, airway, and facial growth, and most importantly, achieving normal speech. Velopharyngeal insufficiency can occur as a result of inadequate velum closure against the pharyngeal walls, resulting in hypernasality and nasal air emission. 2 In most Background: Although some cleft palates show asymmetric palatal shelf length and/or width intraoperatively, the relationship between palate asymmetry and speech outcomes has not been fully investigated. Methods: This study retrospectively reviewed 234 patients who underwent double-opposing Z-plasty (DOZ) for isolated cleft palate (Veau class I and II). Speech outcomes were analyzed to evaluate the association with width and length discrepancy of the palatal shelves using multiple logistic regression adjusting for patient age. Results:The mean age at repair was 14.2 ± 5.26 months. The mean palatal shelf width and length differences were 0.87 ± 0.97 mm and 1.63 ± 1.61 mm, respectively. The mean age at initial and follow-up assessment was 37.6 ± 5.70 months (n = 234) and 66.2 ± 8.81 months (n = 120), respectively. Multivariate logistic regression analysis of initial speech outcomes showed odds ratios in width discrepancy of 1.67 (P = 0.0703), 1.59 (P = 0.0104), and 2.01 (P = 0.0051) for nasal emission, hypernasality, and compensatory articulation, respectively. Additional analysis including follow-up outcomes also revealed that width discrepancy of the palatal shelves had higher odds ratios for nasal emission, hypernasality, and compensatory articulation (OR, 1.49, P = 0.0406; OR, 1.36; P = 0.0660; and OR, 1.65; P = 0.0170, respectively). There was no association between length discrepancy and all speech abnormalities. Conclusions: Greater discrepancies in palatal shelf width, rather than in length, were associated with poorer speech outcomes after DOZ. The authors suggest that DOZ is effective for longitudinally asymmetric cleft palates. (Plast.

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