To investigate possible health effects of mobile phone use, we conducted a double-blind, cross-over provocation study to confirm whether subjects with mobile phone related symptoms (MPRS) are more susceptible than control subjects to the effect of electromagnetic fields (EMF) emitted from base stations. We sent questionnaires to 5,000 women and obtained 2,472 valid responses from possible candidates; from these, we recruited 11 subjects with MPRS and 43 controls. There were four EMF exposure conditions, each of which lasted 30 min: continuous, intermittent, and sham exposure with and without noise. Subjects were exposed to EMF of 2.14 GHz, 10 V/m (W-CDMA), in a shielded room to simulate whole-body exposure to EMF from base stations, although the exposure strength we used was higher than that commonly received from base stations. We measured several psychological and cognitive parameters pre- and post-exposure, and monitored autonomic functions. Subjects were asked to report on their perception of EMF and level of discomfort during the experiment. The MPRS group did not differ from the controls in their ability to detect exposure to EMF; nevertheless they consistently experienced more discomfort, regardless of whether or not they were actually exposed to EMF, and despite the lack of significant changes in their autonomic functions. Thus, the two groups did not differ in their responses to real or sham EMF exposure according to any psychological, cognitive or autonomic assessment. In conclusion, we found no evidence of any causal link between hypersensitivity symptoms and exposure to EMF from base stations.

Using near infrared spectroscopy and repetitive transcranial magnetic stimulation (rTMS), we studied interhemispheric interactions between bilateral motor and sensory cortices in humans. RTMS consisted of a triple-pulse burst (50 Hz) repeated every 200 m for 2 s (10 bursts, 30 pulses); one kind of theta burst TMS (TBS) (Huang et al. in Neuron 45:201-206, 2005). The hemoglobin concentration changes were recorded at the right prefrontal cortex, premotor area (PM), primary hand motor area (M1) and primary sensory area (S1) during and after TBS over the left PM, M1 and S1 or sham stimulation in eight normal volunteers. In addition, motor evoked potentials (MEPs) to TMS over the right M1 were recorded from the left first dorsal interosseous muscle after the conditioning TBS over left S1. TBS over PM induced a significant oxy-Hb decrease at the contralateral PM. TBS over M1 elicited a significant oxy-Hb decrease at the contralateral S1, and TBS over S1 significant oxy-Hb decreases at the contralateral M1 and S1. MEPs to TMS of the right M1 were significantly suppressed by the conditioning TBS over the left S1. These results suggest that there are mainly inhibitory interactions between bilateral PMs and bilateral sensorimotor cortices in humans. Those are partly compatible with the previous findings. In addition to between the primary motor cortices, bilateral connection is requisite for smooth bimanual coordination between the sensory cortices or premotor cortices.

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RAD51 is the only identified autosomal dominant gene to date causative of Fanconi anemia (FA) due to dominant negative effects. Only two patients with RAD51-associated FA have been reported with atypical FA phenotypes without bone marrow failure. We describe a new Asian patient with a novel RAD51 mutation, presenting with multiple congenital anomalies and atypical FA with chromosomal instability. The patient was a 9-year-old Japanese girl. She had strabismus, myopia, submucous cleft palate, bilateral hearing impairment, and scoliosis. She also had growth retardation, developmental delay, and severe intellectual disability. We performed trio whole exome sequencing and Sanger sequencing and identified a de novo RAD51 mutation (c.725A>G, p.Gln242Arg). Isolated lymphocytes from the patient were hypersensitive to chromosomal breakage induced by the DNA cross-linking agent, mitomycin C. Our detailed phenotypic analysis of the RAD51-associated atypical FA revealed clinical manifestations from the diverse population and a consistent FA phenotype characterized by chromosome instability, intellectual disability, radial ray abnormality, and microcephaly, but not bone marrow failure. K E Y W O R D S autosomal dominant, chromosomal instability, Fanconi anemia, intellectual disability, RAD51, radial abnormality

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Disruption of intracortical inhibitory circuits in the motor cortex may, at least in part, be related to severe limb clumsiness in the patients with progressive limb-kinetic apraxia.

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