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The ability to understand the way other people see the world differs from one's own viewpoint is referred to as ''visual perspective-taking'' (VPT). Previous studies have demonstrated the behavioral performance in level 2 VPT (VPT2), the ability to understand that two different observers can have unique visual experiences of the same scene or object depending on the observers' physical location, changes during childhood. However, the developmental aspects underlying the neural mechanisms of VPT2 remains unknown. We measured the hemodynamic responses to a VPT2 task using functional near-infrared spectroscopy, with mental rotation (MR) as a control task in 7- to 11-year-old and 11- to 16-year-old groups. In the VPT2 task, participants were required to mentally compute the perspective of a toy on the turntable from that of a doll placed in a different location from the observer. For the MR task, participants reported their perspectives after the toy was rotated. We found significantly higher oxy-hemoglobin changes during the VPT2 task than the MR task in the 7- to 11-year-old group but not in the 11- to 16-year-old group, in the right middle and superior temporal, angular gyrus and frontal regions. These findings highlight the important role of the right temporoparietal region in processing perspective, up to 11 years.

BACKGROUND The incidence of cerebral palsy (CP) is influenced by perinatal medicine and regional medical systems. We investigated the recent incidence of CP and the current problems of children with CP in living at home under an advanced perinatal medical system in Tochigi Prefecture, Japan. METHODS A clinical datasheet survey was performed among 13 hospitals and six rehabilitation facilities treating children with CP born in Tochigi Prefecture to estimate the incidence of CP among children born between 2009 and 2013. The severity of motor and intellectual impairment, presumed causal factors, complications, and provided medical interventions were investigated and compared between preterm and term-born children with CP. RESULTS The incidence of CP was 1.6 per 1000 live births. Shorter gestation period and lower birthweight were associated with a higher incidence of CP. Fifty-one percent of children with CP were non-ambulatory and 55% had severe to profound intellectual impairment. Episodes of neonatal asphyxia and periventricular leukomalacia were the most frequent causal factors; both were significantly more frequent in preterm than in term-born children. Approximately 30% of children with CP had respiratory disorders, dysphagia, or epilepsy; 62% received medical interventions, including medication, mechanical ventilation, oxygen therapy, tube feeding, and intraoral/intranasal suction. CONCLUSION We found the incidence of CP to be lower in comparison to previous Japanese studies. However, the motor and intellectual impairments were severe, and many children with CP and their families were burdened by daily medical care. Public support systems should be developed, as well as the perinatal medical system.

Autism spectrum disorders (ASD) are associated with face perception atypicalities, and atypical experience with faces has been proposed as an underlying explanation. Studying the own-race advantage (ORA) for face recognition can reveal the effect of experience on face perception in ASD, although the small number of studies in the area present mixed findings. This study probed the ORA in ASD by comparing two cultural groups simultaneously for the first time. Children with ASD in the UK (N = 16) and Japan (N = 26) were compared with age- and ability-matched typically developing (TD) children in the UK (N = 16) and Japan (N = 26). Participants completed a two-alternative forced-choice task, whereby they had to recognize a just seen face from a foil which was manipulated in one of four ways (IC: identity change; EE: easy eyes; HE: hard eyes; HM: hard mouth). Face stimuli were Asian and Caucasian, and thus the same stimuli were own and other race depending on the cultural group. The ASD groups in the UK and Japan did not show impaired face recognition abilities, or impairments with recognizing faces depending on manipulations to the eye region, and importantly they showed an ORA. There was considerable heterogeneity in the presence of the ORA in ASD and TD and also across cultures. Children in Japan had higher accuracy than children in the UK, and TD children in Japan did not show an ORA. This cross-cultural study challenges the view that atypical experiences with faces lead to a reduced/absent ORA in ASD.

Objective: We aimed to clarify the validity of fNIRS measurement for assessing the methylphenidate (MPH) induced neuropharmacological effect in medication-naive children with attention deficit hyperactivity disorder (ADHD) with or without comorbid autism spectrum disorder (ASD), thereby providing the first evidence for differing neurofunctional pathology between the two groups. Methods: We monitored the effects of a single acute clinical dose of MPH on the cortical hemodynamics of 32 medication-naive ADHD children (ADHD with ASD n=11 and ADHD without ASD n=21) performing a go/no-go task before and 1.5 h after MPH or placebo administration, using a randomized, double-blind, placebo-controlled, crossover design. In addition, all subjects’ symptoms were monitored using the Japanese version of the ADHD Rating Scale-IV (ADHDRS- IV-J) before and one month after MPH administration. Results: Medication-naive ADHD children without ASD exhibited reduced right prefrontal activation. MPH medication elicited significant right prefrontal activation except in comparative conditions associated with the placebo effect. Medication-naive ADHD children with ASD exhibited marginal activation before the first day of medication and reduced activation after MPH medication in the right prefrontal area. While the neuropharmacological effects of MPH were different, ADHD-RS-IV-J scores were significantly improved one month after MPH administration in ADHD groups both with and without ASD. Conclusion: Taken together, these results suggest that ADHD with ASD is characterized by a different underlying neurofunctional pathology for inhibition control than that without ASD. To our knowledge, this is the first comparative neuroimaging study between ADHD patients with and without comorbid ASD.

Autism spectrum disorder (ASD) is characterized by impairment in social communication and the presence of restricted and repetitive behaviors and interests. Executive function impairment is reportedly partially responsible for these symptoms. Executive function includes planning, flexibility, and inhibitory control. Although planning and flexibility in ASD have been consistently reported as atypical, the atypicality of inhibitory control remains controversial. As most previous studies have used nonsocial stimuli to investigate inhibitory control in ASD, the effects of socially relevant information on the inhibitory control system in individuals with ASD remain unclear. Therefore, we developed a go/no-go task with gaze stimuli and measured hemodynamic responses in the right prefrontal cortex (PFC), involved in inhibitory processing in both typically developing (TD) children and children with ASD, using functional near-infrared spectroscopy. Direct gaze induced commission errors to similar extents in both groups. Contrary to the behavioral responses, neural activation in the right PFC was modulated by gaze direction only in the TD group. These findings suggest that the gaze-processing mechanisms in the prefrontal region may be affected by atypical gaze processing in other brain regions during an inhibitory control task with socially relevant information in ASD.

The purpose of the present study was to examine the effect of longitudinal habilitation intervention by care staff upon fixation duration in an individual with Rett syndrome using an eye-tracking system. The participant was a 22- year-old woman suffering from Rett syndrome. She could watch television but could not communicate verbally or execute purposeful upper extremity movements. We evaluated whether she could change the pattern of an eye gaze target by learning with the intervention of care staff. Fixation duration to the experimental targets was significantly changed after intervention for 3 weeks compared with before intervention. We consider that this improvement occurred because the patient learned the experimental tasks. Our findings suggest that individuals with Rett syndrome can acquire various abilities using eye gaze. Eye-tracking was shown to be a feasible method for visualizing the learning abilities of individuals with Rett syndrome and judging the outcome of habilitation intervention.

The current study aimed to explore the neural substrate for atomoxetine effects on attentional control in school-aged children with attention deficit hyperactivity disorder (ADHD) using functional near-infrared spectroscopy (fNIRS), which can be applied to young children with ADHD more easily than conventional neuroimaging modalities. Using fNIRS, we monitored the oxy-hemoglobin signal changes of 15 ADHD children (6 to 14 years old) performing an oddball task before and 1.5 h after atomoxetine or placebo administration, in a randomized, double-blind, placebo-controlled, crossover design. Fifteen age-, gender-, and intelligence quotient-matched normal controls without atomoxetine administration were also monitored. In the control subjects, the oddball task recruited the right prefrontal and inferior parietal cortices. The right prefrontal and parietal activation was normalized after atomoxetine administration in ADHD children. This was in contrast to our previous study using a similar protocol showing methylphenidate-induced normalization of only the right prefrontal function. fNIRS allows the detection of differential neuropharmacological profiles of both substances in the attentional network: the neuropharmacological effects of atomoxetine to upregulate the noradrenergic system reflected in the right prefrontal and inferior parietal activations and those of methylphenidate to upregulate the dopamine system reflected in the prefrontal cortex activation.

We studied 17 girls with the complaint of premature breast development. Enlarged breast tissue was confirmed in 15 patients by sonography. Pelvic and breast sonography were also performed in these patients. The sizes of most uteri and ovaries were within the normal range. Nine of the 15 patients (60%) showed follicular cysts in the ovaries. These cysts were ovoid with diameters of up to 10 mm. No relationship was found between the thickness of breast tissue and the ovarian findings. Pelvic sonography was also performed in normally developing girls under 6 years of age. Four of 47 girls (4%) showed small follicular cysts in the ovaries. In summary a high percentage of patients with premature thelarche have relatively large follicular cysts, with normal sized ovaries and uteri. Breast sonography is useful to distinguish swollen subcutaneous tissue from breast development.

In a patient with mitochondrial myopathy, the defect of cytochrome c oxidase activity was restricted to some muscle fibers. To isolate cell lines with or without oxidase activity from a single muscle sample, primary cultured cells were transformed by replication origin-defective simian virus 40, and then cloned. The clones were examined by cytochemical staining for cytochrome c oxidase activity. Eight myogenic clones were completely devoid of activity, while the other myogenic and nonmyogenic clones were not. Deficiency of cytochrome c oxidase was stable in culture for at least a year after serial passaging. The amount of mitochondrial DNA in cytochrome c oxidase-deficient cells was the same as in control cells, and no deletion in the mitochondrial DNA was detected. Protein synthesis in mitochondria of the subunits of cytochrome c oxidase and subunit 6 of the ATP synthase complex was markedly decreased, whereas synthesis of the other subunits encoded by mitochondrial DNA was normal. These cloned cell lines provide an excellent system for clarifying the cause of mitochondrial myopathy and for investigating nuclear-mitochondrial genetic interaction.

Neuron-specific enolase (NSE) is an isoenzyme of the widely distributed glycolytic enzyme 2-phospho-D-glycerate hydrolase expressed by neuronal and neuronendocrine cells of the central and peripheral nervous system. Brain extract contains three forms (α, β, and γ) of enolase, and each form is a dimer of the combination of two distinct subunits α and γ. NSE consists of the two dimers containing subunits, that is, αγ and γγ, existing mainly in neuronal cells an dneuroendocrine cells. Immunohistochemistry and radioimmunoassay have shown NSE in serum from patients with various tumors including neuroblastoma (NB).3.4 In the current study we tried the immunohistochemical staining of the enzyme on the NB cells.