It was aimed to examine the orbital region in children with autism spectrum disorder and comparison with the healthy controls in the present study. A total of 195 children and adolescents (101 of them were in the autism group, 94 of them were in healthy group) were evaluated. Anterior view photographs were taken, and endocanthion (en), exocanthion (ex), and pupil were determined bilaterally on the photographs. Outer canthal (ex-ex), intercanthal (ex-en), inner canthal (en-en) and interpupillary distances were measured and intercanthal index [(en-en / ex-ex) Â 100] was calculated. There was a statistically significant difference between the groups for males for all parameters, while a statistically significant difference was not observed for females. All orbital region distances were higher in male autistic children. Although minor physical anomalies in children and adolescents with autism have been reported before, anthropometric measurements in individuals with autism may differ between genders. Further studies are needed to investigate the differences between genders in autism spectrum disorder.

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Objective: ADHD is associated with increased sleep problems and circadian rhythm disturbances. This study aimed to examine ADHD patients and healthy controls in terms of chronotypic features and expression levels of CLOCK, PER1, lncRNA HULC, lncRNA UCA1. Method: Eighty-three children were included (43 ADHD). Conner’s Parent Rating Scale-Revised Short Form, Childhood Chronotype Questionnaire, Children’s Sleep Disorders Scale were administered. Gene expression levels were studied from peripheral blood. Results: Evening chronotype, sleep initiation/maintenance disorder, sleep-wake transition disorder, excessive sleepiness disorder were higher in the ADHD group compared to the controls in the scales reported by the parents. Expression levels of all examined genes were statistically significantly higher in the ADHD group. There was no significant relationship between genes and sleep parameters in the ADHD group. Conclusion: Our study provides the first evidence that lncRNA HULC and lncRNA UCA1 might have a role in the etiology of ADHD.