The digital child: A cross-sectional survey study on the access to electronic devices in paediatrics.

AIM: To explore the use of electronic devices in children and possible risk factors for smartphone ownership and cyberbullying. METHODS: A cross-sectional survey study was conducted involving 62 Italian general paediatricians who administered a close-ended questionnaire about the use of electronic devices to 1732 parents/caregivers. RESULTS: Data of 2563 children aged 0-14 years were collected. Investigating the electronic device use by parents/caregivers of children aged 0-1 years, 72.5% of mothers were revealed to have the habit to use a smartphone during breastfeeding and bottle-feeding. The ownership of a smartphone was found in 29.5% of children aged 2-14 years, 68.1% considering only children aged 10-14. A higher parental degree level was identified as a protective factor for smartphone ownership by children (OR 0.59; 95% CI 0.36-0.98; p = 0.04 for father; OR 0.51; 95% CI 0.33-0.78; p = 0.002 for mother). A higher risk of cyberbullying was found when caregivers did not use any restrictions on smartphone use (OR 11.92; 95% CI 3.41-41.68; p < 0.001). CONCLUSION: The absence of rules for smartphone use represents a risk factor for cyberbullying. In this context, the general paediatrician might play an important role in helping parents/caregivers and their children adopt safer use of electronic devices.

Genotype-phenotype relationship in three cases with overlapping 19p13.12 microdeletions.

We describe the detailed clinical and molecular characterization of three patients (aged 7, 8(4/12) and 31 years) with overlapping microdeletions in 19p13.12, extending to 19p13.13 in two cases. The patients share the following clinical features with a recently reported 10-year-old girl with a 19p13.12 microdeletion: mental retardation (MR), psychomotor and language delay, hearing impairment, brachycephaly, anteverted nares and ear malformations. All patients share a 359-kb deleted region in 19p13.12 harboring six genes (LPHN1, DDX39, CD97, PKN1, PTGER1 and GIPC1), several of which may be MR candidates because of their function and expression pattern. LPHN1 and PKN1 are the most appealing; LPHN1 for its interaction with Shank family proteins, and PKN1 because it is involved in a variety of functions in neurons, including cytoskeletal organization. Haploinsufficiency of GIPC1 may contribute to hearing impairment for its interaction with myosin VI. A behavioral phenotype was observed in all three patients; it was characterized by overactive disorder associated with MR and stereotyped movements (ICD10) in one patient and hyperactivity in the other two. As Ptger1-null mice show behavioral inhibition and impulsive aggression with defective social interaction, PTGER1 haploinsufficiency may be responsible for the behavioral traits observed in these patients.