Group comprehensive behavioral intervention for tics contribution to broader cognitive and emotion regulation in children.

There is increasing evidence for the effectiveness of behavioral techniques in managing tics in youth with Tourette syndrome and tics disorders (TDs). One such intervention is Comprehensive Behavioral Intervention for Tics (CBIT), which focuses on reducing tic severity by training control and regulation. In view of the regulation deficits characteristic to TDs, in the current study, we aimed to explore the contribution of CBIT beyond tic control, to a wider expression of regulation abilities-cognitive inhibition and emotion regulation.

The phenotype of homozygous EMC10 variant: A new syndrome with intellectual disability and language impairment.

Aim: To explore the cognitive and behavioral phenotype associated with a recently reported variant in endoplasmic reticulum membrane complex EMC10 c.287delG (Gly96Alafs∗9), suggested to cause a novel syndromic neurodevelopmental disorder.

Methods: Homozygous EMC10 variant identified by a combination of autozygosity mapping and exome sequencing was found in five children (aged 7-18) from a large extended family.

Group behavioral interventions for tics and comorbid symptoms in children with chronic tic disorders.

Exposure and Response Prevention (ERP), Habit Reversal Training (HRT) and Comprehensive Behavioral Intervention for Tics (CBIT) are effective in reducing tic severity. ERP and HRT have recently gained primary support in a group setting, while CBIT has not been examined similarly. We compared the efficacy of group-CBIT to group-Educational Intervention for Tics (group-EIT) for tics and comorbid symptoms.

Weak mitochondrial targeting sequence determines tissue-specific subcellular localization of glutamine synthetase in liver and brain cells.

Evolution of the uricotelic system for ammonia detoxification required a mechanism for tissue-specific subcellular localization of glutamine synthetase (GS). In uricotelic vertebrates, GS is mitochondrial in liver cells and cytoplasmic in brain. Because these species contain a single copy of the GS gene, it is not clear how tissue-specific subcellular localization is achieved.