Df(h22q11)/+ mouse model exhibits reduced binding levels of GABA receptors and structural and functional dysregulation in the inhibitory and excitatory networks of hippocampus.

The 22q11.2 hemizygous deletion confers high risk for multiple neurodevelopmental disorders. Inhibitory signaling, largely regulated through GABA receptors, is suggested to serve a multitude of brain functions that are disrupted in the 22q11.

A Review on Planted (, d) Motif Discovery Algorithms for Medical Diagnose.

Personalized diagnosis of chronic disease requires capturing the continual pattern across the biological sequence. This repeating pattern in medical science is called "Motif". Motifs are the short, recurring patterns of biological sequences that are supposed signify some health disorder.

Secure and Efficient High Throughput Medium Access Control for Vehicular Ad-Hoc Network.

The evolution of the internet has led to the growth of smart application requirements on the go in the vehicular ad hoc network (VANET). VANET enables vehicles to communicate smartly among themselves wirelessly. Increasing usage of wireless technology induces many security vulnerabilities.

Channel Allocation for Connected Vehicles in Internet of Things Services.

Based on the existing Internet of Vehicles communication protocol and multi-channel allocation strategy, this paper studies the key issues with vehicle communication. First, the traffic volume is relatively large which depends on the environment (city, highway, and rural). When many vehicles need to communicate, the communication is prone to collision.

Early appearance of developmental alterations in the dendritic tree of the hippocampal granule cells in the Ts65Dn model of Down syndrome.

Down syndrome (DS), a genetic condition caused by triplication of chromosome 21, is characterized by alterations in various cognitive domains, including hippocampus-dependent memory functions, starting from early life stages. The major causes of intellectual disability in DS are prenatal neurogenesis alterations followed by impairment of dendritic development in early infancy. While there is evidence that the Ts65Dn mouse, the most widely used model of DS, exhibits dendritic alterations in adulthood, no studies are available regarding the onset of dendritic pathology.