Abstract: An electronic device is provided. The electronic device includes dynamic random access memory (DRAM), memory, and one or more processors communicatively coupled to the DRAM and the memory, wherein the memory store one or more computer programs including computer-executable instructions that, when executed by the one or more processors, cause the electronic device to generate a first eye diagram based on training the DRAM with a driving voltage, identify a first parameter in a designated format corresponding to the generated first eye diagram, generate a second eye diagram based on training the DRAM with the driving voltage, compare the identified first parameter with a second parameter in the designated format corresponding to the generated second eye diagram, and adjust the driving voltage based on a result of the comparison between the first parameter and the second parameter.

Abstract: The present disclosure relates to controlling an application in a mobile terminal. The present disclosure includes an application control method and apparatus for a mobile terminal, earphone device, and application control system. The method for application control in a mobile terminal may include detecting connection of earphones having a sensor for sensing earphone wearing, sending, upon detection of earphone connection, an interrogation signal to the sensor of the earphones, receiving a response signal, corresponding to the interrogation signal, from the earphones, determining whether the earphones are worn by a user on the basis of the response signal, and controlling, when the earphones are not worn, an application being executed to stop output of an audio signal to the earphones.

Abstract: The present disclosure relates to an ASD genetically engineered model carrying a deletion of Shank2 gene and having reduced NMDA receptor function. According to the present disclosure, genetically engineered mice that show the clinical features of ASD due to the deletion of the Shank2 gene can be obtained, and the genetically engineered mice can be effectively used to screen candidate therapeutic agents.

Abstract: Provided is a method for predicting the risk of attention deficit hyperactivity disorder (ADHD). The method comprises: 1) isolating a nucleic acid species from a biological species derived from a subject; 2) identifying the nucleotide of rs550818 single nucleotide polymorphism (SNP) in the GIT1 gene, which is the 24926101st nucleotide residue on human chromosome 17, from the nucleic acid isolated from stage 1); and 3) determining the risk of ADHD to be high when the genotype of rs550818 SNP that is identified in stage 2) carries T nucleotide; wherein the composition comprising a primer pair for amplifying a rs550818 single nucleotide polymorphism (SNP), wherein the primer pair comprises a primer having a sequence of SEQ ID NO:18 and a primer having a sequence of SEQ ID NO: 45.

Abstract: The present disclosure relates to controlling an application in a mobile terminal. The present disclosure includes an application control method and apparatus for a mobile terminal, earphone device, and application control system. The method for application control in a mobile terminal may include detecting connection of earphones having a sensor for sensing earphone wearing, sending, upon detection of earphone connection, an interrogation signal to the sensor of the earphones, receiving a response signal, corresponding to the interrogation signal, from the earphones, determining whether the earphones are worn by a user on the basis of the response signal, and controlling, when the earphones are not worn, an application being executed to stop output of an audio signal to the earphones.

Abstract: The present disclosure relates to an ASD genetically engineered model carrying a deletion of Shank2 gene and having reduced NMDA receptor function. According to the present disclosure, genetically engineered mice that show the clinical features of ASD due to the deletion of the Shank2 gene can be obtained, and the genetically engineered mice can be effectively used to screen candidate therapeutic agents.

Abstract: Provided is a method of using any mammal except humans, in particular, a mammal as an attention deficit hyperactivity disorder model, wherein genes of G protein-coupled receptor kinase interacting protein 1 (GIT1) as a neuronal synapse protein in the brain are knocked out from the mammal. In addition, disclosed is analysis of GIT1 knock-out mice in aspects of molecular biology, cellular biology, electrical biology and animal behavior and, more particularly, a screening method of novel drug, wherein excessive behavior as an attention deficit hyperactive disorder as well as recovery of theta wave in the frontal lobe are observed by administering a candidate material of the drug, thereby inducing recovery of the attention deficit hyperactivity disorder.

Abstract: The following disclosure relates to a technology of genotyping a particular single nucleotide polymorphism (SNP) having significant association with attention deficit hyperactivity disorder (ADHD) and using the SNP genotypes for predicting the risk of ADHD. The present invention relates to providing a method of predicting ADHD risk by identifying the nucleotide of rs5508181 SNP in GIT1, which is C or T at the 24926101st residue on human chromosome 17, and a linkage disequilibrium block harboring rs5508181. Further, the present invention relates to a composition for diagnosing ADHD risk, including a probe for detecting the SNP or a primer for amplifying the chromosomal region, and a diagnosing kit having the probe immobilized on a surface thereof. Therefore, the method, the composition and the kit for diagnosing ADHD risk according to the following disclosure are useful technologies that can conveniently classify risk groups for ADHD at high sensitivity.

Abstract: Provided is a method of using any mammal except humans, in particular, a mammal as an attention deficit hyperactivity disorder model, wherein genes of G protein-coupled receptor kinase interacting protein 1 (GIT1) as a neuronal synapse protein in the brain are knocked out from the mammal. In addition, disclosed is analysis of GIT1 knock-out mice in aspects of molecular biology, cellular biology, electrical biology and animal behavior and, more particularly, a screening method of novel drug, wherein excessive behavior as an attention deficit hyperactive disorder as well as recovery of theta wave in the frontal lobe are observed by administering a candidate material of the drug, thereby inducing recovery of the attention deficit hyperactivity disorder.