Abstract: To program in a nonvolatile memory device including a cell region including first metal pads and a peripheral region including second metal pads and vertically connected to the cell region by the first metal pads and the second metal pads, a memory block is provided with a plurality of sub blocks disposed in a vertical direction where the memory block includes a plurality of cell strings each including a plurality of memory cells connected in series and disposed in the vertical direction. A plurality of intermediate switching transistors are disposed in a boundary portion between two adjacent sub blocks in the vertical direction. Each of the plurality of intermediate switching transistors is selectively activated based on a program address during a program operation. The selectively activating each of the plurality of intermediate switching transistors includes selectively turning on one or more intermediate switching transistors in a selected cell string based on the program address.

Abstract: A gene for biosynthesis of core structure of ophiobolin, the gene being the AuOS gene of Aspergillus sp. 094102, deposited with the accession number CCTCC No: M208153, the gene sequence thereof being shown as SEQ ID NO. 1. Also provided is a method of preparation of ophiobolin using the gene.

Abstract: A gene for biosynthesis of core structure of ophiobolin, the gene being the AuOS gene of Aspergillus sp. 094102, deposited with the accession number CCTCC No: M208153, the gene sequence thereof being shown as SEQ ID NO. 1. Also provided is a method of preparation of ophiobolin using the gene.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: The present invention relates to a printing through a plurality of printer robot systems. Specifically, the invention provides a mobile printer system which prints letters or pictures inputted by a user without being constrained by the printing region through a plurality of mobile printer robots. The present invention comprises a plurality of mobile printer robot systems which have in-built printer functions and a main body which controls the printer operations through a wireless communication with the printer robot system.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: The present invention relates to a printing through a plurality of printer robot systems. Specifically, the invention provides a mobile printer system which prints letters or pictures inputted by a user without being constrained by the printing region through a plurality of mobile printer robots. The present invention comprises a plurality of mobile printer robot systems which have in-built printer functions and a main body which controls the printer operations through a wireless communication with the printer robot system.