Abstract: There is provided a method of decoding point cloud data, the method comprising: decoding a bitstream to obtain attribute information of point cloud data, acquiring attributes of the point cloud data using the decoded attribute information and reconstructing the point cloud data using the obtained attributes, wherein the attribute information contains bit depth information of each attribute of the point cloud data.

Abstract: Provided are an array antenna apparatus using spatial power spectrum combining and a method of controlling the same. The array antenna apparatus includes a uniform linear array antenna module including antennas which are uniformly and linearly arranged, an array antenna determiner configured to select sub-array antennas arranged at a first distance and sub-array antennas arranged at a second distance from the array antennas in the uniform linear array antenna module in order to derive spatial spectrum components from the uniform linear array antenna module, a spatial spectrum component deriver configured to separately derive spatial power spectrum components from signals received through the selected sub-array antennas selected by the array antenna determiner, and an azimuth calculator configured to calculate an azimuth by performing a calculation with a first spatial spectrum component and a second spatial spectrum component which are separately derived.

Abstract: The present invention relates to a pharmaceutical composition for an anticancer adjuvant comprising a receptor-interacting protein kinase-3 (RIP3) protein expression promotor or activator as an active ingredient. In addition, the present invention provides a method of promoting cancer cell apoptosis, characterized by co-administering an anticancer agent and a RIP3 protein expression promotor or activator to cancer cells. Also, the present invention relates to a method for screening an anticancer adjuvant which promotes RIP3 expression and enhances sensitivity of an anticancer agent, and a method for monitoring sensitivity of an anticancer agent depending on the RIP3 expression. Accordingly, in the case of a patient lacking the expression of RIP3, it is expected to be an effective treatment strategy to pre-treat a demethylating agent to induce the expression of RIP3 and then to use a conventional chemotherapeutic agent.

Abstract: The present disclosure relates to a novel anti-HER2 antibody or an antigen-binding fragment thereof used in the prevention or treatment of cancer, a chimeric antigen receptor including the same, and uses thereof. The antibody of the present disclosure is an antibody that specifically binds to HER2 which is highly expressed in cancer cells (particularly, breast cancer or gastric cancer cells), and binds to an epitope that is different from an epitope to which trastuzumab binds.

Abstract: The present invention relates to methods of preventing or treating skin necroptosis diseases, including administering to subjects receptor-interacting protein kinase-3 (RIP3)-mixed lineage kinase domain-like protein (MLKL) pathway blockers or dabrafenib, and method of diagnosing of skin necroptosis diseases, including detecting phosphorylated MLKL. The RIP3-MLKL pathway blockers according to the present invention directly suppress RIP3 overexpressing in skin necroptosis diseases, or inhibit phosphorylation and translocation to plasma membranes of MLKL, subsequently induced therefrom, thereby effectively preventing skin cell death via necroptosis. Thus, the present invention can prevent or treat a variety of skin diseases caused by necroptosis.

Abstract: There is provided a method of decoding point cloud data, the method comprising: decoding a bitstream to obtain attribute information of point cloud data, acquiring attributes of the point cloud data using the decoded attribute information and reconstructing the point cloud data using the obtained attributes, wherein the attribute information contains bit depth information of each attribute of the point cloud data.

Abstract: The present invention relates to a pharmaceutical composition for an anticancer adjuvant containing a receptor-interacting protein kinase-3 (RIP3) protein expression inducing agent or activator as an active ingredient. The present invention also provides a method for enhancing cancer cell death, comprising administering a RIP3 protein expression inducing agent or activator in combination with an anticancer drug to cancer cells. Additionally, the present invention relates to a method for screening an anticancer adjuvant which enhances anticancer drug sensitivity by promoting RIP3 expression; and a method for monitoring anticancer drug sensitivity based on RIP3 expression. Therefore, in the case of patients lacking RIP3 expression, the use of a conventional chemotherapeutic agent after inducing RIP3 expression by pretreatment with a demethylating agent may be an effective therapeutic strategy.

Abstract: The present invention relates to a pharmaceutical composition for an anticancer adjuvant comprising a receptor-interacting protein kinase-3 (RIP3) protein expression promotor or activator as an active ingredient. In addition, the present invention provides a method of promoting cancer cell apoptosis, characterized by co-administering an anticancer agent and a RIP3 protein expression promotor or activator to cancer cells. Also, the present invention relates to a method for screening an anticancer adjuvant which promotes RIP3 expression and enhances sensitivity of an anticancer agent, and a method for monitoring sensitivity of an anti-cancer agent depending on the RIP3 expression. Accordingly, in the case of a patient lacking the expression of RIP3, it is expected to be an effective treatment strategy to pre-treat a demethylating agent to induce the expression of RIP3 and then to use a conventional chemotherapeutic agent.

Abstract: The present invention relates to methods of preventing or treating skin necroptosis diseases, including administering to subjects receptor-interacting protein kinase-3 (RIP3)-mixed lineage kinase domain-like protein (MLKL) pathway blockers or dabrafenib, and method of diagnosing of skin necroptosis diseases, including detecting phosphorylated MLKL. The RIP3-MLKL pathway blockers according to the present invention directly suppress RIP3 overexpressing in skin necroptosis diseases, or inhibit phosphorylation and translocation to plasma membranes of MLKL, subsequently induced therefrom, thereby effectively preventing skin cell death via necroptosis. Thus, the present invention can prevent or treat a variety of skin diseases caused by necroptosis.

Abstract: The present invention relates to methods of preventing or treating skin necroptosis diseases, including administering to subjects receptor-interacting protein kinase-3 (RIP3)-mixed lineage kinase domain-like protein (MLKL) pathway blockers or dabrafenib, and method of diagnosing of skin necroptosis diseases, including detecting phosphorylated MLKL. The RIP3-MLKL pathway blockers according to the present invention directly suppress RIP3 overexpressing in skin necroptosis diseases, or inhibit phosphorylation and translocation to plasma membranes of MLKL, subsequently induced therefrom, thereby effectively preventing skin cell death via necroptosis. Thus, the present invention can prevent or treat a variety of skin diseases caused by necroptosis.

Abstract: The present invention relates to a pharmaceutical composition for an anticancer adjuvant containing a receptor-interacting protein kinase-3 (RIP3) protein expression inducing agent or activator as an active ingredient. The present invention also provides a method for enhancing cancer cell death, comprising administering a RIP3 protein expression inducing agent or activator in combination with an anticancer drug to cancer cells. Additionally, the present invention relates to a method for screening an anticancer adjuvant which enhances anticancer drug sensitivity by promoting RIP3 expression; and a method for monitoring anticancer drug sensitivity based on RIP3 expression. Therefore, in the case of patients lacking RIP3 expression, the use of a conventional chemotherapeutic agent after inducing RIP3 expression by pretreatment with a demethylating agent may be an effective therapeutic strategy.

Abstract: The present invention relates to methods of preventing or treating skin necroptosis diseases, including administering to subjects receptor-interacting protein kinase-3 (RIP3)-mixed lineage kinase domain-like protein (MLKL) pathway blockers or dabrafenib, and method of diagnosing of skin necroptosis diseases, including detecting phosphorylated MLKL. The RIP3-MLKL pathway blockers according to the present invention directly suppress RIP3 overexpressing in skin necroptosis diseases, or inhibit phosphorylation and translocation to plasma membranes of MLKL, subsequently induced therefrom, thereby effectively preventing skin cell death via necroptosis. Thus, the present invention can prevent or treat a variety of skin diseases caused by necroptosis.

Abstract: A method for setting synchronization between terminals performing device-to-device (D2D) communication based on a cellular communication system is disclosed. The method for setting synchronization between terminals includes receiving a message instructing synchronization setting with an opposite terminal from a base station, selecting a first preamble transmitted for a synchronization setting with the opposite terminal based on the message instructing synchronization setting, transmitting the selected first preamble to the opposite terminal, receiving a second preamble from the opposite terminal, and setting the synchronization with the opposite terminal using a reception timing of the second preamble when the second preamble is a preamble designated in the message instructing synchronization setting.

Abstract: A method of providing service continuity between cellular communication and device-to-device communication is disclosed. A procedure for switching between cellular communication and device-to-device communication according to an example embodiment of the present invention may include transferring, by a gateway, a D2D bearer creation request message to an MME, transferring, by the MME, the D2D bearer creation request message to a base station, mapping, by the base station, D2D bearer QoS to D2D radio bearer QoS and transmitting an RRC connection reconfiguration message to terminals, receiving, by the base station, an RRC connection reconfiguration completion message indicating creation of a D2D radio bearer from the terminals, transmitting, by the base station, a D2D bearer creation response message indicating creation of a D2D bearer to the MME, and transferring, by the MME, the D2D bearer creation response message to the gateway.

Abstract: The present application relates to a composition including gut flora-derived extracellular vesicles, and to an animal disease model using same. In addition, the present application relates to a method for using the gut flora-derived extracellular vesicles to efficiently search for a candidate drug which may prevent or treat diseases that occur due to gut flora-derived extracellular vesicles, and to a vaccine which can efficiently prevent or treat infections caused by gut flora or diseases that occur due to gut flora-derived extracellular vesicles. Further, the development of diagnostic technology to discover, using the gut flora-derived extracellular vesicles of the present application, the etiology of diseases that occur due to gut flora-derived extracellular vesicles, can be achieved.

Abstract: The present application relates to a composition including gut flora-derived extracellular vesicles, and to an animal disease model using same. In addition, the present application relates to a method for using the gut flora-derived extracellular vesicles to efficiently search for a candidate drug which may prevent or treat diseases that occur due to gut flora-derived extracellular vesicles, and to a vaccine which can efficiently prevent or treat infections caused by gut flora or diseases that occur due to gut flora-derived extracellular vesicles. Further, the development of diagnostic technology to discover, using the gut flora-derived extracellular vesicles of the present application, the etiology of diseases that occur due to gut flora-derived extracellular vesicles, can be achieved.

Abstract: A method for setting synchronization between terminals performing device-to-device (D2D) communication based on a cellular communication system is disclosed. The method for setting synchronization between terminals includes receiving a message instructing synchronization setting with an opposite terminal from a base station, selecting a first preamble transmitted for a synchronization setting with the opposite terminal based on the message instructing synchronization setting, transmitting the selected first preamble to the opposite terminal, receiving a second preamble from the opposite terminal, and setting the synchronization with the opposite terminal using a reception timing of the second preamble when the second preamble is a preamble designated in the message instructing synchronization setting.

Abstract: Provided is a composition and a kit for separating a cancer stem cell or a circulating tumor cell, a method of separating a cancer stem cell or a circulating tumor cell in a biological sample, and a method for diagnosing metastatic cancer.

Abstract: The present application relates to a composition including gut flora-derived extracellular vesicles, and to an animal disease model using same. In addition, the present application relates to a method for using the gut flora-derived extracellular vesicles to efficiently search for a candidate drug which may prevent or treat diseases that occur due to gut flora-derived extracellular vesicles, and to a vaccine which can efficiently prevent or treat infections caused by gut flora or diseases that occur due to gut flora-derived extracellular vesicles. Further, the development of diagnostic technology to discover, using the gut flora-derived extracellular vesicles of the present application, the etiology of diseases that occur due to gut flora-derived extracellular vesicles, can be achieved.

Abstract: Provided are a device-to-device (D2D) group communication method and a device using the same. The method includes transmitting a scheduling request for D2D group communication to a base station, receiving first radio resource information for a status report of D2D data to be transmitted from the base station, transmitting a D2D buffer status report to the base station through a first radio resource, receiving second radio resource information including D2D resource allocation information necessary for the D2D group communication from the base station, and transmitting control information for the D2D group communication including a D2D group identifier (ID) as a device ID and D2D user data to two or more communication partner devices belonging to the D2D group.