Abstract: It was revealed that the intravenous administration of HMGB-1 and S100A8 promoted the healing of skin ulcer by recruiting bone marrow-derived cells to the site of skin ulcer. Furthermore, when HMGB-1 was intravenously administered to cerebral infarction model mice after creation of cerebral infarction, bone marrow-derived cells expressing nerve cell markers were detected in their brain. A marked cerebral infarct-reducing effect was observed in mice intravenously administered with HMGB-1 as compared to the control. The post-cerebral infarction survival rate was increased in the intravenous HMGB-1 administration group. The involvement of bone marrow pluripotent stem cells in the process of bone fracture healing was assessed using mice, and the result demonstrated that bone marrow-derived cells distant from the damaged site migrated to the bone fracture site to repair the damaged tissue.

Abstract: It was revealed that the intravenous administration of HMGB-1 and S100A8 promoted the healing of skin ulcer by recruiting bone marrow-derived cells to the site of skin ulcer. Furthermore, when HMGB-1 was intravenously administered to cerebral infarction model mice after creation of cerebral infarction, bone marrow-derived cells expressing nerve cell markers were detected in their brain. A marked cerebral infarct-reducing effect was observed in mice intravenously administered with HMGB-1 as compared to the control. The post-cerebral infarction survival rate was increased in the intravenous HMGB-1 administration group. The involvement of bone marrow pluripotent stem cells in the process of bone fracture healing was assessed using mice, and the result demonstrated that bone marrow-derived cells distant from the damaged site migrated to the bone fracture site to repair the damaged tissue.

Abstract: It was revealed that the intravenous administration of HMGB-1 and S100A8 promoted the healing of skin ulcer by recruiting bone marrow-derived cells to the site of skin ulcer. Furthermore, when HMGB-1 was intravenously administered to cerebral infarction model mice after creation of cerebral infarction, bone marrow-derived cells expressing nerve cell markers were detected in their brain. A marked cerebral infarct-reducing effect was observed in mice intravenously administered with HMGB-1 as compared to the control. The post-cerebral infarction survival rate was increased in the intravenous HMGB-1 administration group. The involvement of bone marrow pluripotent stem cells in the process of bone fracture healing was assessed using mice, and the result demonstrated that bone marrow-derived cells distant from the damaged site migrated to the bone fracture site to repair the damaged tissue.

Abstract: The present invention provides a modified paramyxovirus containing a reduced amount of receptor-binding protein compared with the wild type; a method of preparing a modified paramyxovirus, comprising the following steps: (1) a step for introducing a nucleic acid that suppresses the expression of a receptor-binding protein of a paramyxovirus into an animal cell, (2) a step for infecting the paramyxovirus to the cell, and (3) a step for isolating paramyxovirus particles replicated in the cell; and a modified paramyxovirus prepared by the method of preparation mentioned above.

Abstract: The present invention provides a modified paramyxovirus containing a reduced amount of receptor-binding protein compared with the wild type; a method of preparing a modified paramyxovirus, comprising the following steps: (1) a step for introducing a nucleic acid that suppresses the expression of a receptor-binding protein of a paramyxovirus into an animal cell, (2) a step for infecting the paramyxovirus to the cell, and (3) a step for isolating paramyxovirus particles replicated in the cell; and a modified paramyxovirus prepared by the method of preparation mentioned above.

Abstract: The present invention provides a modified paramyxovirus containing a reduced amount of receptor-binding protein compared with the wild type; a method of preparing a modified paramyxovirus, comprising the following steps: (1) a step for introducing a nucleic acid that suppresses the expression of a receptor-binding protein of a paramyxovirus into an animal cell, (2) a step for infecting the paramyxovirus to the cell, and (3) a step for isolating paramyxovirus particles replicated in the cell; and a modified paramyxovirus prepared by the method of preparation mentioned above.