Japan’s economy lost most of its industrial production force as a result of World War II. However, from 1955 onwards, Japan has achieved rapid economic growth, joining the group of the world’s most developed countri...Japan’s economy lost most of its industrial production force as a result of World War II. However, from 1955 onwards, Japan has achieved rapid economic growth, joining the group of the world’s most developed countries by the early 1970s. The period from 1955 to the early 1970s is generally regarded as a period of High Economic Growth. There are various opinions regarding the factors that enabled Japan to attain such high economic growth, referred to as the Economic Miracle. It can be said that Japan’s post-war economic development was the result of advancements in technological innovation on the basis of financial assistance from the United States, which established Japan’s position in the world economy, loans from the bank, and the introduction of technology from abroad. Needless to say, the “high growth of post-war Japanese capitalism has not been achieved only by giant companies alone. On the contrary, without small businesses, especially in their roles as subcontractors, it would have been impossible to achieve such high growth, which has drawn attention internationally” （Nomura, 1981, p. 126）. The purpose of this presentation is to make clear the role of small businesses in the process of economic development.展开更多
Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that r...Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that results in the phosphorylation and activation of the c-Jun protein. Activation of JNK has been shown to be involved in development, proliferation, inflammation and apoptosis. Recent studies on inactivation of the JNK3 gene in mice leads to deficiency in the kainic acid-induced excitotoxicity, resulting in decreased apoptosis in the hippocampus of the JNK3 knockout mice. In the contrast, in context of nerve growth factor -induced differentiation of PC12 cell, JNK3 expression significantly increased the number and length neuritis. JNK3 has a mirrored function. Our report propose to test whether knockout JNK3 genes provide a protection action in spinal cord injuries of mice and the pathology morphology and mechanisms of the JNK3 knockout mice with spinal cord injures will be discussed. Methods Study used adult female C57B mice and JNK3 knockout mice each 20 (17∽21g) were anesthetized and subjected to laminectomy at (T10).Using 35KD force to impact to the expose cord and 0 KD for sham. After surgery 24 h, and 7 days animal were anesthetized, sacrificed. The spinal cords were picked it out.Make paraffin section. 8 micron each section slices. Section were stained with Luxol fast blue and nuclear fast red. Section were analyzed for per mouse. 4 X condenser microscope images of spinal cord were captured using a Sony digital CCD camera attached to a PPC 7100AV computer allowing lesion areas to be outlined with the use of a mouse. The extent of the lesion was demarcated. The total lesion volume was matter its damage area comparison in number or pathology comparison. The recovery behavior following the injury was poorer in the JNK3 knockout mice than in the wild type mice. (2) Using 35KD force for both groups the JNK3 knockout mice's damaged areas are absolutely bigger than that of the wild type C57B mice at 7 day after their surgery. No matter, damage area comparison in number or pathology comparison. Behaviors recovery from paralysis JNK3 knockout mice are worse than wild type mice. (3) The length of time following the injury, the damage area of the JNK3 and wild type mice at 7 day after injury were all larger than the damage area of both groups at 24 h after injury. Conclusion The knockout JNK3 gene does not decrease the damaged area in the knockout JNK3 mice with spinal cord injury, but it has a worse function. So that we propose an interesting hypothesis that JNK3 may play a role in maintenance of normal neuronal function.展开更多
文摘Japan’s economy lost most of its industrial production force as a result of World War II. However, from 1955 onwards, Japan has achieved rapid economic growth, joining the group of the world’s most developed countries by the early 1970s. The period from 1955 to the early 1970s is generally regarded as a period of High Economic Growth. There are various opinions regarding the factors that enabled Japan to attain such high economic growth, referred to as the Economic Miracle. It can be said that Japan’s post-war economic development was the result of advancements in technological innovation on the basis of financial assistance from the United States, which established Japan’s position in the world economy, loans from the bank, and the introduction of technology from abroad. Needless to say, the “high growth of post-war Japanese capitalism has not been achieved only by giant companies alone. On the contrary, without small businesses, especially in their roles as subcontractors, it would have been impossible to achieve such high growth, which has drawn attention internationally” （Nomura, 1981, p. 126）. The purpose of this presentation is to make clear the role of small businesses in the process of economic development.
文摘Backgroud The JNK3 gene belongs to the c-Jun NH2 -terminal kinases (JNKs) family that is a group of the mitogen - activated protein (MAP) kinases that are activated hy cytokines and other entra-cellular stimuli that results in the phosphorylation and activation of the c-Jun protein. Activation of JNK has been shown to be involved in development, proliferation, inflammation and apoptosis. Recent studies on inactivation of the JNK3 gene in mice leads to deficiency in the kainic acid-induced excitotoxicity, resulting in decreased apoptosis in the hippocampus of the JNK3 knockout mice. In the contrast, in context of nerve growth factor -induced differentiation of PC12 cell, JNK3 expression significantly increased the number and length neuritis. JNK3 has a mirrored function. Our report propose to test whether knockout JNK3 genes provide a protection action in spinal cord injuries of mice and the pathology morphology and mechanisms of the JNK3 knockout mice with spinal cord injures will be discussed. Methods Study used adult female C57B mice and JNK3 knockout mice each 20 (17∽21g) were anesthetized and subjected to laminectomy at (T10).Using 35KD force to impact to the expose cord and 0 KD for sham. After surgery 24 h, and 7 days animal were anesthetized, sacrificed. The spinal cords were picked it out.Make paraffin section. 8 micron each section slices. Section were stained with Luxol fast blue and nuclear fast red. Section were analyzed for per mouse. 4 X condenser microscope images of spinal cord were captured using a Sony digital CCD camera attached to a PPC 7100AV computer allowing lesion areas to be outlined with the use of a mouse. The extent of the lesion was demarcated. The total lesion volume was matter its damage area comparison in number or pathology comparison. The recovery behavior following the injury was poorer in the JNK3 knockout mice than in the wild type mice. (2) Using 35KD force for both groups the JNK3 knockout mice's damaged areas are absolutely bigger than that of the wild type C57B mice at 7 day after their surgery. No matter, damage area comparison in number or pathology comparison. Behaviors recovery from paralysis JNK3 knockout mice are worse than wild type mice. (3) The length of time following the injury, the damage area of the JNK3 and wild type mice at 7 day after injury were all larger than the damage area of both groups at 24 h after injury. Conclusion The knockout JNK3 gene does not decrease the damaged area in the knockout JNK3 mice with spinal cord injury, but it has a worse function. So that we propose an interesting hypothesis that JNK3 may play a role in maintenance of normal neuronal function.
