1.Exploration on Evaluation System for Traditional Medicine Patent
Cong ZHANG ; Junmei QING ; Yanhuai LIU ; Yanbo LI
World Science and Technology-Modernization of Traditional Chinese Medicine 2014;(7):1470-1475
So far, an evaluation system for the patent value of traditional medicine is in absence. For this reason, an evaluation system had been established in this paper, by taking advantage of unique attributes of traditional medicine. This system consisted of 10 key indexes equipped with the algorithm for the calculation of original value and comparative value. The comparative value of patent was easier to show the value difference among patents. In consideration of strong correlation between the legal value, technical value, and economic value of the patent and be-tween evaluation indexes thereof, three kinds of value were combined together without discrimination for integral e-valuation. Besides, with inclusion of specific indexes in this field, the non-specific indexes related or indexes un-available were excluded. Because there is no personal rating involved, this evaluation system is appropriate for the automatic evaluation of patents of traditional medicine and other fields .
2.Study on the event-related potentials P300 of schizophrenic patients with aggressive or violent behaviors
Xiaoming ZHANG ; Fang DU ; Liju QIAN ; Qing YU ; Jianjun WANG ; Peng YANG ; Gongying LI ; Zhong ZHENG ; Junmei HU
Chinese Journal of Behavioral Medicine and Brain Science 2012;21(5):427-429
ObjectiveTo explore the electrophysiological mechanisms of the schizophrenic patients with aggressive or violent behaviors.MethodsAccess the aggressive behaviors of schizophrenic patients being treated in hospitals or clinics with the revised MOAS in accordance with the ICD-10 diagnostic criteria,and sort the qualified patients into two groups:the group of aggressive or violent schizophrenia (Aggressive Group,n=70) and the group of non-aggressive or non-violent schizophrenia ( Non-Aggressive Group,n =65 ) ; 60 age- and gendermatched healthy people were collected as Healthy Group.P300 tests were carried out on patients in these three groups with the MEB-9200 Nicolet Bravo Instrument by the Nihon Kohden Corporation.Results ( 1 ) latency P3a of the Aggressive Group on Cz point exceeded that of the Non-Aggressive Group (P =0.01 ),and that of the Non-Aggressive Group exceeded that of the Healthy Group.All these disparities were of statistical significance (P ＜0.01 ).Latency P3a of the Aggressive Group on Fz point exceeds that of the Non-Aggressive Group,and that of the Non-Aggressive Group exceeded that of Healthy Group.All these disparities are also of stafistical significance (P＜0.01).(2)N2' amplitude of the Aggressive Group on Cz point was higher than those of the Non-Aggressive Group and the Healthy Group.This disparity was of statistical significance(P ＜ 0.05 ) and the disparity between the Non-Aggressive Group and the Healthy Group did not have statistical significance (P =0.985 ).ConclusionCharacteristic electrophysiological changes exist in the event-related potentials P300 of schizophrenic patients with aggressive or violent behaviors.
3.MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
Hui RAN ; Yao LU ; Qi ZHANG ; Qiuyue HU ; Junmei ZHAO ; Kai WANG ; Xuemei TONG ; Qing SU
Diabetes & Metabolism Journal 2021;45(3):439-451
Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear. We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle. MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake. MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
5.MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
Hui RAN ; Yao LU ; Qi ZHANG ; Qiuyue HU ; Junmei ZHAO ; Kai WANG ; Xuemei TONG ; Qing SU
Diabetes & Metabolism Journal 2021;45(3):439-451
Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear. We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle. MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake. MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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