INTRODUCTION Peptic ulcer,as a common disease,seriouslyaffected people’s,work and life.Its occurrence,development and change have close relationshipwith the change of people’s moods.Animalexperiment proved that sign...INTRODUCTION Peptic ulcer,as a common disease,seriouslyaffected people’s,work and life.Its occurrence,development and change have close relationshipwith the change of people’s moods.Animalexperiment proved that significant changes occurredin the endocrine system of the gastric ulcer rats.展开更多
Inspired by the modulation mechanism of neuroendocrine-immune system(NEIs),a novel structure of artificial neural network(ANN) named NEI-NN and its learning method are presented.The NEI-NN includes two parts,i.e.,posi...Inspired by the modulation mechanism of neuroendocrine-immune system(NEIs),a novel structure of artificial neural network(ANN) named NEI-NN and its learning method are presented.The NEI-NN includes two parts,i.e.,positive subnetwork(PSN) and negative sub-network(NSN).The neuron functions of PSN and NSN are designed according to the increased and decreased secretion functions of hormone,respectively.In order to make the novel neural network learn quickly,the novel neuron based on some characteristics of NEIs is also redesigned.Besides the normal input signals,two control signals are considered in the proposed solution.One is the enable/disable signal,and the other is the slope control signal.The former can modify the structure of NEI-NN,and the later can regulate the evolutionary speed of NEINN.The NEI-NN can obtain the optimized network structure by using error back-propagation(BP) learning algorithm.Since the modeling of the beam pumping unit is very difficult by using the conventional method,the modeling of bean bump unit is chosen to examine the performance of the NEI-NN.The experiment results show that the optimized structure and learning speed of NEI-NN are better than those of the conventional neural network.展开更多
Objective: To observe the changes of vascular endothelial functions and general neuroendocrine-immunity (NEI) network under the state of qi-deficiency syndrome induced by excessive idleness and to approach their in...Objective: To observe the changes of vascular endothelial functions and general neuroendocrine-immunity (NEI) network under the state of qi-deficiency syndrome induced by excessive idleness and to approach their internal relevance and illuminate initially the pathophysiological mechanism of vascular lesion induced by excessive idleness. Methods: A total of 100 male Wistar rats were randomly divided into the control group and the qi-deficiency syndrome model group, 50 rats in each group. The qi-deficiency syndrome model was established by feeding the animals with hyper-alimentation diet in combination with restricting movement for 10 weeks. Changes of common chemical signal molecules related to NEI and vascular endothelial functions were measured by the end of the experiment. Furthermore, their internal relevance was analyzed by the method of canonical correlation analysis. Results: The vascular endothelial structure and function were obviously injured in the model group. Compared with the control group, the chemical signal molecules, such as 5-hydroxytryptamine (5-HT), corticosterone (CORT), triiodothyronine (T3), tetraiodothyronine (T4), angiotensin Ⅱ (Ang Ⅱ), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α) in peripheral blood of the model group (n=43) were changed significantly (P〈0.05 or P〈0.01). Canonical correlation analysis showed that vascular endothelial dysfunction was correlated to the changes of these signal molecules in the NEI network. Conclusions: Comfortbased lifestyle induced not only vascular endothelial dysfunction but also an imbalance of the NEI network. Vascular endothelial dysfunction and the imbalanced NEI network interacted with each other, and an imbalance of the NEI network may be the pathophysiologic basis for the genesis and development of vascular endothelial dysfunction, even diseases of the blood vessel.展开更多
基金the Foundation of Shandong Educational Committee
文摘INTRODUCTION Peptic ulcer,as a common disease,seriouslyaffected people’s,work and life.Its occurrence,development and change have close relationshipwith the change of people’s moods.Animalexperiment proved that significant changes occurredin the endocrine system of the gastric ulcer rats.
基金the Key Project of the National Natural Science Foundation of China(No.61134009)National Natural Science Foundations of China(Nos.61473078,61271001)+5 种基金Program for Changjiang Scholars from the Ministry of Education,ChinaSpecialized Research Fund for Shanghai Leading Talents,ChinaProject of the Shanghai Committee of Science and Technology,China(No.13JC1407500)the Fundamental Research Funds for the Central Universities,China(No.09CX04026A)Excellent Youth and Middle Age Scientists Fund of Shandong Province,China(No.BS2010DX038)Fundamental Research Funds for the Central Universities,China(No.14CX02171A)
文摘Inspired by the modulation mechanism of neuroendocrine-immune system(NEIs),a novel structure of artificial neural network(ANN) named NEI-NN and its learning method are presented.The NEI-NN includes two parts,i.e.,positive subnetwork(PSN) and negative sub-network(NSN).The neuron functions of PSN and NSN are designed according to the increased and decreased secretion functions of hormone,respectively.In order to make the novel neural network learn quickly,the novel neuron based on some characteristics of NEIs is also redesigned.Besides the normal input signals,two control signals are considered in the proposed solution.One is the enable/disable signal,and the other is the slope control signal.The former can modify the structure of NEI-NN,and the later can regulate the evolutionary speed of NEINN.The NEI-NN can obtain the optimized network structure by using error back-propagation(BP) learning algorithm.Since the modeling of the beam pumping unit is very difficult by using the conventional method,the modeling of bean bump unit is chosen to examine the performance of the NEI-NN.The experiment results show that the optimized structure and learning speed of NEI-NN are better than those of the conventional neural network.
基金Supported by the National Basic Research Program of China (973 Program,No.2005CB523301)the International Science and Technology Cooperation Program(No.2006DFB32460)
文摘Objective: To observe the changes of vascular endothelial functions and general neuroendocrine-immunity (NEI) network under the state of qi-deficiency syndrome induced by excessive idleness and to approach their internal relevance and illuminate initially the pathophysiological mechanism of vascular lesion induced by excessive idleness. Methods: A total of 100 male Wistar rats were randomly divided into the control group and the qi-deficiency syndrome model group, 50 rats in each group. The qi-deficiency syndrome model was established by feeding the animals with hyper-alimentation diet in combination with restricting movement for 10 weeks. Changes of common chemical signal molecules related to NEI and vascular endothelial functions were measured by the end of the experiment. Furthermore, their internal relevance was analyzed by the method of canonical correlation analysis. Results: The vascular endothelial structure and function were obviously injured in the model group. Compared with the control group, the chemical signal molecules, such as 5-hydroxytryptamine (5-HT), corticosterone (CORT), triiodothyronine (T3), tetraiodothyronine (T4), angiotensin Ⅱ (Ang Ⅱ), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α) in peripheral blood of the model group (n=43) were changed significantly (P〈0.05 or P〈0.01). Canonical correlation analysis showed that vascular endothelial dysfunction was correlated to the changes of these signal molecules in the NEI network. Conclusions: Comfortbased lifestyle induced not only vascular endothelial dysfunction but also an imbalance of the NEI network. Vascular endothelial dysfunction and the imbalanced NEI network interacted with each other, and an imbalance of the NEI network may be the pathophysiologic basis for the genesis and development of vascular endothelial dysfunction, even diseases of the blood vessel.