A 2nd-order spline wavelet convolution method in resolving overlapped peaks is developed. It determines the number of peaks, peak positions and width through wavelet? convolution, then uses spline function to construc...A 2nd-order spline wavelet convolution method in resolving overlapped peaks is developed. It determines the number of peaks, peak positions and width through wavelet? convolution, then uses spline function to construct the resoluter, which is used to resolve overlapped peaks. Theoretical proof is given, and the selections of wavelets and parameters are discussed. It is proven that baseline separation can be achieved after processed, the relative errors of peak position and area are less than 0.2% and 4.0% respectively. It can be directly applied to seriously overlapped signals, noisy signals and multi-component signals, and the results are satisfactory. It is a novel effective method for resolution.展开更多
机械性痛觉过敏是痛觉过敏的一种,表现为机械刺激引起的周围正常组织感觉敏感性增强,其传导机制十分复杂,目前尚未能完全阐明。近年来,有研究发现在真核生物中,多种力敏感离子通道(mechanosensitive ion channel, MSC)在机械痛觉过敏的...机械性痛觉过敏是痛觉过敏的一种,表现为机械刺激引起的周围正常组织感觉敏感性增强,其传导机制十分复杂,目前尚未能完全阐明。近年来,有研究发现在真核生物中,多种力敏感离子通道(mechanosensitive ion channel, MSC)在机械痛觉过敏的传导中发挥着重要作用,其中主要包括瞬时受体电位(transient receptor potential, TRP)家族及压电(Piezo)离子通道家族等。位于外周神经末梢的MSC能被机械性刺激激活,从而参与疼痛信号的转导过程。而抑制MSC的开放,将有助于阻止这一信号的转导。由此,文章对不同类型MSC参与机械性痛觉过敏的机制做进一步的总结以及深入理解MSC参与机械性痛觉过敏的过程,从而为机械性痛觉过敏的治疗提供新的药物靶点。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This work was supported by the National Natural Science Foundation of China(Grant No.29975033)the Natural Science Foundation of Guangdong Province(Grant Nos.980340 and 001237).
文摘A 2nd-order spline wavelet convolution method in resolving overlapped peaks is developed. It determines the number of peaks, peak positions and width through wavelet? convolution, then uses spline function to construct the resoluter, which is used to resolve overlapped peaks. Theoretical proof is given, and the selections of wavelets and parameters are discussed. It is proven that baseline separation can be achieved after processed, the relative errors of peak position and area are less than 0.2% and 4.0% respectively. It can be directly applied to seriously overlapped signals, noisy signals and multi-component signals, and the results are satisfactory. It is a novel effective method for resolution.
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.