In order to research on the design and implementation of a modernized GPS civil signals simulation system,a brief review of the modernized GPS signals is introduced,including the signal structure and characteristics o...In order to research on the design and implementation of a modernized GPS civil signals simulation system,a brief review of the modernized GPS signals is introduced,including the signal structure and characteristics of L2C,L5 and L1C signals.The design and implementation of the main modules of the simulation system is described in detail.The simulation system is mainly composed of parameter setting,system initialization,signal generator,noise generator,disturbance generator,signal synthesis,low-pass filter,A/D conversion and storage.The simulation results based on Matlab are then presented,and the power spectral density（PSD） of all navigation signals is analyzed.The simulation system completes the physical layer simulation of a modernized GPS new civil signal and can provide a controllable signal source for designing and testing of modernized GPS civil receivers,especially for the signal processing algorithm design of the GPS software receiver.展开更多
目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮...目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮瓣组织病理学变化,TUNEL法染色观察皮瓣组织细胞凋亡,ELISA法检测血清中TNF-α、IL-6水平,用黄嘌呤氧化酶法和硫代巴比妥酸TBA比色法分别测定皮瓣组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,Westernblot法检测皮瓣组织中Nrf-2、HO-1、γ-GCS蛋白表达水平。结果:与模型组比较,治疗组皮瓣红肿、坏死程度、病理损伤程度减弱;TUNEL法染色观察,与模型组比较,治疗组皮瓣组织细胞凋亡率减少(P<0.05);ELISA法检测发现,与模型组比较,治疗组血清中TNF-α、IL-6降低(P<0.05);与模型组比较,治疗组SOD活性升高(P<0.05),MDA含量降低(P<0.05);Westernblot法检测发现,与模型组比较,治疗组Nrf-2、HO-1、γ-GCS蛋白相对表达水平上升(P<0.05)。结论:APC能改善大鼠皮瓣缺血再灌注损伤,其机制可能与激活Nrf-2/HO-1信号通路,抑制氧化应激反应和减少细胞凋亡、炎症反应有关。展开更多
Cartilage defects may lead to severe degenerative joint diseases.Tissue engineering based on type I collagen hydrogel that has chondrogenic potential is ideal for cartilage repair.However,the underlying mechanisms of ...Cartilage defects may lead to severe degenerative joint diseases.Tissue engineering based on type I collagen hydrogel that has chondrogenic potential is ideal for cartilage repair.However,the underlying mechanisms of chondrogenic differentiation driven by type I collagen hydrogel have not been fully clarified.Herein,we explored potential collagen receptors and chondrogenic signaling pathways through bioinformatical analysis to investigate the mechanism of collagen-induced chondrogenesis.Results showed that the super enhancer-related genes induced by collagen hydrogel were significantly enriched in the TGF-b signaling pathway,and integrin-b1(ITGB1),a receptor of collagen,was highly expressed in bone marrow mesenchymal stem cells(BMSCs).Further analysis showed genes such as COL2A1 and Tenascin C(TNC)that interacted with ITGB1 were significantly enriched in extracellular matrix(ECM)structural constituents in the chondrogenic induction group.Knockdown of ITGB1 led to the downregulation of cartilage-specific genes(SOX9,ACAN,COL2A1),SMAD2 and TNC,as well as the downregulation of phosphorylation of SMAD2/3.Knockdown of TNC also resulted in the decrease of cartilage markers,ITGB1 and the SMAD2/3 phosphorylation but overexpression of TNC showed the opposite trend.Finally,in vitro and in vivo experiments confirmed the involvement of ITGB1 and TNC in collagen-mediated chondrogenic differentiation and cartilage regeneration.In summary,we demonstrated that ITGB1 was a crucial receptor for chondrogenic differentiation of BMSCs induced by collagen hydrogel.It can activate TGF-SMAD2/3 signaling,followed by impacting TNC expression,which in turn promotes the interaction of ITGB1 and TGF-SMAD2/3 signaling to enhance chondrogenesis.These may provide concernful support for cartilage tissue engineering and biomaterials development.展开更多
A new code concept is used for the L1 civil（L1C） signal of the global positioning system（GPS）.The generation of L1C codes is quite different from the generation of traditional ranging codes.Thus,it is necessary to...A new code concept is used for the L1 civil（L1C） signal of the global positioning system（GPS）.The generation of L1C codes is quite different from the generation of traditional ranging codes.Thus,it is necessary to find a method for the correct generation to pave the way for future research.L1C codes are based on only one Legendre sequence which consists of Legendre symbols.To calculate these Legendre symbols,the Euler criterion is always used to evaluate quadratic residues.However,due to the great length of L1C codes,this procedure causes overflow problems.Therefore,the quadratic reciprocity law,some related theorems and properties are introduced to solve the problems.Moreover,if the quadratic reciprocity law,some related theorems and properties are used to calculate different Legendre symbols,the combination modes may vary,which causes a complex generation process.The proposed generation method deals with this complex generation process effectively.In addition,through simulations,it is found that the autocorrelation features of obtained Legendre sequences and L1C codes are in accordance with theoretical results,which proves the correctness of the proposed method.展开更多
Objective:To investigate the modulatory effects of bitter gourd extract on the insulin signaling pathway in the liver and skeletal muscle tissues of diabetic rats.Methods:The ethanolic extract of bitter gourd was prep...Objective:To investigate the modulatory effects of bitter gourd extract on the insulin signaling pathway in the liver and skeletal muscle tissues of diabetic rats.Methods:The ethanolic extract of bitter gourd was prepared and its contents of total polyphenols and flavonoids were assayed.A neonatal streptozotocin-induced diabetic rat model was established and the diabetic rats were assigned into different groups and were treated with different doses of bitter gourd extract(100,200,400,or 600 mg/kg)or with glibenclamide(0.1 mg/kg)for 30 d.Fasting blood glucose,insulin,and lipid profile were evaluated and the insulin signaling pathway in the liver and skeletal muscle of rats was investigated.The correlations between homeostasis model assessment(HOMA)and the components of insulin signaling pathway were also evaluated.Results:Different doses of bitter gourd extract significantly ameliorated fasting blood glucose level and HOMA index for insulin resistance.Moreover,bitter gourd extract increased serum insulin and improved disrupted serum lipid profile.The levels of insulin receptor substrate-1(IRS-1),p-insulin receptorβ(p-IR-β),protein kinase C(PKC),GLUT2,and GLUT4 were improved by treatment with bitter gourd extract.The best results were obtained with 400 mg/kg dose of the extract,the effect of which was equivalent to that of glibenclamide.HOMA in the bitter gourd treated rats was negatively correlated with p-IR-β,IRS-1 and PKC in hepatic and skeletal muscle.HOMA was also negatively correlated with skeletal muscle GLUT4.Conclusions:Bitter gourd extract improves glucose homeostasis and lipid profile in diabetic rats via enhancement of insulin secretion and sensitivity.Therefore,bitter gourd can be used as a potential pharmacological agent for the treatment of type 2 diabetes mellitus.展开更多
The activation of the mitogen-activated protein(MAP) kinases extracellular signal-regulated kinase(ERK)1/2 was traditionally used as a readout of signaling of G protein-coupled receptors(GPCRs) via arrestins, as oppos...The activation of the mitogen-activated protein(MAP) kinases extracellular signal-regulated kinase(ERK)1/2 was traditionally used as a readout of signaling of G protein-coupled receptors(GPCRs) via arrestins, as opposed to conventional GPCR signaling via G proteins. Several recent studies using HEK293 cells where all G proteins were genetically ablated or inactivated, or both non-visual arrestins were knocked out, demonstrated that ERK1/2 phosphorylation requires G protein activity, but does not necessarily require the presence of non-visual arrestins. This appears to contradict the prevailing paradigm. Here we discuss these results along with the recent data on gene edited cells and arrestinmediated signaling. We suggest that there is no real controversy. G proteins might be involved in the activation of the upstream-most MAP3Ks, although in vivo most MAP3K activation is independent of heterotrimeric G proteins, being initiated by receptor tyrosine kinases and/or integrins. As far as MAP kinases are concerned, the best-established role of arrestins is scaffolding of the three-tiered cascades(MAP3K-MAP2 K-MAPK). Thus, it seems likely that arrestins, GPCRbound and free, facilitate the propagation of signals in these cascades, whereas signal initiation via MAP3K activation may be independent of arrestins. Different MAP3Ks are activated by various inputs, some of which are mediated by G proteins, particularly in cell culture, where we artificially prevent signaling by receptor tyrosine kinases and integrins, thereby favoring GPCR-induced signaling. Thus, there is no reason to change the paradigm: Arrestins and G proteins play distinct non-overlapping roles in cell signaling.展开更多
基金The National Natural Science Foundation of China (No.41104015)Foundation of Key Laboratory of Micro-Inertial Instrument and Advanced Navigation Technology of Ministry of Education (No.201011)
文摘In order to research on the design and implementation of a modernized GPS civil signals simulation system,a brief review of the modernized GPS signals is introduced,including the signal structure and characteristics of L2C,L5 and L1C signals.The design and implementation of the main modules of the simulation system is described in detail.The simulation system is mainly composed of parameter setting,system initialization,signal generator,noise generator,disturbance generator,signal synthesis,low-pass filter,A/D conversion and storage.The simulation results based on Matlab are then presented,and the power spectral density（PSD） of all navigation signals is analyzed.The simulation system completes the physical layer simulation of a modernized GPS new civil signal and can provide a controllable signal source for designing and testing of modernized GPS civil receivers,especially for the signal processing algorithm design of the GPS software receiver.
文摘目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮瓣组织病理学变化,TUNEL法染色观察皮瓣组织细胞凋亡,ELISA法检测血清中TNF-α、IL-6水平,用黄嘌呤氧化酶法和硫代巴比妥酸TBA比色法分别测定皮瓣组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,Westernblot法检测皮瓣组织中Nrf-2、HO-1、γ-GCS蛋白表达水平。结果:与模型组比较,治疗组皮瓣红肿、坏死程度、病理损伤程度减弱;TUNEL法染色观察,与模型组比较,治疗组皮瓣组织细胞凋亡率减少(P<0.05);ELISA法检测发现,与模型组比较,治疗组血清中TNF-α、IL-6降低(P<0.05);与模型组比较,治疗组SOD活性升高(P<0.05),MDA含量降低(P<0.05);Westernblot法检测发现,与模型组比较,治疗组Nrf-2、HO-1、γ-GCS蛋白相对表达水平上升(P<0.05)。结论:APC能改善大鼠皮瓣缺血再灌注损伤,其机制可能与激活Nrf-2/HO-1信号通路,抑制氧化应激反应和减少细胞凋亡、炎症反应有关。
基金supported by the Guangxi Scientific Research and Technological Development Foundation(grant number GuikeAB23026049)Guangxi Natural Science Foundation(grant number 2023GXNSFBA026034)the National Natural Science Foundation of China(grant number 82360426).
文摘Cartilage defects may lead to severe degenerative joint diseases.Tissue engineering based on type I collagen hydrogel that has chondrogenic potential is ideal for cartilage repair.However,the underlying mechanisms of chondrogenic differentiation driven by type I collagen hydrogel have not been fully clarified.Herein,we explored potential collagen receptors and chondrogenic signaling pathways through bioinformatical analysis to investigate the mechanism of collagen-induced chondrogenesis.Results showed that the super enhancer-related genes induced by collagen hydrogel were significantly enriched in the TGF-b signaling pathway,and integrin-b1(ITGB1),a receptor of collagen,was highly expressed in bone marrow mesenchymal stem cells(BMSCs).Further analysis showed genes such as COL2A1 and Tenascin C(TNC)that interacted with ITGB1 were significantly enriched in extracellular matrix(ECM)structural constituents in the chondrogenic induction group.Knockdown of ITGB1 led to the downregulation of cartilage-specific genes(SOX9,ACAN,COL2A1),SMAD2 and TNC,as well as the downregulation of phosphorylation of SMAD2/3.Knockdown of TNC also resulted in the decrease of cartilage markers,ITGB1 and the SMAD2/3 phosphorylation but overexpression of TNC showed the opposite trend.Finally,in vitro and in vivo experiments confirmed the involvement of ITGB1 and TNC in collagen-mediated chondrogenic differentiation and cartilage regeneration.In summary,we demonstrated that ITGB1 was a crucial receptor for chondrogenic differentiation of BMSCs induced by collagen hydrogel.It can activate TGF-SMAD2/3 signaling,followed by impacting TNC expression,which in turn promotes the interaction of ITGB1 and TGF-SMAD2/3 signaling to enhance chondrogenesis.These may provide concernful support for cartilage tissue engineering and biomaterials development.
基金supported by the National High Technology Research and Development Program of China(863Program)(2011AA110101)the National Basic Research Program of China(973Program)(2009CB724002)
文摘A new code concept is used for the L1 civil（L1C） signal of the global positioning system（GPS）.The generation of L1C codes is quite different from the generation of traditional ranging codes.Thus,it is necessary to find a method for the correct generation to pave the way for future research.L1C codes are based on only one Legendre sequence which consists of Legendre symbols.To calculate these Legendre symbols,the Euler criterion is always used to evaluate quadratic residues.However,due to the great length of L1C codes,this procedure causes overflow problems.Therefore,the quadratic reciprocity law,some related theorems and properties are introduced to solve the problems.Moreover,if the quadratic reciprocity law,some related theorems and properties are used to calculate different Legendre symbols,the combination modes may vary,which causes a complex generation process.The proposed generation method deals with this complex generation process effectively.In addition,through simulations,it is found that the autocorrelation features of obtained Legendre sequences and L1C codes are in accordance with theoretical results,which proves the correctness of the proposed method.
文摘Objective:To investigate the modulatory effects of bitter gourd extract on the insulin signaling pathway in the liver and skeletal muscle tissues of diabetic rats.Methods:The ethanolic extract of bitter gourd was prepared and its contents of total polyphenols and flavonoids were assayed.A neonatal streptozotocin-induced diabetic rat model was established and the diabetic rats were assigned into different groups and were treated with different doses of bitter gourd extract(100,200,400,or 600 mg/kg)or with glibenclamide(0.1 mg/kg)for 30 d.Fasting blood glucose,insulin,and lipid profile were evaluated and the insulin signaling pathway in the liver and skeletal muscle of rats was investigated.The correlations between homeostasis model assessment(HOMA)and the components of insulin signaling pathway were also evaluated.Results:Different doses of bitter gourd extract significantly ameliorated fasting blood glucose level and HOMA index for insulin resistance.Moreover,bitter gourd extract increased serum insulin and improved disrupted serum lipid profile.The levels of insulin receptor substrate-1(IRS-1),p-insulin receptorβ(p-IR-β),protein kinase C(PKC),GLUT2,and GLUT4 were improved by treatment with bitter gourd extract.The best results were obtained with 400 mg/kg dose of the extract,the effect of which was equivalent to that of glibenclamide.HOMA in the bitter gourd treated rats was negatively correlated with p-IR-β,IRS-1 and PKC in hepatic and skeletal muscle.HOMA was also negatively correlated with skeletal muscle GLUT4.Conclusions:Bitter gourd extract improves glucose homeostasis and lipid profile in diabetic rats via enhancement of insulin secretion and sensitivity.Therefore,bitter gourd can be used as a potential pharmacological agent for the treatment of type 2 diabetes mellitus.
基金Supported by National Institutes of Health RO1 grants,No.EY011500National Institutes of Health R35 grants,No.GM122491Cornelius Vanderbilt Endowed Chair(Vanderbilt University),No.NS065868(to Gurevich VV)and No.DA030103(to Gurevich EV)
文摘The activation of the mitogen-activated protein(MAP) kinases extracellular signal-regulated kinase(ERK)1/2 was traditionally used as a readout of signaling of G protein-coupled receptors(GPCRs) via arrestins, as opposed to conventional GPCR signaling via G proteins. Several recent studies using HEK293 cells where all G proteins were genetically ablated or inactivated, or both non-visual arrestins were knocked out, demonstrated that ERK1/2 phosphorylation requires G protein activity, but does not necessarily require the presence of non-visual arrestins. This appears to contradict the prevailing paradigm. Here we discuss these results along with the recent data on gene edited cells and arrestinmediated signaling. We suggest that there is no real controversy. G proteins might be involved in the activation of the upstream-most MAP3Ks, although in vivo most MAP3K activation is independent of heterotrimeric G proteins, being initiated by receptor tyrosine kinases and/or integrins. As far as MAP kinases are concerned, the best-established role of arrestins is scaffolding of the three-tiered cascades(MAP3K-MAP2 K-MAPK). Thus, it seems likely that arrestins, GPCRbound and free, facilitate the propagation of signals in these cascades, whereas signal initiation via MAP3K activation may be independent of arrestins. Different MAP3Ks are activated by various inputs, some of which are mediated by G proteins, particularly in cell culture, where we artificially prevent signaling by receptor tyrosine kinases and integrins, thereby favoring GPCR-induced signaling. Thus, there is no reason to change the paradigm: Arrestins and G proteins play distinct non-overlapping roles in cell signaling.
