Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization...Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization is the process of identifying the target node’s location.In this research work,a Received Signal Strength Indicator(RSSI)-based optimal node localization approach is proposed to solve the complexities in the conventional node localization models.Initially,the RSSI value is identified using the Deep Neural Network(DNN).The RSSI is conceded as the range-based method and it does not require special hardware for the node localization process,also it consumes a very minimal amount of cost for localizing the nodes in 3D WSN.The position of the anchor nodes is fixed for detecting the location of the target.Further,the optimal position of the target node is identified using Hybrid T cell Immune with Lotus Effect Optimization algorithm(HTCI-LEO).During the node localization process,the average localization error is minimized,which is the objective of the optimal node localization.In the regular and irregular surfaces,this hybrid algorithm effectively performs the localization process.The suggested hybrid algorithm converges very fast in the three-dimensional(3D)environment.The accuracy of the proposed node localization process is 94.25%.展开更多
AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the...AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the proliferation of NIH 3T3 cells was measured by incorporation of 3H-TdR. Receptor-binding assay of 125I-AFP was performed to detect the properties of AFP receptor in NIH 3T3 cells. The influences of AFP on the [cAMP]i and the activities of protein kinase A (PKA) were determined. Western blot was used to detect the change of K-ras P21 protein expression. RESULTS: The proliferation of NIH 3T3 cells treated with 0-80 mg/L of AFP was significantly enhanced. The Scatchard analysis indicated that there were two classes of binding sites with KD of 2.722 x 10(-9)M (Bmax=12810 sites per cell) and 8.931 x 10(-8)M (Bmax=119700 sites per cell) respectively. In the presence of AFP (20 mg/L), the content of cAMP and activities of PKA were significantly elevated . The level of K-ras P21 protein was upregulated by AFP at the concentration of 20 mg/L. The monoclonal antibody against AFP could reverse the effects of AFP on the cAMP content, PKA activity and the expression of K-ras p21 gene. CONCLUSION: The effect of AFP on the cell proliferation was achieved by binding its receptor to trigger the signal transduction pathway of cAMP-PKA and alter the expression of K- ras p21 gene.展开更多
In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al....In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein展开更多
Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into ...Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into the mouse NIH3T3 cells by liposome.Immunohistochemistry was used to detect the expression of VEGF protein of mouse NIH/3T3 cells in vitro.The NIH3T3 cell were stained with CM-DiI before the transplantation.展开更多
NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal...NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal bovina serum (FBS) or lower coneentrafcion of calf serum (CS). The transformation takes the form of foci of multiplying cells among the surrounding cells which have stopped cell division. However, no focus of transformed cells could be seen in medium containing high concentration (10%) of OS. Further experiments indicated that the frequency of transformation is highly dependent on the concentration of serum and the transformation in OS is changeable when the cells are passaged in FBS. 8H-thymidine autoradiography has been proved to be a sensitive measurement indicator for foous formation. Our results suggest that the high frequency of transformation and its dependence on confmenoy as well as on medium composition are characteristics of cell differentiation rather than mutation. The role of the NIH 3T3 cell line as a cancer-initiated cell population and its accelerated transformation by rat oncogene might be considered as a form of tumor promotion is discussed.展开更多
基金appreciation to King Saud University for funding this research through the Researchers Supporting Program number(RSPD2024R918),King Saud University,Riyadh,Saudi Arabia.
文摘Wireless Sensor Network(WSNs)consists of a group of nodes that analyze the information from surrounding regions.The sensor nodes are responsible for accumulating and exchanging information.Generally,node local-ization is the process of identifying the target node’s location.In this research work,a Received Signal Strength Indicator(RSSI)-based optimal node localization approach is proposed to solve the complexities in the conventional node localization models.Initially,the RSSI value is identified using the Deep Neural Network(DNN).The RSSI is conceded as the range-based method and it does not require special hardware for the node localization process,also it consumes a very minimal amount of cost for localizing the nodes in 3D WSN.The position of the anchor nodes is fixed for detecting the location of the target.Further,the optimal position of the target node is identified using Hybrid T cell Immune with Lotus Effect Optimization algorithm(HTCI-LEO).During the node localization process,the average localization error is minimized,which is the objective of the optimal node localization.In the regular and irregular surfaces,this hybrid algorithm effectively performs the localization process.The suggested hybrid algorithm converges very fast in the three-dimensional(3D)environment.The accuracy of the proposed node localization process is 94.25%.
基金This work was supported by National NaturalScience Fundation of China(No.39760077).
文摘AIM: The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS: The effect of AFP on the proliferation of NIH 3T3 cells was measured by incorporation of 3H-TdR. Receptor-binding assay of 125I-AFP was performed to detect the properties of AFP receptor in NIH 3T3 cells. The influences of AFP on the [cAMP]i and the activities of protein kinase A (PKA) were determined. Western blot was used to detect the change of K-ras P21 protein expression. RESULTS: The proliferation of NIH 3T3 cells treated with 0-80 mg/L of AFP was significantly enhanced. The Scatchard analysis indicated that there were two classes of binding sites with KD of 2.722 x 10(-9)M (Bmax=12810 sites per cell) and 8.931 x 10(-8)M (Bmax=119700 sites per cell) respectively. In the presence of AFP (20 mg/L), the content of cAMP and activities of PKA were significantly elevated . The level of K-ras P21 protein was upregulated by AFP at the concentration of 20 mg/L. The monoclonal antibody against AFP could reverse the effects of AFP on the cAMP content, PKA activity and the expression of K-ras p21 gene. CONCLUSION: The effect of AFP on the cell proliferation was achieved by binding its receptor to trigger the signal transduction pathway of cAMP-PKA and alter the expression of K- ras p21 gene.
文摘In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein
文摘Objective To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps.Methods Plasmid PcDNA3.1（-）/VEGF165 containing VEGF gene was transduced into the mouse NIH3T3 cells by liposome.Immunohistochemistry was used to detect the expression of VEGF protein of mouse NIH/3T3 cells in vitro.The NIH3T3 cell were stained with CM-DiI before the transplantation.
文摘NIH 3T3 cells, a mouse fibroblast cell line used as routine target cells for transfection experiments, undergo spontaneous transformation in our experiments after they form a confluent sheet in medium containing fetal bovina serum (FBS) or lower coneentrafcion of calf serum (CS). The transformation takes the form of foci of multiplying cells among the surrounding cells which have stopped cell division. However, no focus of transformed cells could be seen in medium containing high concentration (10%) of OS. Further experiments indicated that the frequency of transformation is highly dependent on the concentration of serum and the transformation in OS is changeable when the cells are passaged in FBS. 8H-thymidine autoradiography has been proved to be a sensitive measurement indicator for foous formation. Our results suggest that the high frequency of transformation and its dependence on confmenoy as well as on medium composition are characteristics of cell differentiation rather than mutation. The role of the NIH 3T3 cell line as a cancer-initiated cell population and its accelerated transformation by rat oncogene might be considered as a form of tumor promotion is discussed.
