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Sensor-based degradation signals measure the accumulation of damage of an engineering system using sensor technology. Degradation signals can be used to estimate, for example, the distribution of the remaining life of partially degraded systems and/or their components. In this paper we present a nonparametric degradation modeling framework for making inference on the evolution of degradation signals that are observed sparsely or over short intervals of times. Furthermore, an empirical Bayes approach is used to update the stochastic parameters of the degradation model in real-time using training degradation signals for online monitoring of components operating in the field. The primary application of this Bayesian framework is updating the residual lifetime up to a degradation threshold of partially degraded components. We validate our degradation modeling approach using a real-world crack growth data set as well as a case study of simulated degradation signals.

Sensor-based degradation signals measure the accumulation of damage of an engineering system using sensor technology. Degradation signals can be used to estimate, for example, the distribution of the remaining life of partially degraded systems and/or their components. In this paper we present a nonparametric degradation modeling framework for making inference on the evolution of degradation signals that are observed sparsely or over short intervals of times. Furthermore, an empirical Bayes approach is used to update the stochastic parameters of the degradation model in real-time using training degradation signals for online monitoring of components operating in the field. The primary application of this Bayesian framework is updating the residual lifetime up to a degradation threshold of partially degraded components. We validate our degradation modeling approach using a real-world crack growth data set as well as a case study of simulated degradation signals.

Sensor-based degradation signals measure the accumulation of damage of an engineering system using sensor technology. Degradation signals can be used to estimate, for example, the distribution of the remaining life of partially degraded systems and/or their components. In this paper we present a nonparametric degradation modeling framework for making inference on the evolution of degradation signals that are observed sparsely or over short intervals of times. Furthermore, an empirical Bayes approach is used to update the stochastic parameters of the degradation model in real-time using training degradation signals for online monitoring of components operating in the field. The primary application of this Bayesian framework is updating the residual lifetime up to a degradation threshold of partially degraded components. We validate our degradation modeling approach using a real-world crack growth data set as well as a case study of simulated degradation signals.

Sensor-based degradation signals measure the accumulation of damage of an engineering system using sensor technology. Degradation signals can be used to estimate, for example, the distribution of the remaining life of partially degraded systems and/or their components. In this paper we present a nonparametric degradation modeling framework for making inference on the evolution of degradation signals that are observed sparsely or over short intervals of times. Furthermore, an empirical Bayes approach is used to update the stochastic parameters of the degradation model in real-time using training degradation signals for online monitoring of components operating in the field. The primary application of this Bayesian framework is updating the residual lifetime up to a degradation threshold of partially degraded components. We validate our degradation modeling approach using a real-world crack growth data set as well as a case study of simulated degradation signals.

The purpose of our research was the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation could be assessed. Our primary efforts have been aimed at overcoming longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We initially focused on development of tightly controlled expression systems using vector- and retroviral-based ecdysone systems and a tetracycline-regulated amplicon system in established NIH3T3 murine fibroblasts and neurofibromin-deficient primary mouse embryo fibroblasts (MEFs). Our progress has been limited by technical difficulties with all three systems that prevented establishment of reliably inducible exogenous neurofibromin expression in either cell type. We have utilized a recently developed modified tetracycline-regulated amplicon system that affords tighter control of exogenous gene expression. Our preliminary analyses in NIH3T3 fibroblasts, neurofibromin-deficient MEFs, and human Schwann cells derived from NFl-associated tumors show improved control of tetracycline-inducible gene expression and suggest that this amplicon system will be a valuable tool in analysis of neurofibromin function in a broad spectrum of cell types, including those that are pathologically relevant to the NFl phenotype. We expect that further studies utilizing the amplicon system will help to clarify the complex role of neurofibromin in cellular growth control.

The purpose of our research was the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation could be assessed. Our primary efforts have been aimed at overcoming longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We initially focused on development of tightly controlled expression systems using vector- and retroviral-based ecdysone systems and a tetracycline-regulated amplicon system in established NIH3T3 murine fibroblasts and neurofibromin-deficient primary mouse embryo fibroblasts (MEFs). Our progress has been limited by technical difficulties with all three systems that prevented establishment of reliably inducible exogenous neurofibromin expression in either cell type. We have utilized a recently developed modified tetracycline-regulated amplicon system that affords tighter control of exogenous gene expression. Our preliminary analyses in NIH3T3 fibroblasts, neurofibromin-deficient MEFs, and human Schwann cells derived from NFl-associated tumors show improved control of tetracycline-inducible gene expression and suggest that this amplicon system will be a valuable tool in analysis of neurofibromin function in a broad spectrum of cell types, including those that are pathologically relevant to the NFl phenotype. We expect that further studies utilizing the amplicon system will help to clarify the complex role of neurofibromin in cellular growth control.

The purpose of our research is the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation can be readily assessed. Our primary efforts have been aimed at overcoming the longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We have focused on the development of tightly controlled expression systems using both a vector-based ecdysone system and a tetracycline-regulated HSV amplicon system in established NIH3T3 murine fibroblasts and primary neurofibromin-deficient mouse embryo fibroblasts. Our progress has been severely limited by technical difficulties with both systems that have prevented the establishment of reliably inducible exogenous neurofibromin expression in either cell type. We are now utilizing a recently described retroviral based ecdysone expression system since stable trans-activator-expressing NIH3T3 lines in this system are available. Additionally, expanded transgene delivery into poorly transfected cell lines is afforded by retrovirus infection. These important features will overcome the two major obstacles that have hampered our progress to date. The revised experiments outlined in this report will lay the foundation for further investigation of the complex role of neurofibromin in cellular growth control mediated through its Ras-dependent and Ras-independent functions.

The purpose of our research is the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation can be readily assessed. Our primary efforts have been aimed at overcoming the longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We have focused on the development of tightly controlled expression systems using both a vector-based ecdysone system and a tetracycline-regulated HSV amplicon system in established NIH3T3 murine fibroblasts and primary neurofibromin-deficient mouse embryo fibroblasts. Our progress has been severely limited by technical difficulties with both systems that have prevented the establishment of reliably inducible exogenous neurofibromin expression in either cell type. We are now utilizing a recently described retroviral based ecdysone expression system since stable trans-activator-expressing NIH3T3 lines in this system are available. Additionally, expanded transgene delivery into poorly transfected cell lines is afforded by retrovirus infection. These important features will overcome the two major obstacles that have hampered our progress to date. The revised experiments outlined in this report will lay the foundation for further investigation of the complex role of neurofibromin in cellular growth control mediated through its Ras-dependent and Ras-independent functions.

The purpose of our research is the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation can be readily assessed. Our primary efforts have been aimed at overcoming the longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We have focused on the development of tightly controlled expression systems using both a vector-based ecdysone system and a tetracycline-regulated HSV amplicon system in established NIH3T3 murine fibroblasts and primary neurofibromin-deficient mouse embryo fibroblasts. Our progress has been severely limited by technical difficulties with both systems that have prevented the establishment of reliably inducible exogenous neurofibromin expression in either cell type. We are now utilizing a recently described retroviral based ecdysone expression system since stable trans-activator-expressing NIH3T3 lines in this system are available. Additionally, expanded transgene delivery into poorly transfected cell lines is afforded by retrovirus infection. These important features will overcome the two major obstacles that have hampered our progress to date. The revised experiments outlined in this report will lay the foundation for further investigation of the complex role of neurofibromin in cellular growth control mediated through its Ras-dependent and Ras-independent functions.

The purpose of our research is the generation of relevant biological assay systems in which Ras-independent effects of neurofibromin on cellular proliferation can be readily assessed. Our primary efforts have been aimed at overcoming the longstanding difficulties of manipulating normal and mutant forms of neurofibromin in mammalian cells. We have focused on the development of tightly controlled expression systems using both a vector-based ecdysone system and a tetracycline-regulated HSV amplicon system in established NIH3T3 murine fibroblasts and primary neurofibromin-deficient mouse embryo fibroblasts. Our progress has been severely limited by technical difficulties with both systems that have prevented the establishment of reliably inducible exogenous neurofibromin expression in either cell type. We are now utilizing a recently described retroviral based ecdysone expression system since stable trans-activator-expressing NIH3T3 lines in this system are available. Additionally, expanded transgene delivery into poorly transfected cell lines is afforded by retrovirus infection. These important features will overcome the two major obstacles that have hampered our progress to date. The revised experiments outlined in this report will lay the foundation for further investigation of the complex role of neurofibromin in cellular growth control mediated through its Ras-dependent and Ras-independent functions.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.

This article is from Clinics , volume 68 . Abstract OBJECTIVE:: Advances in graft reepithelialization and revascularization have renewed interest in airway transplantation. This study aims to determine whether topically applied preservation solutions can ameliorate ischemic injury to tracheal grafts. We analyzed 1) the effects of cold ischemia on the mucociliary clearance of tracheal grafts and 2) the impact of topically applied preservation solutions on the effects of cold ischemia on mucociliary clearance. METHOD:: Tracheal segments (n = 217) from 109 male Wistar rats were harvested, submerged in low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, or saline solution (saline group), and stored at 4°C for 6, 10, 16, or 24 hours. A control group (not submerged) was analyzed immediately after harvesting. In situ mucociliary transport and ciliary beating frequency were measured using a stroboscope. Epithelial integrity, cellular infiltration, and mucus storage were quantified by light microscopy and image analysis software, along with transmission electron microscopy. RESULTS:: 1) The effects of cold ischemia: in situ mucociliary transport and ciliary beating frequency were greater in the control group than after cold ischemia. Microscopic analysis results were similar between groups. 2) The effects of preservation solutions: there was no difference between the low-potassium-dextran-glucose, histidine-tryptophan-ketoglutarate, and saline groups in functional or light microscopy analysis. The saline group presented stronger signs of ischemic injury with transmission electron microscopy. CONCLUSIONS:: Cold ischemia diminished the mucociliary clearance of the tracheal respiratory epithelium. Topically applied preservation solutions did not ameliorate the injury caused by cold ischemia to the tracheal respiratory epithelium.