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Includes bibliographies and index

Includes bibliographies and index

"The Mechanism of Evolution. In the Light of Heredity and Development. II" is an article from The Scientific Monthly, Volume 10 . View more articles from The Scientific Monthly . View this article on JSTOR . View this article's JSTOR metadata . You may also retrieve all of this items metadata in JSON at the following URL: https://archive.org/metadata/jstor-6888

"The Mechanism of Evolution. In the Light of Heredity and Development. II" is an article from The Scientific Monthly, Volume 10 . View more articles from The Scientific Monthly . View this article on JSTOR . View this article's JSTOR metadata . You may also retrieve all of this items metadata in JSON at the following URL: https://archive.org/metadata/jstor-6888

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

Precise developmental control of jaw length is critical for survival, but underlying molecular mechanisms remain poorly understood. The jaw skeleton arises from neural crest mesenchyme (NCM), and we previously demonstrated that these progenitor cells express more bone-resorbing enzymes including Matrix metalloproteinase 13 ( Mmp13 ) when they generate shorter jaws in quail embryos versus longer jaws in duck. Moreover, if we inhibit bone resorption or Mmp13, we can increase jaw length. In the current study, we uncover mechanisms establishing species-specific levels of Mmp13 and bone resorption. Quail show greater activation of and sensitivity to transforming growth factor beta (TGFβ) signaling than duck; where intracellular mediators like SMADs and targets like Runt-related transcription factor 2 ( Runx2 ) , which bind Mmp13 , become elevated. Inhibiting TGFβ signaling decreases bone resorption, and overexpressing Mmp13 in NCM shortens the duck lower jaw. To elucidate the basis for this differential regulation, we examine the Mmp13 promoter. We discover a SMAD-binding element and single nucleotide polymorphisms (SNPs) near a RUNX2-binding element that distinguish quail from duck. Altering the SMAD site and switching the SNPs abolish TGFβ sensitivity in the quail Mmp13 promoter but make the duck promoter responsive. Thus, differential regulation of TGFβ signaling and Mmp13 promoter structure underlie avian jaw development and evolution.

"Publication #: 13231-107-50-5-83- C.R."

"Publication #: 13231-107-50-5-83- C.R."

Book digitized by Google from the library of the University of Michigan and uploaded to the Internet Archive by user tpb.

"This essay represents the expansion of a dissertation offered for the degree of Ph. D. in the University of Chicago."--Pref

This report describes the Palenque Project, a highly interactive, multimedia, optical disc research prototype which was developed for home use and tested by observing 25 children in the 9 to 14 year age range and their families and 8 12-year-olds in pairs. It is noted that the project was intended to create a rich, multimedia database environment for children and their families that would pique their curiosity and foster self-guided exploration, information seeking, and decision making as they explore a Mayan ruin in the Yucatan called Palenque. Following an overview of the project and a description of the design and development team, the report provides descriptions of: (1) the components of the prototype design; (2) the target audience and context for use; and (3) the two phases of design, development, and research which produced the preliminary and final prototypes. It is noted that the research and development project involved concurrent and iterative processes of design, research, production, and programming over the course of a 2-year time frame. It is further noted that since the final goal was to produce research prototypes rather than products, collective research efforts in the development of design conventions that reflected chosen pedagogical biases in content and theme development, interface design, production techniques, and technical implementation, were the essence of the project rather than by-products or activities conducted after product completion. (8 references) (GL)

This report describes the Palenque Project, a highly interactive, multimedia, optical disc research prototype which was developed for home use and tested by observing 25 children in the 9 to 14 year age range and their families and 8 12-year-olds in pairs. It is noted that the project was intended to create a rich, multimedia database environment for children and their families that would pique their curiosity and foster self-guided exploration, information seeking, and decision making as they explore a Mayan ruin in the Yucatan called Palenque. Following an overview of the project and a description of the design and development team, the report provides descriptions of: (1) the components of the prototype design; (2) the target audience and context for use; and (3) the two phases of design, development, and research which produced the preliminary and final prototypes. It is noted that the research and development project involved concurrent and iterative processes of design, research, production, and programming over the course of a 2-year time frame. It is further noted that since the final goal was to produce research prototypes rather than products, collective research efforts in the development of design conventions that reflected chosen pedagogical biases in content and theme development, interface design, production techniques, and technical implementation, were the essence of the project rather than by-products or activities conducted after product completion. (8 references) (GL)

The Royal College of Surgeons of England

The Royal College of Surgeons of England

The rules by which anatomical size and shape are generated have intrigued scientists for centuries. In 1638, Galileo suggested a mathematical relationship between proportional changes in the shape of bones as animals increase in size, which he argued was a functional necessity for weight bearing (1914). The formalism of Galileo, whereby, physical forces and mathematical laws became integrated with studies of size and shape in biology, was most conspicuously encapsulated over a hundred years ago in the 1917 monumental tome by D’Arcy Thompson entitled, On Growth and Form (Thompson 1917). In a breathtakingly comprehensive manner, Thompson synthesized the observations of numerous predecessors and contemporaries, and through countless examples built a theoretical and experimental framework for describing changes in morphology that persists to this day (Stern and Emlen 1999; Arthur 2006).

We present a model of decentralized growth for Artificial Neural Networks (ANNs) inspired by the development and the physiology of real nervous systems. In this model, each individual artificial neuron is an autonomous unit whose behavior is determined only by the genetic information it harbors and local concentrations of substrates modeled by a simple artificial chemistry. Gene expression is manifested as axon and dendrite growth, cell division and differentiation, substrate production and cell stimulation. We demonstrate the model's power with a hand-written genome that leads to the growth of a simple network which performs classical conditioning. To evolve more complex structures, we implemented a platform-independent, asynchronous, distributed Genetic Algorithm (GA) that allows users to participate in evolutionary experiments via the World Wide Web.

We present a model of decentralized growth for Artificial Neural Networks (ANNs) inspired by the development and the physiology of real nervous systems. In this model, each individual artificial neuron is an autonomous unit whose behavior is determined only by the genetic information it harbors and local concentrations of substrates modeled by a simple artificial chemistry. Gene expression is manifested as axon and dendrite growth, cell division and differentiation, substrate production and cell stimulation. We demonstrate the model's power with a hand-written genome that leads to the growth of a simple network which performs classical conditioning. To evolve more complex structures, we implemented a platform-independent, asynchronous, distributed Genetic Algorithm (GA) that allows users to participate in evolutionary experiments via the World Wide Web.

We present a model of decentralized growth for Artificial Neural Networks (ANNs) inspired by the development and the physiology of real nervous systems. In this model, each individual artificial neuron is an autonomous unit whose behavior is determined only by the genetic information it harbors and local concentrations of substrates modeled by a simple artificial chemistry. Gene expression is manifested as axon and dendrite growth, cell division and differentiation, substrate production and cell stimulation. We demonstrate the model's power with a hand-written genome that leads to the growth of a simple network which performs classical conditioning. To evolve more complex structures, we implemented a platform-independent, asynchronous, distributed Genetic Algorithm (GA) that allows users to participate in evolutionary experiments via the World Wide Web.

Gift of Arthur G. Humes

xiv, 456 p. 22 cm

Following World War II, the steadily increasing Government investment in R & D activities focused national attention on the controversial issue of patent rights. Several decades of debate notwithstanding, no uniform Government patent policy exists today. The 1980 amendments to the U.S. patent and trademark laws represent a compromise between the advocates of the 'title' and 'license' schools of thought. The interaction of the Executive, Legislative, and Judicial Branches in attempting to establish a uniform Government patent policy applicable to all Federal agencies and departments has been unsuccessful. This situation provides the impetus for future legislative efforts in this area. This thesis provides recommendations for evaluating the impact of the 1980 amendments and insuring that the agency patent policy provisions are promptly implemented.

120 p. :

Since its origination under NASA's previous Human System Research and Technology program, the Lunar Simulant Development Program has undergone several changes. NASA recognized as early as the Apollo Program, and even more so as a result of the Apollo missions, that a viable dust and lunar simulant program is critical to the success of its space exploration goals. Unfortunately, this program has suffered the same problems that all programs share from time to time including uncertain budgets, shifting of priorities, and schedule fluctuations. To compound the problem, the process for developing simulants is being redefined and is not a trivial pursuit. Before now, NASA had not attempted to develop a suitable standard simulant since the 1990s when JSC-1 was produced. Although several other simulants have been developed by various groups both before and after the production of JSC-1, JSC-1 had become the de facto standard even though it has some limitations. The development and production of new simulants will address some of these limitations by starting with an assessment of NASA's needs and understanding the required processing in order to make these simulants.

Since its origination under NASA's previous Human System Research and Technology program, the Lunar Simulant Development Program has undergone several changes. NASA recognized as early as the Apollo Program, and even more so as a result of the Apollo missions, that a viable dust and lunar simulant program is critical to the success of its space exploration goals. Unfortunately, this program has suffered the same problems that all programs share from time to time including uncertain budgets, shifting of priorities, and schedule fluctuations. To compound the problem, the process for developing simulants is being redefined and is not a trivial pursuit. Before now, NASA had not attempted to develop a suitable standard simulant since the 1990s when JSC-1 was produced. Although several other simulants have been developed by various groups both before and after the production of JSC-1, JSC-1 had become the de facto standard even though it has some limitations. The development and production of new simulants will address some of these limitations by starting with an assessment of NASA's needs and understanding the required processing in order to make these simulants.

The geomagnetic field (GMF) is a natural component of our environment. Plants, which are known to sense different wavelengths of light, respond to gravity, react to touch and electrical signaling, cannot escape the effect of GMF. While phototropism, gravitropism, and tigmotropism have been thoroughly studied, the impact of GMF on plant growth and development is not well-understood. This review describes the effects of altering magnetic field (MF) conditions on plants by considering plant responses to MF values either lower or higher than those of the GMF. The possible role of GMF on plant evolution and the nature of the magnetoreceptor is also discussed.

280 pages : 22 cm

280 pages : 22 cm

Search for possible relationships between phylogeny and ontogeny is one of the most important issues in the field of evolutionary developmental biology. By representing developmental dynamics of spatially located cells with gene expression dynamics with cell-to-cell interaction under external morphogen gradient, evolved are gene regulation networks under mutation and selection with the fitness to approach a prescribed spatial pattern of expressed genes. For most of thousands of numerical evolution experiments, evolution of pattern over generations and development of pattern by an evolved network exhibit remarkable congruence. Here, both the pattern dynamics consist of several epochs to form successive stripe formations between quasi-stationary regimes. In evolution, the regimes are generations needed to hit relevant mutations, while in development, they are due to the emergence of slowly varying expression that controls the pattern change. Successive pattern changes are thus generated, which are regulated by successive combinations of feedback or feedforward regulations under the upstream feedforward network that reads the morphogen gradient. By using a pattern generated by the upstream feedforward network as a boundary condition, downstream networks form later stripe patterns. These epochal changes in development and evolution are represented as same bifurcations in dynamical-systems theory, and this agreement of bifurcations lead to the evolution-development congruences. Violation of the evolution-development congruence, observed exceptionally, is shown to be originated in alteration of the boundary due to mutation at the upstream feedforward network. Our results provide a new look on developmental stages, punctuated equilibrium, developmental bottlenecks, and evolutionary acquisition of novelty in morphogenesis.

Search for possible relationships between phylogeny and ontogeny is one of the most important issues in the field of evolutionary developmental biology. By representing developmental dynamics of spatially located cells with gene expression dynamics with cell-to-cell interaction under external morphogen gradient, evolved are gene regulation networks under mutation and selection with the fitness to approach a prescribed spatial pattern of expressed genes. For most of thousands of numerical evolution experiments, evolution of pattern over generations and development of pattern by an evolved network exhibit remarkable congruence. Here, both the pattern dynamics consist of several epochs to form successive stripe formations between quasi-stationary regimes. In evolution, the regimes are generations needed to hit relevant mutations, while in development, they are due to the emergence of slowly varying expression that controls the pattern change. Successive pattern changes are thus generated, which are regulated by successive combinations of feedback or feedforward regulations under the upstream feedforward network that reads the morphogen gradient. By using a pattern generated by the upstream feedforward network as a boundary condition, downstream networks form later stripe patterns. These epochal changes in development and evolution are represented as same bifurcations in dynamical-systems theory, and this agreement of bifurcations lead to the evolution-development congruences. Violation of the evolution-development congruence, observed exceptionally, is shown to be originated in alteration of the boundary due to mutation at the upstream feedforward network. Our results provide a new look on developmental stages, punctuated equilibrium, developmental bottlenecks, and evolutionary acquisition of novelty in morphogenesis.

Click here to view the University of Florida catalog record

Click here to view the University of Florida catalog record

Click here to view the University of Florida catalog record

Click here to view the University of Florida catalog record

pt. 1. v.1-8. History of man--pt. 2. v.9-16. History of events

pt. 1. v.1-8. History of man--pt. 2. v.9-16. History of events

Overview: Challenges of securing open architecture (OA) systems. Specifying security requirements for software systems. Case study: Securing the development and evolution of an OA C2 system within an agile, adaptive software ecosystem. Discussion and conclusions.

Following World War II, the steadily increasing Government investment in R & D activities focused national attention on the controversial issue of patent rights. Several decades of debate notwithstanding, no uniform Government patent policy exists today. The 1980 amendments to the U.S. patent and trademark laws represent a compromise between the advocates of the 'title' and 'license' schools of thought. The interaction of the Executive, Legislative, and Judicial Branches in attempting to establish a uniform Government patent policy applicable to all Federal agencies and departments has been unsuccessful. This situation provides the impetus for future legislative efforts in this area. This thesis provides recommendations for evaluating the impact of the 1980 amendments and insuring that the agency patent policy provisions are promptly implemented.

Following World War II, the steadily increasing Government investment in R & D activities focused national attention on the controversial issue of patent rights. Several decades of debate notwithstanding, no uniform Government patent policy exists today. The 1980 amendments to the U.S. patent and trademark laws represent a compromise between the advocates of the 'title' and 'license' schools of thought. The interaction of the Executive, Legislative, and Judicial Branches in attempting to establish a uniform Government patent policy applicable to all Federal agencies and departments has been unsuccessful. This situation provides the impetus for future legislative efforts in this area. This thesis provides recommendations for evaluating the impact of the 1980 amendments and insuring that the agency patent policy provisions are promptly implemented.

Following World War II, the steadily increasing Government investment in R & D activities focused national attention on the controversial issue of patent rights. Several decades of debate notwithstanding, no uniform Government patent policy exists today. The 1980 amendments to the U.S. patent and trademark laws represent a compromise between the advocates of the 'title' and 'license' schools of thought. The interaction of the Executive, Legislative, and Judicial Branches in attempting to establish a uniform Government patent policy applicable to all Federal agencies and departments has been unsuccessful. This situation provides the impetus for future legislative efforts in this area. This thesis provides recommendations for evaluating the impact of the 1980 amendments and insuring that the agency patent policy provisions are promptly implemented.

Following World War II, the steadily increasing Government investment in R & D activities focused national attention on the controversial issue of patent rights. Several decades of debate notwithstanding, no uniform Government patent policy exists today. The 1980 amendments to the U.S. patent and trademark laws represent a compromise between the advocates of the 'title' and 'license' schools of thought. The interaction of the Executive, Legislative, and Judicial Branches in attempting to establish a uniform Government patent policy applicable to all Federal agencies and departments has been unsuccessful. This situation provides the impetus for future legislative efforts in this area. This thesis provides recommendations for evaluating the impact of the 1980 amendments and insuring that the agency patent policy provisions are promptly implemented.

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