Colin J. Barnstable – författare

Leading academic and pharmaceutical researchers and clinicians from many disciplines synthesize and summarize current clinical and basic knowledge concerning abnormal growth of blood vessels in the eye, the cause of major neovascular eye diseases. The authors also identify and assess the most promising approaches with potential for commercial exploitation and discuss the challenges encountered in developing therapeutics for ocular neovascular diseases. Highlights include illuminating chapters on gene therapy and novel drug delivery systems and excellent summaries of the newest therapeutic approaches.

Comprehensive and penetrating, The Visual Transduction Cascade: Basic and Clinical Principles brings together the developmental, structural, and molecular mechanisms of the visual transduction cascade and is an invaluable text for everyone conducting research in the visual system.

Perhaps the oldest surviving record of ancient ophthalmic practices is the Babylonian code of Hammurabi that over 4000 years ago, mentioned fees for eye surgery—and penalties for unsuccessful operations that led to loss of the eye.

An exciting contribution to the field, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement is designed with two overriding objectives: to help readers understand the impact of vision impairment in people living daily with diabetes rather than considering diabetic retinopathy solely as a medical problem, and to explore what we know and don't know about the ways diabetes affect the eye.  With the plethora of new information being generated, there are still a series of fundamental questions that must be addressed if effective treatments for diabetic retinopathy are to be found and applied.  Developed by a renowned group of authorities, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement offers responses and context for a range of questions, such as: do metabolic factors beyond glucose contribute to vision-threatening diabetic retinopathy? If so, how do these lead to vision impairment?  Is diabetic retinopathy a response to systemic metabolic abnormalities or are there unique ocular problems related to insulin resistance? What is the relationship between the neural, vascular, and inflammatory abnormalities in diabetic retinopathy? Do they represent a pathological cascade induced sequentially or simultaneous responses to one or more metabolic perturbations?  The authors note that if we do not address these types of questions, it is possible that the long process of developing new therapeutics will target only one arm of the pathology and leave the retina open to damaging consequences of the others. State-of-the-art, comprehensive, and an invaluable addition the research and clinical literature, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement offers guidance and a significant step toward new scientific approaches that can lessen the devastating vision impairment associated with diabetes.

Leading academic and pharmaceutical researchers and clinicians from many disciplines synthesize and summarize current clinical and basic knowledge concerning abnormal growth of blood vessels in the eye, the cause of major neovascular eye diseases.

For centuries, humans have tried to explain the complex process of vision and find effective treatments for eye diseases. Perhaps the oldest surviving record of ancient ophthalmic practices is the Babylonian code of Hammurabi that over 4000 years ago, mentioned fees for eye surgery—and penalties for unsuccessful operations that led to loss of the eye. Babylonian medicine was controlled by priests who directed the work of skilled surgeons. The earliest records of Egyptian medicine date from almost the same time. The Ebers Papyrus, dating back to more than 3500 years ago is a superbly preserved document in which a section outlines a relatively advanced system of diagnosis and treatment of various ocular pathologies. The text reveals that ancient Greek and Egyptian physicians prescribed “liver juice” for night blindness. This was obtained from roasted and crushed ox liver. We now know that their prescription contained a remarkable amount of vitamin A. It was only within the last century, however, that we have recognized the importance of vitamin A to the function of photoreceptors and visual acuity and that its deficiency can result in night blindness. Egyptian ophthalmological practices were held in high esteem in the ancient world and so were their medical institutes, called “peri-ankh,” which existed since the first dynasty. Herodotus, the fifth century BC Greek historian, comments on the specialization of the physicians: “Each physician treats just one disease.

The mechanisms of the various forms of glaucoma were unknown at the outset of the twentieth century. Late in the twentieth century, two nascent areas of research were beginning to provide glimpses of what the twenty-first century held in store for the future of glaucoma: the mechanisms of glaucomatous optic neuropathy and the molecular basis of the glaucomas. In Mechanisms of the Glaucomas: Disease Processes and Therapeutic Modalities, the authors review the most current knowledge available in the field and provide a basis in which researchers can effectively study the glaucomas. The intent of the book is not primarily to describe the clinical appearances of the glaucomas nor how to manage them. Rather, it is to provide basic scientists, who are working in the field of glaucoma, with a current understanding of the clinical aspects of glaucoma, and to provide clinician scientists with the basic knowledge, as they attempt to translate it into rational treatments for glaucoma. In this important new book leaders in the various fields of glaucoma review our current understanding of glaucoma from epidemiology and genetics through molecular, cellular and tissue responses to the mechanisms of the glaucomas and the mechanisms by which we manage them. Mechanisms of the Glaucomas: Disease Processes and Therapeutic Modalities will be of great value as its contents will aid the reader in prevention of blindness from glaucoma.

Remarkable advances have contributed to revolutionizing the study of vertebrate vision. The first step to identifying objects and establishing spatial relationships is the visual transduction cascade, a process that underpins a wide range of ocular diseases and therapies. Toward that, The Visual Transduction Cascade: Basic and Clinical Principles reveals not only how the eye evolved into an organ of vision, but also describes how molecular mechanisms of key molecules (such as transducins, phosphodiesterases, and CyclicGMP metabolizing enzymes) operate in the phototransduction cascade. In this groundbreaking text, experts also explain mechanisms for sensing radiation outside of the visible wavelengths -- a good example of the limitations of the human sensory systems. Comprehensive and penetrating, The Visual Transduction Cascade: Basic and Clinical Principles brings together the developmental, structural, and molecular mechanisms of the visual transduction cascade and is an invaluable text for everyone conducting research in the visual system.

Detection and responses to light are common features found throughout the plant and animal kingdoms. In most primitive life forms, a patch of light-sensitive cells make up a region containing a cell sheet devoid of any specialized anatomical structure. With the development of the eyes in more advanced life forms, light-sensing structures became more complex but primitive eyes are still in contiguity with other body tissues and fluids. The evolution of the eyeball promoted an increase in visual acuity and visual processing that, in turn, allowed vision to become the dominant sensory system for many species, including humans. The formation of a totally enclosed structure, however, required a unique set of solutions to enable the eye to control its environment. Like most organs, the eye evolved a series of homeostatic mechanisms to regulate its environment within tightly controlled limits. Unlike most organs, however, this advanced light-sensing structure has a series of requirements that place a tremendous burden on molecules that are responsible for controlling ocular homeostasis. There are many sig naling molecules and pathways that work in parallel or through crosstalk to maintain the normal ocular environment required for visual function. Perhaps none are so critical as the group of membrane molecules that are collectively termed transporters. These molecules are responsible for the controlled and selective movements of ions, nutrients, and fluid across various ocular layers necessary to optimize the internal milieu to p- serve visual function.

An exciting contribution to the field, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement is designed with two overriding objectives: to help readers understand the impact of vision impairment in people living daily with diabetes rather than considering diabetic retinopathy solely as a medical problem, and to explore what we know and don't know about the ways diabetes affect the eye.  With the plethora of new information being generated, there are still a series of fundamental questions that must be addressed if effective treatments for diabetic retinopathy are to be found and applied.  Developed by a renowned group of authorities, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement offers responses and context for a range of questions, such as: do metabolic factors beyond glucose contribute to vision-threatening diabetic retinopathy? If so, how do these lead to vision impairment?  Is diabetic retinopathy a response to systemic metabolic abnormalities or are there unique ocular problems related to insulin resistance? What is the relationship between the neural, vascular, and inflammatory abnormalities in diabetic retinopathy? Do they represent a pathological cascade induced sequentially or simultaneous responses to one or more metabolic perturbations?  The authors note that if we do not address these types of questions, it is possible that the long process of developing new therapeutics will target only one arm of the pathology and leave the retina open to damaging consequences of the others. State-of-the-art, comprehensive, and an invaluable addition the research and clinical literature, Visual Dysfunction in Diabetes: The Science of Patient Impairment and Improvement offers guidance and a significant step toward new scientific approaches that can lessen the devastating vision impairment associated with diabetes.

Detection and responses to light are common features found throughout the plant and animal kingdoms. In most primitive life forms, a patch of light-sensitive cells make up a region containing a cell sheet devoid of any specialized anatomical structure. With the development of the eyes in more advanced life forms, light-sensing structures became more complex but primitive eyes are still in contiguity with other body tissues and fluids. The evolution of the eyeball promoted an increase in visual acuity and visual processing that, in turn, allowed vision to become the dominant sensory system for many species, including humans. The formation of a totally enclosed structure, however, required a unique set of solutions to enable the eye to control its environment. Like most organs, the eye evolved a series of homeostatic mechanisms to regulate its environment within tightly controlled limits. Unlike most organs, however, this advanced light-sensing structure has a series of requirements that place a tremendous burden on molecules that are responsible for controlling ocular homeostasis. There are many sig naling molecules and pathways that work in parallel or through crosstalk to maintain the normal ocular environment required for visual function. Perhaps none are so critical as the group of membrane molecules that are collectively termed transporters. These molecules are responsible for the controlled and selective movements of ions, nutrients, and fluid across various ocular layers necessary to optimize the internal milieu to p- serve visual function.

Collectively, these three discoveries armed physicians with the knowledge and means to substantially reduce the prevalence of infectious disease, which was and still remains the leading cause of death throughout the world, and to perform a much wider range of surgeries with greatly improved survivals.

The mechanisms of the various forms of glaucoma were unknown at the outset of the twentieth century. Late in the twentieth century, two nascent areas of research were beginning to provide glimpses of what the twenty-first century held in store for the future of glaucoma: the mechanisms of glaucomatous optic neuropathy and the molecular basis of the glaucomas. In Mechanisms of the Glaucomas: Disease Processes and Therapeutic Modalities, the authors review the most current knowledge available in the field and provide a basis in which researchers can effectively study the glaucomas. The intent of the book is not primarily to describe the clinical appearances of the glaucomas nor how to manage them. Rather, it is to provide basic scientists, who are working in the field of glaucoma, with a current understanding of the clinical aspects of glaucoma, and to provide clinician scientists with the basic knowledge, as they attempt to translate it into rational treatments for glaucoma. In this important new book leaders in the various fields of glaucoma review our current understanding of glaucoma from epidemiology and genetics through molecular, cellular and tissue responses to the mechanisms of the glaucomas and the mechanisms by which we manage them. Mechanisms of the Glaucomas: Disease Processes and Therapeutic Modalities will be of great value as its contents will aid the reader in prevention of blindness from glaucoma.