Preface Open angle glaucoma (OAG) is one of the leading causes of impaired vision worldwide. The pathogenesis of glaucomatous optic neuropathy remains poorly understood, and several pathogenic mechanisms are proposed to coexist. As the world population ages, OAG will become more prevalent and advances in the diagnosis and treatment of glaucomatous optic neuropathy are important to protect and improve the quality of life of our aging population. Treatment of OAG has been directed at lowering intraocular pressure (IOP) which is the only current therapeutic strategy available to patients with glaucoma. While a wide variety of studies have demonstrated that lowering IOP decreases the risk of glaucoma development and/or progression, many studies have also shown that some patients continue to lose vision despite significant lowering of IOP. There have been many attempts to elucidate the etiology for the deterioration in glaucomatous optic neuropathy despite low levels of IOP. Over the past several decades, deficits in the ocular circulation of patients with OAG have become well established and these may explain the continued progression of OAG patients despite lowered IOP. The purpose of the present publication is to provide an updated view of ocular blood flow and vascular dysregulation in OAG. The importance of the topic was demonstrated by the focus of the 2009 6th Consensus meeting of the World Glaucoma Association which focused entirely on blood flow deficits in patients with OAG. Although a great deal of knowledge on vascular risk factors in glaucoma has already been established, many questions remain. Do ocular blood flow deficits precede glaucoma progression? How does ocular perfusion pressure fit into the IOP and blood flow paradigm? What conclusions can be drawn from recent evidence showing the fluctuation of OAG risk factors including IOP, blood pressure and ocular perfusion pressure? We hope this update d current prospective will serve as a foundation for future investigations which will be designed to answer these and other important considerations in the management of glaucoma. Alon Harris, MS, PhD, FARVO Director of Clinical Research Lois Letzter Professor of Ophthalmology Professor of Cellular and Integrative Physiology
Preface Open angle glaucoma (OAG) is one of the leading causes of impaired vision worldwide. The pathogenesis of glaucomatous optic neuropathy remains poorly understood, and several pathogenic mechanisms are proposed to coexist. As the world population ages, OAG will become more prevalent and advances in the diagnosis and treatment of glaucomatous optic neuropathy are important to protect and improve the quality of life of our aging population. Treatment of OAG has been directed at lowering intraocular pressure (IOP) which is the only current therapeutic strategy available to patients with glaucoma. While a wide variety of studies have demonstrated that lowering IOP decreases the risk of glaucoma development and/or progression, many studies have also shown that some patients continue to lose vision despite significant lowering of IOP. There have been many attempts to elucidate the etiology for the deterioration in glaucomatous optic neuropathy despite low levels of IOP. Over the past several decades, deficits in the ocular circulation of patients with OAG have become well established and these may explain the continued progression of OAG patients despite lowered IOP. The purpose of the present publication is to provide an updated view of ocular blood flow and vascular dysregulation in OAG. The importance of the topic was demonstrated by the focus of the 2009 6th Consensus meeting of the World Glaucoma Association which focused entirely on blood flow deficits in patients with OAG. Although a great deal of knowledge on vascular risk factors in glaucoma has already been established, many questions remain. Do ocular blood flow deficits precede glaucoma progression? How does ocular perfusion pressure fit into the IOP and blood flow paradigm? What conclusions can be drawn from recent evidence showing the fluctuation of OAG risk factors including IOP, blood pressure and ocular perfusion pressure? We hope this update d current prospective will serve as a foundation for future investigations which will be designed to answer these and other important considerations in the management of glaucoma. Alon Harris, MS, PhD, FARVO Director of Clinical Research Lois Letzter Professor of Ophthalmology Professor of Cellular and Integrative Physiology
This two volume set is a complete guide to the diagnosis and treatment of paediatric skin conditions. With its first edition having published more than 33 years ago, this reference is renowned amongst clinicians practising in the field of paediatric dermatology. The fifth edition has been thoroughly revised and updated to provide all the latest techniques and therapeutic advances for daily practice. More than 2000 clinical and histologic pictures, the majority new to this edition, illustrate all the skin conditions described in the comprehensive text covering 2500 pages, across the two volumes. Detailed references offer suggestions for further reading. Divided into 22 sections, the book begins with an introduction to basic science and discussion on diagnosis in paediatric dermatology. The following chapters cover a multitude of conditions, from genetic diseases, eczema, and pigmentary disorders, to vascular anomalies, tumours and cysts, skin infections, and many more. The book concludes with a section on the principles of treatment. A complete section is dedicated to neonatal disorders. The book is edited by Madrid-based Antonio Torrelo, with contributions from numerous other experts in the field. The previous edition (9780723435402) published in 2010.
This second edition offers a fully revised and updated work on a rapidly growing field of knowledge, and was prepared by two experts whose goal was to explain the molecular basis of mosaic skin disorders in a language that is accessible for practicing physicians and medical students alike. It presents a timely and comprehensive overview of the strikingly manifold patterns and peculiarities of mosaic skin disorders in a straightforward, reader-friendly way that will help physicians to further improve genetic counseling and treatment outcomes. The first two parts of the book are devoted to the mechanisms and patterns of cutaneous mosaicism, and include an explanation of genomic and epigenetic mosaicism and a description of the archetypical segmental patterns including the lines of Blaschko and the flag-like, phylloid and lateralization pattern, the non-segmental pattern of large congenital melanocytic nevi, and the sash-like arrangement as noted in a particular type of cutis tricolor. The concept of lethal mutations surviving as mosaics has now been confirmed by molecular analysis in many sporadically occurring phenotypes. The difference between monoallelic and biallelic traits has deepened our understanding of hereditary mosaics, especially of multiple benign skin tumors. Moreover, recognition of the fundamental difference between the simple segmental and the superimposed types of mosaicism is important for the purpose of genetic counseling. In the third part, the various mosaic skin disorders are examined in depth, including nevi, didymotic disorders, other binary genodermatoses, mosaic manifestations of autosomal skin disorders, and nevoid skin disorders such as phenotypes reflecting functional X-chromosome mosaicism or a superimposed mosaic manifestation of common skin diseases with a polygenic background. Reader-friendly and clearly structured, Mosaicism in Human Skin will appeal to both experienced dermatologists and residents in training, as well as to medical geneticists and pediatricians.
Thank you for visiting our website. Would you like to provide feedback on how we could improve your experience?
This site does not use any third party cookies with one exception — it uses cookies from Google to deliver its services and to analyze traffic.Learn More.