The carotid body (CB) is in charge of adjusting ventilatory and cardiovascular function during changes in arterial blood gases. Regardless this essential function, the CB has been implicated in the sensing of other physiological signals such as changes in blood flow and glucose levels. More important, malfunction of the CB chemoreceptors has been associated with the progression and deterioration of several disease states such as hypertension, heart failure, renal failure, insulin resistance, diabetes and sleep apnea. Although the mechanisms involved in the alterations of the CB function in pathophysiology are currently under intense research, the development of therapeutic approaches to restore normal CB chemoreflex function remains unsolved. Recent studies showing the effect of CB denervation in pathophysiology have unveiled a key role of these arterial chemoreceptors in the development of autonomic imbalance and respiratory disturbances, and suggest that targeting the CB could represent a novel strategy to improve disease outcome. Unfortunately, classical pharmacotherapy intended to normalize CB function may be hard to establish since several cellular pathways are involved in the CB dysfunction. Augmented levels of angiotensin II, endothelin-1, cytokines and free radicals along with decreases in nitric oxide had all been related to the CB dysfunction. Moreover, changes in expression of angiotensin receptors, nitric oxide synthases and cytokines that take place within the CB tissue in pathological states also contribute to the enhanced CB chemoreflex drive. It has been shown in heart failure, hypertension and obstructive sleep apnea that the CB becomes tonically hyper-reactive. During the progression of the disease this CB chemosensory facilitation process induces central nervous system plasticity. The altered autonomic-respiratory control leads to increased cardiorespiratory distress and the deterioration of the condition. The focus of this e-book will be to cover the role of the CB in pathophysiology and to provide new evidence of the pathways involved in the maladaptive potentiation of the CB chemoreflex function. In memory of Professor Mashiko Shirahata and Professor Constancio Gonzalez.

Known for its clear writing style, easy-to-navigate format, and authoritative coverage of tumor pathology, Dr. Christopher Fletcher’s Diagnostic Histopathology of Tumors, 5th Edition, remains your go-to source for accurate, efficient evaluation and interpretation of histopathology specimens. This highly regarded reference provides superbly illustrated information on pathogenesis, diagnostic criteria, molecular/cytogenetic findings, and prognosis on the neoplastic diseases most likely to be encountered by general surgical pathologists, and helps you stay current with the latest diagnostic tumor markers to assist in daily sign-out. Discusses the latest developments in immunohistochemistry, molecular genetics, targeted therapy/personalized medicine, and prognostic/predictive markers to assist in the diagnosis of the complete range of neoplastic entities. Includes coverage of newly described variants and new histologic entities. Covers all modern diagnostic techniques while retaining a strong emphasis on morphologic diagnosis, which remains the cornerstone of diagnosis for most lesions. Features thousands of high-quality photographs, photomicrographs, and artwork throughout. Incorporates the latest TNM and WHO classification and staging systems. Contains diagnostic flow charts, correlations of gross appearances to microscopic findings, and differential diagnosis tables for better recognition and evaluation of similar-looking entities. Shares the knowledge and expertise of internationally renowned experts in tumor pathology, including Dr. Christopher Fletcher, as well as numerous global authorities in the field.

The carotid body (CB) is in charge of adjusting ventilatory and cardiovascular function during changes in arterial blood gases. Regardless this essential function, the CB has been implicated in the sensing of other physiological signals such as changes in blood flow and glucose levels. More important, malfunction of the CB chemoreceptors has been associated with the progression and deterioration of several disease states such as hypertension, heart failure, renal failure, insulin resistance, diabetes and sleep apnea. Although the mechanisms involved in the alterations of the CB function in pathophysiology are currently under intense research, the development of therapeutic approaches to restore normal CB chemoreflex function remains unsolved. Recent studies showing the effect of CB denervation in pathophysiology have unveiled a key role of these arterial chemoreceptors in the development of autonomic imbalance and respiratory disturbances, and suggest that targeting the CB could represent a novel strategy to improve disease outcome. Unfortunately, classical pharmacotherapy intended to normalize CB function may be hard to establish since several cellular pathways are involved in the CB dysfunction. Augmented levels of angiotensin II, endothelin-1, cytokines and free radicals along with decreases in nitric oxide had all been related to the CB dysfunction. Moreover, changes in expression of angiotensin receptors, nitric oxide synthases and cytokines that take place within the CB tissue in pathological states also contribute to the enhanced CB chemoreflex drive. It has been shown in heart failure, hypertension and obstructive sleep apnea that the CB becomes tonically hyper-reactive. During the progression of the disease this CB chemosensory facilitation process induces central nervous system plasticity. The altered autonomic-respiratory control leads to increased cardiorespiratory distress and the deterioration of the condition. The focus of this e-book will be to cover the role of the CB in pathophysiology and to provide new evidence of the pathways involved in the maladaptive potentiation of the CB chemoreflex function. In memory of Professor Mashiko Shirahata and Professor Constancio Gonzalez.