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New opportunities for stroke prevention and therapeutics: a hope from anti-inflammatory drugs?.- Inflammation in stroke and CNS trauma - experimental and clinical evidence.- Clinical evidence of inflammation as a risk factor in ischemic stroke.- Inflammation as a risk factor for stroke: evidence from experimental models.- Inflammatory and immune responses to CNS injury: beneficial and detrimental components.- Salutary effect of autoimmune T cells after central nervous system injury.- Traumatic brain injury: is head trauma an inflammatory disease?.- Cyclic activation and inactivation of brain vessels involving inflammatory mediators - implications for stroke.- Inflammatory cells in stroke.- Do leukocytes play a role in focal ischemia in the brain? An objective review of the literature.- The role of microglia in ischemic brain injury.- Inflammatory activation of brain cells by hypoxia: transcription factors and signaling pathways.- Inflammatory cytokines, interleukins and chemokines in stroke and CNS trauma.- Cytokine effects on CNS cells: implications for the pathogenesis and prevention of stroke.- Interleukin-10 in cerebral ischemia and stroke.- Chemokines and ischemic stroke.- Biphasic activity of tumor necrosis factor in stroke and brain trauma: interaction with reactive oxygen species.- Interleukin-1 and IL-1 receptor antagonist in stroke: mechanisms and potential therapeutics.- Inflammatory cytokines in CNS trauma.- Inflammation in cerebral thrombosis, angiogenesis and matrix regulation: a new perspective in stroke research and therapeutics.- Microvessel integrin expression during focal cerebral ischemia.- The inflammatory response in focal cerebral ischemia.- Chronic neuronal perturbation mediated by RAGE, a receptor for ?-sheet fibrils and S100/calgranulins.- Mediators of inflammation and blood-brain barrier permeability in cerebral ischemia.- Inflammatory proteases and oxygen radicals in stroke.- The role of metalloproteinases on blood-brain barrier breakdown after ischemic stroke.- Matrix metalloproteinases and their inhibitors in hypoxia/reoxygenation and stroke.- Extracellular matrix-degrading metalloproteinases and neuroinflammation in stroke.- Anti-oxidant strategies to treat stroke.- Inflammatory adhesion molecules, kinins, nitric oxide complement factors and lipid mediators in stroke.- Selectin-and complement-mediated mechanisms of tissue injury in stroke.- The kallikrein-kinin system in ischemic and traumatic brain injury.- Nitric oxide, nitric oxide synthases and cyclooxygenase-2 in experimental focal stroke.
Historically, 20% of all injured combatants die on the battlefield before they can be evacuated to a field hospital. Blood lossâ€"hemorrhageâ€"is the single major cause of death among those killed in action whose lives might otherwise be saved. Fluid resuscitation and the treatment of hypovolemia (the abnormally decreased volume of circulating fluid in the body) offer the greatest opportunity for reducing mortality and morbidity associated with battlefield casualties. In Fluid Resuscitation, a committee of experts assess current resuscitation fluids and protocols for the treatment of combat casualties and make recommendations for future research. Chapters focus on the pathophysiology of acute hemorrhagic shock, experience with and complications of fluid resuscitation, novel approaches to the treatment of shock, protocols of care at the site of injury, and future directions for research. The committee explicitly describes the similarities and differences between acute medical care during combat and civilian emergency trauma care. Fluid Resuscitation should help energize and focus research in both civilian and military emergency care and help save the lives of citizens and soldiers alike.
Vascular Responses to Pathogens focuses on the growing research from leaders in the field for both the short and long-term impact of pathogens on the vasculature. It discusses various organisms, including bacteria, parasites, and viruses, and their role in key events leading to vascular disease. Formatted to discuss the topic of the interaction of pathogens with the vascular rather than individual diseases described separately, this reference demonstrates that common mechanisms are at play in many different diseases because they have a similar context, their vasculature. This all-inclusive reference book is a must-have tool for researchers and practicing clinicians in the areas of vascular biology, microvasculature, cardiology, and infectious disease. Covers a wide spectrum of organisms and provides analysis of pathogens and current therapeutic strategies in the context of their vasculature Provides detailed perspectives on key components contributing to vascular pathogens from leaders in the field Interfaces between both vascular biology and microbiology by encompassing information on how pathogens affect both macro and microvasculature Includes coverage of the clinical aspects of sepsis and current therapeutic strategies and anti-sepsis drugs
Cutting edge research in cell and tissue research abounds in this review of the latest technological developments in the area. The chapters are written by excellent scientists on advanced, frontier technology and address scientific questions that require considerable engineering brainpower. The aim is to provide students and scientists working in academia and industry new information on bioengineering in cell and tissue research to enhance their understanding and innovation.
A large number of cardiovascular diseases are accompanied by inflammation. This volume on the molecular basis of microcirculatory disorders gives a comprehensive summary of key steps in the inflammatory cascade. Leading investigators present a state-of-the-art analysis of the molecular determinants of leukocyte-endothelial cell adhesion, mechanotransduction in endothelial and inflammatory cells, mechanisms of cell activation, microvascular apoptosis with applications to ischemia-reperfusion in the brain, the heart and in venous disease, diabetes and hypertension. The book provides the latest thinking in these important cardiovascular problems, with the most contemporary literature and a look at the increasingly complex events during inflammation. Molecular biology tools, microvascular and modern bioengineering analysis are seamlessly integrated into the analysis of clinical problems. The book helps not only newcomers to gain entry into the interesting problems associated with microvascular disorders, but lays the foundation for the design of new therapeutic interventions.
Hypertension is a condition which affects millions of peopleworldwide and its treatment greatly reduces the risk of strokes andheart attacks. This fully revised and updated edition of the ABCof Hypertension is an established guide providing all thenon-specialist needs to know about the measurement of bloodpressure and the investigation and management of hypertensivepatients. This new edition provides comprehensively updated andrevised information on how and whom to treat. The ABC of Hypertension will prove invaluable to generalpractitioners who may be screening large numbers of patients forhypertension, as well as nurse practitioners, midwives and otherhealthcare professionals.
The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References
The aim of this treatise is to summarize the current understanding of the mechanisms for blood flow control to skeletal muscle under resting conditions, how perfusion is elevated (exercise hyperemia) to meet the increased demand for oxygen and other substrates during exercise, mechanisms underlying the beneficial effects of regular physical activity on cardiovascular health, the regulation of transcapillary fluid filtration and protein flux across the microvascular exchange vessels, and the role of changes in the skeletal muscle circulation in pathologic states. Skeletal muscle is unique among organs in that its blood flow can change over a remarkably large range. Compared to blood flow at rest, muscle blood flow can increase by more than 20-fold on average during intense exercise, while perfusion of certain individual white muscles or portions of those muscles can increase by as much as 80-fold. This is compared to maximal increases of 4- to 6-fold in the coronary circulation during exercise. These increases in muscle perfusion are required to meet the enormous demands for oxygen and nutrients by the active muscles. Because of its large mass and the fact that skeletal muscles receive 25% of the cardiac output at rest, sympathetically mediated vasoconstriction in vessels supplying this tissue allows central hemodynamic variables (e.g., blood pressure) to be spared during stresses such as hypovolemic shock. Sympathetic vasoconstriction in skeletal muscle in such pathologic conditions also effectively shunts blood flow away from muscles to tissues that are more sensitive to reductions in their blood supply that might otherwise occur. Again, because of its large mass and percentage of cardiac output directed to skeletal muscle, alterations in blood vessel structure and function with chronic disease (e.g., hypertension) contribute significantly to the pathology of such disorders. Alterations in skeletal muscle vascular resistance and/or in the exchange properties of this vascular bed also modify transcapillary fluid filtration and solute movement across the microvascular barrier to influence muscle function and contribute to disease pathology. Finally, it is clear that exercise training induces an adaptive transformation to a protected phenotype in the vasculature supplying skeletal muscle and other tissues to promote overall cardiovascular health. Table of Contents: Introduction / Anatomy of Skeletal Muscle and Its Vascular Supply / Regulation of Vascular Tone in Skeletal Muscle / Exercise Hyperemia and Regulation of Tissue Oxygenation During Muscular Activity / Microvascular Fluid and Solute Exchange in Skeletal Muscle / Skeletal Muscle Circulation in Aging and Disease States: Protective Effects of Exercise / References