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| Author | : Hellmut G. Augustin-Voss |
| Publisher | : |
| Total Pages | : 388 |
| Release | : 1992 |
| Genre | : |
| ISBN | : |
| Author | : Derek J. Chadwick |
| Publisher | : John Wiley & Sons |
| Total Pages | : 260 |
| Release | : 2007-08-20 |
| Genre | : Science |
| ISBN | : 0470319429 |
The formation of blood vessels is an essential aspect of embryogenesis in vertebrates. It is a central feature of numerous post-embryonic processes, including tissue and organ growth and regeneration. It is also part of the pathology of tumour formation and certain inflammatory conditions. In recent years, comprehension of the molecular genetics of blood vessel formation has progressed enormously and studies in vertebrate model systems, especially the mouse and the zebrafish, have identified a common set of molecules and processes that are conserved throughout vertebrate embryogenesis while, in addition, highlighting aspects that may differ between different animal groups. The discovery in the past decade of the crucial role of new blood vessel formation for the development of cancers has generated great interest in angiogenesis (the formation of new blood vessels from pre-existing ones), with its major implications for potential cancer-control strategies. In addition, there are numerous situations where therapeutic treatments either require or would be assisted by vasculogenesis (the de novo formation of blood vessels). In particular, post-stroke therapies could include treatments that stimulate neovascularization of the affected tissues. The development of such treatments, however, requires thoroughly understanding the developmental properties of endothelial cells and the basic biology of blood vessel formation. While there are many books on angiogenesis, this unique book focuses on exactly this basic biology and explores blood vessel formation in connection with tissue development in a range of animal models. It includes detailed discussions of relevant cell biology, genetics and embryogenesis of blood vessel formation and presents insights into the cross-talk between developing blood vessels and other tissues. With contributions from vascular biologists, cell biologists and developmental biologists, a comprehensive and highly interdisciplinary volume is the outcome.
| Author | : Sophie Kate Hidden |
| Publisher | : |
| Total Pages | : |
| Release | : 2010 |
| Genre | : |
| ISBN | : |
All classes of leukocytes must be able to move from the circulation into tissue to carry out their protective functions. To achieve this transfer, the flowing cells must adhere to the endothelium and migrate through the vessel wall. Though this process follows common stages during recruitment in different organs, there is also specialisation in underlying molecular mechanisms. The main aim was to further elucidate these organ specific phenotypic differences and relate them to the functional ability of EC to recruit subsets and total leukocytes from flow. Murine models of human disease are an incredibly useful experimental tool allowing investigation of whole diseases to the effect of one gene on a disease outcome. Isolation of primary human endothelial cell populations is well-defined (hLSEC/HUVEC) however obtaining and culturing the murine counterparts is more challenging. Primary mLSEC were isolated from murine livers using [alpha]-CD146 magnetic beads and the phenotype compared to immortalised cell lines from heart (mUCEC-1), skin (s. END) and brain (b. End. 5). The expression of a number of adhesion molecules and endothelial markers varied within cell type in response to pro-inflammatory insult (Endoglin, CD34, CD31). Some artefacts of immortalisation were also apparent (VCAM-1 expression in mUCEC-1 and LYVE-1 in s. END). Functional assays indicated small differences in cell types and further microarray analysis elucidated further candidates, including chemokines, which could be involved in regulating leukocyte recruitment processes in the different organs examined.
| Author | : Florence Rena Sabin |
| Publisher | : |
| Total Pages | : 100 |
| Release | : 1913 |
| Genre | : Lymphatics |
| ISBN | : |
| Author | : Mohit Kumar Jolly |
| Publisher | : MDPI |
| Total Pages | : 512 |
| Release | : 2020-12-29 |
| Genre | : Medical |
| ISBN | : 3039367242 |
Recent studies have highlighted that epithelial-mesenchymal transition (EMT) is not only about cell migration and invasion, but it can also govern many other important elements such as immunosuppression, metabolic reprogramming, senescence-associated secretory phenotype (SASP), stem cell properties, therapy resistance, and tumor microenvironment interactions. With the on-going debate about the requirement of EMT for cancer metastasis, an emerging focus on intermediate states of EMT and its reverse process mesenchymal-epithelial transition (MET) offer new ideas for metastatic requirements and the dynamics of EMT/MET during the entire metastatic cascade. Therefore, we would like to initiate discussions on viewing EMT and its downstream signaling networks as a fulcrum of cellular plasticity, and a facilitator of the adaptive responses of cancer cells to distant organ microenvironments and various therapeutic assaults. We hereby invite scientists who have prominently contributed to this field, and whose valuable insights have led to the appreciation of epithelial-mesenchymal plasticity as a more comprehensive mediator of the adaptive response of cancer cells, with huge implications in metastasis, drug resistance, tumor relapse, and patient survival.
| Author | : D. Neil Granger |
| Publisher | : Morgan & Claypool Publishers |
| Total Pages | : 99 |
| Release | : 2010 |
| Genre | : Medical |
| ISBN | : 1615041656 |
The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References
| Author | : Bohuslav Ostadal |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 467 |
| Release | : 2012-10-12 |
| Genre | : Medical |
| ISBN | : 1461452031 |
This book summarizes present knowledge of different mechanisms involved in the development of positive and negative consequences of cardiac adaptation. Particular attention is paid to the still underestimated adaptive cardiac responses during development, to adaptation to the frequently occurring pressure and volume overload as well as to cardiac changes, induced by enduring exercise and chronic hypoxia. Cardiac Adaptations will be of great value to cardiovascular investigators, who will find this book highly useful in their cardiovascular studies for finding solutions in diverse pathological conditions; it will also appeal to students, fellows, scientists, and clinicians interested in cardiovascular abnormalities.
| Author | : Józef Dulak |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 414 |
| Release | : 2014-02-10 |
| Genre | : Medical |
| ISBN | : 3709114284 |
The book presents the overview of the current knowledge in some fields of vascular biology, addressing cellular and molecular aspects of blood-vessel formation and their role in health and disease. The major factors involved in the formation of blood vessels are presented by scientists actively involved in this area of research. Special emphasis is put on the presentation of various molecular mechanisms not addressed in similar works to date. The book is divided into three parts. The first part describes the cells and mediators in angiogenesis. The significance of various populations of potential endothelial progenitors is particularly highlighted. The chapters of the second part focus on molecular mechanisms, with special emphasis on the role of hypoxia, gasotransmitters and reactive oxygen species as well as microRNAs in regulation of angiogenic processes. In the third part, the pathological aspects of disturbed – aggravated or impaired – vascularization are discussed and new modalities for potential therapies are presented. The book is intended for scientists and PhD students in the fields of vascular biology and cancer research. It may be of interest for medical professionals in the fields of cardiovascular disease, diabetes, oncology and rheumatoid arthritis.
| Author | : Robert Fitridge |
| Publisher | : University of Adelaide Press |
| Total Pages | : 589 |
| Release | : 2011 |
| Genre | : Medical |
| ISBN | : 1922064009 |
New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.
| Author | : Eric A. Jaffe |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 471 |
| Release | : 2012-12-06 |
| Genre | : Medical |
| ISBN | : 146132825X |
The participation of endothelial cells in various physiologic and pathologic processes has been hypothesized since before the turn of the century. However, until recently, direct evidence for endothelial involvement in these processes has been extremely difficult to obtain due to the inability to study endothelial cell function in vitro. Though the possibility of using cultured endothelial cells to study endothelial cell function in vitro was recognized many years ago, the inability to culture unambiguously identifiable endothelial cells limited investigators in their studies of endothelial function. As a result, the field of endothelial cell biology lay relatively fallow for many years. The development in the early 1970's of routine and easily implemented methods for culturing human endothelial cells and the demonstration that cultured endothelial cells synthesized a physiologically relevant protein, Factor VIII/von Willebrand Factor, quickly changed this state of affairs. Over the following decade the scope of endothelial cell research rapidly widened, spreading in a number of directions. First, methods were developed to culture endothelial cells from a variety of species. Second, methods were developed to culture endothelial cells from different organs and types of blood vessels (arteries, veins, and capillaries) within a single species. Third, and most important, investigators began using cultured endothelial cells as tools to study the potential involvement of endothelial cells in a wide assortment of biologically interesting processes. The net result has been a tremendous increase in our understanding of endothelial cell function.
