ISBN-13: 9780195124507 / Angielski / Twarda / 2001 / 56 str.
Hematopoiesis, or the process of blood formation, has been extensively studied at both basic and clinical levels. Human diseases such as thalassemia, immunodeficiency, and leukemia represent defects in this process. Approaches to treat these disorders have required a basic understanding of the biology of blood cells. For instance, hemapoietic stem cell replacement or bone marrow transplantation has been used to ameliorate disease. This volume focuses on hematopoiesis at a cellular and molecular level, and establishes the basis for clinical manipulation of hematopoietic cells for therapeutic benefit. In Part I, the cellular characteristics of progenitors and stem cells are explored. Emphasis is placed on purification of stem cells and both in vitro and in vivo assays. The regulation of normal and leukemis stem cells is illustrated. An excellent discussion of potential use of these cells for gene therapy concludes this section. Hemapoiesis is easily studied during embryogenesis. Part II develops the concept of the waves of hemapoiesis during development. Comparative hematology is making a major comeback as a field in the 1990's. One hope is that general principles of hematopoiesis will be established by studying many models and systems. Part III delves into critical factors that regulate hematopoiesis, including both intracellular and extracellular signals. Part IV and V describe lineage programs for myeloid and lymphoid lineages. These chapters are meant to be illustrative of the different cell fates, but are not exhaustive. Part VI examines the genetics of hematopoisis, particularly in animal models. The hematopoietic system is in constant contact with stromal cells and endothelial cells during development and in the adult. Evidence suggests that endothelial cells and blood cells may arise from a common progenitor, the hemangioblast. Part VII and VIII discuss the stromal and endothelial cells with the emphasis on their interaction with hematopoietic cells.