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Hematopoiesis refers to the continuous production and release of blood cells into the circulation. As blood cells become old or injured, self-renewing hematopoietic stem cells (HSC) proliferate and differentiate to replenish multiple hematopoietic lineages. This process produces nearly 200 billion red blood cells, 10 billion white blood cells, and 400 billion platelets every day. In addition to the requirement for high cell production, the concentration of individual blood cell lineages is precisely regulated in the peripheral blood and tissues. The production and use of circulating blood cells increase during periods of altered homeostasis such as defense against infection or replenishment of circulating red cells after hemorrhage. When the tightly regulated production of blood cells fails, the host may encounter life-threatening anemia or other cytopenias or suffer from excessive neoplastic growth of blood cells manifesting as leukemia.
Hematopoiesis refers to the continuous production of circulating blood cells. From early in embryonic life to our final days on Earth, newly formed cells enter the circulation while injured, senescent, and tissue-recruited cells are withdrawn. Nearly 200 billion red blood cells, 10 billion white blood cells, and 400 billion platelets are produced daily throughout a normal lifetime. In addition to the requirement for high cell production, the concentration of individual blood cell lineages is precisely regulated in the peripheral blood and tissues. The production and use of circulating blood cells increase during periods of altered homeostasis such as defense against infection or replenishment of circulating red cells after hemorrhage. When the tightly regulated production of blood cells fails, the host may encounter life-threatening anemia or other cytopenias or suffer from excessive neoplastic growth of blood cells manifesting as leukemia.
Blood cell production is developmentally regulated and tissue specific. Blood cells are produced in several different tissues during human development, with each tissue having a characteristic pattern of blood cell production that is regulated in part by the nonhematopoietic cells in residence. This important relationship between nonhematopoietic tissue stromal elements and hematopoietic cells in regulating tissue-specific cell proliferation and differentiation is most evident during the embryonic period.
VASCULAR BED/ORGAN STRUCTURE AND FUNCTION IN HEALTH AND DISEASE
David A. Ingram, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis,
Mervin C. Yoder, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis
The level of endothelial cell (EC) proliferation in normal, mature vessels in most mammals remains poorly defined but in general is reported to be extremely low, if not nonexistent. In fact, until approximately 50 years ago, the predominant view held that ECs lining vessels do not undergo mitosis. However, the advent of tritiated thymidine labeling studies and modifications of the Hautchen preparation permitted direct analysis of EC mitosis in vessels recovered after labeling in vivo (1). In some experimental animals, such as rats, guinea pigs, pigs, and dogs, the tritiated thymidine labeling studies demonstrated 0.1% to 3.0% EC turnover daily (2, 3). Endothelial proliferation rates were correlated with the age of the subject and appeared to decline rapidly after birth with most adult vessel endothelium displaying mitosis in <1% of the cells daily (4). Furthermore, the sites of endothelial replication were not homogenously distributed but appeared to occur in clustered areas nearest vessel bifurcations where flow was disturbed and often turbulent (2). Whether these dividing ECs were unique and possessed proliferative potential that was lacking in other mature endothelium or these focal areas of replicating cells merely represented the sites of greatest vessel injury and endothelial turnover has not yet been determined. It has been well documented that EC division may reach 50% of the cells in the thoracic aorta following experimentally induced hypertension, re-endothelialization of organized clots or injured vessels after arterial denudation, or following experimentally induced vascular constriction (5).
In marked contrast to the slow turnover of ECs in normal vessels, in vitro plating of ECs derived from human or animal vessels is associated with brisk EC proliferation.
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