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Biomedical subjects

E D Gol'dberg

Publications and source records attributed to E D Gol'dberg.

At least 19 recordsLinked to original sources
PubMed1998

[Mechanisms of hemopoiesis cytostatic damage and regeneration].

Bone marrow hemopoiesis, a state of the committed precursor cell pool and the nature of their interaction with hemopoiesis-inducing microenvironment (HIM) elements, the level of humoral stimulants of secretion, was studied following a single injection of 5-fluorouracil (5-FU), cyclophosphamide (CF) or adriamycin (A) to mice in maximum tolerance doses. Cytostatic-related changes in hemopoietic recovery were shown to depend primarily on the proliferation-differentiation relationships in the hemopoietic cells, which is in its turn determined by the status of HIM cells after cytostatic exposure. The enhanced functional activity of HIM elements in response to hemopoietic tissue damage induced by A or CF promotes rapid hemopoietic recovery which becomes much more accelerated while using recombinant colony-stimulating factor (CSF) and, to a lesser degree, glycyrrham, a plant drug. At the same time 5-FU that caused prolonged bone marrow hypoplasia impaired the function of microenvironment cells. The use of this model demonstrated a lower efficiency of CSF than glycyrrham that normalized the structure of HIM.

Animals↗
PubMed1997

[Results of studies of regulatory mechanisms of hematopoiesis in health and disease].

Local and distant hemopoietic regulatory mechanisms were studied under various emergencies (immobilization, cytostatic injection, radiation, etc.). There were common processes (cell migration, destruction, T-lymphocyte accumulation, activation of the microenvironment and hemopoietic precursors) forming the local basis for compensatory and adaptive reactions of bone marrow hemopoietic tissue. Emphasis is laid on the association of local mechanisms with the neuroendocrine system which inevitably becomes activated under extreme exposures. On exposure to irritants having no myeloinhibitory effect, neurotransmitters and hormones, mainly glucocorticoids and catecholamines cause the development of erythro- and granulocytopoietic hyperplasia due to stimulation of the hemopoiesis-inducing microenvironment (HIM). Under hemopoiesis-suppressing influences, catecholamine-induced activations of HIM's resistant elements is accompanied by simultaneous inhibition of hemopoietic cells and HIN's factors damaged by an irritant. Under these conditions hemopoietic separation caused by the heterogeneous effect of transmitters on the cell leads to imbalance of hemopoietic precursor proliferation and differentiation and, finally, to delayed hemopoietic tissue regeneration. At the same time, the neuroendocrine system does not seem to play a leading role as compared to the control intact hemopoiesis.

Antineoplastic Agents↗