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Biomedical subjects

L W Sullivan

Publications and source records attributed to L W Sullivan.

At least 55 records · Page 3Linked to original sources
PubMed1990

Oral testimony.

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Community Participation↗
PubMed1978

Humoral regulation of thrombopoiesis in man.

Plasma was obtained before and after plateletpheresis-induced thrombocytopenia from two healthy male subjects during periods of ethanol ingestion and abstinence. Autologous reinfusion of these plasmas was performed at a later date when both subjects were hematologically normal. Eight thrombopoietically active plasmas produced an increased percent of immature megakaryocytes 24 hr after reinfusion and a peak rise in platelet count (averaging 148% of baseline values) at 5.8 days. Similar changes were not found with inactive plasmas, plasma collected at the end of a "sham" plateletpheresis, or plasma collected after 8 hr of ingestion of 296 gm of ethanol. A transient increase in TSA was found in plasmas collected at the end of plateletpheresis during abstinence, but this activity was not detected 12 hr later. The rapid disappearance of TSA, despite persistent thrombocytopenia, coincided with the appearance of an increased percent of immature magakaryocytes in the bone marrow. Elevated TSA was also noted at the end of plateletpheresis during ethanol ingestion but, in contrast to events during abstinence, remained elevated as long as ethanol ingestion continued.

Blood Cell Count↗
PubMed1977

Induction of thrombocytopenia by thrombopheresis in man: patterns of recovery in normal subjects during ethanol ingestion and abstinence.

Using the technique of thrombophoresis (TP), platelet and megakaryocyte dynamics following acute thrombocytopenia were studied in two normal subjects during periods of ethanol ingestion and abstinence. Thrombocytopenia was induced over a period of 12 hr. A logarithmic decline in platelet count during TP and the serial morphologic changes in megakaryocytes during recovery from thrombocytopenia are described. Although these parameters were not affected by ethanol ingestion, platelet counts after TP did not return to normal until ethanol was discontinued. 51Cr-labeled platelet survival was normal in one subject studied, and no evidence of increased platelet sequestration was found. It is concluded that heavy ethanol ingestion induces, augments, or sustains thrombocytopenia by impairing megakaryocytopoiesis in man. The mechanism by which ethanol induces thrombocytopenia may be due, in part, to "ineffective thrombopoiesis," impairment of the differentiation of precursor cells into the megakaryocytic compartment, or a combination of these factors.

Adult↗
PubMed1975

Ultrastructural studies of the bone marrow in sickle cell anaemia. I. The structure of sickled erythrocytes and reticulocytes and their phagocytic destruction.

Marrow aspirates from sickle cell patients were examined without prior deoxygenation and revealed the presence of a variable proportion (10-30%) of sickled red cells and reticulocytes. The main feature of sickled red cells was the presence of 17.6 nm fibres arranged in hexagonal order, and to a lesser extent in square or rectangular array, to form bundles of varying size and compactness which occupied the entire cytoplasm. The sickling pattern in reticulocytes was more variable. Some reticulocytes contained highly-ordered bundles of 17.6 nm fibres whose structure and distribution was identical to that in red cells from whiich they could be distinguished only by their content of organelles. Many reticulocytes exhibited less-organized fibre patterns ranging from localized aggregates to poorly-ordered regions of short fibres and filaments lacking apparent preferential orientation. In these cells, the bulk of the cytoplasm was not polymerized. Haemoglobin polymerization in reticulocytes led to entrapment of ribosomes in concentrated foci among the fibres. Frequently, iron-laden mitochondria were associated with sickled reticulocytes. The variation in pattern of sickling seen in reticulocytes is attributed to possible differences in concentration of Hb S. Correlative studies have shown that fibres were not induced by fixation procedures. Marked phagocytic degradation of sickled cells by macrophages was observed. The results are interpreted to indicate the possible intramedullary phagocytosis of red cells and reticulocytes, predisposed to sickling in the marrow. However, the data are also consistent with the removal of sickled elements from the circulating blood.

Anemia, Sickle Cell↗
PubMed1975

Ultrastructural studies of the bone marrow in sickle cell anaemia. II. The morphology of erythropoietic cells and their response to deoxygenation in vitro.

Electron microscopic studies of bone marrow aspirates obtained from patients with homozygous sickle cell anaemia (HbSS) were fixed immediately without attempts to deoxygenate the samples. Erythroblasts and normoblasts in these preparations were devoid of haemoglobin polymers or other indications of sickling. Furthermore, the nucleated erythroid cells from sickle-cell patients presented an ultrastructural morphology indistinguishable from that of identically-processed erythroid cells in marrow samples from normal human volunteers. This report presents a description of the ultrastructural features of pronormoblasts and normoblasts in normal and sickle-cell marrows and stresses the essentially normal appearance of nucleated erythroid elements in sickle cell anaemia. Exposure of sickle-cell marrow aspirates to nitrogen at 37 degrees C for 30 min resulted in haemoglobin polymerization in most erythrocytes and reticulocytes but only in 10-20% of the nucleated erythroid cells. Haemoglobin polymers in the form of intertwining fibre meshworks were observed in reticulocytes, orthochromatic and polychromatophilic normoblasts, but were absent in basophilic normoblasts and pronormoblasts. The results suggest that the concentration of haemoglobin in intramedullary normoblasts may be the limiting factor determining the predisposition of these cells to undergo sickling as well as the pattern of haemoglobin aggregation. Under the physiological conditions prevailing in the marrow, haemoglobin concentration in normoblasts may be insufficient to result in aggregation and polymerization.

Anemia, Sickle Cell↗