Neil I. Gallagher
Saint Louis University
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Featured researches published by Neil I. Gallagher.
Annals of Internal Medicine | 1960
Neil I. Gallagher; John M. Mccarthy; Robert D. Lange
Excerpt During the last decade the clinical and experimental observations of numerous investigators have established the concept that erythropoiesis is regulated in part by humoral factors. Recent ...
Experimental Biology and Medicine | 1965
D. L. Mann; M. L. Sites; R. M. Donati; Neil I. Gallagher
Summary Serial observations were made on plasma erythropoietin levels of infants during the first 90 days of life. Results indicate variable erythropoietin titers and are suggestive of a physiologic control of erythro-poiesis during the newborn period by erythro-poietin.
Annals of Internal Medicine | 1967
Dean L. Mann; Neil I. Gallagher; Robert M. Donati
Excerpt Erythrocytosis as an unusual complication of cancer has been documented in an increasing number of reports. The prevalence and the pathogenesis of this association have recently been review...
Experimental Biology and Medicine | 1973
Robert M. Donati; J. W. Fletcher; M. A. Warnecke; Neil I. Gallagher
Summary The purpose of this study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. The oxygen consumption was again measured and the experiments initiated 8 weeks thereafter. The 18-hr red cell radioiron incorporation was used as an index of erythropoiesis. The gastrointestinal absorption of radioiron and the 24-hr urinary erythropoietin levels were assessed. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D-triiodo-thyronine, L-triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L-triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L-triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.
Annals of Internal Medicine | 1965
Robert M. Donati; Mary Anne Warnecke; Neil I. Gallagher
Excerpt Alteration of thyroid function influences the synthesis and life span of the red blood cell. Anemia occurs in hypothyroid patients (1, 2) and in animals after thyroid ablation when there ha...
Experimental Biology and Medicine | 1964
R. M. Donati; M. A. Warnecke; Neil I. Gallagher
Summary LT3 administration produced an increase in erythrocyte radioiron incorporation in rats. This response was not modified by administration of reserpine. Animals given LT3 or DT3 showed comparable increases in erythrocyte radioiron incorporation, however rats given LT3 demonstrated a marked increase in oxygen utilization when compared to DT3 treated rats.
Experimental Biology and Medicine | 1966
D. L. Mann; R. M. Donati; Neil I. Gallagher
Summary Erythrocyte radioiron incorporation following administration of renin, angiotensin II or aldosterone was not altered suggesting that these substances do not have erythropoietic stimulating properties. In addition, maintenance of rats on a sodium-deficient diet for a 3-week period in order to effect increased endogenous renin and aldosterone production produced no alteration in the red blood cell mass. The significance of these results in relation to the renal origin of erythropoietin is discussed.
Experimental Biology and Medicine | 1973
J. W. Fletcher; Neil I. Gallagher; M. A. Warnecke; Robert M. Donati
Summary Exposure to a 50% oxygen environment produced a decrease in erythropoiesis which was paralleled by a decrease in plasma erythropoietic stimulating activity. Similar results were obtained following exposure to a 100% oxygen environment. Marrow depression produced by hyperoxia could be reversed by erythropoietic stimulants. The suppression of erythropoiesis in both partners of parabiots maintained so that one breathed 20% and the other 90-95% oxygen suggests that a humoral inhibitor is produced in the hyperoxic animal and supports the hypothesis that erythropoiesis is regulated by the dynamic interaction of erythropoietin and an erythropoietic inhibitor.
Experimental Biology and Medicine | 1964
R. M. Donati; C. W. Chapman; M. A. Warnecke; Neil I. Gallagher
Summary Iron metabolism was studied in acutely starved and erythropoietically stimulated rats. Acute starvation did not alter blood volume or gastrointestinal absorption of radioiron. However, prolongation of the plasma iron clearance with concomitant diminution in plasma iron turnover and radioiron in the bone marrow was demonstrated in starved animals. These results can be explained by diminished erythropoiesis. Eryth-ropoietin administration reversed these changes, augmenting plasma iron turnover, gastrointestinal absorption of radioiron and bone marrow radioiron content. Approximately equal increases in plasma iron turnover were produced in both the fed and starved animal by injection of equal amounts of erythropoietin.
International Archives of Allergy and Immunology | 1974
Raymond G. Slavin; Neil I. Gallagher
Lymphocytopenia is a common accompaniment of renal failure. To study this phenomenon, guinea pigs were made uremic by ureteral ligation. In one day, peripheral lymphocytes had decreased by 44%. The phenomenon is not species-specific since both rats and rabbits exhibited early peripheral blood lymphocytopenia after bilateral nephrectomy or ureteral ligation. Lymphocytopenia due to the markedly elevated blood cortisol levels following ureteral ligation is unlikely for two reasons. Normal guinea pigs injected with large amounts of corticosteroids showed no lymphocytopenia. Adrenalectomized rats underwent bilateral nephrectomy with resultant increase in plasma creatinine and marked fall in peripheral lymphocytes. The rapid development of the lymphocytopenia associated with uremia would favor increased destruction rather than decreased production.