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Biomedical subjects

W H Adams

Publications and source records attributed to W H Adams.

At least 37 records · Page 2Linked to original sources
PubMed1989

Early renal ultrasonographic findings in dogs with experimentally induced ethylene glycol nephrosis.

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary junction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.

Animals↗
PubMed1989

Prophylaxis of cyanobacterial and mushroom cyclic peptide toxins.

The pathogenicity of virulent cyclic peptide toxins of the cyanobacterium, Microcystis aeruginosa, and the mushroom, Amanita phalloides, was prevented in mice by pretreatment with a variety of chemically unrelated agents including hydrocortisone, shellac, certain diazo and triazine dyes and cyclosporine. A. Despite the diverse nature of the protective agents, a feature commonly associated with protection was the ability to impair hepatic uptake of 51Cr-labeled sheep erythrocytes, a function of hepatic macrophages (Kupffer cells). In addition, several of the protective agents are known to affect other aspects of reticuloendothelial cell function. Therefore it seems likely that the hepatic macrophage is involved in the observed protection, although by what mechanism(s) is unknown. The most remarkable prophylaxis was seen with a single injection of Trypan red, which provided nonimmunologic protection against a lethal dose of a cyanobacterial toxin, cyanoginosin-LR, for periods up to 3 months.

Amanitins↗
PubMed1988

Pathophysiology of cyanoginosin-LR: in vivo and in vitro studies.

Cyanoginosin-LR, one of the group of virulent cyclic heptapeptide toxins (cyanoginosins) isolated from some strains of the cyanobacterium, Microcystis aeruginosa, kills mice within 1-2 hr after iv or ip injection. Although the liver is a target organ of the toxin, the rapidity of lethality is incompatible with metabolic death from failure of hepatocellular function. However, disintegration of sinusoidal endothelium causes massive intrahepatic hemorrhage. The loss of the structural integrity of hepatic sinusoids provides a previously undescribed mechanism for embolization of disintegrating cells from the liver to the lung. No injury to either cultured bovine pulmonary artery endothelial cells or mouse peritoneal macrophages was observed following prolonged incubation with high concentrations of the toxin, and there was no increase in vascular permeability to 125I-labeled albumin detected before intrahepatic hemorrhage. However, plasma fibronectin increased transiently after toxin injection. Acute, severe thrombocytopenia, a characteristic of cyanoginosin-LR toxicity, remains unexplained since platelets did not concentrate in the lungs, liver, or spleen. There are similarities between the effects of cyanoginosin-LR and of the lipopolysaccharide endotoxins, such as elevations of plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha.

Animals↗
PubMed1988

Effects of deuteration on hematopoiesis in the mouse.

Mice ingesting 30 to 50% D2O (heavy water, deuterium oxide) developed a dose-dependent depression of formed peripheral blood elements in 4 to 9 days. The principal mechanism of anemia and thrombocytopenia is impaired hematopoiesis. Despite pancytopenia in the peripheral blood, bone marrow cellularity and morphology remained normal. Upon replacement of D2O with tap water, platelet and neutrophil concentrations returned to normal within 48 to 72 hr. In contrast, blood lymphocyte concentrations remained low for several weeks. B-lymphocytes may be more affected by deuteration than other lymphocyte subsets. In vivo reticuloendothelial cell function, as assessed by 51Cr-labeled sheep erythrocyte clearance, was unaffected by D2O. Although a dose-dependent decrease in fluid intake occurred during deuteration, hematocytopenia was not a consequence of dehydration. In view of the known kinetics of D2O in biological systems, the rapid response of myeloid elements to deuteration must be due primarily to the solvent (nonmetabolic) isotope effect. Prolonged deuteration has proven toxic when included in regimens for treatment of neoplasia, including leukemia, in animal models. The present study shows that modulation of hematopoiesis by D2O is possible without invoking the toxicities associated with prolonged deuteration.

Animals↗
PubMed1987

Normal hematologic values and prevalence of anemia in children living on selected Pacific atolls.

The hematologic status of infants and children living on the small islands of the Pacific basin has been poorly documented. This report determines the normal ranges for hemoglobin (Hb) and mean corpuscular volume (MCV) for children residing on four of the small atolls of the Republic of the Marshall Islands in the archipelago of Micronesia. The difficulty in establishing normal hematologic values in pediatric populations is discussed and a methodology suggested that does not exclude any Hb value above the mean in determining the normal range for Hb. The study population was comprised of 563 Marshallese children representing approximately 3.4% of all children less than 16 years of age living in the Marshall Islands. The local prevalence of anemia and iron deficiency was also established.

Adolescent↗
PubMed1987

Toxoplasma antibodies and retinochoroiditis in the Marshall Islands and their association with exposure to radioactive fallout.

Nearly universal serologic evidence of Toxoplasma gondii infection was found to have occurred by adulthood in 517 Marshallese tested in 1981-1982. The prevalence and incidence of retinal lesions compatible with toxoplasmosis were 3.9% and 273 cases/year/100,000 seropositive persons, respectively, thus indicating a significant public health problem. Seronegativity was significantly more common in a subgroup of Marshallese that had received 110-190 rads of total-body gamma radiation as a consequence of accidental exposure to radioactive fallout in 1954. Despite this finding there was no evidence of an increase in clinically significant lesions in exposed persons.

Adolescent↗
PubMed1986

Blood bromine levels in a Pacific atoll population.

Serum and red cells from 20 Marshallese on two atolls and from 10 subjects in New York were compared for their elemental composition employing an energy dispersive X-ray fluorescence technique. The elements analyzed in serum included Cl, Zn, and Br, whereas red cells were analyzed for Cl, K, Fe, Zn, Br, and Rb. Both Marshallese groups showed statistically significant (P less than 0.01) elevations in serum Br (51 and 96%) and in red cell Br (393 and 478%) as compared to the New York group. The Marshallese Br/Cl ratio in serum and in red cells was elevated when compared to that of the New York group, whereas the Rb/K ratios were equivalent. The red cell Br/serum Br ratio was also elevated in the Marshallese subjects. There were no similar differences noted among the other elements tested. Drinking liquids in the Marshall Islands were analyzed for Br but did not provide a clear source for the elevated Br levels.

Adult↗
PubMed1986

Serologic markers for hepatitis B among Marshallese accidentally exposed to fallout radiation in 1954.

At least one serologic marker of prior hepatitis B infection (hepatitis B surface antigen, antibody to surface antigen, or antibody to core antigen) was found in 91.7% of 314 Marshallese tested. The prevalence of hepatitis B surface antigenemia (3.3%) in a subpopulation that had resided on Rongelap Atoll at the time of accidental exposure to radioactive fallout from a thermonuclear test in 1954 did not differ significantly from the prevalence in a selected unexposed population (10.5%).

Adolescent↗
PubMed1985

Pathophysiologic effects of a toxic peptide from Microcystis aeruginosa.

Toxin-LR, a hexapeptide produced by Microcystis aeruginosa, causes marked hepatic vascular congestion, thrombocytopenia, microscopic pulmonary thrombi and death in 50-70 min when injected into mice. Although it is considered an hepatotoxin, we report that sublethal hepatocellular damage produced by CCl4 given 24 hr prior to toxin-LR administration prevents the acute deaths. However, CCl4-treated mice surviving toxin-LR acute effects often died during the subsequent three days. Pretreatment of mice with the microsomal enzyme inhibitors SKF 525A or cobaltous chloride did not alter the acute lethality of toxin-LR, but pharmacologic doses of hydrocortisone prevented both the acute and delayed deaths. X irradiation-induced thrombocytopenia or thrombocytopenia and leukopenia did not significantly affect the toxin's lethality. In vitro platelet aggregation or lysis did not occur during incubation with toxin-LR, nor was a humoral aggregating factor detected in plasma from toxin-injected mice.

Animals↗
PubMed1984

Pediatrics in the Marshall Islands.

The delivery of health care to children living on isolated island communities presents unique challenges to health professionals. An evolved method of providing longitudinal services to infants and children residing on islands of the Marshall Island chain--a central Pacific portion of the Micronesian archipelago--is presented. The difficulties associated with provision of comprehensive health care in a vast ocean area are discussed.

Adolescent↗
PubMed1983

Atypical pulmonary thrombosis caused by a toxic cyanobacterial peptide.

Parenteral injection into mice of a toxic pentapeptide isolated from the cyanobacterium Microcystis aeruginosa induced thrombocytopenia, pulmonary thrombi, and hepatic congestion. The lethality of the toxin was unaffected by several anticoagulants. The acute liver damage that follows injection of the toxin has been attributed to direct action on liver cells but may be due to hypoxemia, heart failure, and shock.

Animals↗
PubMed1982

Periodic neutropenia and monocytopenia.

A patient with periodic neutropenia exhibited simultaneous monocytopenia, and epinephrine infusion revealed no monocytes in the marginating pool during neutropenia. Lymphocytes, eosinophils, and platelets also fluctuated periodically, but serial bone marrow studies and epinephrine infusion data indicate these fluctuations could have represented epiphenomena rather than a more global form of periodic hematopoiesis. Bone marrow descriptions of most cases of periodic neutropenia have indicated a "maturation arrest" at the promyelocyte or myelocyte stage prior to development of neutropenia; peripheral blood monocytes are usually normal or fluctuate out of phase with neutrophils. In this present case, "maturation arrest" occurred at the myeloblast stage, and neutrophils and monocytes cycled together. Morphologically normal eosinophilopoiesis with a mean eosinophil to erythroid ratio in the marrow of 0.27 +/- 0.10 (SD) persisted despite a sustained disappearance of promyelocytes.

Agranulocytosis↗
PubMed1981

Correlations and cumulative frequency distributions of maternal and newborn hematologic data.

Nonparametric correlation coefficients and cumulative frequency distributions of hematologic data and birth weight obtained from 151 mothers and most of their newborns have been analyzed. Taken overall, the data reaffirm considerable fetal autonomy in maintaining hematologic homeostasis; a dissociation was found between maternal and newborn hemoglobin (Hb) levels, there was no evidence for an effect of maternal iron deficiency on the fetus, nor was birth weight correlated with maternal Hb levels. However, the lack of significance of the latter two correlations was apparent only when three maternal-newborn pairs with alpha-thalassemia were excluded from analysis. An inverse relation was found between birth weight and Hb level in the newborn, and this was present over the entire birth weight range, rather than being restricted to small-for-gestational-age newborns.

Anemia, Hypochromic↗
PubMed1978

Thrombocytopenia and intravenous heroin use.

Five young male heroin users presented with a syndrome resembling acute immune thrombocytopenic purpura. Although a viral, autoimmune, or toxic origin cannot be conclusively excluded at present, data are most consistent with the hypothesis that the thrombocytopenia was due to a drug-related immunologic mechanism that resulted in peripheral platelet destruction. Epidemiologic considerations suggest the common agent involved in their illnesses was present in the heroin they used. Although glucocorticoid therapy was followed by clinical recovery in four of the five patients (one was lost to follow-up), it is not certain that this represented a causal relation.

Adult↗
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↗