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Biomedical subjects

C Waterhouse

Publications and source records attributed to C Waterhouse.

At least 19 recordsLinked to original sources
PubMed1988

Plasmodium relictum as a cause of avian malaria in wild-caught magellanic penguins (Spheniscus magellanicus).

Avian malaria (Plasmodium relictum) caused significant mortality in wild-caught Magellanic penguins (Spheniscus magellanicus) in 1986 at the Blank Park Zoo in Des Moines, Iowa (USA). In early winter, wild birds were captured off the southern coast of Chile and flown to Detroit, Michigan for a 38 day quarantine. After quarantine, 18 birds were dispersed to Lansing, Michigan, six to a facility in Maine, and 46 to Des Moines, Iowa. Upon arrival in Des Moines, several penguins became weak and inactive, had to be force-fed, and died after 2 days. Gross lesions at postmortem included splenomegaly, hepatomegaly, and pulmonary edema. Histopathological examination revealed numerous intraendothelial schizonts in spleen, lung, liver, heart and kidney. Schizonts were generally 16 to 28 micron by 11 to 16 micron and contained merozoites of two distinct sized (macromerozoites, nuclei 1.0 micron; micromerozoites, nuclei 0.5 micron). Based on the morphology of the abundant exoerythrocytic forms, a tentative diagnosis of avian malaria (Plasmodium sp.) was made. Subsequent transmission electron microscopic examination of schizonts in formalized tissue revealed merozoites with tear-shaped rhoptries. Antimalarial therapy was initiated early but deaths continued for 5 mo. Mortality, which eventually totaled 83%, occurred in three distinct waves, each separated by a hiatus of approximately 1 mo. Despite examinations of repeated blood smears, intraerythrocytic Plasmodium relictum was not detected until late in the outbreak. Diagnosis was based on morphologic characteristics including schizonts with eight to 12 merozoites/segmenter and round gametocytes that displaced and turned the infected erythrocyte nucleus. In addition to malaria, penguins showed evidence of aspergillosis, bacterial enteritis (Escherichia coli; Proteus sp.; and Edwardsiella sp.), and helminthiasis (Contracaecum sp. and Tetrabothrius sp.). Based on gross and histological lesions, disease prevalence in this group of penguins was malaria 58%, aspergillosis 61%, enteritis 60%, helminthiasis 26%. Epidemiologic investigation including group transport history, disease prevalence in co-quarantined birds not sent to Des Moines and climatological data implicated Des Moines as the likely site for initial exposure, although information is not conclusive. Stress and concurrent disease certainly contributed to the severe mortality in this group of penguins infected with P. relictum.

Animals↗
PubMed1981

Leucine metabolism in patients with malignant disease.

Studies of the metabolism of the amino acid, leucine, have been carried out in six patients with progressive cancer and compared to similar studies in a group of control subjects. U-14C leucine was given by the single injection technique and the disappearance of radioactive leucine from the plasma as well as the appearance of the label in expired air was determined over a 3-hour interval in both the overnight fasting state and during glucose ingestion. Plasma leucine levels in the basal state were higher in the patients with malignant disease (193 +/- 17 mumol/L vs 135 +/- 16 mumol/L) as was the flux or rate of appearance of unlabeled leucine molecules into the plasma (136 +/- 5 mumol/kg hour vs 79 mumol/kg/hour). Oxidation of leucine resulted in the appearance of about 19% of the injected label in expired CO2 of control subjects with almost twice that amount being found in progressive cancer patients. When the irreversible disposal of leucine to a metabolic fate other than oxidation was calculated (perhaps an indicator of protein synthesis), this was also increased in the progressive cancer patients. Exogenous glucose administration resulted in a fall in both leucine level and flux in the control subjects, while these parameters were less affected in three of the cancer patients. The fall in oxidation when glucose was given was more pronounced in the control subjects. These data are interpreted to mean that all aspects of leucine metabolism, presumably an example of branched chain amino acid metabolism, appear to be accelerated in subjects with cancer and weight loss. In addition, the peripheral control of the metabolism of this group of amino acids, as affected by glucose and insulin, appears to be impaired.

Body Weight↗
PubMed1979

Free amino acid levels in the blood of patients undergoing parenteral alimentation.

Free amino acid levels were determined in the blood of patients undergoing parenteral alimentation. During amino acid infusions, alanine, valine, glycine, isoleucine, leucine, proline, threonine, serine, methionine, phenylalanine, and lysine levels increased. Bivariate regression analysis was then done to determine the average rise in each amino acid when 1 mmole/hr of that amino acid was infused and when 1 mmole/hr of glucose was infused. This analysis was done on both arterial plasma and arterial wh-le blood increments. The average rise in the amino acid level with 1 mmole of infusion per hour varied from 32 to 133 mumole/liter. Only alanine levels were positively correlated with glucose infusion, while the branched chain levels were all negatively correlated. In no instance could a significant positive arteriovenous difference across the forearm be correlated with the infusion of an amino acid, despite amino acid levels as much as five times normal. Methionine, proline, valine, threonine, and lysine showed the greatest rise in blood concentration per millimole of amino acid infused per hour suggesting that their degradation or use in protein synthesis was limited. While the blood concentration rise in glycine was only about half as much per millimole per hour infused as was found in the previously mentioned group of amino acids, high rates of infusion of this amino acid resulted in large increments inglycine levels. It may be desirable to reduce the amounts of these amino acids in parenteral amino acid formulations.

Amino Acids↗
PubMed1979

Glucocorticoid effects in vitamin D intoxication.

Calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin D intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. Prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. Calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.

Calcium↗
PubMed1979

Gluconeogenesis from alanine in patients with progressive malignant disease.

We have studied by tracer technique the conversion of the carbon skeleton of alanine to glucose in patients with progressive malignant disease. These data have been compared to similar studies done in patients with chronic undernutrition from other causes. The results show increased conversion of alanine to glucose in the overnight fasting state as compared to the control group. Whereas the percentage increases are comparable to those found with pyruvate-glucose cycling in such subjects, the total amount of carbon conversion is considerably less (alanine carbon, 5.6 mmol/hr, versus pyruvate carbon, 39 mmol/hr). Exogenous glucose resulted in good suppression of alanine-to-glucose conversion as it does in normal subjects. It did, however, result in increased glucose-to-alanine conversion, increased alanine levels, and increased flux of alanine from the circulation. Although these latter data may not have specificity for the patient with advanced cancer, a strong dependence for carbohydrate and protein metabolism is suggested. We conclude that uncontrolled gluconeogenesis from alanine is probably not significant in terms of energy expenditure in the patient with uncontrolled cancer.

Adult↗
PubMed1979

Lactic acidosis and liver disease.

Both acute and chronic hepatic insufficiency can result in lactate accumulation and lactic acidosis; data from both types of patients were compared. In the chronic group, an acute precipitating event was identified in seven of nine subjects. Four had sepsis and three had gastrointestinal hemorrhage. In these patients, results from most tests of hepatic function were not altered dramatically. There were no long-term survivors in this group. In contrast, patients with acute hepatic failure had striking alterations in their results of hepatic function tests. Notable prolongation of the prothrombin time was always present initially and antedated other abnormalities of hepatic function. Three of seven patients in this group survived. Hypoglycemia was seen in both groups and in two subjects with acute hepatic insufficiency, glucose administration alone resulted in rapid lowering of lactate levels.

Acidosis↗
PubMed1978

Peripheral amino acid levels in patients with cancer.

Peripheral arterial and venous whole blood amino acid concentrations were determined in four groups of subjects after an overnight fast 1) normal people, 2) patients with cancer who had not lost body weight, 3) subjects with cancer who had lost more than 20% of body weight and 4) patients who had lost more than 20% of body weight from diminished intake due to cause other than cancer. Comparison of the arterial blood levels in the four groups showed that patients with cancer and weight loss had amino acid patterns different from patients who were malnourished for other reasons. Branched chain amino acids were normal in patients with malignant disease. Some gluconeogenic amino acids were reduced as in other subjects with weight loss but the characteristic rise in glycine seen with malnutrition was not present. Arterio venous differences in whole blood across the forearm showed no evidence of increase in venous excess in patients with progressive malignant disease, indicating no excessive protein catabolism in muscle tissue. The data are consistent with increased gluconeogenesis in malnourished cancer subjects, probably due to intrinsic change in hepatic metabolism.

Amino Acids↗
PubMed1978

Treatment of alcoholic acidosis: the role of dextrose and phosphorus.

We have made serial metabolic observations in 18 acute episodes of alcoholic ketoacidosis in ten patients. Data from patients treated with only saline initially were compared to data from patients who received modest amounts of intravenous dextrose (7.0 to 7.5 gm/hr). More rapid improvement in the acidotic state was seen in the latter group (P less than .001). The quicker decline in absolute levels and ratio of beta-hydroxybutyrate to acetoacetate when glucose was given suggests that this treatment induced mitochondrial oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH). Since phosphorus is a critical cofactor necessary for NADH oxidation and the glucose-induced correction of the acidosis was associated with a rapid decline in serum phosphorus from an initial mean of 6.79 +/- .82 mg/100 ml SEM to 0.96 +/- 0.12 mg/100 ml in 24 hours, we propose that glucose enhanced the mitochondrial capacity to oxidize NADH by increasing hepatocyte phosphorus. This effect combined with decline in free fatty acid levels results in reversal of acidosis. Our data suggest that glucose provides the safest, most effective treatment for this disorder; addition of either insulin or bicarbonate is usually unnecessary.

Acetoacetates↗
PubMed1978

The contribution of glucose to alanine metabolism in man.

We have studied by tracer technique the interconversion of the carbon skeleton of alanine with that of glucose. The data analysis is in terms of renewal theory rather than traditional compartmental analysis. This eliminates the need for estimation of compartment size, which is particularly difficult to determine in the case of alanine. In addition, the conversion rates between the two substances are found by considering the two components which are responsible for the determined radioactivity curves, namely, the first conversion of the labeled carbon and its subsequent movement in the product compound. The subjects of the study were for the most part underweight but had been hospitalized and eating a standard hospital diet for at least 3 days prior to the studies. Our data indicate that nearly twice as much carbon from glucose is cycled to alanine as is recycled from alanine back to glucose after a 14 hr overnight fast. Small amounts of glucose suppress the alanine-glucose arm of the cycle but probably do not change the glucose-alanine conversion. The contribution of glucose carbon to alanine metabolism is significant and appears to be immediately influenced by the magnitude of glycolysis.

Adult↗
PubMed1976

Vitamin D resistance in magnesium deficiency.

Four patients with gastrointestinal disorders, and one patient with chronic alcoholism presented with both hypocalcemia and hypomagnesemia. Pharmacological doses of either ergocalciferol or dihydrotachysterol did not correct the hypocalcemia except in one patient who had a minimal rise in serum calcium. Parathormone levels were high in three patients and exogenous parathormone given to the fourth subject failed to elicit a rise in serum calcium, implying impairment of the calcemic response to parathormone. Magnesium repletion simultaneously corrected the hypomagnesemia and hypocalcemia. Balance data suggested that the rise in serum calcium was in part, at least, due to increased mobilization of minerals from bone. While the mechanism remains speculative, it appears that magnesium facilitates the release of calcium from bone in the presence of adequate amounts of vitamin D and parathormone.

Adolescent↗
PubMed1975

The effect of potassium loading on sodium excretion and plasma renin activity in Addisonian man.

Potassium has been shown to suppress plasma renin activity (PRA). This study was designed to study the role of increased aldosterone production in the mediation of such a response. Five patients with adrenal insufficiency were placed on a diet of 60 meq potassium and 100-150 meq of sodium while receiving a constant amount of cortisone acetate and Florinef. Upright PRA was determined each day for 2-3 days in the control period and then for 3-4 days after potassium intake had been increased to 200-300 meq/day. Potassium loading induced a natriuresis. Hence, patients were either sodium replaced (six studies in four patients) or allowed to become sodium depleted (three patients). Potassium loading without replacement was associated with a decrease in weight, negative sodium balance, hyperkalemia, and a positive potassium balance. PRA rose during the experimental period. Potassium loading with sodium replacement was associated with little change in weight or sodium balance. Hyperkalemia and positive potassium balance were present to the same degree as found in the studies without sodium replacement. When all PRA values are considered (both morning and evening values) there was no significant change with potassium loading (+ 1.31 ng/ml per h; range + 6.9 to -2.0). We conclude that hyperkalemia or a positive potassium balance did not suppress PRA in Addisonian man in these studies when sodium balance was maintained, nor did it prevent a rise in PRA when sodium balance was negative.

Addison Disease↗
PubMed1975

GammaG-globulin production and light-chain metabolism in patients with metastatic cancer.

GammaG-Globulin and excess light-chain metabolism were studied in eight subjects with progressive metastatic malignant disease by determining the plasma radioactivity curves following the administration of appropriately labeled substances. In addition to the plasma die-away curves, which required about 3 weeks for full expression for gamma-globulin, but only 3 to 4 days for light-chain, urinary excretion of the label from metabolized protein was determined. The data are compared to similar studies in control individuals. The metabolism of excess light chain was similar to normal in all respects. The total synthesis of gammaG-globulin was increased with a mean value about twice normal. The mean survival time of a circulating immunoglobulin molecule was short, indicating rapid loss from the system. Other aspects of immunoglobulin metabolism were similar to normal with a normal percentage of the labeled protein appearing in the urine, suggesting no abnormality in the utilization pattern but simply an increased rate of turnover. The capability of malnourished patients with cancer to produce large quantities of immunoglobulin is not specific for this disease, since similar patterns may be seen in response to infections in protein-depleted individuals. However, there is the possibility that the cancer itself acts as an inciting agent in these subjects. Furthermore, such sustained protein synthesis may place an additional burden on already compromised host metabolism.

Humans↗