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Biomedical subjects

I Gray

Publications and source records attributed to I Gray.

At least 55 records · Page 3Linked to original sources
PubMed1968

Leukocyte lactate dehydrogenase changes as an indicator of infection prior to overt symptoms.

Lactic acid dehydrogenase (LDH) concentration of rabbit serum and leukocytes was followed during the course of an acute infection with Diplococcus pneumoniae. Control values were obtained prior to infection, and again 4, 24, and 48 hr later. LDH isozymes were characterized by acrylamide gel electrophoresis and quantitated by densitometry. An increase in serum LDH was observed as early as 4 hr after infection. These levels returned to normal in 24 hr and rose again 48 hr after infection. The LDH level of leukocytes, from 10 of 12 infected rabbits, rose rapidly during the 24-hr period after exposure. The levels were two to three times the original preinoculation level for that animal. In six of these rabbits, this LDH elevation occurred 4 hr after inoculation and preceded the onset of fever. Change in the type of leukocyte did not account for the increase in cellular LDH. All infected rabbits showed approximately the same increase in polymorphonuclear leukocytes, but not all developed comparable increases in LDH. The isozyme patterns obtained, when defined amounts of enzyme were applied to the gel for electrophoresis, were characterized for the most part by a three-enzyme pattern. Increasing amounts of enzyme occasionally revealed a fourth, more cathodal, enzyme. The more cathodic enzymes appear to be the most responsive when sudden shifts in enzyme concentration occur within the cell.

Animals↗
PubMed1967

Metabolic changes in nicotinamide adenine dinucleotide in response to anthrax toxin.

Bacillus anthracis produces a toxin both in vitro and in vivo which, when injected intravenously into rats, brings about the death of the animals accompanied by gross pulmonary edema. Lung tissue removed prior to death showed, in vitro, a 30% reduction in overall oxidative metabolism (Q(o2)), whereas the nicotinamide adenine dinucleotide (NAD)-independent succinic dehydrogenase remained unaffected. The NAD concentration in the lungs of injected animals was reduced by 50%. Upon addition of NAD, the Q(o2) of lung tissue from injected animals rose to control values. At 45 min after toxin injection, the serum lactate concentration began to rise, showing about a 3.5-fold increase over controls after 75 min. No changes occurred in the pyruvate concentration. These changes may be explained by increased use of the pyruvate for glycolytic energy production with further loss of NAD. Additional experiments with liver, spleen, kidney, and brain tissues showed that the toxin-induced reduction of Q(o2) is an effect specific for lung tissue. Brain tissue showed a significant increase in oxidative metabolism upon the addition of the toxin, whereas the other tissues remained unaffected. It is suggested that a principal effect of the toxin is to inhibit, in lung tissue, the regeneration of NAD in the respiratory chain.

Animals↗
PubMed1966

Clinical chemistry of staphylococcal enterotoxin poisoning in monkeys.

Clinical chemistry values were examined in 90 monkeys administered a purified preparation of staphylococcal enterotoxin, type B, intravenously. These studies showed an early release of epinephrine accompanied by a mild increase in blood glucose. This was followed by progressively developing prolonged hypoglycemia. An early increase in bloodurea nitrogen occurred, presumably as a result of both prerenal azotemia and functional renal failure seen in association with the observed hypotension. Serum protein, Ca, and Cl concentrations decreased with time. Pi levels increased, whereas Na and K concentrations in serum remained unchanged. Serum enzyme concentrations were unchanged, with the exception of serum glutamic oxaloacetic transaminase, which rose rapidly when compared with prechallenge control observations or with values from sham-challenged monkeys. These changes were statistically significant. These results suggested that enterotoxin administered intravenously produced early change in glucose metabolism, possibly related initially to catecholamine release and later to increased utilization of glucose and metabolic acidosis. Other findings were compatible with tissue breakdown at as yet undetermined locations and with loss of endothelial membrane integrity, as evidenced by loss of protein from the vascular space.

Animals↗
PubMedDate not supplied

Cadmium modification of the response in Balb/c mice to MOPC-104E tumor.

The immunotoxicological effects of cadmium suggest that it may alter immunosurveillance. However, the studies contributing to this conclusion have been conducted at relatively high cadmium concentrations and for extended periods of exposure. Cadmium was administered in the drinking water of Balb/c mice at 0.01, 0.10, and 1.0 ppm for 4 to 5 wk. Under these conditions, there was a cadmium dose-dependent change in the mortality rate of mice when challenged with an intraperitoneal injection of 5 X 10(3), 5 X 10(4), or 5 X 10(5) MOPC-104E plasmacytoma cells. There was a maximum decrease in mortality at the 0.01 ppm dose level, while at the higher cadmium concentrations there was little or no change. At the two highest tumor cell doses, there was a decrease in the incubation time of the illness in animals exposed to 0.01 ppm cadmium. This returned to control values at the higher concentration of cadmium. The data indicate that at very low concentrations cadmium can alter tumor growth by more than one mechanism that may involve immunocompetence.

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