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L J Berry

Publications and source records attributed to L J Berry.

88 records · Page 5Linked to original sources
PubMed1966

Inhibition of inducible liver enzymes by endotoxin and actinomycin D.

Berry, L. Joe (Bryn Mawr College, Bryn Mawr, Pa.), Dorothy S. Smythe, and Louise S. Colwell. Inhibition of inducible liver enzymes by endotoxin and actinomycin D. J. Bacteriol. 92:107-115. 1966.-Bacterial endotoxin at the ld(50) level lowers liver tryptophan pyrrolase in mice, it prevents for 16 to 20 hr the induction of the enzyme by a concurrent injection of cortisone, it lowers significantly but does not prevent substrate induction, and it reduces the enzymatic activity promptly and significantly when administered during the course of hormonal induction. The ld(50) amount of actinomycin D has a similar effect on tryptophan pyrrolase, except that its inhibition of induction by cortisone persists for a longer period of time. Endotoxin in the intact mouse induces tyrosine-alpha-ketoglutarate transaminase almost as well as cortisone, but not in the adrenalectomized animal, a fact that suggests induction of this enzyme is due to release of endogenous adrenal hormones. Actinomycin D, on the other hand, has an effect on this transaminase similar to that on tryptophan pyrrolase. The site of action of endotoxin and actinomycin D would appear to be similar for one of the two enzymes studied and different for the other, a relationship that requires a specificity difficult to imagine for a material as complex as endotoxin.

Adrenalectomy↗
PubMed1965

Some metabolic aspects of tolerance to bacterial endotoxin.

Berry, L. Joe (Bryn Mawr College, Bryn Mawr, Pa.), and Dorothy S. Smythe. Some metabolic aspects of tolerance to bacterial endotoxin. J. Bacteriol. 90:970-977. 1965.-The tolerance to bacterial endotoxins which is produced in mice given a series of daily injections of heat-killed Salmonella typhimurium failed to occur when actinomycin D was administered with the heat-killed cells. Neither ethionine nor 2-thiouracil, when given with endotoxin, altered the development of tolerance. An injection of endotoxin, actinomycin D, or ethionine lowered the activity of the liver enzyme tryptophan pyrrolase more significantly at either 4 or 17 hr postinjection in normal mice than in tolerant mice. Similarly, an injection of either saccharated iron oxide or Thorotrast lowered liver tryptophan pyrrolase activity more extensively in normal than in tolerant animals. Activation of the reticuloendothelial system (RES) of tolerant mice, as determined by an accelerated rate of carbon clearance from the blood, was observed, but this was prevented by the appropriate dose of actinomycin D. Similar results were obtained when saccharated iron oxide, rather than endotoxin, was used to activate the RES, but these animals were not resistant to endotoxin and their tryptophan pyrrolase was normally diminished after an injection of endotoxin. Thus, RES activation may occur without tolerance developing. A more nearly normal level of enzyme activity appears to be characteristic of the tolerant state.

Cortisone↗
PubMed1963

POSSIBLE SOURCE OF SECONDARY INVADING STAPHYLOCOCCI IN MICE EXPOSED TO ACUTE COLD.

Miraglia, Gennaro J. (Bryn Mawr College, Bryn Mawr, Pa.) and L. Joe Berry. Possible source of secondary invading staphylococci in mice exposed to acute cold. J. Bacteriol. 85:345-348. 1963.-In an effort to determine the origin of the staphylococci known to invade the deep tissues (liver, spleen, kidneys, lungs, and heart) of mice exposed continuously to 5 C in individual compartments without bedding, the intestinal tract was freed of these organisms, as judged by absence of growth when fecal suspensions were inoculated into selective media. Substitution of 0.01 n hydrochloric acid for drinking water eliminated staphylococci within a few days, yet the incidence of tissue invasion was unaltered. The coagulase-negative strains normally present in feces and in tissues persisted in tissues even though the intestine was seeded with a coagulase-positive strain by feeding contaminated food. Cultures from the external nares continued unaltered. This suggests that the respiratory tract is a possible origin of the staphylococci found in tissues of the cold-stressed mice.

Journal Article↗
PubMed1962

ENHANCEMENT OF SALMONELLOSIS AND EMERGENCE OF SECONDARY INFECTION IN MICE EXPOSED TO COLD.

Miraglia, Gennaro J. (Bryn Mawr College, Bryn Mawr, Pa.) and L. Joe Berry. Enhancement of salmonellosis and emergence of secondary infection in mice exposed to cold. J. Bacteriol. 84:1173-1180. 1962.-The ld(50) dose for mice of Salmonella typhimurium, strain RIA, is 4.1 x 10(5) for animals individually housed without bedding and maintained at 25 C. It is 3.8 x 10(3) for animals similarly housed but kept at 5 C. An intravenous injection of 0.1 ml of Proferrin 2 hr prior to infection with RIA lowers the ld(50) to 4.9 x 10(3) and to 4.0 x 10(1) for mice kept, respectively, at 25 and at 5 C. Low environmental temperature and "blockade" of the reticuloendothelial system (RES) lower the resistance of mice to about the same degree, but low temperature and RES impairment together lower resistance as if each were acting independently. No effect of cold could be detected in mice infected with the highly virulent SR-11 strain of S. typhimurium, since all animals died after infection with only a few cells. Mice that were natural carriers of salmonellae, as judged by fecal discharge, were highly resistant to challenge and responded to cold in a manner similar to normal mice infected with RIA. Strain RIA could be isolated from the tissues of infected animals with greater frequency and persisted longer in mice maintained at 5 C than those at 25 C. Staphylococci were isolated from livers of animals that survived salmonella infection for 14 days at 5 C, and the incidence of staphylococci was proportional to the number of salmonellae injected. At 25 C, only a small percentage of mice had staphylococci in tissues and these occurred independent of the infectious dose of salmonellae. These observations were made on normal mice infected with RIA and on carrier mice infected with SR-11.

Journal Article↗
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Bacterial toxins.

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Animals↗