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L S Colwell

Publications and source records attributed to L S Colwell.

7 recordsLinked to original sources
PubMed1990

An evaluation of external cause-of-injury codes using hospital records from the Indian Health Service, 1985.

To evaluate the usefulness of International Classification of Diseases external cause-of-injury and poisoning codes (E codes) for public health surveillance of nonfatal injuries, we analyzed E codes from Indian Health Service (IHS) hospital records. E codes for unknown or unspecified causes were used for 25 percent of records. At two hospitals, 63 percent of E codes assigned by independent coders agreed; another 18 percent matched on general cause-of-injury groups. With uniform guidelines and increased training, E coding could provide a valuable, cost-effective method of quantifying and characterizing severe, nonfatal injuries.

Health Services Administration↗
PubMed1990

Playground hazards in Atlanta child care centers.

We identified 684 playground hazards in 66 child care centers despite regulations mandating that the grounds be hazard-free. Of 21 centers with less than or equal to 5 hazards, 42.9 percent reported a playground-related injury in the previous year; of 25 centers with 6-11 hazards, 52.0 percent reported a playground-related injury; and of 20 centers with greater than or equal to 12 hazards, 60.0 percent reported a playground-related injury. Climbing equipment greater than or equal to 6 feet tall generally had inadequate impact-absorbing undersurfacing and had over twice the rate of fall injuries as climbing equipment less than 6 feet.

Child Day Care Centers↗
PubMed1971

Comparison of the effects of a synthetic polyribonucleotide with the effects of endotoxin on selected host responses.

An injection of a small dose (1 to 50 mug) of synthetic polyriboinosinic acid complexed with polyribocytidylic acid (poly I:poly C) inhibited the induction of tryptophan oxygenase by cortisone acetate; it induced tyrosine amino transferase, and it accelerated the loss of liver glycogen reserves. It also resulted in first a suppression followed by an activation of the reticuloendothelial system as judged by the rates of carbon clearance from blood. All of these responses are elicited by comparable doses of endotoxin. Pretreatment of mice with poly I:poly C did not, or only marginally, increased their nonspecific resistance to infection with several bacterial pathogens, and it failed to result in the development of tolerance to endotoxin, effects known to be produced by endotoxin when given under similar conditions.

Journal Article↗
PubMed1968

Inhibition of hepatic enzyme induction as a sensitive assay for endotoxin.

Bacterial endotoxins in mice reduced the induction by cortisone of two hepatic enzymes, tryptophan oxygenase, and phosphoenolpyruvate carboxykinase, they prevented the glyconeogenesis in liver induced by the same hormone, and they induced in intact animals the liver enzyme tyrosine-alpha-ketoglutarate transaminase, all in proportion to their ld(50). When cortisone was given in the least amount (100 mug), it resulted in near maximal induction of tryptophan oxygenase; a smaller amount of endotoxin reduced significantly the level of enzyme than that required when 5 mg of hormone was injected. The smallest amount of endotoxin that prevented tryptophan oxygenase induction was given intravenously to adrenalectomized mice in which 25 mug of cortisone was administered. The amount (0.01 mug) is 1/40,000th of the ld(50). The other metabolic processes subject to alteration by endotoxin required at least 100 to 400 times as much. This property of endotoxin can serve as a sensitive bioassay, although the dose-response curve is steep.

Adrenalectomy↗
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↗