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M Callaham

Publications and source records attributed to M Callaham.

31 records · Page 2Linked to original sources
PubMed1985

Epidemiology of fatal tricyclic antidepressant ingestion: implications for management.

Although there is a large body of literature documenting the lethal cardiotoxic complications of tricyclic antidepressant (TCA) overdose, the absence of reliable predictive signs has led to a policy of admitting even trivial-appearing overdoses for inpatient observation. A study of 18 fatal cases revealed that with the exception of two that received clearly inadequate medical care, all fatal ingestions developed major signs of toxicity mandating admission within two hours of arrival at the hospital, and the mean time from arrival to death was only 5.43 hours. All patients who died of direct TCA toxicity did so within 24 hours of arrival. In addition, half the fatal cases presented with only trivial signs of poisoning, but deteriorated catastrophically within one hour. These data lead to an algorithm to guide admission of serious cases.

Adult↗
PubMed1982

Induction of differentiation of human promyelocytic leukemia (HL-60) cells by teleocidin and phorbol-12-myristate-13-acetate.

Human promyelocytic leukemia cells (HL-60) were induced to differentiate into macrophage-like cells in a dose-dependent manner by the tumor promoters phorbol-12-myristate-13-acetate and teleocidin, a non-phorbol ester promoter. An HL-60 cell variant, designated as R-59, which is resistant to differentiation induction by phorbol-12-myristate-13-acetate was also resistant to differentiation induction by teleocidin. Differentiation was determined by increases in the percent of morphologically mature cells and in lysozyme and nonspecific esterase activities. Both compounds inhibited the growth of HL-60 cells by blocking them from entering the synthesis phase of the cell cycle with an accumulation of cells after 48 h in G1 phase. No such effects were observed in the R-59 cells. They were, however, as susceptible as the parent HL-60 cells, to inducers which are not considered to be tumor promoters such as dimethylsulfoxide and retinoic acid. However, these inducers cause the HL-60 and R-59 cells to differentiate into granulocyte-like cells. These results indicate that teleocidin produces in both the HL-60 and R-59 cells effects which are similar to those cause by phorbol-12-myristate-13-acetate. The possibility that agents producing such effects in these two cell types may represent potential tumor promoters is discussed.

Alkaloids↗
PubMed1981

Dog bit wounds.

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Aerobiosis↗
PubMed1981

Alterations in polyamine levels induced by phorbol diesters and other agents that promote differentiation in human promyelocytic leukemia cells.

Polyamine levels were evaluated in human HL-60 promyelocytic leukemia cells after treatment with inducers of terminal differentiation. Differentiation in these cells was determined by increases in the percentage of morphologically mature cells and in lysozyme activity. Treatment of the HL-60 cells with phorbol 12-myristate-13-acetate (PMA), phorbol 12,13-didecanoate or other inducers of terminal differentiation such as dimethylsulfoxide and retinoic acid resulted in increased levels of putrescine. However, no increase in putrescine could be detected after PMA treatment of a HL-60 cell variant that exhibited a decreased susceptibility to PMA-induced terminal differentiation. Similarly, no increase in putrescine was observed with two non-tumor-promoters (phorbol 12,13-diacetate and 4-O-methyl-PMA) or with anthralin, a non-phorbol tumor promoter. In addition to enhancing putrescine levels, PMA also increased the amount of spermidine and decreased the amount of spermine. The increase in putrescine and spermidine preceded the expression of the various differentiation markers. Unlike the changes observed in the polyamine levels after PMA treatment, the activities of ornithine and S-adenosylmethionine decarboxylases, which are polyamine biosynthetic enzymes, did not significantly change. alpha-Methylornithine and alpha-difluoromethylornithine and methylglyoxal bis(guanylhydrazone), which are inhibitors of the polyamine biosynthetic enzymes, did not affect differentiation in control or PMA-treated cells. Because of these observations, we suggest that the change in polyamine levels involve biochemical pathways other than the known biosynthetic ones. By-products of these pathways may perhaps be the controlling factors involved in the induction of terminal differentiation in the HL-60 and other cell types as well.

Cell Differentiation↗
PubMed1981

Down regulation of specific binding of [20-3H]phorbol 12,13-dibutyrate and phorbol ester-induced differentiation of human promyelocytic leukemia cells.

Binding of [20-3H]phorbol 12,13-dibutyrate ([3H]PDB) to intact human promyelocytic leukemia cells susceptible (HL-60) or resistant (R-35) to phorbol ester-induced differentiation was characterized. Specific binding of [3H]PDB to both HL-60 and R-35 cells at 37 degrees C reached a maximum within 15-20 min. Maximal specific [3H]PDB binding to HL-60 cells was followed by a decline (down regulation) of radioactivity. This down regulation was temperature dependent, because no loss of radiolabel occurred by 1 hr at 4 degrees C. The down regulation of bound [3H]PDB seen in HL-60 cells at 37 degrees C was not observed with R-35 cells. Prior exposure of the HL-60 cells but not of R-35 cells to 1 microM phorbol 12-myristate 13-acetate for 90 min at 37 degrees C caused a marked reduction in the specific binding of [3H]PDB. When [3H]PDB binding was carried out at 4 degrees C, [3H]PDB bound to both cell types in a rapid, specific, and reversible manner. At equilibrium, HL-60 and R-35 cells were found to contain almost the same number of binding sites, which had dissociation constants of about 50 nM, indicating that the failure of R-35 cells to undergo PDB-induced differentiation was not associated with any change in the affinity or in the number of [3H]PDB binding sites. These results indicate that the down regulation of specific [3H]PDB binding may be a crucial early event in the control of phorbol ester-induced terminal differentiation in HL-60 cells. Furthermore, we suggest that such down regulation may be involved in other cellular and biochemical effects of phorbol diester tumor promoters.

Binding Sites↗
PubMed1980

Dog bite wounds.

Dog bite wounds are a common problem with an infection rate only slightly higher than that for lacerations in general. Wounds may be sutured after debridement and thorough irrigation, unless they are located on the hand, where infection is common. Infection is caused by a variety of organisms. A penicillinase-resistant penicillin or cephalexin monohydrate is the drug of choice; studies suggest prophylactic antibiotic therapy may be useful, especially in high-risk wounds.

Animals↗
PubMed1980

Prophylactic antibiotics in common dog bite wounds: a controlled study.

A double-blind prospective study of 98 patients was carried out, but 57 (58%) returned for follow-up and form the basis of this report. Wound irrigation and debridement were found to be important in reducing infection. Hand wounds were most likely to become infected; face and scalp wounds were at low risk. Puncture wounds became infected more often than did lacerations. Suturing wounds did not increase the likelihood of infection except on the hand, where the data were equivocal. Prophylactic penicillin decreased the incidence of infection in high-risk wounds; there was no difference in low-risk wounds. Cultures of wounds showed many different organisms but were of no predictive value. Pasteurella multocida was found very rarely. Staphylococcus aureus accounted for 10% of all infections, a finding which makes use of a penicillinase-resistant penicillin logical.

Adolescent↗
PubMed1979

Animal bites.

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Animals↗