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Biomedical subjects

R McLeod

Publications and source records attributed to R McLeod.

At least 127 records · Page 7Linked to original sources
PubMed1980

Necrotizing vasculitis and Sarcocystis: a cause-and-effect relationship?

We have described a patient with an unusual infection with Sarcocystis and a necrotizing vasculitis with subcutaneous nodules, and have discussed the possibility of a cause-and-effect relationship between these two entities and the available diagnostic methods and therapeutic measures.

Adult↗
PubMed1980

Inhibition or killing of an intracellular pathogen by activated macrophages is abrogated by TLCK or aminophylline.

Agents that are known to inhibit certain metabolic pathways or cell functions were evaluated to determine their effects on the capacity of activated macrophages to inhibit or kill obligate intracellular pathogens. Tosyllysine chloromethyl ketone (TLCK) and aminophylline abrogate inhibition or killing of Toxoplasma gondii by activated macrophages.

Amino Acid Chloromethyl Ketones↗
PubMed1979

A method to evaluate the capacity of monocytes and macrophages to inhibit multiplication of an intracellular pathogen.

A new method to assess intracellular inhibition of multiplication or killing by normal and activated mouse peritoneal macrophages, human peripheral blood monocytes, and human monocyte-derived macrophages is described. This method involves measurement of incorporation of [3H]uracil into nucleic acids of the obligate intracellular parasite Toxoplasma gondii. The method utilizes the observation by Pfefferkorn and Pfefferkorn (1977) that [3H]uracil is incorporated in substantially greater amounts by T. gondii than by certain mammalian cell types. Differential uptake of [3H]uracil by Toxoplasma-infected and uninfected cultures allows for evaluation of the ability of macrophages or monocytes to inhibit or kill this organism. This method has been adapted to microsystem.

Animals↗
PubMed1979

Probable transmission of Toxoplasma gondii by organ transplantation.

Two heart transplant recipients developed toxoplasmosis shortly after surgery. As neither recipient had serologic evidence of exposure to Toxoplasma gondii before transplantation, infection was acquired from an exogenous source. Of the possible modes of transmission of Toxoplasma to the recipients, infection by the oral route or through transfusion of blood or blood products seems remote. Since both heart donors had serologic evidence of recently acquired toxoplasma infection at the time of transplantation and the myocardium is known to be infected with the organism during acute infection, we considered these facts to be a strong implication that the donors' hearts were the most likely source of toxoplasma infection in the recipients.

Adult↗
PubMed1978

Pseudomonas maltophilia causing heroin-associated infective endocarditis.

The association of Pseudomonas maltophilia endocarditis in three patients with recent history of intravenous drug abuse is reported. All three patients had abnormal heart valves (two prosthetic and one rheumatic). A prominent characteristic of this uncommon pathogen is its in vitro resistance to the commonly used antimicrobials. Cure was achieved in all three cases. In two cases, synergistic antibiotic combinations were used. In one case, plasmid-mediated resistance to amikacin sulfate (Amikan, British; no comparable US product) emerged during therapy. The two patients with prosthetic valves received combined surgical and antibiotic therapy.

Adult↗
PubMed1977

A new method for evaluation of intracellular inhibition of multiplication or killing by mononuclear phagocytes.

A new method for evaluation of the capacity of mononuclear phagocytes to inhibit intracellular microorganisms is described. The system provides a means for assessing this effect of macrophages without concern for multiplication of extracellular organisms, effect of antibiotics, and the potential observer bias which may result from visual evaluation. It involves measurement of amount of [6-3H]UdR incorporated by Toxoplasma gondii. Differences between uptake of [6-3H]UdR by infected and uninfected macrophages can be augmented by cytosine arabinoside as this agent inhibits macrophage DNA synthesis but does not substantially alter DNA synthesis by the test organism, T. gondii.

Animals↗