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S J Stewart

Publications and source records attributed to S J Stewart.

52 records · Page 3Linked to original sources
PubMed1984

Immunochemical analysis of the released Leu-2 (T8) molecule.

We recently have found that the human T cell antigen Leu-2 was specifically released from Leu-2-bearing cells. The preliminary study showed that the released Leu-2 (RLeu-2) from HPB-ALL cells was composed of a single polypeptide chain of 27,000 molecular weight (mol wt), which was smaller than the subunit of the homodimeric molecule found on the cell surface. In the present study, RLeu-2 was further characterized and compared with cellular Leu-2 (CLeu-2). Metabolically radiolabeled Leu-2 was released from HPB-ALL cells and this released Leu-2 molecule had a mol wt of 27,000. Cell surface radioiodinated HPB-ALL cells were found to release radioactive Leu-2 molecules and this antigen also had the same mol wt of 27,000. In both experiments, the CLeu-2 was reconfirmed to be composed of a 33,000-mol wt subunit under reducing conditions. These experiments establish that the 27,000-mol wt single polypeptide chain of Leu-2 released from the cell is derived directly from the homodimeric Leu-2 molecule on the cell surface, presumably by a specific proteolytic cleavage. Two-dimensional gel analysis showed that CLeu-2 exhibited extensive charge heterogeneity with predominantly basic isoelectric points, whereas RLeu-2 was a group of more acidic proteins with less charge heterogeneity. Although CLeu-2 and RLeu-2 showed several different immunochemical characteristics, the homology between these two antigens was confirmed by the following results: CLeu-2 and RLeu-2 were found to share at least three different antigenic determinants, Leu-2a and Leu-2b, and those which were detected by a polyvalent rabbit antiserum. Significant similarities between CLeu-2 and RLeu-2 were demonstrated by peptide mapping analysis of these antigens. Therefore, RLeu-2 appears to be the specific, physiological product of the CLeu-2 protein.

Animals↗
PubMed1983

Quantum differences in oral susceptibility of voles, Microtus pennsylvanicus, to virulent Francisella tularensis type B, in drinking water: implications to epidemiology.

Shedding nephritis in voles with chronic tularemia is the probable source of frequent contamination of streams over wide areas of the northern hemisphere. However, voles inoculated parenterally with as few as one dex viable cells of Francisella tularensis palaearctica succumb uniformly to acute tularemia, whereas voles, beavers, and muskrats often thrive in waters contaminated with the organism. Nevertheless, water-borne epizootics do occur in these animals, and at these times streams are heavily contaminated. In attempts to determine the lethal dose, per os, of the bacteria to voles, it was found that there are stable, 'order-of-magnitude' differences in susceptibility of individual weaned voles reared under uniform conditions. Also, voles thus infected often became chronically infected with bacteriuria. It is proposed that the most susceptible voles are responsible for amplification of water contamination and thus for initiation of water-borne epizootics in hygrocolic mammals and for frequent mild infections in man.

Animals↗
PubMed1983

Biosynthesis, glycosylation, and in vitro translation of the human T cell antigen Leu-4.

Two families of polypeptides were found in immunoprecipitates formed from human T cell lines by using the monoclonal antibody anti-Leu-4. When analyzed by one- and two-dimensional SDS-PAGE, the first family consisted of members with m.w. of 26,000 and isoelectric points that varied from very basic to acidic. The second family consisted of members with m.w. of 22,000 to 23,000 and isolectric points that varied from neutral to very acidic. The biosynthetic processing and intracellular glycosylation of several of these polypeptides were examined. Some, but not all, intracellular forms of the Leu-4 antigen contained N-linked oligosaccharides of the high mannose type. By using messenger RNA from human T cell lines, intracellular forms of Leu-4 were shown to be accurately translated and properly processed by Xenopus oocytes in vitro.

Animals↗
PubMed1981

Amphotericin B-induced resistance to Schistosoma mansoni.

Amphotericin B (AmB) increases host resistance against several infectious agents and tumors. We evaluated its effect on infections with the helminth Schistosoma mansoni. A single dose of 500 microgram i.p. or 25 microgram i.v. increased resistance in mice to a challenge with 500 or 100 S. mansoni cercariae. Schistosomula recovery from the lungs, 5 days after challenge, was reduced 33 to 40%. Adult worm recovery 8 wk after infection was reduced 36 to 43%, AmB was effective in protecting mice when given from 9 days before until the day of cercarial challenge but was ineffective 2 wk before or at all intervals after S. mansoni infection. To examine the mechanism of this resistance, we obtained peritoneal exudate cells (PEC) from animals treated with AmB and assessed their ability to kill schistosomula, the migrating larval stage of the parasite. Killing by adherent PEC 1 or 2 days after AmB treatment was the same as that of resident macrophages from untreated animals. Adherent PEC from animals 3 to 7 days after AmB treatment showed enhanced killing of schistosomula (38.0 plus or minus 3.0% at day 4, which exceeded control of 8.1 plus or minus 4.0%, p less than 0.01). These PEC also displayed increased killing of Staphylococcus aureus. When AmB was added to cultures of resident peritoneal adherent cells from untreated mice at 0.5 microgram/ml to 2.0 microgram/ml (concentrations not toxic to the organism), schistosomula killing was increased 1- to 6- fold. These findings demonstrate activation of murine macrophages by AmB in vitro and in vivo, which results in greater killing of this multicellular parasite and potentially contributes to enhanced resistance to infection.

Amphotericin B↗
PubMed1979

Resistance to tick-borne Francisella tularensis by tick-sensitized rabbits: allergic klendusity.

Mammals become hypersensitive to ticks that feed upon them. That hypersensitivity was thought responsible for an observation that a large number of Francisella tularensis-infected Dermacentor variabilis failed to infect a rabbit previously exposed to ticks of that species. In a series of tests of that hypothesis, rabbits sensitized to ticks were often significantly more resistant than control animals to tick-borne tularemia. The conditions that determine the klendusity are thought to be variable and complex but the phenomenon must be of importance in the epidemiology of some arthropod-borne agents.

Animals↗
PubMed1978

Mutagenicity testing of benomyl, methyl-2-benzimidazole carbamate, streptozotocin and N-methyl-N'-nitro-N-nitrosoguanidine in Salmonella typhimurium in vitro and in rodent host-mediated assays.

The fungicide benomyl and its commercial preparations Fundazol 50WP and Benlate 50WP and the benomyl metabolite methyl-2-benzimidazole carbamate and its commercial preparation MBC 50WP were tested for mutagenicity in in vitro spot tests, in microsomal plate assay, in liquid-culture treatments, or in rodent host-mediated assay. The base-pair substitution Salmonella typhimurium mutant hisG46 and the hisG46-bearing uvrB excision-repair-deficient mutants TA100, TA1530, TA1535 or TA1950 were used as test organisms. Complete genotypic information of these mutants is given in Ames et al. [2]. Captain 50WP, streptozotocin (SZN), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 2-aminopurine and N-acetylaminofluorene were used as positive control compounds. In nonoverlay spot tests Benlate 50WP was not mutagenic over a dose range of 50-5000 microgram/spot in hisG46 and TA1535. In overlay spot tests 50 or 100 microgram/spot Benomyl, MBC, Fundazol 50WP, Benlate 50WP and MBC 50WP were tested in hisG46, TA1530 or TA1950. Only a non-commercial MBC sample at 100 microgram/spot showed weak mutagenic activity in hisG46. In microsomal activation plate assay MBC, benomyl, Fundazol 50WP and Benlate 50WP were tested in TA100 over a dose range of 50-2000 microgram/plate. None of the compounds showed mutagenicity. In a 20-h liquid-culture treatment 10, 100, 1000 and 10 000 microgram/ml Fundazol 50WP were not mutagenic in TA 30. In 1-h liquid-culture treatments benomyl, Benlate 50WP or Fundazol 50WP failed to induce mutations in hisG46, TA100 or TA1950 over a dose range of 0.25-1000 microgram/ml. Appropriate positive controls were mutagenic in each experiment. The consistently negative results in this study with commercial MBC and benomyl preparations are contrary to positive results reported earlier with similar methods and similar commercial preparations. Possible reasons to explain the different results are presented. The alkylating agents SZN and MNNG induced fewer mutations in TA1530 and TA1950 uvrB excision-repair-deficient strains than in the hisG46 excision-proficient strain, indicating that with these mutagens excision-repair is also a mutation-prone process. In rodent host-mediated assays with Fundazol 50WP in mice 3 consecutive subcutaneous hourly doses of 500 mg/kg in hisG46 and TA1950 and in rats or mice an oral dose of 4000 mg/kg in TA1950 were not mutagenic. The positive control SZN was mutagenic.

Animals↗
PubMed1977

Dissimilar courses of twins with leukemia.

Twin girls, genetically identical, probably experienced different leukemogenic events and presented with acute lymphocytic leukemia 6 years apart. Their clinical presentations were similar, but they received significantly different therapy. The first twin died 34 months after diagnosis following multiple remissions and relapses, having received single-drug maintenance. The second twin remains free of apparent disease 60 months after diagnosis, following vincristine and prednisone induction, 6-mercaptopurine maintenance, methotrexate and prednisone reinforcement, and central nervous system treatment of occult disease. Their dissimilar clinical courses may have been due to different leukemogenic events and/or markedly different therapeutic programs.

Antineoplastic Agents↗
PubMed1975

Chronic shedding tularemia nephritis in rodents: possible relation to occurrence of Francisella tularensis in lotic waters.

Contamination of streams by Francisella tularensis, a fastidious pathogen, was discovered by Miller in Russia. Subsequently that contamination was found to be the source of extensive human outbreaks, and to occur as well in North America. Circumstantial evidence supports a hypothesis that infected voles are responsible for the contamination, but when freshly isolated F. tularensis palaearctica is inoculated parenterally, only acute illness and death result whereas long-term contamination of streams would seem to demand a more chronic process. Laboratory studies have demonstrated that voles have an apparent predilection to tularemic nephritis when partially immunized before parenteral infection, but also when naive voles are infected orally. Associated chronic bacteriuria would seem to fulfill requirements for protracted contamination of watersheds.

Animals↗