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Biomedical subjects

T C Jones

Publications and source records attributed to T C Jones.

At least 109 records · Page 6Linked to original sources
PubMed1975

Assessment in vitro of immunity against Toxoplasma gondii.

Studies have been made on humoral and cellular immune respones in mice immunized with an attenuated strain of Toxoplasma gondii. Heat-inactivated antitoxoplasma serum did not cause morphologic changes in the organisms, but did markedly influence their interactions with host cells. Toxoplasma exposed to antibody were no longer capable of entering fibroblasts or HeLa cells. They were readily engulfed by macrophages, but the antibody treatment strikingly altered the intracellular fate of the parasites leading to killing and digestion of the toxoplasmas in phagolysosomes. Addition of antitoxoplasma antibody immediately after infection of macrophages in vitro had no effect on intracellular multiplication of the organism. The division time of virulent toxoplasmas in mouse peritoneal macrophages in vitro was markedly prolonged in cells from immunized mice. During the first 2-3 mo after immunization, the macrophages harvested from the peritoneal cavity demonstrated this cellular immunity directly; thereafter exposure of the macrophages to immune lymphocytes and toxoplasma antigen, or to supernates from such an interaction was required for induction of the maximal capacity to inhibit growth of toxoplasmas. Induction of the alternation in macrophages by the lymphocyte product was detectable in 6 h and maximal at 18-24 h. Cultivation in vitro of macrophages from immunized animals for periods longer than 48 h rendered the cells nonresponsive to the immune lymphocyte-toxoplasma product. Macrophages from the peritoneal cavities of normal, nonimmunized mice were also incapable of developing the capacity to inhibit growth of toxoplasmas in response to this product. The nonresponsiveness of normal macrophages, or of macrophages cultured for several days in vitro was not changed by exposure of the cells to antitoxoplasma serum.

Animals↗
PubMed1975

Imported mucocutaneous leishmaniasis in New York City. Report of a patient treated with amphotericin B.

A case of mococutaneous leishmaniasis in a patient referred to Memorial Sloan-Kettering Cancer Center, New York, with a presumptive diagnosis of lethal mid-line granuloma is described. The patient had lived in Bolivia and had been treated with antimony during and after which his mucosal lesions progressed. These lesions completely healed with 971 mg of amphotericin B. Mucocutaneous leishmaniasis is endemic in many areas of Central and South America and may occur in patients in the United States who have lived in or traveled to these areas. Organisms may be difficult to identify, and multiple biopsies and cultures may be necessary. The use of amphotericin B for the treatment of leishmaniasis is reviewed. It is an effective alternative to antimony therapy, and in some cases resistant to antimony, it may be the drug of choice.

Adult↗
PubMed1975

A technique for isolating and concentrating microfilariae from peripheral blood by gradient centrifugation.

A method for isolating microfilariae from blood cells by Ficoll-Hypaque centrifugation, followed by concentration by conventional centrifugation, is described. A 30 fold concentration and quantitative recovery of parasites was achieved. This technique should be of value for documenting low levels of parasitaemia, and for obtaining relatively pure suspensions of microfilariae for metabolic studies and antigen analysis.

Blood↗
PubMed1975

Effect of glucocorticosteroids on phagosome-lysosome interaction.

The effects of hydrocortisone on fusion of thorotrast-labeled lysosomes with phagosomes containing killed toxoplasmas was studied. Mouse peritoneal macrophages from glucocorticosteroid-treated animals fromed phagolysosomes just as effectively as macrophages from untreated animals (72% thorotrast-positive vacuoles in hydrocortisone-treated animals; 78% in controls). The electron microscopic appearence of macrophages from treated or untreated animals was similar. This observation complements studies which show no change in intracellular microbicidal activity in macrophages treated with glucocorticosteriods.

Animals↗
PubMed1975

Y-autosome translocation in the howler monkey, Alouatta palliata.

Two modal diploid chromosome numbers were encountered in a population sample of howler monkeys, Alouatta palliata. The modal diploid number of males was 53, females: 54. Karyotypes prepared by G-band and C-band techniques identified a Y-auto-some translocation in the males.

Alouatta↗
PubMed1975

Phylogeny of complement components in non-human primates.

The antigenic properties and functional activities of complement components were analyzed in primates to determine their relative evolutionary development. The sera of eight different sub-human primate species were examined by double diffusion in agar and compared to a pool of human serum with rabbit and goat antisera to human complement components Clq, Cls, C4, C2 C3, C5, C6, C8, C9, properdin, factor B (B), and C1 inhibitor. There are no apparent antigenic differences in complement proteins between man and the apes except for C1q. Old world monkeys are antigenically deficient in Clq,C1s, C9, and variably deficient in C4, C3, and C8. New World monkeys are antigenically deficient in all components (measured) except C5, C6, and properdin factor B. Prosimians are antigenically deficient in all components. Functional analyses of complement components showed similar levels in man and primates, except in prosimians. There is a dissociation between hemolytic assays and antigenic analyses, suggesting that functional sites may be separate from antigenic sites.

Absorption↗
PubMed1972

The interaction between Toxoplasma gondii and mammalian cells. I. Mechanism of entry and intracellular fate of the parasite.

Macrophage, fibroblast, and HeLa cell cultures have been infected with Toxoplasma gondii, and observations have been made on parasite entry and fate. A special procedure was devised for studying the entry of toxoplasmas by electron microscopy. Toxoplasmas were centrifuged onto the cells in the cold; fixation 1-3 min after warming yielded specimens showing numerous examples of parasites in the process of entering cells. The mechanism of entry into macrophages, fibroblasts, and HeLa cells was in all cases by phagocytosis. Micropseudopods were extended by the cells to envelop the attached parasites in a typical phagocytic vacuole. Apparently the toxoplasmas stimulated this response of HeLa cells and fibroblasts, cell types not usually phagocytic. No instance was seen of penetration of toxoplasmas through the cell membrane, or of parasites located free in the cytoplasm. Essentially all of the toxoplasmas that entered HeLa cells divided with a generation time of 9 hr; the parasites formed large rosettes situated in vacuoles, eventually leading to host cell rupture. Macrophages took in larger numbers of toxoplasmas than did HeLa cells, but approximately half of the parasites inside of macrophages degenerated within a few hours. The surviving toxoplasmas in macrophages divided every 8 hr, forming rosettes and eventually rupturing the cells.

Animals↗
PubMed1972

The interaction between Toxoplasma gondii and mammalian cells. II. The absence of lysosomal fusion with phagocytic vacuoles containing living parasites.

Electron microscope methods have been used to study delivery of macrophage primary or secondary lysosomal contents to phagocytic vacuoles containing living or dead toxoplasmas. Secondary lysosomes were labeled by culturing the cells in colloidal thorium dioxide (thorotrast) or in ferritin. Acid phosphatase cytochemistry was employed for detection of primary as well as secondary lysosomal constituents. These various lysosomal labels were present in nearly all vacuoles containing toxoplasmas killed with glutaraldehyde, or in vacuoles containing those parasites undergoing degeneration 1 hr after the uptake of living toxoplasmas. In contrast, at times ranging from 1 to 20 hr after infection, no vacuoles containing morphologically normal, apparently viable toxoplasmas were thorotrast or ferritin positive, and only rarely did these vacuoles react for acid phosphatase. In many instances vacuoles containing viable toxoplasmas and no lysosomal markers were situated in the same cell nearby to vacuoles containing degenerating toxoplasmas and lysosomal constituents, thus indicating that the determinants of lysosomal fusion were operating locally in the immediate vicinity of the phagocytic vacuole, and not operating to influence general cell function. Thus, some toxoplasmas are able to prevent the delivery of lysosomal contents, and apparently the phagocytic vacuole provides for these parasites a sheltered microenvironment ideal for their growth. Morphologic evidence indicated that living toxoplasmas altered the phagocytic vacuolar membrane in macrophages, fibroblasts, and HeLa cells. Within minutes after phagocytosis, the vacuole became surrounded by closely apposed strips of endoplasmic reticulum and mitochondria; somewhat later, microvillous protrusions of the membrane into the vacuole were seen. These morphologic features of phagocytic vacuoles containing living toxoplasmas may be of importance in relation to the absence of lysosomal fusion, or they may serve some function in protecting the host cell or in nourishing the parasite.

Acid Phosphatase↗