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Biomedical subjects

L Jackson

Publications and source records attributed to L Jackson.

At least 181 records · Page 10Linked to original sources

Survey of human lymphoblastoid cell lines and primary cultures of normal and leukaemic leukocytes for oncornavirus production.

Velocity sedimentation of uridine-labelled cultures was found to be more reliable than isopycnic sedimentation in detecting oncornavirus production in lymphoid cells. Of 13 cell lines (including six derivea from Burkitt's lymphomas and two from leukaemic leukocytes) only one, the leukaemia-derived, Epstein-Barr virus-producing line QIMR-WIL, showed any activity. The nature of the QIMR-WIL particles was further defined by isolation of uridine-labelled 70S RNA and by the simultaneous assay for reverse transcriptase and 70S RNA, but production of such particles was detected in only three of 10 assays. Pretreatment of cells with 5'-iododeoxyuridine or culture in arginine-free medium did not induce particle production. Syncytia assays using XC cells were negative. Of 13 primary cultures (nine samples of leukaemic leukocytes and four of cord leukocytes) treated with mitogens and subjected to inducing conditions, one (leukocytes from a patient with acute myelogenous leukaemia) showed evidence in successive assays of oncornavirus synthesis. The low and transient yield of oncornavirus-like particles obtained in this work parallels that reported in previous studies of fresh lymphoid cells and primary cultures.

Burkitt Lymphoma↗

Spleno-hepatic tuberculosis due to Mycobacterium kansasii.

A case of tuberculosis of the spleen and liver is described. The organism involved was Mycobacterium kansasii, one of the atypical mycobacteria. The lack of evidence in the literature of primary splenic or hepatic involvement by this organism suggests that it is rare. In this instance it complicated a case of myeloproliferative disease, megakaryocytic myelosis with extra-medullary haemopoiesis, and was not diagnosed until autopsy.

Autopsy↗

Effect of phenobarbitone on plasma lipids in normal subjects.

1. Phenobarbitone in a dose of 180 mg daily was administered to ten normal subjects for 3 weeks. There was a significant increase in total plasma cholesterol, plasma low-density-lipoprotein cholesterol, plasma low-density-lipoprotein (LDL) triglycerides and plasma LDL protein. The increase in plasma LDL cholesterol accounted for the increase in total plasma cholesterol. There was a significant reduction in the ratio of LDL cholesterol to LDL protein. 2. No significant changes were observed in total plasma triglycerides, plasma very-low-density-lipoprotein (VLDL) triglycerides, plasma VLDL cholesterol or plasma VLDL protein. 3. Evidence that drug-metabolizing enzymes were induced by phenobarbitone was provided by an increase in antipyrine clearance. No relationship was observed between changes in plasma cholesterol and changes in antipyrine clearance. Serum gamma-glutamyl transpeptidase was also increased after phenobarbitone administration, the increase being unrelated to changes in antipyrine clearance or plasma cholesterol.

Adult↗

The relationship between liver volume, antipyrine clearance and indocyanine green clearance before and after phenobarbitone administration in man.

Liver volume and the clearances of antipyrine and indocyanine green have been measured before and after administration of phenobarbitone (180 mg/day) for 3 weeks to ten healthy subjects. The measurement of liver volume by an ultrasound scanning technique yielded reproducible results which were consistent with predictions of liver size by allometric methods. Before phenobarbitone, antipyrine clearance correlated with liver volume, but there was no correlation between indocyanine green clearance and liver volume. Phenobarbitone administration increased the clearance of antipyrine significantly by 90 +/- 14% but there was no significant change in indocyanine green clearance or liver volume. After phenobarbitone the correlation between antipyrine clearance and liver volume persisted. There was no correlation between indocyanine green clearance and liver volume. These results suggest that in non-medicated subjects some of the difference in antipyrine clearance is due to difference in functional hepatic parenchymal mass and that phenobarbitone increases the drug metabolising capacity per unit of hepatic mass but not total liver size.

Adult↗

Lymphocyte stimulation with skin cells. A function of maturation.

Cell monolayers grown from trypsin dispersions of whole rat embryos were tested for their capacity to stimulate allogeneic rat thymus cells in mixed cell cultures. Cells from whole embryos of only 15-days gestation were virtually ineffective at stimulating allogeneic thymus cells. Cells from 19-day-old whole embryos produced definite stimulation and stronger stimulation was obtained with skin cell monolayers prepared from these embryos. The average amount of allogeneic stimulation obtained with rat skin cells increased with the age of the donor animals. The greatest degree of stimulation occurred when the skin cells were obtained from rats about 1 week postpartum. Thereafter, the stimulating potential of allogeneic skin cells declined and was found to stabilize at the levels observed when adult skin cells were used as the stimulator cells. Neither rat brain cells nor rat kidney cells (taken from embryos, neonates, and adults) were capable of inducing allogeneic rat thymocytes to undergo significant transformation in culture. We conclude that the in vitro lymphocyte response to skin cell stimulation is a function of skin cell maturation, and that the inability of kidney cells or brain cells to provoke the same sort of stimulation is not attributable to antigen loss during or after foetal development, but exists as a feature of these cells at the earliest stages of differentiation.

Animals↗

T lymphocyte-enriched murine peritoneal exudate cells. I. A reliable assay for antigen-induced T lymphocyte proliferation.

The in vitro activation of murine thymus-derived (T) lymphocytes by soluble protein and synthetic antigens has been difficult to assess because of the lack of a specific and reliable proliferation assay. The present report describes the development of an assay system which overcomes these problems by making use of a population of nylon wool column-purified T lymphocytes obtained from thioglycollate-induced peritoneal exudates of immunized mice. PETLES (peritoneal exudate, T lymphocyte-enriched cells) were composed mainly of T lymphocytes, eosinophils and small numbers of macrophages. Contamination with bone marrow-derived (B) lymphocytes averaged only 2%. When PETLES from immunized mice were stimulated in microtiter cultures with the immunizing antigen, large degrees of proliferation ensued as measured by incorporation of 3H-methyl-thymidine 5 days after initiation. As few as 1.25 x 10(4) cells and as little as 50 ng/ml of antigen gave significant stimulation. Maximum responses were obtained witn a series of 10 experiments under these optimal conditions, gave a mean incorporation of 70,900 cpm while the controls cultured without antigen showed only 3,600 cpm. PETLES from nonimmunized mice or from mice immunized to other antigens did not respond to DNP5OVA although they did respond to mitogens. The antigen-induced proliferation was shown to require the presence of immune T lymphocytes by two criteria: elimination of the response by treatment with anti-Thy 1.2 serum plus complement and failure to reconstitute the response when the few remaining immune B lymphocytes left after anti-Thy 1.2 treatment were added to nonimmune T lymphocytes. In addition, the system exhibited carrier specificity. Because of the paucity of B lymphocytes in the population, their contribution to the overall magnitude of the proliferative response was negligible as demonstrated by the small response to B cell mitogens. Thus, the assay appears to be a quantitative as well as a qualitative assay for one aspect of T lymphocyte function. This technique should prove useful for the study of murine T lymphocytes in vitro.

Animals↗