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Biomedical subjects

J D Marshall

Publications and source records attributed to J D Marshall.

At least 73 records · Page 4Linked to original sources
PubMed1984

B cell maturation factor: effects on various cell populations.

B cell maturation factor (BMF) is a lymphokine that promotes the maturation of resting murine splenic B lymphocytes, and the analogous B cell tumor line WEHI-279, to the state of active immunoglobulin (Ig) secretion. All subsets of normal B cells examined, including neonatal and adult B cells, B cells from various organs, and B cells from CBA/N mice, are inducible by BMF. Induction of Ig secretion is independent of thymus-derived cells, LPS receptors, and MHC haplotype, because nude, C3H/He, and mice of many strains are equally responsive to BMF. Purified B cells prepared by using a fluorescence-activated cell sorter also respond to BMF, showing that BMF directly interacts with and triggers Ig secretion by B cells. In limiting dilution cultures, most normal resting splenic B cells or WEHI-279 B tumor cells are inducible by BMF. By using the WEHI-279 cells as a model system, specific aspects of the BMF response have been analyzed. In terms of the degree of stimulation observed, the primary mechanism for the induction of Ig secretion by BMF is an enhanced and balanced synthesis of Ig heavy (H) and light (L) chains. A less significant component of the induced Ig secretion is an increase in the ratio of secretory to membrane H chains produced. Kinetically, the shift in the ratio of secretory to membrane H chain forms occurs first, and this is followed by the increased synthesis of both L and H chains. Responding B cells also die during this induction process. Although the changes in the ratio of H chain forms, H and L synthesis, and cell viability take several days to occur, BMF will program significant later responses after only 1 or a few hr of interaction with target B cells.

Animals↗
PubMed1983

Suppression of endocytosis in polyclonally activated Con A-stimulated T lymphocytes by 25-hydroxycholesterol.

Endocytosis in polyclonally activated, Con A-stimulated spleen cell cultures was analyzed. It was found that as lymphocytes differentiate to acquire cytotoxic capability their endocytic activity also increases, reaching a plateau at 48 hr. Inhibition of sterol synthesis reduced endocytic rates by as much as 50% when 25-hydroxycholesterol was added during the first 24 hr of culture, the time at which sterol synthesis is at its maximum. When 25-hydroxycholesterol was added after the cycle of sterol synthesis, little or no suppression of endocytosis was seen. Compactin, which is an allosteric, competitive inhibitor of HMG-CoA reductase (the rate-limiting enzyme in the sterol biosynthetic pathway), produced a similar abrogation of endocytic rate. The effect of inhibition of sterol synthesis on endocytosis can be counteracted by the addition of cholesterol to the cultures. It is hypothesized that the dynamic process of endocytosis plays a role in the reorganization of membrane components necessary for the expression of the differentiated state of cytotoxicity.

Animals↗
PubMed1982

Cholesterol synthesis in polyclonally activated cytotoxic lymphocytes and its requirement for differentiation and proliferation.

The kinetics of sterol synthesis and DNA synthesis in polyclonally activated, concanavalin A-stimulated spleen cell cultures were analyzed. Inhibition of DNA synthesis by 1-beta-D-arabinofuranosylcytosine (Ara-C) did not abrogate the formation of cytotoxic effector cells. However, inhibition of sterol synthesis by 25-hydroxycholesterol inhibited formation of cytotoxic effector cells as well as cellular proliferation. The inhibition of cytotoxicity correlated well with the dose of 25-hydroxycholesterol administered and was dependent on the time of administration. The agent had to be present when sterol synthesis occurred normally during the time lapse before DNA synthesis began. Compactin had the same effect as 25-hydroxycholesterol. The effects of inhibition of sterol biosynthesis on cytotoxicity could be counteracted by addition of cholesterol-containing liposomes. Based on these experiments, the links between proliferation and differentiation in lymphocytes are discussed.

Animals↗
PubMed1979

High affinity Concanavalin A binding to sterol-depleted L cells.

Binding of Concanavalin A to mouse L cells which were grown in serum free, chemically defined medium and depleted of their membrane sterol by blocking their de novo sterol synthesis was investigated. Kinetic analysis of binding data implied positive cooperativity, with two different affinities for Con A, in both experimental and control cultures. The amount of Con A bound to the cell surface at saturation was approximately 0.5 picomoles per mg cellular protein in controls and approximately 1.0 picomoles per mg cellular protein in 25-hydroxycholesterol treated cultures (which had a reduced sterol concentration of up to 50% in their plasma membranes). This phenomenon was reversed when cholesterol or mevalonate was added to the inhibited cultures to compensate for their inability to synthesize sterol. Our findings indicate that lectin binding to specific glycoprotein receptors is influenced by membrane lipid composition.

Animals↗
PubMed1979

Pinocytosis in L cells: its dependence on membrane sterol and the cytoskeleton.

Pinocytosis in L-cells, grown in serum-free medium, was depressed when cultures were treated with oxygenated derivatives of cholesterol which inhibited sterol synthesis and reduced the sterol concentration of the plasma membranes. Noninhibitory sterols, such as cholesterol or desmosterol counteracted the effects of the inhibitors. Treatment with polylysine increased the rate of pinocytosis in sterol-depleted cells to a level similar to the enhanced rate found in polylysine treated control cells. Drugs which interfere with cytoskeletal systems (microfilaments, microtubules) also depressed pinocytosis but their effect could not be overcome by treatment with polylysine.

Animals↗
PubMed1979

Totally implantable dimension telemetry.

A totally implantable dimension telemetry system has been developed to instrument animals for chronic physiological research. Implantable signal processing electronics allow free-roaming animals with no percutaneous leads while retaining the long-term redproducibility of fixed implanted transducers. Two low-powered, custom-integrated circuits have been developed and assembled into an implantable package capable of measuring one dimension channel. The system has been operated in the amplitude modes of through-transmission and reflection as well as in a new Doppler-power configuration and aimed at determining interfaces between blood and surrounding structures. In a addition to single channel systems, these ICs are key elements in multimode, multidimensional implants capable of more accurate characterization of deep body structures.

Anatomy↗