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Biomedical subjects

G S Johnson

Publications and source records attributed to G S Johnson.

At least 145 records · Page 8Linked to original sources
PubMed1977

Social-services support for multiple sclerosis patients in West of Scotland.

A survey has been carries out of 104 patients with multiple sclerosis (m.s.) in West-Central-Scotland. All patients were living at home, and success of services to assist them in the community was examined. The partients were aged 16-65 years and had permanent disability, many being severely handicapped. Regular hospital follow-up was more common among the least disabled. 24 patients had never seen a social worker. Many patients had experienced problems with employment but 37 per cent of these had never registered with a disablement resettlement officer. After advice 10 additional patients applied successfully for an attendance allowance. Legislation requires local authorities to compile a register of the disabled and give information on services available to them. Only 19 patients were registered, however, and no one had received any information from a local authority. Many of these M.S. patients had failed to establish or maintain contact with available services. These results indicate a need for reorganisation of the support for the chronically disabled, possibly by setting up regular clinics for assessment and management, as recommended by the Tunbridge report (1972).

Adolescent↗
PubMed1977

Control of growth by picolinic acid: differential response of normal and transformed cells.

Picolinic acid reversibly inhibits the growth of cultured cells. Fourteen other pyridine derivatives were ineffective or toxic. Untransformed normal rat kidney (NRK) cells are reversibly arrested in the G(1) stage of the growth cycle as shown by cell counts, mitotic index, [(3)H]thymidine incorporation, and flow microfluorometry. Flow microfluorometry was used to monitor the effects of picolinic acid on numerous other cell lines. Normal cells are blocked in G(1), whereas transformed cells show responses that are dependent upon the transforming virus and independent of species or origin of the cell line. Kirsten sarcoma virus-transformed cells are blocked in G(1). Simian virus 40-transformed cells progress to a G(2) block. Cells transformed by polyoma or Harvey sarcoma virus with Moloney virus coat have flow microfluorometry profiles that indicate blocks in both G(1) and G(2). Cells transformed with Moloney sarcoma virus are not blocked in a specific phase of the cell cycle. Picolinic acid does not change the levels of NAD(+) plus NADH; however, the growth inhibition by picolinic acid is partially overcome by nicotinamide. These results suggest that picolinic acid interacts with a specific growth control mechanism that may involve NAD(+) and that this control mechanism is altered by different transforming viruses in different manners.

Cell Division↗
PubMed1977

Selective toxicity induced by picolinic acid in simian virus 40-transformed cells in tissue culture.

When cultured normal and SV40-transformed normal rat kidney and BALB/3T3 cells were exposed to picolinic acid, cell proliferation ceases. Most of the normal cells remained in a quiescent G1 (G0) state and viable for prolonged periods of time. In contrast, SV40-transformed cells progressed to the S and G2 phases of the cell cycle and remained viable only up to 90 to 120 hr. Then, most of the cells began to die. However, a very small fraction of the cell population (approximately 0.01 percent) developed into variants resistant to picolinic acid. Prevention of development of variants, and therefore destruction of all transformed cells, was obtained by addition of glycerol to picolinic acid-treated cells. Untransformed cells were unaffected by the same treatment. These results suggest that differential tumor toxicity should be feasible.

Cell Cycle↗
PubMed1973

Transformation of chick-embryo fibroblasts by wild-type and temperature-sensitive Rous sarcoma virus alters adenylate cyclase activity.

The activity of the enzyme adenylate cyclase, a component of the plasma membrane, has been determined in chick-embryo fibroblasts and in cells transformed by either Bryan high-titer strain of Rous sarcoma virus (RSV-BH) or a temperature-sensitive mutant of this virus (RSV-BH-Ta). Adenylate cyclase activity is reduced in cells transformed by the wild-type virus and also by the temperature-sensitive mutant when the cells are grown at the permissive temperature (37 degrees ). Transformation results in an altered affinity (K(m)) for the substrate (Mg ATP). The apparent K(m) ATP is 0.23 mM in normal cells and 1.1 mM in cells transformed with wild-type virus. The K(m) ATP of the cells infected with RSV-BH-Ta is 0.67-1.0 mM at 37 degrees and 0.28 mM at 42 degrees . The enzyme from normal cells appears to have two binding sites for Mg(++), one at the catalytic site and a second at a regulatory site. Transformation by RSV-BH or RSV-BH-Ta (37 degrees ) apparently alters this second Mg(++) site. A decrease in adenylate cyclase activity occurs within 10 min after cells infected with RSV-BH-Ta are shifted from 42 degrees to 37 degrees ; the activity falls to one-half that of normal cells 30 min after the temperature shift. Our observations indicate that a viral function lowers cyclic AMP content by lowering the activity of adenylate cyclase, probably through some modification of the plasma membrane.

Adenosine Triphosphate↗