Biomedical subjects

J E Cope

Publications and source records attributed to J E Cope.

4 recordsLinked to original sources

PubMed1989

Medical Research Council AIDS Directed Program: program plan and research opportunities.

In 1987 the U.K. Medical Research Council established a Directed Programme of AIDS Research, the primary objective of which is the development of vaccines and therapeutic approaches against HIV infection and AIDS. The Programme's activities have been rapidly built up and by mid-1989 comprised some 130 individual research projects. The Programme provides the framework for a cohesive approach to AIDS research, comprising a clearly defined scientific development plan, the central provision of resources including laboratory reagents and specialized laboratory facilities and special arrangements for interaction with industry and for international collaboration and training. This article describes the organization, scientific strategies and progress of the Programme.

Acquired Immunodeficiency Syndrome↗

PubMed1980

Mode of action of miconazole on Candida albicans: effect on growth, viability and K+ release.

Miconazole at 10 micrograms ml-1 inhibited the growth of exponential phase cultures of Candida albicans and released intracellular K+. Higher concentration of miconazole were, however, required to cause cell death: at neutral pH, complete killing occurred at 30 micrograms ml-1, while at pH 3.0 or 4.5, there was only partial killing with miconazole up to 80 micrograms ml-1. Efficient killing of C. albicans by miconazole occurred both at low temperature and when cells were incubated in buffer alone. It is proposed that both the fungistatic and fungicidal actions of miconazole are due to its direct interaction with the cellular membranes of C. albicans rather than to an inhibition of biochemical reactions. Divalent cations protected C. albicans from both the fungistatic and fungicidal effects of miconazole and this was probably due to a competition between the ions and miconazole in its positively charged form for negatively charged binding sites. Candida albicans increased in resistance to miconazole-induced K+ release during the stationary phase of a batch culture. Development of this resistance required efficient aeration.

Candida albicans↗

PubMed1980

The porosity of the cell wall of Candida albicans.

Polyethylene glycols of different molecular sizes have been used to study the penetrability of the cell wall of Candida albicans harvested at the end of the growth phase and after prolonged incubation in the stationary phase. No differences were found which could account for the greater resistance of cells from stationary phase cultures of C. albicans to the antimycotic agents amphotericin B methyl ester and miconazole.

Amphotericin B↗

PubMed1980

The interaction of [3H]miconazole with Candida albicans.

During the stationary phase of a batch culture, Candida albicans develops the ability to take up large amounts of [3H]miconazole, and this occurs over the same period of time as the cells become resistant to miconazole-induced K+ release. Cell walls isolated from C. albicans also take up [3H]miconazole, and it is likely that the cell wall is the site of the association of [3H]miconazole with intact cells. Miconazole interaction with C. albicans is freely reversible and relatively nonspecific, and evidence suggests the involvement of hydrophobic bonding. Although fractionation studies were not exhaustive, results suggest that [3H]miconazole associates with glycoprotein and lipid in the matrix of the cell wall. Development of the ability to take up [3H]miconazole requires a low pH in the culture medium at the end of the growth phase, and efficient aeration, and was found to occur most rapidly in the presence of 0.3 mM sodium azide. The nature of the changes that occur during incubation through the stationary phase, and also similar changes that take place during cell wall preparation, and their relationship to phenotypic miconazole resistance are discussed.

Candida albicans↗