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Biomedical subjects

M Porter

Publications and source records attributed to M Porter.

88 records · Page 5Linked to original sources
PubMed1976

The chemotherapy of rodent malaria, XXVI. The potential value of WR 122,455 (a 9-phenanthrenemethanol) against drug-resistant malaria parasites.

The phenanthrenemethanol compound WR 122,455 is an effective blood schizontocide against lines of Plasmodium berghei that are highly resistant to primaquine, sulphonamides, pyrimethamine and cycloguanil. It is also active against the NS line that is moderately resistant to chloroquine. WR 122,455 is inactive against the RC line which is highly resistant to chloroquine. Resistance to WR 122,455 is fairly readily developed by the drug-sensitive N strain of P. berghei, using a relapse technique. Resistance develops very readily to the NS line of P. berghei. Both resistant lines exhibit cross-resistance to quinine, but a roughly normal response to chloroquine, primaquine, sulphonamides, dapsone, pyrimethamine and cycloguanil. Resistance to WR 122,455 is stable through cyclical transmission and through cryopreservation, as well as in the absence of drug selection pressure. The resistant parasites have an essentially normal morphology and virulence. A warning is given against the widescale use of WR 122,455 or similar new drugs for human malaria other than in a suitable combination, in order to minimize the danger of the development of resistance to them.

Animals↗
PubMedDate not supplied

Intracellular expression of Kluyveromyces lactis toxin gamma subunit mimics treatment with exogenous toxin and distinguishes two classes of toxin-resistant mutant.

The Kluyveromyces lactis toxin is a heterotrimeric protein which irreversibly arrests proliferation of sensitive Saccharomyces cerevisiae cells in the G1 phase of the cell cycle. By expressing the gamma subunit of the toxin in sensitive yeast cells from a conditional promoter, it was previously demonstrated that it alone is required for inhibition (Tokunaga et al. (1989). Nucleic Acids Res. 17, 3435-3446). Here we show that, like native exogenous toxin, intracellular gamma subunit expression promotes a striking arrest of sensitive cells in G1. However, unlike the G1 arrest caused by native toxin, that induced by the gamma subunit alone does not result in reduced cellular viability and is fully and rapidly reversible, suggesting that the G1 arrest and the irreversibility of action may reflect different aspects of the toxin's interaction with sensitive cells. We have selected a large number of S. cerevisiae mutants which are highly resistant to the toxin in order to study its mode of action in more detail. Complementation analysis demonstrated that all but one of the mutants were recessive and these defined four separate genes. Members of two complementation groups concurrently acquired resistance to intracellular gamma subunit expression, suggesting that they contain a modified toxin target site. The other two genes appear to be required for entry of the gamma subunit into the sensitive cells since these mutants, while refractory to exogenous toxin, were fully sensitive to intracellular gamma subunit expression.

Culture Media↗
PubMedDate not supplied

A comparison of men's and women's professional basketball injuries.

Injuries sustained by male and female professional basketball teams were compared. Injuries from two consecutive seasons were coded, and computer-based cross-tabulations comparing sex, body part, and type of injury were performed. The women's injury frequency was 1.6 times that of men. The body part most frequently injured on both teams was the ankle. Women sustained significantly more knee and thigh injuries as well as sprains, strains, and contusions. Men had significantly more muscle spasms. Other injuries occurred in similar patterns in both sexes. Alterations in training programs are suggested with emphasis on women's strengthening and men's flexibility.

Ankle Injuries↗
PubMedDate not supplied

Happysurfing.

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Health Education↗
PubMedDate not supplied

Automated testing of arrhythmia monitors using annotated databases.

Arrhythmia-algorithm performance is typically tested using the AHA and MIT/BIH databases. The tools for this test are simulation software programs. While these simulations provide rapid results, they neglect hardware and software effects in the monitor. To provide a more accurate measure of performance in the actual monitor, a system has been developed for automated arrhythmia testing. The testing system incorporates an IBM-compatible personal computer, a digital-to-analog converter, an RS232 board, a patient-simulator interface to the monitor, and a multi-tasking software package for data conversion and communication with the monitor. This system "plays" patient data files into the monitor and saves beat classifications in detection files. Tests were performed using the MIT/BIH and AHA databases. Statistics were generated by comparing the detection files with the annotation files. These statistics were marginally different from those that resulted from the simulation. Differences were then examined. As expected, the differences were related to monitor hardware effects.

Algorithms↗