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James Whyte Black was a Scottish pharmacologist who trained in medicine at St Andrews University and had a career in drug invention and academic pharmacology, moving several times between universities and the pharmaceutical industry. He was awarded the 1988 Nobel Prize in Physiology or Medicine for his drug invention method, which was to build molecules around the structure of a natural chemical activator of a pathway involved in the aetiology of a disease. This produced two extremely useful drug categories, beta-blockers and histamine H2-antagonists, with huge impact on the previously intractable diseases of angina, hypertension and stomach ulcers. In 2000 he was awarded the UK's highest honour, the Order of Merit (OM). His ideas on analytical pharmacology had a significant effect on the development of the discipline in the late twentieth century.

Illusory line motion (ILM) has been shown to occur when a line is presented with one end next to a previously stimulated location. The line appears to be drawn away from the site of stimulation. It has been suggested that this is because of the allocation of attention to the stimulated site. Using an endogenous attentional manipulation (a central arrow cue) with no differences in the display between the two ends of the line at the time of line presentation or immediately prior, no ILM was detected, though there was a small effect in the opposite direction. Those who have found endogenously induced ILM have used an endogenous cue based on a property of a location marker that indicated the cued location. Changing the method of cuing to one based on a property of a peripheral marker instead of a central arrow produced a small but significant report of ILM. The small magnitude of the effect, participant self-reports, and the absence of the effect in the purely endogenous condition, suggest that this was merely a bias. ILM is not generated by endogenous attention shifts. [ABSTRACT FROM AUTHOR]

Phe-activated Ca2+signals recorded from single rat-1 fibroblasts stably expressing the bovine α1a-adrenoceptor (AR) were characterized and used to analyze functional agonist-antagonist interactions. The response to Phe was initiated by the mobilization of stored Ca2+and subsequently sustained by receptor-regulated Ca2+influx. The selective α1A-AR agonist (R)-A-61603 was 141-fold more potent as an agonist than Phe. This potency ratio was consistent with the pharmacology of the native α1A-ARs. Functional responses evoked by concentrations of Phe of more than 0.3 μM displayed fade, which could be explained by agonist-dependent depletion of Ca2+stores. The antagonists tested did not conform to the predictions of the Schild equation for competitive antagonism as expected from the nonequilibrium nature of the response. The antagonist potency series WB4101 ≥ prazosin ≫ BMY7378, however, was consistent with α1A-ARs. Antagonism exhibited by WB4101 and prazosin was compatible with a model in which antagonists dissociate so slowly from the receptor that this is a major factor in their inhibition of the transient agonist-mediated response, leading to the appearance of insurmountable antagonism. A consequence of this phenomenon was that an inverse concentration-response relationship at high agonist concentrations was abolished by low concentrations of antagonists. Overall, the results indicate that quantitative pharmacology can be studied successfully in single cells even though equilibrium could not be achieved in the agonist-antagonist-response relationship in this particular cell phenotype. The study also showed a form of fade that could be readily explained.