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Biomedical subjects

J D Allen

Publications and source records attributed to J D Allen.

At least 145 records · Page 8Linked to original sources
PubMed1976

Subsite mapping of enzymes: collecting and processing experimental data--a case study of an amylase-malto-oligosaccharide system.

Two research groups have independently developed the theory and experimental methodology for quantitatively assessing substrate monomer-subsite binding-energies for depolymerases. When the two approaches are applied to the same enzyme-substrate system they yield surprisingly divergent results. This paper outlines the application of the two approaches to an amylase-maltooligosaccharide system and points out the more important areas of disagreement. We show that by proper data-management, the conflicts between the tow laboratories are basically resolved. The complexities of the subsite model demand extensive data-gathering and exacting data-processing and verification that the computed model-parameters can faithfully reproduce the experimental data.

Amylases↗
PubMed1976

Schedule-induced drinking as a function of interreinforcement interval in the rhesus monkey.

Lever presses by two rhesus monkeys produced food pellets that were assigned by both an ascending and descending series of fixed-interval schedules whose values varied between 1 and 512 sec. The amount of schedule-induced drinking was bitonically related to interreinforcement interval, reaching a maximum at approximately 120 sec and declining at longer fixed intervals. The relation between water intake and interreinforcement interval was complexly related to two drinking measures: (1) the probability of drinking following a pellet and (2) the amount drunk per bout. Drinking rate was also bitonically related to interreinforcement interval.

Journal Article↗
PubMed1975

The effects of practolol on the dysrhythmias complicating acute ischemic heart disease.

The cardioselective beta-adrenoceptor blocking agent practolol was used in the management of ventricular and supraventricular dysrhythmias associated with acute myocardial infarction in 134 patients, and in the management of these dysrhythmias in 19 atients with acute myocardial ischemia. Practolol was frequently effective in controlling ventricular dysrhythmias which occurred within the first 24 hours after the onset of symptoms of acute myocardial infarction. It was also effective in controlling the ventricular dysrhythmias which occurred after resuscitation from ventricular fibrillation. It was of particular value when therapeutic doses of lidocaine had been ineffective. Practolol was much less effective in controlling ventricular dysrhythmias which occurred more than 24 hours after acute infarction. Atrial fibrillation and atrial flutter were infrequently abolished by practolol in undigitalized patients after acute myocardial infarction. There was no correlation between the effectiveness of practolol and the blood concentration of the drug. One adverse effect of practolol was the occurence of sinus bradycardia with or without an increase in the frequency of ventricular ectopic beats. Bradycardia was sometimes accompanied by hypotension. Severe hypotension occasionally occurred in the absence of bradycardia.

Aged↗
PubMed1975

Effects of variable and fixed second-order schedules on schedule-induced polydipsia in the rat.

Schedule-induced polydipsia was studied in rats on a variable second-order schedule in Experiments 1 and 2. Drinking occurred only following presentations of the pellet reinforcer and was not induced by a stimulus that was associated with pellet delivery. Moreover, it was shown that lever pressing for food was not competing with the opportunity to drink following the stimulus during non-reinforced intervals. In Experiment 3 a fixed second-order schedule was used, and only one animal drank following the presentation of the stimulus. A positive contrast effect was obtained with schedule-induced drinking in Experiments 1 and 2, and it was suggested that schedule-induced polydipsia shows behavioral interactions similar to those seen with food reinforced operants.

Animals↗
PubMed1975

Schedule-induced drinking as a function of percentage reinforcement.

Drinking was recorded in rats while lever pressing was maintained on a series of percentage reinforcement schedules in which the per cent of 1-min fixed intervals terminating with food was 100, 90, 30, 70, 10, 50, and 100%. Intervals in which a pellet was omitted were terminated by brief light flash and click stimuli that were also correlated with food presentations. Drinking failed to develop in five of six subjects following intervals in which the brief stimuli were presented regardless of percentage reinforcement. Postpellet drinking, which followed intervals terminated with pellet delivery, however, increased in both duration and amount ingested per interval as percentage reinforcement was systematically decreased. The increase in postpellet drinking above that produced by 100% reinforcement was interpreted as an analogue of the positive-contrast effect observed with food-reinforced operants.

Journal Article↗
PubMed1974

Effects of tiprenolol, practolol and propranolol on experimental ventricular tachyarrhythmias.

1 Low doses of tiprenolol (0.01-0.02 mg/kg) and propranolol (0.05 mg/kg) abolished the ventricular arrhythmias produced by the intravenous injection of adrenaline in anaesthetized dogs respired with halothane.2 Larger doses of tiprenolol (2.0-4.0 mg/kg) restored sinus rhythm in four of five dogs with ventricular tachycardia produced by toxic doses of ouabain. Propranolol (2.0-4.0 mg/kg) had the same effect in each of four dogs.3 Both tiprenolol (4.0-8.0 mg/kg) and propranolol (4.0 mg/kg) increased the frequency of sinus beats and reduced the ventricular rate in dogs with ventricular tachycardia 20-44 h after ligation of a coronary artery.4 Practolol (0.5-16.0 mg/kg) did not reduce the ventricular rate or increase the frequency of sinus beats in dogs with ventricular tachycardia after ligation of a coronary artery.5 In dogs with ouabain-induced ventricular tachycardia mean arterial pressure was reduced after the administration of tiprenolol (0.5-8.0 mg/kg) or propranolol (4.0-8.0 mg/kg). Depression of sinus and atrioventricular nodal function, and of intraventricular conduction developed in some of the dogs given tiprenolol (4-8 mg/kg) or propranolol (8.0 mg/kg).6 The administration of tiprenolol (1.0-8.0 mg/kg) or propranolol (4.0-8.0 mg/kg) depressed the arterial pressure and caused the deaths of some dogs in which a coronary artery had been ligated. Such deaths did not occur in the group which had been given toxic doses of ouabain.

Adrenergic beta-Antagonists↗