Redundancy in the perception of bilateral symmetry in dot textures.
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Biomedical subjects
Publications and source records attributed to B Jenkins.
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Size constance is a term used to refer to the fact that objects seem to maintain size as their distance from an observer changes, despite change in image size. It is known that size constancy has limits. People seen from the top of tall buildings look small. By observing objects, including the Moon, and after-images, we demonstrate here that size constancy holds when image size is above half a degree, and breaks down when it is less. In other words, image size is scaled for distance only when image size is above half a degree.
A gene sequence for the fowl plague virus (FPV) haemagglutinin molecule has been inserted into a bacterial plasmid such that its transcription is under the control of a promoter derived from the tryptophan operon. Such plasmids direct the synthesis of a protein that reacts specifically with antisera to FPV haemagglutinin. Evidence is also presented that in some cases DNA inserted at the HindIII site of pBR322 is expressed.
SK&F 29661 is an effective, reversible inhibitor of both central nervous system and adrenal phenylethanolamine N-methyl-transferase in vitro; its Ki values in our standard assay systems were 6 X 10(-7) M (central nervous system) and 3 X 10(-7) M (adrenal), respectively. In vivo, the drug inhibited the conversion of [3H]norepinephrine to [3H]epinephrine in the rat adrenal gland and upon chronic administration decreased the endogenous adrenal epinephrine/norepinephrine ratio in both the rat and squirrel monkey. SK&F 29661 did not, however, reduce rat brain stem PNMT activity after systemic administration; subsequent radioautographic studies indicated that the compound did not enter the central nervous system, presumably because of its high polarity. This drug may be useful in defining the physiological importance of peripheral phenylethanolamine N-methyltransferase inhibition.
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SK&F 64139, an inhibitor of adrenal phenylethanolamine N-methyltransferase (PNMT), was found to significantly decrease 2-deoxy-D-glucose (2-DG) induced epinephrine excretion in the conscious rat under conditions where the former agent was administered chromically at 50 and 200 mg/kg/day over a 12-day period and 2-DG was administered after 3, 7 and 11 days of treatment. The reduced epinephrine output caused by SK&F 64139 in response to 2-DG was accompanied by an increased norepinephrine excretion pattern at 200 mg/kg/day of the compound. The reductions in epinephrine excretion were also associated with significant decreases in adrenal epinephrine and increases in the norepinephrine content.
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We have found that the potency of SK&F 64139 in inhibiting rabbit adrenal phenylethanolamine N-methyltransferase (PNMT) is a function of protein concentration when high concentrations of the latter are employed. At lower enzyme levels, however, the degree of inhibition produced by the drug becomes independent of PNMT, allowing for the proper calculation of an inhibition constant. The Ki for the compound under these circumstances was 3 nM. Inhibitor dissociation constants within the same order of magnitude were subsequently obtained using the adrenal enzyme obtained from the rat, cow, dog, human and squirrel monkey. These data provide evidence that the PNMT receptor sites for SK&F 64139 do not differ substantially from species to species and suggest the general utility of this drug as an inhibitor of adrenal epinephrine biosynthesis.
Chronic administration of SK&F 64139, an inhibitor of phenylethanolamine N-methyltransferase (PNMT), initially resulted in a lowered adrenal epinephrine content in both the rat and squirrel monkey adrenal gland. With continued dosing, however, these levels returned toward control. The latter changes were accompanied by increased adrenal levels of norepinephrine and PNMT, but not by decreased plasma drug levels. These results suggest that long-term pharmacological PNMT inhibition may evoke compensatory mechanisms to maintain adrenal epinephrine biosynthesis under basal laboratory conditions.
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To test the hypothesis that chronic neurologic sequelae are associated with cholinesterase depression short of frank organophosphate poisoning, we compared 45 male subjects who had a history of moderate cholinesterase inhibition with 90 male subjects who had neither past cholinesterase inhibition nor current pesticide exposure. Cholinesterase-inhibited subjects were defined as having had a history of (a) red blood cell cholinesterase at 70% or less of baseline or (b) plasma cholinesterase at 60% or less of baseline absent symptoms of frank poisoning. In the subject comparison evaluation, only 1 of 27 neurologic tests (i.e., serial digit performance) was significant statistically, but it was opposite of the direction hypothesized. In a companion study for which the same battery of neurologic tests and the same subjects were used, neurologic sequelae were related to high exposures among subjects who sought treatment for organophosphate poisoning. The data in the current study, in which the subjects experienced lower exposures short of frank poisoning, provide some evidence that preventing acute organophosphate poisoning also prevents neurologic sequelae.
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Twentyseven patients admitted for surgery for primary hyperparathyroidism were studied preoperatively. Fifteen were normotensive and 12 were either hypertensive, diastolic blood pressure > 95 mmHg or had a raised serum creatinine measuring 109.7 (55-171) mumol/l. The beta 2 microglobulin (beta 2M) urinary excretion was measured on all patients. The beta 2M levels were raised in all patients preoperatively even in those patients who had normal values for conventional renal function tests. Following curative surgery the values are returned to the normal range. The patients were followed up for a mean of 4.2 (2.8-5.6) years. Six patients who were initially normotensive subsequently developed hypertension and the initial beta 2M ratio was significantly higher 386 (122-680) micrograms/l compared to those who remained normotensive 186 (95-340) micrograms/l (p < 0.05). Even higher preoperative beta 2M excretion was found in the initial hypertensive group 505 (87-1160) micrograms/l compared to those who later developed hypertension 386 (122-680) micrograms/l, p < 0.001. This preliminary study suggests that preoperative beta 2M urinary excretion may be of value in identifying those patients who will subsequently develop hypertension, an identified long term cause of death in patients operated on for primary hyperparathyroidism. Further studies are indicated.