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Biomedical subjects

M Nickerson

Publications and source records attributed to M Nickerson.

At least 19 recordsLinked to original sources
PubMed1992

Perceived credibility of children's sexual abuse allegations: effects of gender and sexual attitudes.

We investigated whether sex role stereotyping, adversarial sexual beliefs, acceptance of interpersonal violence, sex of the subject, characteristics of the child (age, sex), and characteristics of the alleged perpetrator (stranger, father) affect judgments of the credibility of children's reports that they have been sexually abused. Two hundred and fifty-five college students in a 3 x 2 x 2 factorial arrangement were given the Burt (1980) scales and asked to read a short vignette in which a child alleged that he/she was sexually abused and the accused male denied the abuse. Although the vast majority of subjects indicated that they believed the child was telling the truth, females rated the child's credibility significantly higher than males F(1, 253) = 6.29, p = .01226. No other significant relationships were found. The results imply that the vast majority of individuals in a college sample tended to believe children's sexual abuse allegations and that this credibility assessment is not influenced by characteristics of the child or perpetrator examined in this study. Implications of the truncated range of the dependent variable and of the Burt scales are discussed.

Adolescent↗
PubMed1981

Beta-adrenoreceptors of the cat nictitating membrane.

1. The relaxant effects of isoprenaline, salbutamol, adrenaline and noradrenaline on the partially contracted isolated nictitating membrane of the cat were determined in the absence and the presence of alpha-adrenoreceptor blockade. 2. It was possible to demonstrate significant relaxant effects of isoprenaline and salbutamol in the absence as well as in the presence of alpha-adrenoreceptor blockade. However, the relaxant effects of adrenaline and noradrenaline could not be demonstrated in the absence of alpha-adrenoreceptor blockade. 3. Molar concentrations (EC30) of isoprenaline, salbutamol and adrenaline causing 30% relaxation of the tone did not significantly differ from each other; EC30 of each of these agents was significantly less than that of noradrenaline. 4. Beta 1-Adrenoreceptor antagonist metoprolol was less potent than beta 2-antagonist H 35/25 in antagonizing the effect of salbutamol; metoprolol was more potent than H 25/35 in antagonizing noradrenaline. Both these agents were effective antagonists of isoprenaline; however, metoprolol and H 25/35 in combination produced greater antagonism of isoprenaline than did each antagonist separately. 5. It is concluded that the cat nictitating membrane possesses both beta 1- and beta 2-adrenoreceptors which are responsible for the relaxant effects of sympathomimetic agents. A study of these receptors is, however, complicated by concomitant stimulation of alpha-adrenoreceptors.

Acetylcholine↗
PubMed1981

Denervation and beta-adrenoreceptors of the cat nictitating membrane.

1. Dose-response curves to the relaxant effects of isoprenaline, salbutamol, adrenaline and noradrenaline were determined on the partially contracted smooth muscles of the cat nictitating membrane following alpha-adrenoreceptor blockade in order to test the hypothesis of a causal relationship between the inhibition of neuronal uptake and denervation supersensitivity. 2. Denervation did not produce supersensitivity of the nictitating membrane to the beta-adrenoreceptor-mediated relaxant effects of any of the four agents studied. 3. The sensitivity of the inferior muscle was greater than that of the medial muscle to agents which were good substrates for neuronal uptake (adrenaline and noradrenaline) as well as to those which were not (isoprenaline and salbutamol). 4. Denervation did not alter the antagonist activity of beta-adrenoreceptor blockers propranolol (nonselective) and metoprolol (beta 1-blocker) against isoprenaline or of H 35/25 (beta 2-blocker) against salbutamol. 5. These results do not support the hypothesis of a casual relationship between inhibition of neuronal uptake and supersensitivity to sympathomimetic amines.

Adrenergic beta-Antagonists↗
PubMed1977

Effects of sympathetic innervation and temperature on the properties of rat heart adrenoceptors.

1. The pharmacological characteristics of adrenoceptors at different temperatures were assessed on the basis of the effects of various alpha- and beta-adrenoceptor agonists and antagonists on electrically-driven left atria and spontaneously-beating pairs of atria from rats. 2. Phenoxybenzamine (Pbz) potentiated inotropic responses of left atria to noradrenaline (NA) at 31 degrees C, produced significantly less potentiation at 24 degrees C and inhibited responses at 17 degrees C; it had little effect on responses to CaCl2. Both Pbz and phentolamine inhibited responses to phenylephrine more effectively at 17 than at 31 degrees C. N-cyclohexylmethyl-N-ethyl-beta-chloroethylamine hydrochloride (GD-131), a haloalkylamine with negligible alpha-adrenoceptor blocking activity, caused only potentiation of responses to NA at 17 degrees C. 3. The presence of phentolamine during incubation with Pbz eliminated block of responses to NA and revealed a potentiation that was equivalent at all three temperatures tested. Phentolamine did not alter the block of responses to 5-hydroxytryptamine by Pbz. Protection of alpha-adrenoceptors by phentolamine during exposure to [3H]-Pbz significantly decreased the amount of label bound to the myocardium at 17 degrees C, but did not alter binding at 31 degrees C. 4. Inhibition of responses to NA by propranolol decreased with temperature, and the magnitude of the change increased with the concentration of propranolol. Compared to 31 degrees C, the effect of the highest concentration of propranolol. (4.0 micronM) was significantly decreased at 24 degrees C, and the effects of all except the lowest concentration (0.04 micronM) were significantly decreased at 17 degrees C. 5. The potency of isoprenaline decreased and that of phenylephrine increased at low temperatures, and their potency ratio was much lower at 17 than at 31 degrees C for both the inotropic and chronotropic responses of spontaneously-beating atria. However, the ratio was unaffected by temperature in electrically-driven left atria. A similar difference between spontaneously-beating and driven preparations is apparent in the data of other workers, but its basis is not clear. 6. Atria from rats pretreated with 6-hydroxydopamine (6-OHDA) were sensitized to the effects of NA, and there was no increase in alpha-adrenoceptor properties at low temperatures. Little alpha-adrenoceptor activity could be demonstrated in chemically denervated atria at any temperature, 6-OHDA pretreatment did not alter the binding of [3H]-Pbz at 31 degrees C, but decreased it significantly at 17 degrees C. Pretreatment with reserpine caused some sensitization, but not significantly after the characteristics of the adrenoceptors or their responses to temperature. 7. It is concluded that the adrenoceptors of atria are affected by temperature in much the same way as those of frog hearts, although the transition from beta- to alpha-adrenoceptor properties may begin at a slightly higher temperature...

Animals↗
PubMed1976

Temperature-induced interconversion of alpha-and beta-adrenoceptors in the frog heart.

1. The effect of ambient temperature on the properties of adrenoceptors mediating inotropic responses was assessed in isolated frog hearts on the basis of the effects and tissue uptake of alpha- and beta-adrenoceptor antagonists. 2. At temperatures of 23degree C and above inotropic responses to adrenaline were antagonized by propranolol (0-4-4-0muM), but were unaffected by phentolamine (26-5muM) and were potentiated by phenoxybenzamine (POB) (0-7-29-5muM). Below 17degree C the activity of propranolol was reduced at least tenfold, and the alpha-adrenoceptor antagonists inhibited responses to both adrenaline and isoprenaline, but not those to CaCL2. 3. The responses of hearts exposed to POB at 14degree C and then tested, after thorough washing, at both 14 and 24degree C were similarly inhibited at both temperatures, i.e. the usual beta-adrenoceptor response did not appear at the higher temperature. Conversely, exposure to POB at 24degree C produced only potentiation at both test temperatures. 4. Parallel to the reciprocal changes in their blocking actions, significantly more (14C)propranolol was retained by hearts exposed at high temperatures and significantly more (3H)POB was bound to the myocardium at low temperatures. Changes in binding and in the pharmaco logical effects of both blocking agents occurred entirely within a relatively narrow temperature range (17-22degree C) Parallel to the change from alpha- to beta-adrenoceptor characteristics with increasing temperature, the sensitivity of the hearts to adrenaline increased about tenfold. 5. Phentolamine (26-5muM) effectively protected hearts from block by (3H)POB at 14degree C, unmasked a potentiation of responses to adrenaline equivalent to that produced by POB at 24degree C, and reduced binding of the label to approximately the level found in unprotected hearts exposed at the higher temperature. At 24degree C, phentolamine did not alter the potentiation produced by (3H)POB, and reduced binding only slightly. There was no significant temperature differential in the amount of (3H)POB bound in the presence of phentolamine. 6. The results presented indicate a close functional and, probably, morphological association of alpha- and beta-adrenoceptors in the frog heart. It is suggested that the two classes of adrenoceptors may represent allosterie conformations of the same structure.

Animals↗
PubMed1974

Dissociation of cardiac inotropic and adenylate cyclast activating adrenoceptors.

1 At higher temperatures, near the physiological range for mammals and nonhibernating frogs, the adrenoceptors for both inotropic responses to adrenaline and noradrenaline and for cyclic 3',5'-adenosine monophosphate (cyclic AMP) production in rat and frog isolated heart preparations, had typical beta characteristics. Phenoxybenzamine potentiated the inotropic response and the accumulation of cyclic AMP; conversely, propranolol inhibited the two responses.2 When the ambient temperature was reduced, the adrenoceptors mediating cyclic AMP production changed very little; they were blocked as effectively as at the higher temperature by propranolol and were not blocked by phenoxybenzamine. However, the adrenoceptors mediating the inotropic response were markedly changed by the decrease in temperature; phenoxybenzamine now inhibited this response and the inhibitory activity of propranolol was reduced about tenfold.3 These results indicate that the adrenoceptors that mediate cardiac inotropic responses at physiological temperatures are distinct from those that mediate the production of cyclic AMP, and that the activation of adenylate cyclase and the accumulation of cyclic AMP are probably not intermediate steps in cardiac inotropic responses to catecholamines.

Adenine↗