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Biomedical subjects

R E Whalen

Publications and source records attributed to R E Whalen.

At least 19 recordsLinked to original sources
PubMed1991

Premenstrual syndrome.

The Premenstrual Syndrome (PMS) was described as a unique entity meriting therapeutic attention in 1931. Although researchers in the area have failed to develop a widely accepted definition of PMS, substantial progress has been made in describing the variety of psychobiological profiles encompassed by this syndrome, particularly with respect to its typical symptoms, cyclical nature, symptoms recurrence and severity. Therapies ranging from diet and exercise to vitamin, hormone and drug treatment have been proposed. While none is more efficacious than placebo, several have been popularized. Our failure to develop adequate treatment may reflect our lack of understanding of either the psychosocial or biological factors involved in PMS. This, in turn, may reflect inadequate theoretical development in this research area. We provide a critical assessment of research on PMS, suggest a framework for theoretical development and advocate research strategies that might provide insights into the etiology of the premenstrual syndrome.

Adult↗
PubMed1989

Aggression in male mice: rapid-onset attack of lactating female mice following termination of hyperphysiological testosterone treatment.

Gonadally-intact or castrated and testosterone-(T) treated male mice display aggressive behavior towards olfactory-bulbectomized male (OBM) stimuli, but not towards lactating female (LF) stimuli. By comparison, T-treated female mice display aggressive behavior towards both OBM and LF stimuli. The purpose of the present experiment was to determine if male mice given hyperphysiological T-treatment would display "female-typical" attack of OBM and LF stimuli. Hyperphysiological T-stimulation did not lead to the display of aggressive behavior towards OBM and LF stimuli; only OBM stimuli were attacked, suggesting a qualitative behavioral sex difference in response to T. However, the major finding of this study occurred following the termination of T-treatment. Castrated males that had previously received hyperphysiological T-treatment began to attack LF stimuli within 48 hr of treatment termination. By comparison, castrated males that had previously received physiological T-stimulation, as well as a gonadally-intact control group, generally began to attack LF stimuli 3-4 weeks following treatment-termination/castration. It is suggested that this unusual treatment-termination-induced behavioral display occurs via neurochemical mediation.

Aggression↗
PubMed1988

Muscarinic receptors in preoptic area and hypothalamus: effects of cyclicity, sex and estrogen treatment.

Cholinergic muscarinic receptor binding was measured in the preoptic area (POA) and whole hypothalamus (HTH) of adult Sprague-Dawley rats using the tritiated antagonist quinuclidinyl benzilate ([3H]QNB) as the ligand. Binding of [3H]QNB expressed as fmol/mg protein was 30% higher in POA than in HTH from gonadectomized rats. Cyclic changes were observed in the POA with the highest binding at proestrus and the lowest binding at diestrus. In HTH, no significant changes occurred over the estrous cycle. Estrogen treatment (10 micrograms of estradiol benzoate (EB)/120 g b. wt./48 and 24 h before sacrifice) increased [3H]QNB binding by 42% in the POA and 17% in HTH, relative to the ovariectomized controls. The enhancement of [3H]QNB binding in POA as compared with controls was evident with both the filtration and the centrifugation methods, although binding levels were higher when centrifugation assay was used. A lower estrogen dose (2 micrograms EB/rat/48 and 24 h before sacrifice) which is routinely used to activate lordotic behavior in female rats increased muscarinic binding by 26% in the POA but had no appreciable effect in HTH. A significant sex difference was found in the ability of estrogen to induce [3H]QNB binding in the central nervous system (CNS). Estrogen was ineffective in altering [3H]QNB binding in either brain region of castrated males, although the level and pattern of cholinergic binding between untreated gonadectomized males and females were similar.2+ These data suggest that physiological changes in estrogen secretion over the estrous cycle are capable of modulating cholinergic muscarinic binding in the POA and these changes may be of physiological relevance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Muscarinic cholinergic modulation of hypothalamic estrogen binding sites.

Studies from other laboratories have demonstrated that agents which interact with the dopaminergic and noradrenergic neurotransmitter systems alter the concentrations of cytosolic hypothalamic estrogen receptors. These results have led to the hypothesis that catecholamine systems are involved intimately with the regulation of brain estrogen receptors. The present study was undertaken to determine if agents from a different neurotransmitter system similarly affect [3H]estradiol binding. The data presented here show that the muscarinic cholinergic agonist, bethanechol, increases the number of cytosolic hypothalamic estradiol binding sites in ovariectomized female rats by as much as 38% above control values. Pretreatment with atropine sulfate, a highly specific muscarinic antagonist, blocked the bethanechol effect. Interestingly, bethanechol failed to alter the concentration of estradiol binding sites in castrated male rats. The results of the present experiments show not only that pharmacological modulation of cytosolic hypothalamic estradiol binding sites is not limited to drugs which interact with catecholaminergic systems, but that such effects may be sex-specific.

Animals↗
PubMed1988

Aggression in adult female mice: chronic testosterone treatment induces attack against olfactory bulbectomized male and lactating female mice.

Ovariectomized adult female CFW mice were given a series of tests for fighting behavior against olfactory bulbectomized male and lactating female mice prior to (for 2 weeks), and during (for 4 weeks) chronic treatment with testosterone propionate. While ovariectomized, 40% attacked the lactating female and 13.3% attacked the olfactory bulbectomized male. While ovariectomized and testosterone-treated, 73.3% attacked the lactating female and 60% attacked the olfactory bulbectomized male. However, during the initial 2 weeks of testosterone treatment there was an inhibition of attack against the lactating female. This was followed by a facilitation of attack against the olfactory bulbectomized male and the lactating female during the third and fourth weeks of testosterone treatment. When compared with a previous experiment showing that male mice, gonadally-intact or castrated and testosterone-treated, discriminate between these two stimuli (only the bulbectomized male is attacked), the present data do not support the notion that sexual differentiation of mouse aggression is due solely to the development of a limited sensitivity to testosterone in females.

Aggression↗
PubMed1988

Testicular hormones reduce individual differences in the aggressive behavior of male mice: a theory of hormone action.

A chronology of theoretical development in studies of the role of testicular hormones in murine aggression is presented. Evidence which brings into question the generality of current theory is reviewed, and the implications of this evidence for the direction of future research are discussed. A new method by which to characterize individual differences in aggressive behavior is described, and recent data which provide the basis for the development of a new theory are presented. It is theorized that testicular hormones reduce individual differences in the aggressive behavior of male mice, and that this behavioral "homogenization" is mediated by a testicular-hormone regulated "discrimination mechanism," possibly localized within the mouse olfactory system. The generality of this theory and the implications for other hormone/behavior systems are also discussed.

Aggression↗
PubMed1987

Sexual differentiation of androgen-sensitive and estrogen-sensitive regulatory systems for aggressive behavior.

CF-1 female mice were treated with either testosterone (T), diethylstilbestrol (DES), or methyltrienolone (R1881) on the day of birth and were subsequently tested for their responsiveness to the aggression-promoting property of androgen or estrogen during adulthood. The results showed that neonatal exposure to androgen enhanced subsequent sensitivity to androgenic stimulation but did not alter responsiveness to estrogens. Neonatal estrogen treatment established the capacity to exhibit aggression in response to estrogenic stimulation in adulthood but had little effect on responsiveness to androgens. These data indicate that the androgenic and estrogenic metabolites of T have distinct roles in masculinization of the neural substrate for aggressive behavior.

Aggression↗
PubMed1987

Individual differences in the attack behavior of male mice: a function of attack stimulus and hormonal state.

Male CFW mice were tested for fighting behavior directed against olfactory bulbectomized male mice and against lactating female mice. Some males were tested with each stimulus type before and after castration. Some males were tested first following castration and then after testosterone treatment. All gonadally intact males attacked bulbectomized males and 25% attacked lactating females. After castration 81% attacked males on at least one occasion and 62% began to attack lactating females, although individual differences in the pattern of post-castration behavior were large. Individual differences in attack behavior were also large in males whose first tests followed castration. Of these, 60% attacked both stimuli. Following testosterone treatment, attack against males increased while attack against females was inhibited. Hormonal stimulation reduced individual differences in behavior and increased males' discrimination between the two types of stimuli.

Aggression↗
PubMed1986

Predicting outcome in coronary disease. Statistical models versus expert clinicians.

To study the accuracy with which long-term prognosis can be predicted in patients with coronary artery disease, prognostic predictions from a data-based multivariable statistical model were compared with predictions from senior clinical cardiologists. Test samples of 100 patients each were selected from a large series of medically treated patients with significant coronary disease. Using detailed case summaries, five senior cardiologists each predicted one- and three-year survival and infarct-free survival probabilities for 100 patients. Fifty patients appeared in multiple samples for assessing interphysician variability. Cox regression models, developed using patients not in the test samples, predicted corresponding outcome probabilities for each test patient. Overall, model predictions correlated better with actual patient outcomes than did the doctors' predictions. For three-year survival, rank correlations were 0.61 (model) and 0.49 (doctors). For three-year infarct-free survival predictions, correlations with outcome were 0.48 (model) and 0.29 (doctors). Comparisons by individual doctor revealed Cox model three-year survival predictions were better than those of four of five doctors (model predictions added significant [p less than 0.05] prognostic information to the doctor's predictions, whereas the converse was not true). For infarct-free survival, the Cox model was superior to all five doctors. Where predictions were made by multiple doctors, the interphysician variability was substantial. In coronary artery disease, statistical models developed from carefully collected data can provide prognostic predictions that are more accurate than predictions of experienced clinicians made from detailed case summaries.

Coronary Disease↗
PubMed1986

Lordotic behavior in male rats: genetic and hormonal regulation of sexual differentiation.

The male offspring of Long-Evans rats treated with the aromatization inhibitor ATD (1,4,6-androstatriene-3,17-dione) during pregnancy show high levels of lordotic behavior when treated with estrogen and progesterone in adulthood. The male offspring of Sprague-Dawley dams treated in the same way show only a slight facilitation of lordotic potential. These strain differences could reflect strain differences in gestation length and therefore differences in the timing of the sensitive period of sexual differentiation; they could reflect differences in the sensitivity to the defeminizing actions of gonadal hormones; or they could reflect differences in the sensitivity to ATD treatment. We therefore directly compared the effects of prenatal and early postnatal treatment with ATD on the potential of male Long-Evans and Sprague-Dawley rats to show lordosis when given estrogen and progesterone in adulthood. In both strains ATD treatment facilitated adult lordotic behavior. Treatment appeared to have a greater effect in the Long-Evans strain. However, control Long-Evans males were substantially more responsive to hormone treatment in adulthood than were Sprague-Dawley males. In the Long-Evans strain short-term ATD treatment (Days 20-23 of pregnancy) was as effective as long-term treatment (Days 10-23). In the Sprague-Dawley strain, ATD treatment was most effective when given prenatally and postnatally. Strain differences in hormonal sensitivity best account for the present findings.

Androstatrienes↗
PubMed1986

Progesterone substitutes: cGMP mediation.

Over the past 20 years many investigators have shown that one can facilitate sexual receptivity in estrogen-primed rats either by giving progesterone or a drug which stimulates or inhibits a neurotransmitter system. Drugs which have been reported to substitute for progesterone include cholinergic agonists, serotonergic agonists and antagonists, dopaminergic agonists and antagonists, opiate antagonists, neurohormones, pituitary, ovarian and adrenal hormones and drugs that interact with cyclic nucleotide systems. Most of the drugs that are active are known to increase neural levels of cyclic GMP either by acting on guanylate cyclase or on phosphodiesterase. We propose that the cGMP system mediates the common behavioral effect of the wide variety of drugs that facilitate receptivity.

Adrenalectomy↗
PubMed1985

Induction of male-typical aggression by androgens but not by estrogens in adult female mice.

Ovariectomized adult CF-1 female mice were implanted with silastic capsules containing either testosterone (T), dihydrotestosterone (DHT), methyltrienolone (R1881), estradiol (E2), diethylstilbestrol (DES), or oil vehicle and were tested for aggressive behavior. The androgenic treatments (T, DHT, R1881) were highly effective in promoting male-like aggression while the estrogens (DES, E2) were completely ineffective. Subsequent receptor-binding studies confirmed assumptions about the specificity of DES, DHT, and R1881 binding to estrogen and androgen receptors in mouse hypothalamus.

Aggression↗
PubMed1984

Multiple actions of steroids and their antagonists.

Our scientific language is often misleading. We speak, for example, of virilizing progestins when we should be speaking of "dihydrotestosterone-like" progestins because genital virilization is normally brought about by DHT. We speak of the anti-libidinal properties of antiandrogens as though we knew that their mechanism of action was through the blockage of androgen receptors; some of these agents are antiestrogenic and progestational as well. Until we know the mechanism of action of androgens, estrogens, antiandrogens, antiestrogens, aromatase inhibitors, and reductase inhibitors we should be cautious in our terminology. All hormones and their antagonists have multiple effects.

Androgen Antagonists↗
PubMed1984

Dihydrotestosterone activates male mating behavior in castrated King-Holtzman rats.

Having previously found that King-Holtzman rats respond behaviorally to dihydrotestosterone (DHT), this strain was used to compare the effectiveness of DHT and dihydrotestosterone propionate (DHTP) in maintaining and reinstating copulatory behavior. The 5 alpha-reduced androgens were capable of stimulating mating behavior in these castrated male rats. DHT and DHTP were equally effective in maintaining ejaculatory behavior, whereas DHT was slightly more potent behaviorally than DHTP in restoring mating responses. It was found that as little as 200 micrograms hormone/day restored ejaculatory behavior in 78% of the DHT-treated and 50% of the DHTP-treated rats. In both the maintenance and restoration paradigms, the mating performance of the DHT(P) treated males declined over time. The present data suggest that the conversion of androgen to estrogen may not be critical for the activation of male mating behavior.

Adrenal Cortex↗
PubMed1984

Congenital endodermal heterotopia of the atrioventricular node: evidence for the endodermal origin of so-called mesotheliomas of the atrioventricular node.

A case of so-called mesothelioma of the atrioventricular node is presented. Controversy exists as to whether this lesion is of mesodermal or endodermal origin. The light and electron microscopic morphologic characteristics in this case were identical to those reported previously. The glandular component produced mucin that resisted digestion with both hyaluronidase and diastase; this staining pattern is characteristic of endodermal rather than of mesodermal tissue. Immunohistochemical methods demonstrated abundant carcinoembryonic antigen (CEA) in the cytoplasm of the cells composing the lesion. The presence of CEA strongly argues for an endodermal origin, since this antigen characterizes tissue derived from endoderm and is generally absent from mesoderm. The lesion probably represents endodermal foregut tissue that is displaced during embryogenesis. As such, it is not a true neoplasm. It is proposed that this lesion be designated "congenital endodermal heterotopia of the atrioventricular node."

Atrioventricular Node↗