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PubMed2002

Apoptosis and leucocyte-endothelium interactions contribute to the delayed effects of cryotherapy on tumours in vivo.

In dermatology, cryotherapy is commonly used to treat benign and malignant skin lesions. However, studies investigating the time-course of the direct and delayed effects on the microvasculature and subsequent tissue destruction are lacking. Amelanotic melanomas (A-Mel-3) were implanted into the dorsal skinfold chamber of Syrian Golden hamsters (n=51). Tumour and normal tissue were frozen to -20 masculine C (cooling rate 150 masculine C/min). Intravital fluorescence microscopy was performed to assess microvascular changes and leucocyte-endothelium interactions up to 24 h. The relative degrees of necrosis and apoptosis and the accumulation of leucocytes were investigated by histology and immunohistochemistry. Apoptosis was quantified using the TUNEL assay in combination with computer-assisted image analysis. After cryotherapy, red blood cell velocity (RBCV) decreased in postcapillary venules and tumour vessels, whereas functional vessel density (FVD) was significantly reduced in tumour vessels as compared with postcapillary venules. Leucocyte-endothelium interaction increased first in normal and tumour tissue, and then after 24 h leucocytes accumulated in normal tissue close to the tumour margin. Necrosis was induced in the cryolesions directly after freezing and remained constant over the entire observation period. In contrast, apoptosis increased in the periphery of the tumour tissue up to 24 h following cryotherapy. In conclusion, tissue destruction by cryotherapy is not only induced by direct necrosis and microvascular stasis, but also by the inflammatory infiltrate and subsequent apoptosis. This could be an important finding regarding the generation of an immune response.

Animals↗
PubMed1998

Distribution of heterochromatin on the mitotic chromosomes of Musca domestica L. in relation to the activity of male-determining factors.

In the housefly, male sex is determined by a dominant factor, M, located either on the Y, on the X, or on any of the five autosomes. M factors on autosome I and on fragments of the Y chromosome show incomplete expressivity, whereas M factors on the other autosomes are fully expressive. To test whether these differences might be caused by heterochromatin-dependent position effects, we studied the distribution of heterochromatin on the mitotic chromosomes by C-banding and by fluorescence in situ hybridization of DNA fragments amplified from microdissected mitotic chromosomes. Our results show a correlation between the chromosomal position of M and the strength of its male-determining activity: weakly masculinizing M factors are exclusively located on chromosomes with extensive heterochromatic regions, i.e., on autosome I and on the Y chromosome. The Y is known to contain at least two copies of the M factor, which ensures a strong masculinizing effect despite the heterochromatic environment. The heterochromatic regions of the sex chromosomes consist of repetitive sequences that are unique to the X and the Y, whereas their euchromatic parts contain sequences that are ubiquitously found in the euchromatin of all chromosomes of the complement.

Animals↗
PubMed2006

Associations among gender-linked toy preferences, spatial ability, and digit ratio: evidence from eye-tracking analysis.

Eye-tracking technology was used to monitor eye-movements in 64 adults (age range, 18-22 years) during simultaneous presentation of "masculine" and "feminine" toys. Women and men who showed more visual fixations on male-typical toys compared to female-typical toys had significantly better targeting ability and smaller (i.e., more masculine) digit ratios, a putative marker of prenatal androgen levels. In contrast, individuals with visual preferences for female-typical or male-typical toys did not differ in mental rotations ability and in their retrospective reports of childhood gender-linked activities. The finding that targeting ability and digit ratios varied according to visual preferences for gender-linked toys suggests that prenatal androgens promote enduring preferences for male-typical objects and indicate further that some gender-linked traits vary according to the direction of a visual preference for gender-linked toys. Visual preferences derived from eye-tracking, therefore, may be a useful supplement to current measures of psychosexual differentiation in hormone-behavior research, particularly because eye-movements are not dependent on verbal abilities or subjective evaluations of behavior.

Adult↗
PubMed1988

Sex differences in fatty acid composition of rat liver phosphatidylcholine are regulated by the plasma pattern of growth hormone.

The effects of continuous and intermittent (at 12 h intervals) administration of growth hormone (GH), and the effects of gonadal steroids on the regulation of the fatty acid composition of liver phosphatidylcholine were studied in gonadectomized and hypophysectomized adult female Sprague-Dawley rats. Gonadal steroids have been shown to influence the fatty acid composition of liver phosphatidylcholine in the rat. It is shown in the present study that neither testosterone nor estradiol had any effects on liver phosphatidylcholine in hypophysectomized rats. There was a 'masculinizing' effect of hypophysectomy of female rats on the fatty acid composition of liver phosphatidylcholine (i.e., an increase in the proportion of palmitic, oleic and linoleic acids and a decrease in the proportion of stearic and arachidonic acids). Continuous infusion of human GH and bovine GH partly reversed the 'masculinizing' effect of hypophysectomy. In contrast, there were no effects of intermittent administration of human GH. Also, there was no effect of prolactin infusion. It is concluded that the sexually dimorphic secretory pattern of GH may be involved in the regulation of the sexual differentiation of the fatty acid composition of liver phosphatidylcholine in the rat.

Animals↗
PubMed1994

Men are innocent until proven guilty: a comment on the examination of sex differences by Pierce and Kirkpatrick (1992).

Pierce and Kirkpatrick (1992, Behaviour Research and Therapy, 30, 415-418) addressed the finding that men reported lower levels of fear than women in response to specific fear items and concluded on the basis of their experiment that this was because the men were lying. Their conclusion is questioned on various grounds, including inappropriate statistical analyses, inadequate treatment of physiological data, failure to address the possibility of sample selection bias (signalled by the high drop-out rate) and the inadequacy of self-assessed fear measures based on a small number of single items. An alternative interpretation of their data is offered, based on the inverse correlation between initial response level and size of increment, demonstrable in their study in males but not in females. It is argued here that the increments may have been due to anticipatory arousal, a mediating factor that would also account for the facilitation of generalization between certain specific items. It is further suggested that, if this explanation is correct, the men were acting with more rather than less honesty, and it may on the other hand be the reports of the females that were affected by their sex-role stereotype. Another possible explanation of the findings is discussed. If men relatively high in masculinity had a greater tendency to drop out, the experimental sample at the second testing would be biased towards men relatively low in masculinity and reporting higher fear levels.

Arousal↗
PubMed1984

Changes in the activities of microsomal enzymes involved in hepatic steroid metabolism in the rat after administration of androgenic, estrogenic, progestational, anabolic and catatoxic steroids.

Several steroids (5 beta-dihydrotestosterone, 19-nortestosterone, methyltrienolone, norethisterone, medroxyprogesterone acetate, cyproterone acetate, chlormadinone acetate and 16 alpha-cyanopregnenolone) were tested for their ability to influence the activities of three sexually differentiated hepatic microsomal enzymes (3 alpha- and 3 beta-hydroxysteroid dehydrogenase and 5 alpha-reductase) in male and female gonadectomized and intact female rats. Of the steroids tested only 5 beta-dihydrotestosterone was completely ineffective. The other tested steroids elicited varying degrees of "masculinization" with a distinct gradation of effect according to the enzyme activity measured and animal model used. 5 alpha-Reductase was the most sensitive enzyme activity and 3 alpha-hydroxysteroid dehydrogenase the least. Male castrates responded better than female castrates, and these in turn better than intact females. The mechanism of action of three of the steroids (methyltrienolone, medroxyprogesterone acetate and norethisterone) was examined. Both flutamide and estradiol were able to block the action of methyltrienolone and medroxyprogesterone acetate, but not that of norethisterone. It is concluded that methyltrienolone and medroxyprogesterone acetate probably masculinize the enzyme activities by the same mechanisms as androgens, whereas the repression of 5 alpha-reductase activity elicited by norethisterone administration involves a different route.

Aminopyrine N-Demethylase↗
PubMed1989

Growth hormone regulation of hepatic drug-metabolizing enzymes in the mouse.

Hepatic microsomal hexobarbital hydroxylase and aminopyrine N-demethylase activities increased in adult male mice following hypophysectomy to female-like levels, eliminating the normal sexually dimorphic pattern of these enzymes. Exogenous growth hormone replacement (0.08 I.U./100 g body weight/day) re-established the lower masculine activities only when administered subcutaneously once every 12 hr. Enzyme activities remained elevated at female-like levels when the same total dose of growth hormone was infused continuously using osmotic pumps or was injected once every 6 hr. These data suggest that, despite the reversed orientation of sex differences in hepatic drug-metabolizing enzymes between rats and mice (i.e. higher enzyme activities in female mice and male rats), the basic hormonal regulatory axis is similar in the two species. Cyclic fluctuations of systemic growth hormone concentrations masculinize kinetic parameters of hepatic hexobarbital hydroxylase and aminopyrine N-demethylase in both species. Rats and mice differ in that these similar hormonal signals lower the apparent Vmax in male mice, while markedly increasing the enzyme activities in male rats. It appears more likely, therefore, that species- and sex-specific differences in the total hepatic cytochrome P-450 isoenzyme populations produce the reversed sex-dependent pattern of hexobarbital hydroxylase and aminopyrine N-demethylase.

Animals↗
PubMed1991

Differential effects of neonatally administered glutamate on the ultradian pattern of circulating growth hormone regulating expression of sex-dependent forms of cytochrome P450.

Neonatal male rats were treated with monosodium glutamate (MSG) at either 0.5, 1.0, 2.0, 3.0 or 4.0 mg/g body weight on alternate days during the first 9 days of life. As adults, rats were catheterized to obtain unstressed, serial blood samples for the determination of ultradian patterns of circulating growth hormone. In addition, the levels of drug-metabolizing enzymes (i.e. hexobarbital hydroxylase, cytochromes P450 and b5, NADPH-cytochrome P450 reductase and ethoxyresorufin O-deethylase) as well as sex-dependent forms of cytochrome P450 [i.e. male-dependent cytochromes P450 2c (IIC11), 2a (IIIA2) and RLM2 (IIA2) and female-dependent cytochromes P450 2d (IIC12) and 3 (IIA1)] and/or their catalytic activities were measured in the hepatic microsomes of the treated rats. The results demonstrated a dose-dependent, graded response to MSG treatment. As the dose of MSG increased from 0.5 to 4.0 mg, there was a concurrent decline in the amplitudes of the characteristically masculine, episodic bursts of growth hormone, until at the highest dose (4 mg), the pulses were no longer detectable. Associated with this dose-dependent alteration in the ultradian pattern of growth hormone secretion was a measurable change in the activities of the sex-dependent hepatic enzymes. As the pulse heights of the hormone declined to 10-20% of their normal amplitudes, the levels of the male-dependent enzymes (i.e. the drug-metabolizing enzymes, as well as the male forms of cytochrome P450 and their specific steroid hydroxylases) were maintained, and in some cases, exceeded the levels normally found in males. However, as the hormone pulse heights declined, there appeared an accompanying increase in the activities of some of the female-dependent enzymes. Finally, with the loss of all detectable levels of circulating growth hormone, the normal masculine profile of hepatic enzymes was reversed to an apparently normal (with the exception of cytochrome P450 2d) feminine profile. Summarizing, the results indicate that (1) neonatal administration of MSG can produce dose-dependent, graded, long-term developmental defects in the ultradian rhythm of circulating growth hormone and associated sex-dependent hepatic enzymes, and (2) while the male-dependent hepatic enzymes can be maintained at normal or even higher levels in the face of an up to 90% reduction in the pulse heights of plasma growth hormone, the activities of the female-dependent enzymes may begin to increase.

Animals↗
PubMed1982

Behavioral correlates of sexual differentiation in the zebra finch song system.

The capacity for song is masculinized in female zebra finches by exposure to 17 beta-estradiol at hatching, and requires continual exposure to androgen for its behavioral expression in the adult. The stereotypy of the song developed by estrogenized females can be as good as that of male song. The sexual dimorphism in behavioral capacity for song parallels morphological sex differences in the efferent motor pathway which participates in the production of song. Estradiol induces the cytoarchitectonic masculinization of the telencephalic nuclei within the motor system for song, and renders them able to respond morphologically when song is induced in estrogenized females by exposure to androgen as adults.

Animals↗
PubMed1982

Sexual dimorphism and the influence of neonatal androgen in the dorsolateral motor nucleus of the rat lumbar spinal cord.

There is a sexually dimorphic motor nucleus, the spinal nucleus of the bulbocavernosus (SNB) in the fifth and sixth lumbar segments of the rat spinal cord. We now report a second sex difference in the dorsolateral nucleus (DLN) in the ventral horn of the rat lumbar cord, which includes motoneurons innervating the ischiocavernosus muscle, a sexually dimorphic perineal muscle. Adult females possess fewer motoneurons in the DLN, probably because of an absence of neurons innervating the ischiocavernosus muscle, which females lack. The effect of a single dose of testosterone propionate on day 2 of life was confined to a specific rostrocaudal region of the adult DLN in which it partially masculinized the female DLN. Masculinized females have more DLN neurons than control females. The direction of change induced in DLN neuron number by the neonatal hormone treatment is compatible with the hypothesis that androgens are involved with the sexually dimorphic development of the DLN. In another motor nucleus, the retrodorsolateral nucleus, a small sex difference in neuron number was found in one study, but was not replicated in a second experiment.

Androgens↗
PubMed1985

Reversal of the sexually dimorphic distribution of serotonin-immunoreactive fibers in the medial preoptic nucleus by treatment with perinatal androgen.

The effect of perinatal androgen exposure on the sexually dimorphic distribution of serotonin (5-HT)-immunoreactive fibers in the medial preoptic nucleus (MPN) of the rat was evaluated with an indirect immunohistochemical method. Female animals treated with testosterone propionate (TP) perinatally, postnatally or with oil vehicle alone were gonadectomized as adults and the 5-HT fiber distributions compared with those of intact male and female animals. In the adult female rat, the TP treatments resulted in a significant masculinization of both the 5-HT-stained fiber distribution and the sexually dimorphic cytoarchitectonic features of the MPN. This masculinization appears to be complete only in the animals exposed to TP perinatally, suggesting that the critical period for the sexual differentiation of this nucleus may extend into the late prenatal period.

Animals↗
PubMed1992

SDN-MPOA volume in male rats is decreased by prenatal stress, but is not related to ejaculatory behavior.

A computer-assisted image analysis technique was used to measure the adult volume of the sexually dimorphic nucleus of the medial preoptic area (SDN-MPOA) in prenatally stressed male rats and in groups of non-stressed males and females. The SDN-MPOA of male offspring from dams stressed daily (i.e. three 45-min exposures to physical restraint and bright light) during the last week of pregnancy was significantly smaller than in males not exposed to stress, but was larger than in females. Maternal stress has been shown to attenuate the surge in fetal plasma testosterone (T) which normally occurs on days 18 and 19 of gestation in male rats. The present results suggest that suppression of T during prenatal development leads to an incomplete masculinization of the SDN-MPOA in male rats. There was no difference in SDN-MPOA volume between males that exhibited the ejaculatory pattern when tested with estrous females and males that failed to ejaculate in either the control or prenatal stress group. SDN-MPOA volume does not appear to be predictive of masculine ejaculatory performance.

Analysis of Variance↗
PubMed1995

Sexually dimorphic areas in the rat medial amygdala: resistance to the demasculinizing effect of prenatal stress.

Exposure to prenatal stress blocks full masculinization of several sexually dimorphic nuclei in the brain and spinal cord of male rats. We now compare the adult volume of the medical amygdala (MA) and two of its component cell groups, posterodorsal (MePD) and posteroventral (MePV), in prenatally stressed male rats and nonstressed males and females. Previous reports of sex differences (male > female) in the overall size of the MA and the MePD component were confirmed, and we identified a previously unreported sex difference (male > female) in MePV. Prenatal stress had no effect on the size of the total MA, or of the MePD or MePV in males. Maternal stress attenuates the surge in plasma testosterone (T) which normally occurs on days 18 and 19 of gestation in male rats. This brief suppression of T during prenatal development leads to incomplete masculinization of some sexually dimorphic features of the CNS (i.e. the SDN-MPOA of the hypothalamus, and SNB and DLN of the spinal cord) but not others (i.e. the MA, MePD, and MePV). The selective effects of prenatal stress on neural differentiation may be due to differences in the onset and duration of the periods when each of these structures in most sensitive to T and/or its metabolites.

Amygdala↗
PubMed1994

Post-hatching inhibition of aromatase activity does not alter sexual differentiation of the zebra finch song system.

Hatchling zebra finches were treated with fadrozole, an aromatase (estrogen synthesis) inhibitor, to test whether estrogen is required for normal masculine development of the song system. Injections on posthatching days 1-30 had no effect on the volumes of the robust nucleus of the archistriatum (RA) and area X or on neuron soma size in RA and high vocal center (HVC) measured on day 31. These results argue against the importance of estrogen in masculinization of the song system in males after hatching.

Animals↗
PubMed1986

Development of interstitial cells in experimentally sex-reversed gonads of genetically female chick embryos.

A testis graft implanted in young genetically female embryos induced a male gonadal differentiation. The interstitial cell percentage and actual content were strongly lowered in masculinized gonads compared to normal female embryos and became similar to those observed in the normal developing embryonic testis. This effect was enhanced by the association of a graft and an antiestrogenic drug, and was not observed after administration of the drug alone. This inhibiting influence of the graft on interstitial cell formation may be considered as resulting in an inhibition of estrogen production. Its possible causative role in gonadal masculinization is discussed in the light of previous and present results.

Animals↗
PubMed1990

Aromatization mediates aggressive behavior in quail.

Although testosterone (T) stimulates aggressive and reproductive behaviors in males of many vertebrate species, it is now known that the full expression of T action in the brain requires aromatization to estradiol (E2) and subsequent interaction of locally formed E2 with nuclear estrogen receptors. In experiments reported here, we used a behavioral test which quantifies the response of an individual male Japanese quail (Coturnix coturnix japonica) to the visual stimulus of a conspecific. We have called this behavior aggression because it shares many features in common with traditional measures of aggression, e.g., predicting dominance and subordinance. Nevertheless, the behavior probably also combines a complex steroid-sensitive masculine behavior. The advantage of this test is that it allows the discrimination of individual differences in masculine behavior but avoids fighting and sexual encounters per se, thereby reducing effects of learning, a problem with previous tests of avian aggression. In addition, this test has been applied usefully to identify neuroendocrine correlates to male behavior. Using this test, the arousal of reproductively inactive males (hereafter referred to as aggression) is activated by administration of T or estradiol benzoate (EB), but not by 5 alpha-dihydrotestosterone (DHT). T-induced aggression was blocked by the aromatase inhibitor 4-hydroxyandrostenedione (OHA), an effect partially reversed by treatment with EB. In addition, OHA or the estrogen receptor blocker CI-628 reduced aggressiveness of reproductively active males whereas the androgen receptor blocker flutamide had no effect. Results with the 5 alpha-reductase inhibitor N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 alpha-carboxyamide (4-MA) were equivocal. Additionally, treatment of reproductively inactive quail with T or E2 but not DHT increased aromatase activity in the hypothalamus-preoptic area (HPOA). We conclude, therefore, that T to E2 conversion is essential for the activation of aggressiveness in this species. Although locally formed estrogen exerts its effects on aggression in part by increasing activity of aromatase per se, analysis of the time course of behavioral induction or suppression by the various treatments suggests that the response has multiple components, including both short latency, receptor-independent and long latency, receptor-dependent events.

5-alpha Reductase Inhibitors↗
PubMed1983

Neonatal neural organizing effects of exogenous corticosteroids on sexual differentiation of the brain in the female rat.

Testosterone, deoxycorticosterone, or vehicle was administered neonatally to female Long-Evans rats. Parameters expressing the reproductive physiology and behavior of the adult animals were studied. It was found that neonatal administration of testosterone produced the expected "defeminization" and "masculinization" of the brain, affecting both the reproductive behavior and cyclicity of these females. In contrast, neonatal administration of the adrenal steroid did not affect cyclicity although it "defeminized" and "masculinized" sexual behavior, albeit to a lesser degree than testosterone. The results suggest a dichotomy in the neuroregulation of reproductive physiology and sexual behavior.

Animals↗
PubMed1985

Effects of testosterone on ontogeny of urinary behavior in male and female dogs.

Development of urinary behavior from birth to adulthood was observed in six groups of beagles including normal males (NM), normal females (NF), males castrated soon after birth (CM), males castrated soon after birth and treated with testosterone (T) for the next 90 days (CMT), females exposed to T in utero (FTU), and females exposed to T in utero and during infancy, i.e., the first 30-40 days postpartum (FTUI). Prenatal treatment with T had masculinizing effects on juvenile urinary behavior in FTU and FTUI. On the other hand normal development of fully adult masculine urinary patterns in males and females necessitated both prenatal and postnatal androgenic stimulation. It was not necessary that T be present at the time the overt behavior developed. For example, adult male behavior appeared in FTUI at the same time as in NM, i.e., 6-10 months, although the supply of exogenous androgen in FTUI had been exhausted within 30-40 days after birth. CMT showed precocious development of all components of the adult male pattern. Development of adult responses was markedly retarded in most CM, and their performance did not equal that of NM at 23 months. They were then injected with TP which promptly evoked completely normal male urinary behavior. It is tentatively concluded that T acting before birth and during the juvenile period "prepares" critical CNS mechanisms so that when general maturation reaches the appropriate point adult male behavior develops. Although the preparatory role of T is essential, the behavior is not dependent on T after it has developed.

Animals↗