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PubMed2003

[Clinical and cytogenetic evaluation of patients with disorders of somato-sexual development].

UNLABELLED: Congenital somato-sexual disturbances include wide range of classic syndromes, as well as different types of numerous or isolated developmental defects. 28 women with disorders of sexual development were clinically and cytogenetically analyzed. AIM: Clinical and cytogenetic evaluation of patients with disorders of somato-sexual development. MATERIAL AND METHODS: 28 women, 17-35 years old, were included in the study. Analysis data were performed on the basis of clinical records from Department of Obstetrics and Woman's Diseases of Medical University in Bydgoszczy. Cytogenetic investigations were carried out on standard lymphocyte culture method. RESULTS: Turner's syndrome was found in 12 women; 45, X in 7 mosaic karyotype 45, X/46, XX in 4, isochromosome i(Xq) in 1.3 women had normal, male karyotype, 46, XY. One of them had dysgenetic gonads of malignant dysplesia transformation. One patient's karyotype was 47, XXX. 12 women with gonadal dysgenesis--karyotype 46, XX. CONCLUSIONS: 1. Patients with congenital disorders of somato-sexual development are a heterogenous group. 2. Laparoscopy an effective diagnostic and treatment method in women with disorders of congenital somato-sexual development.

Adolescent↗
PubMed2000

Expression of Plasmodium falciparum trimeric G proteins and their involvement in switching to sexual development.

Both cholera and pertussis toxins were used to label and study the expression of heterotrimeric G protein alpha subunits in Plasmodium falciparum extracts. Expression of these proteins is developmentally regulated throughout the erythrocytic cycle with peak expression during early asexual development and in mature sexual stages. Treatment of P. falciparum cultures with cholera toxin causes an increase in conversion to sexual development, and at the same concentration has a marginal inhibitory effect on asexual growth and division. Through precise synchronisation of the parasites' asexual cell cycle, we have defined the period of sensitivity to this induction at around the time of invasion, one cycle before the development of the sexual form. Fluorescent microscopy confirmed that access of the toxin to the parasite is limited to the invasive form - the free merozoite, while further labelling studies revealed expression of a single G protein alpha subunit in these stages. These observations are consistent with the view that a G protein-dependent signal transduction pathway is involved in coupling the parasite's environment to commitment to sexual development (gametocytogenesis). This means of artificially stimulating the pathways leading to sexual development can now be used to biochemically follow the activation of the signalling pathways involved.

Animals↗
PubMed2000

Expression of Plasmodium falciparum trimeric G proteins and their involvement in switching to sexual development.

Both cholera and pertussis toxins were used to label and study the expression of heterotrimeric G protein alpha subunits in Plasmodium falciparum extracts. Expression of these proteins is developmentally regulated throughout the erythrocytic cycle with peak expression during early asexual development and in mature sexual stages. Treatment of P. falciparum cultures with cholera toxin causes an increase in conversion to sexual development, and at the same concentration has a marginal inhibitory effect on asexual growth and division. Through precise synchronisation of the parasites' asexual cell cycle, we have defined the period of sensitivity to this induction at around the time of invasion, one cycle before the development of the sexual form. Fluorescent microscopy confirmed that access of the toxin to the parasite is limited to the invasive form--the free merozoite, while further labelling studies revealed expression of a single G protein alpha subunit in these stages. These observations are consistent with the view that a G protein-dependent signal transduction pathway is involved in coupling the parasite's environment to commitment to sexual development (gametocytogenesis). This means of artificially stimulating the pathways leading to sexual development can now be used to biochemically follow the activation of the signalling pathways involved.

Animals↗
PubMed2001

Abnormalities of sexual development in male rats with in utero and lactational exposure to the antiandrogenic plasticizer Di(2-ethylhexyl) phthalate.

Several members of the phthalate ester family have antiandrogenic properties, yet little is known about how exposure to these ubiquitous environmental contaminants early in development may affect sexual development. We conducted experiments to determine effects of in utero and lactational exposure to the most prevalent phthalate ester, di(2-ethylhexyl) phthalate (DEHP), on male reproductive system development and sexual behavior. Sprague-Dawley rats were dosed with corn oil or DEHP (0, 375, 750, or 1,500 mg/kg/day, per os) from gestation day 3 through postnatal day (PND) 21. Dose-related effects on male offspring included reduced anogenital distance, areola and nipple retention, undescended testes, and permanently incomplete preputial separation. Testis, epididymis, glans penis, ventral prostate, dorsolateral prostate, anterior prostate, and seminal vesicle weights were reduced at PND 21, 63, and/or 105-112. Additional dose-related effects included a high incidence of anterior prostate agenesis, a lower incidence of partial or complete ventral prostate agenesis, occasional dorsolateral prostate and seminal vesicle agenesis, reduced sperm counts, and testicular, epididymal, and penile malformations. Many DEHP-exposed males were sexually inactive in the presence of receptive control females, but sexual inactivity did not correlate with abnormal male reproductive organs. These results suggest that in utero and lactational DEHP exposure also inhibited sexually dimorphic central nervous system development. No major abnormalities were found in any of eight control litters, but DEHP caused severe male reproductive system toxicity in five of eight litters at 375 mg/kg/day, seven of eight litters at 750 mg/kg/day, and five of five litters at 1,500 mg/kg/day. These results demonstrate that the male reproductive system is far more sensitive to DEHP early in development than when animals are exposed as juveniles or adults. The effects of DEHP on male reproductive organs and sexual behaviors and the lack of significant effects on time to vaginal opening and first estrus in their littermates demonstrate that DEHP (and/or its metabolites) affects development of the male reproductive system primarily by acting as an antiandrogen. The pattern of effects of in utero and lactational DEHP exposure differed from patterns caused by other phthalate esters, and the preponderance of anterior prostate agenesis appears to be unique among all chemicals. These results suggest that DEHP acts partly by mechanisms distinct from those of other antiandrogens.

Androgen Antagonists↗
PubMed2001

The nsdD gene encodes a putative GATA-type transcription factor necessary for sexual development of Aspergillus nidulans.

The ability to reproduce both sexually and asexually is one of the characteristics of the homothalic ascomycete Aspergillus nidulans. Unlike the other Aspergillus species, A. nidulans undergoes sexual development that seems to be regulated by internal and external stimuli. To begin to understand the sexual reproduction of A. nidulans we previously isolated and characterized several NSD (never in sexual development) mutants that failed to produce any sexual reproductive organs, and identified four complementation groups, nsdA, nsdB, nsdC, and nsdD. The nsdD gene has been isolated, and it is predicted to encode a GATA-type transcription factor with the type IVb zinc finger DNA-binding domain. The mRNA of the nsdD gene started to accumulate in the early phase of vegetative growth, and the level increased as sexual development proceeded. However, it decreased during asexual sporulation and no nsdD mRNA was detected in conidia. Deletion of nsdD resulted in no cleistothecia (fruiting bodies) formation, even under the conditions that preferentially promoted sexual development, indicating that nsdD is necessary for sexual development. In contrast, when the nsdD gene was over-expressed, sexual-specific organ (Hülle cell) was formed even in submerged culture, which normally completely blocked sexual development, and the number of cleistothecia was also dramatically increased on solid medium. These results lead us to propose that the nsdD gene functions in activating sexual development of A. nidulans. Multiple copies of the nsdD gene could suppress nsdB5 and veA1, indicating that either nsdD acts downstream of these genes or possibly functions in overlapping pathway(s).

Aspergillus nidulans↗
PubMed1991

[The role of echography in the complex dynamic examination of patients with retardation of sexual development].

Seventy-nine patients with sexual development retardation were examined, 24 of these suffered from ovarian genesis condition and 55 from central genesis condition. The findings evidence that detection of the uterus and gonads presenting as cords is one of the diagnostic criteria indicating gonadal dysgenesis. Echographic examinations carried out over the course of therapy yield a more accurate picture of ovarian function. No increase in uterine size on the echogram after discontinuation of hormonal therapy and the appearance of follicles in the ovaries after treatment point to normally functioning ovaries and helps specify the origin of sexual development retardation. In sexual development retardation of a central origin ultrasonic scanning helps assess the therapy efficacy and predict its outcome.

Adolescent↗
PubMed1992

Reduction in the intracellular cAMP level triggers initiation of sexual development in fission yeast.

Schizosaccharomyces pombe initiates sexual development in response to nutritional starvation. The level of cAMP in S. pombe cells changed during the transition from exponential growth to stationary phase. It also changed in response to a shift from nitrogen-rich medium to nitrogen-free medium. A decrease of approximately 50% was observed in either case, suggesting that S. pombe cells contain less cAMP when they initiate sexual development. S. pombe cells that expressed the catalytic domain of Saccharomyces cerevisiae adenylyl cyclase from the S. pombe adh1 promoter contained 5 times as much cAMP as the wild type and could not initiate mating and meiosis. These observations, together with previous findings that exogenously added cAMP inhibits mating and meiosis and that cells with little cAMP are highly derepressed for sexual development, strongly suggest that cAMP functions as a key regulator of sexual development in S. pombe. The pde1 gene, which encodes a protein homologous to S. cerevisiae cAMP phosphodiesterase I, was isolated as a multicopy suppressor of the sterility caused by a high cAMP level. Disruption of pde1 made S. pombe cells partially sterile and meiosis-deficient, indicating that this cAMP phosphodiesterase plays an important role in balancing the cAMP level in vivo.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2000

Luteinizing hormone receptor mutations in disorders of sexual development and cancer.

Human male sexual development is regulated by chorionic gonadotropin (CG) and luteinizing hormone (LH). Aberrant sexual development caused by both activating and inactivating mutations of the human luteinizing hormone receptor (LHR) have been described. All known activating mutations of the LHR are missense mutations caused by single base substitution. The most common activating mutation is the replacement of Asp-578 by Gly due to the substitution of A by G at nucleotide position 1733. All activating mutations are present in exon 11 which encodes the transmembrane domain of the receptor. Constitutive activity of the LHR causes LH releasing hormone-independent precocious puberty in boys and the autosomal dominant disorder familial male-limited precocious puberty (FMPP). Both germline and somatic activating mutations of the LHR have been found in patients with testicular tumors. Activating mutations have no effect on females. The molecular genetics of the inactivating mutations of the LHR are more variable and include single base substitution, partial gene deletion, and insertion. These mutations are not localized and are present in both the extracellular and transmembrane domain of the receptor. Inactivation of the LHR gives rise to the autosomal recessive disorder Leydig cell hypoplasia (LCH) and male hypogonadism or male pseudohermaphroditism. Severity of the clinical phenotype in LCH patients correlates with the amount of residual activity of the mutated receptor. Females are less affected by inactivating mutation of the LHR. Symptoms caused by homozygous inactivating mutation of the LHR include polycystic ovaries and primary amenorrhea.

Disorders of Sex Development↗
PubMed1972

Serum follicular-stimulating hormone and luteinizing hormone as measured by radioimmunoassay correlated with sexual development in hypopituitary subjects.

Serum follicular-stimulating hormone (FSH) and luteinizing hormone (LH) as determined by radioimmunoassay, were correlated with sexual development in 29 patients with hypopituitarism (ages 14.2-29.9 yr).16 of 25 idiopathic hypopituitary patients (20 males and 5 females) exhibited some degree of sexual development. Stage III of sexual development or beyond was achieved by 12 of the 16. Of 13 patients with growth hormone (GH), adrenocortical-stimulating hormone (ACTH), and thyroid-stimulating hormone (TSH) deficiency, 8 did not develop beyond stage I. In contrast, five of six patients with GH deficiency without ACTH or TSH deficiency developed to stage III of sexual development or beyond. The mean (+/-sd) serum LH concentration while in stage I (4.3 +/-0.9 mIU/ml) of eight patients (seven males and one female) who developed beyond stage I was significantly (P < 0.005) greater than the mean serum LH concentration (2.3 +/-0.9 mIU/ml) in nine patients (seven males and two females) who had not developed beyond stage I. Mean serum FSH concentrations were not different. Three of four males with organic hypopituitarism did not develop beyond stage I of sexual development. Serum FSH and LH concentrations in the idiopathic and organic hypopituitary patients were more compatible with stage of sexual development than with age. A serum LH concentration below the range of normal for stage I of sexual development in a prepubertal patient suggests that the patient will remain sexually infantile as an adult.

Adolescent↗
PubMed1980

The effect of the Kn gene of the sexual development of cockerels.

The sexual development of cockerels of three feather growth rate genotypes, k+/k+, Kn/k+, and Kn/Kn, was studied at 2-week intervals from ages 1 to 31 weeks. Body, testis, and comb weights were collected. Histologic evaluation of testes and semen fertility tests were also made. The Kn gene, when homozygous, delayed body growth, and testis growth and development in homozygous males, thus delaying their sexual maturity 2 to 3 weeks. Body weights, relative testis weights, and seminiferous tubule diameters were similar for the k+/k+ and Kn/k+ males but significantly different from the Kn/Kn males. Stages of spermatozoic development were not significantly different between males of any of the genotypes. Regressions of relative testis weight on body weight and of seminiferous tubule size and stage of spermatozoic development on relative testis weight were not different for any of the genotypes. Relative comb size was significantly different between males of all three genotypes. When regressed against relative testis weight, the Kn/Kn males were significantly different from the other two groups of males. The Kn gene exerted an influence, directly or indirectly, which appeared to reduce testosterone production in the Kn/Kn males. The nature of the Kn gene's action was not evident from these data, nor was it clear whether it was acting on the Leydig cells of the testes or on the lutinizing hormone producing cells of the pituitary.

Animals↗
PubMed2003

Altered sexual characteristics in guppies (Poecilia reticulata) exposed to 17beta-estradiol and 4-tert-octylphenol during sexual development.

The effects of estrogenic compounds on the development of sexual characteristics in juvenile guppies (Poecilia reticulata) were examined. After exposure for 3 months, the sex ratio was female biased in guppies exposed to 0.5 microg/L 17beta-estradiol (E2) or higher but unaffected by exposure to 4-tert-octylphenol (OP). When exposed to 100 microg/L OP, the male guppy sexual behavior and sperm count were increased. In contrast, the male sperm count was markedly reduced after exposure to a high concentration of E2. The length of the gonopodium (copulatory organ) was increased when exposed to 100 microg/L OP and at all the tested concentrations of E2. Similar concentrations of OP and E2 reduced the gonad weight of the females. The results demonstrate that the development of sexual characteristics in guppies can be disturbed by environmentally realistic concentrations of E2 but higher concentrations of OP are needed to induce similar alterations.

Animals↗
PubMed1995

Effect of pinealectomy and melatonin treatment during pregnancy on the sexual development of the female and male rat offspring.

Sexual development of female and male rat offspring of control, pinealectomized (PIN-X) or melatonin (MEL 250 micrograms/100 g body wt)-treated mother rats during pregnancy was studied. Newborns were studied at the following phases of sexual development: neonate (5 days old), infantile (15 days old), juvenile (25 and 30 days old) and pubertal phase (55 days). In female offspring, MEL treatment during pregnancy significantly increased plasma luteinizing hormone (LH) in 15- and 25-day-old rats; however, at the end of the prepubertal period (30 days) the concentration of plasma LH decreased significantly as compared to control rats. This hormonal pattern was different from that observed in offspring of control and PIN-X rats, which had low LH levels at 25 days of age and higher LH levels at 30 days of age. Follicle-stimulating hormone (FSH) did not vary significantly among the three groups. Plasma prolactin levels were affected by PIN-X of the mother, showing significantly higher levels in the 5-day-old offspring than in the controls; plasma prolactin levels were also affected by MEL treatment of the mother, producing hyperprolactinemia in the 30-day-old female offspring. In male offspring, sexual development in control male rats progressed rapidly with significantly increased LH and FSH levels at 25 and 30 days compared to those measured during the neonatal and infantile periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Sexual development and life of obese women].

The authors examined by means of a structured interview and four questionnaires (heterosexual development of women, sexual activity of women, sexual function of women and N5 assessing the incidence and intensity of neurotic symptoms 100 obese women, mostly aged 21-40 years, who had a regular sex life. 73 of them had BMI values of 22 to 30. In the remaining 27 morbid obesity was involved with BMI values above 30. In the group as a whole the course of sexual development and life did not differ markedly from that of average women. A retarding trend with lower values in questionnaires on sexual activity and sexual function was found in women with primary and morbid obesity. In these sub-groups the number and intensity of neurotic symptoms was elevated. Their intensity in the group as a whole was significantly higher than in the ordinary population.

Adult↗
PubMed2001

The IsdA gene is necessary for sexual development inhibition by a salt in Aspergillus nidulans.

Using one of 17 expressed sequence tags (ESTs) previously identified as specific to the late sexual developmental (LSD) stage of Aspergillus nidulans, a gene for the subject EST was isolated. The determined DNA sequences revealed an open reading frame encoding a 356 amino acid polypeptide which does not share a sequence similarity to previously identified genes or proteins. The isolated gene was named lsdA (late sexual development), since it was expressed abundantly at the LSD stage. The lsdA gene expression began earlier than at the LSD stage. Disruption of the lsdA gene in the veA+ background strongly induced sexual development under conditions where sexual development in wild-type strains is almost completely inhibited. In contrast, in the veA1 background, an lsdA null mutant failed to show any phenotypic difference in sexual development under the various conditions tested. These results indicate that the lsdA gene may be responsible for inhibiting the sexual development of veA+ strains by a high concentration of a salt.

Amino Acid Sequence↗
PubMed1984

The sexual development and life of female schizophrenic patients.

The sexual development of 51 female schizophrenics, their attitudes toward sex, and their sexual activity and arousability were investigated. The control group consisted of 101 gynecological patients. The sexual development of the female schizophrenics was significantly retarded, and their sexual activity and arousability significantly lowered in adult life compared with the control group. The hypothesis is advanced that the retarded development may be caused by some biological factor, while sexuality in adult life is negatively affected primarily by social isolation.

Adult↗
PubMed1998

Novel factor highly conserved among eukaryotes controls sexual development in fission yeast.

In the fission yeast Schizosaccharomyces pombe, the onset of sexual development is controlled mainly by two external signals, nutrient starvation and mating pheromone availability. We have isolated a novel gene named rcd1+ as a key factor required for nitrogen starvation-induced sexual development. rcd1+ encodes a 283-amino-acid protein with no particular motifs. However, genes highly homologous to rcd1+ (encoding amino acids with >70% identity) are present at least in budding yeasts, plants, nematodes, and humans. Cells with rcd1+ deleted are sterile if sexual development is induced by nitrogen starvation but fertile if it is induced by glucose starvation. This results largely from a defect in nitrogen starvation-invoked induction of ste11+, a key transcriptional factor gene required for the onset of sexual development. The striking conservation of the gene throughout eukaryotes may suggest the presence of an evolutionarily conserved differentiation controlling system.

Amino Acid Sequence↗
PubMed1971

Sexual development, normal and abnormal.

An understanding of normal sexual development is essential to understanding abnormal sexual development. Normal differentiation of the bipotential external genitalia, reproductive ducts, and gonads are dependent upon the presence or absence of androgens from any source, the presence or absence of mullerian inhibiting factor from the fetal testes, and the number and type of sex chromosomes present respectively. Abnormal differentiation results from an imbalance of one or more of these factors or peripheral resistance to these factors.

Adrenal Hyperplasia, Congenital↗