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PubMed1977

Anatomical analysis of the developmental effects of aneuploidy in man--the 18-trisomy syndrome: I. Anomalies of the head and neck.

This paper describes the anatomical variations observed in the head and neck in eight infants with the 18-trisomy syndrome that were dissected and studied in detail. Of the usual muscles of facial expression, occipitofrontalis and the auricular and nasal muscles were hypolastic in all eight bodies and each subject showed extensive fusion of the muscles around the corner of the mouth. In each body there was a supernumerary muscle band that extended from the region near the corner of the mouth to the occipital attachment of trapezius. The otomandibular region in each body showed a variable spectrum of muscular, skeletal, arterial, and salivary gland variations bilaterally. Three of the bodies had infrahyoid muscle variations. The sum of these observations provides a more complete delineation of the variations that occur in the 18-trisomy syndrome. Tentative pathogenetic hypotheses for several of the defects are discussed, based on observations from human descriptive embryology. Poswillo's teratological model [1973] implicating hemorrhaging as a causal mechanism in human first and second branchial arch malformations is suggested as a possible mechanism to explain the bilateral otomandibular defects.

Chromosomes, Human, 16-18↗
PubMed1978

Anatomical analysis of the developmental effects of aneuploidy in man--the 18-trisomy syndrome: II. Anomalies of the upper and lower limbs.

We report the anatomical variations of the limbs in eight infants with the trisomy-18 syndrome that were dissected and studied in detail. In each case, the upper limbs showed defects which further define the specific influence of this aneuploidy on the development of its preaxial (radial) component, and the tendency towards reduction defects. Abnormalities included muscle variations concentrated along the radial margin of the forearm and hand, the absence of the definitive musculocutaneous nerve in all of the limbs, and reductions of the radial artery in four of the bodies. Pathogenetic mechanisms explaining the observed defects are discussed, and include: 1) a defect in peripheral nerve development; or 2) tissue necrosis. The characteristic flexion deformities of the fingers seem to be due to a displacement of the tendons of extensors digitorum and digiti minimi. The lower limbs did not show a consistent pattern of defects, except for the absence of some muscles (psoas minor, the tendon of flexor digitorum brevis to digit V), and the presence of several supernumerary muscles. These variations are discussed as possible nonspecific effects of 18-trisomy on development. The additional anatomical data from this and the first paper in this series [Bersu and Ramirez-Castro, 1977] provide a more detailed picture of the trisomy-18 phenotype which may be useful in corroborating an unconfirmed clinical diagnosis of the syndrome.

Abnormalities, Multiple↗
PubMed2001

Letter to the editor: Chronicle for an orphan trait: comment on Hofer, Shair, Masmela, & Brunelli, "Developmental effects of selective breeding for an infantile trait: the rat pup ultrasonic isolation call".

Hofer, Brunelli, Shair, and Masmela (2001) examined several behavioral and physiological measures in low, high, and unselected lines obtained from a divergent selection for ultrasound production (USP) in young rats. Although the response to selection was clear-cut, few correlated responses appeared. This surprising result could be explained by two reasons. USP has polygenic correlates in this population, and most of the chromosomal regions that are linked with these measures only contribute to a small part of the genetic variance. Therefore, correlated responses to selection might exist, but the common genetic variance between the trait under selection and the indirectly selected trait is too small to be detected by a selective breeding strategy.

Age Factors↗
PubMed1989

Developmental effects of modifiers of the vg mutant in Drosophila melanogaster.

An analysis of the modifiers affecting the expression of the vg gene was performed. We selected for weak and strong expression of the vg mutant in F2 segregating populations obtained by crossing a vestigial stock with an Oregon laboratory stock (O) and with a wild strain (B) captured near Bologna, Italy. The selection for enlarged wings was more effective in the vg B population where wild wings appeared from the 10th generation. The assay of the three major chromosomes showed that the modifiers are located on chromosomes 2 and 3. The mutant imaginal disc cell death phenotype is evident in vg/vg strains that have a wild-type wing phenotype. It is suggested that the selected modifiers do not prevent cell death but induce regenerative growth.

Animals↗
PubMed1988

Developmental effect of dimethyl sulfoxide on hypothalamo-neurohypophysial neurons in vitro.

Primary dissociated cultures were established from diencephalic tissue of 14-day-old fetal rats. Neurons exhibiting immunocytochemical staining for neurophysin appeared in these cultures after 6 days of cultivation. Addition of dimethyl sulfoxide (DMSO) to the culture medium resulted in a slight decrease in total neuronal cell mass as assessed by immunocytochemistry and radio-immunometric quantitation of neuron-specific enolase. In contrast, in DMSO-treated cultures the number of neurophysin-immunoreactive neurons was more than doubled as compared to control cultures. [3H]Thymidine labeling and autoradiography in conjunction with immunocytochemistry for neurophysin showed that this was not due to a mitogenic effect of DMSO on precursor cells. Time-course analysis of the action of DMSO revealed a 6-day time lag between the initiation of treatment and the appearance of increased numbers of neurophysin-immunoreactive cells. These findings suggest that DMSO, which has previously been reported to have a differentiation-inducing effect on malignant transformed cells, may also modulate cellular processes that control differentiation in specific types of neurons in primary culture.

Animals↗
PubMed1995

Changes in dopamine uptake and developmental effects of dopamine receptor inactivation in the sea urchin.

[3H]-dopamine ([3H]-DA) uptake was measured in the presence or absence of the catecholamine uptake inhibitor nomifensine in both unfertilized and fertilized eggs. Specific [3H]-DA uptake depended on time and [3H]-DA concentration; it was high in unfertilized eggs, declined 20-30 min after fertilization, and rose again during cleavage. Irreversible inactivation of dopamine receptors by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) resulted in a complete loss of sensitivity of egg adenylate cyclase to dopamine stimulation. In fertilized eggs treated with EEDQ for 1 hr, restoration of adenylate cyclase activity sensitive to dopamine stimulation could be observed 4 hr after the end of treatment, thus suggesting the appearance of new dopamine receptors in cleaving eggs. Short-term EEDQ treatment on unfertilized eggs, although not impairing fertilization, resulted in cleavage inhibition; the same treatment carried out soon after fertilization, on the other hand, elicited no effect on development. On the contrary, in embryos subjected to continuous treatment with EEDQ, development was impaired independent of the stage at which the treatment was started.

Adenylyl Cyclases↗
PubMed1987

Developmental effects of isotretinoin and 4-oxo-isotretinoin: the role of metabolism in teratogenicity.

Previous observations have indicated that isotretinoin (IT), a drug in common use for therapy of cystic acne, is teratogenic in humans but possesses low embryotoxicity in pregnant mice, probably because of its shorter half-life and limited placental transfer in rodents. In human volunteers and patients, one major blood metabolite of IT is 4-oxo-isotretinoin (4-oxo-IT) which undergoes slower elimination than IT and may itself be a participant in teratogenesis. To investigate the problem of species differences displayed by IT and the role of its metabolism, embryotoxic effects of 4-oxo-IT were examined after its single or repeated intubations into pregnant ICR mice and compared with the effects of a similar regimen of IT. The two compounds were also tested for their relative ability to suppress chrondrogenesis in the in vitro cell and organ culture assays. We found that a single dose of 4-oxo-IT, 100 mg/kg, given on day 11 of gestation (plug day = day 0 of gestation) produced a moderate incidence of limb reduction defects and cleft palate (39% and 27% of surviving fetuses, respectively), while a dose of 150 mg/kg affected virtually every fetus. IT, on the other hand, produced no defects in fetuses exposed to similar dose levels. Repeated intubations with IT, however, resulted in increasing the frequencies of limb reduction defects and cleft palate to levels obtained after 4-oxo-IT administration. We found that a 3-hour interval between IT intubations was more effective in this regard than an 8-hour interval. Repeated IT intubations also uncovered sharper stage-dependency of limb and palatal defects than obtained otherwise.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed1987

Reproductive and developmental effects on rats after prenatal, postnatal, or pre- and postnatal exposure to the hypotensive agent losulazine.

Losulazine was administered orally to 21 bred Sprague-Dawley rats per group at 0, 4, and 8 mg/kg/day by three dosing schedules: gestation day 15 until term (prenatal section); postnatal days 1 to 21 (postnatal section); and gestation day 15 until postnatal day 21 (pre- and postnatal section). Dams were allowed to deliver and the number of live and dead pups recorded. Each pup was sexed and weighed on days 0, 4, and 21. Also, pinna detachment and eye opening were monitored. Randomly selected offspring were allowed to mature and then cohabited for assessment of reproductive performance. Dam body weight gain during dosing was reduced in the high dose group of the pre- and postnatal section. Treated dams in the postnatal and pre- and postnatal sections had litters with reduced body weight, delayed development, and decreased survival. In the F1 mating portion of the postnatal and pre- and postnatal sections, F1 offspring from losulazine-treated dams had reduced body weights over the entire study. A dose-related decrease was found for both the percentage of F1 males that bred and the conception rate of bred F1 females. All F1 females entered estrus at least once, and those that conceived delivered normal litters. Neither microscopic examination of F1 male reproductive organs nor analyses of serum prolactin, luteinizing hormone (LH), and testosterone levels indicated the cause of impaired fertility. Thus, although prenatal exposure only did not result in adverse effects, postnatal exposure to losulazine via lactation affected offspring growth, development, and reproductive capacity.

Administration, Oral↗
PubMed1995

Placental transfer and developmental effects of 9-cis retinoic acid in mice.

9-cis retinoic acid (RA) is a naturally occurring isomer of all-trans RA. While both isomers can bind with high affinity and activate RA receptors, only 9-cis RA is the specific ligand for the retinoid X receptors. 9-cis RA has also been shown to be much more potent than all-trans RA in inducing digit duplication in the chick embryo wing bud. To gain further insight into its mechanisms, here we investigated the teratogenic activity in pregnant mice of 9-cis RA and compared it with those of all-trans RA and 13-cis RA. Using frequency and severity of limb reduction defects as well as palatal clefts in the resultant fetuses as indicators, we found that orally administered 9-cis RA was one-half as potent a teratogen as all-trans RA. That 9-cis RA was intrinsically less active than all-trans RA was deduced by comparing the inhibitory activities of the two retinoids in the limb bud mesenchymal cell micromass cultures using chondrogenesis as an end-point. Since placental transfer of cis isomers of RA is generally poor, we monitored the identities and amounts of retinoids in the embryo after administration of 9-cis RA to the mother. We found that 9-cis RA undergoes extensive metabolism and isomerization during absorption resulting in a number of metabolites in the maternal circulation within 30 min after administration. Although some of these metabolites remain to be identified, the most abundant RA isomers in the plasma coeluted with 13-cis RA.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗
PubMed2001

Prolactin, growth hormone, and epidermal growth factor activate Stat5 in different compartments of mammary tissue and exert different and overlapping developmental effects.

Prolactin (Prl)-induced phosphorylation of Stat (signal transducer and activator of transcription) 5 is considered a key event in functional mammary development and differentiation. We now demonstrate that not only Prl, but also growth hormone (GH) and epidermal growth factor (EGF), can activate Stat5 in mammary tissue. We investigated the roles of these hormones in mammary development using mice in which the respective receptors had been inactivated. Although Prl receptor (PrlR)-null mice are infertile, we were able to maintain pregnancies in a few mice by treatment with progesterone. Mammary tissue in these mice was severely underdeveloped and exhibited limited differentiation as assessed by the phosphorylation status of Stat5 and the expression of milk protein genes. PrlR +/- mice showed impaired mammary development and alveolar differentiation during pregnancy, which corresponded with reduced phosphorylation levels of Stat5a and 5b, and impaired expression of milk protein genes. Development of the glands in these mice was arrested at around day 13 of pregnancy. While Prl activated Stat5 only in the epithelium, GH and EGF activated Stat5 preferentially in the stroma. To assess the relevance of the GH receptor (GHR) in the mammary gland, we transplanted GHR-null epithelium into cleared fat pads of wild-type mice. These experiments demonstrated that the GHR in the epithelium is not required for functional mammary development. Similarly, the EGFR in the epithelium is not required for alveolar development. In contrast, epithelial PrlR is required for mammary development and milk protein gene expression during pregnancy. Although GH is not required for alveolar development, we were able to demonstrate its lactogenic function in cultured mammary epithelium from PrlR-null mice. However, ductal development in GHR-null mice was impaired, supporting the notion that GH signals through the stromal compartment. Our findings demonstrate that GH, Prl, and EGF activate Stat5 in separate compartments, which in turn reflects their specific roles in ductal and alveolar development and differentiation.

Animals↗
PubMed2002

Developmental effects of ambient UV-B light and landfill leachate in Rana blairi and Hyla chrysoscelis.

This study assessed the effects of ambient UV light on the development of two native species of anurans, Rana blairi and Hyla chrysoscelis, during their normal breeding season in Oklahoma. Additionally, the effects of ambient UV light and water contaminated with landfill leachate in Rana blairi were examined. Embryos were collected from the field and distributed equally among replicates of four filter treatments of ambient UV light in experimental tubs filled with either FETAX solution or landfill leachate diluted to 25, 10, and 5% concentrations. Three endpoints (mortality, teratogenesis, and growth) were compared between filter treatments. By itself, UV-B caused no significant effects. Leachate at 10 and 25% concentrations caused 100% mortality across all filter treatments. There was a significant interaction between filter treatment and water toxicity at leachate concentrations of 5% for both malformation and growth. Increased UV-B exposure decreased the malformation rate and increased growth in the leachate treatments.

Animals↗
PubMed2001

Developmental effects of testosterone on behavior in male and female green anoles (Anolis carolinensis).

This study addressed the role of testosterone (T) in the development of sexually dimorphic behavior in the green anole lizard, Anolis carolinensis. We documented the pattern of endogenous T concentrations during ontogeny and we determined the behavioral effects of experimentally elevated T in juvenile males and females. T concentrations were measured in the plasma of hatchlings from eggs incubated in the laboratory, in juveniles of all sizes sampled in the field, and in the yolks of freshly laid eggs in the laboratory and were compared to plasma T in adult females (measured in this study) and adult males. There were no sex differences in plasma T in hatchling and small juvenile (<26-mm snout-vent length, SVL; <14 days old) males and females, concentrations of which in both sexes tended to decline over the 14-day posthatching period. Plasma T sharply increased in juvenile males, but not females, after approximately 14 days posthatching (>25-mm SVL), and it became significantly higher after approximately 38 days posthatching (>30-mm SVL). Plasma T for juvenile males was within the range detected in breeding adult females, but it was 20- to 45-fold lower than that of adult males, breeding or postbreeding. All eggs contained detectable yolk T, but eggs that gave rise to males contained nearly twice as much yolk T as those that gave rise to females. We do not know whether this yolk T comes from the mother, embryo, or both. In behavior trials conducted in the laboratory, juveniles (36- to 42-mm SVL) with T implants, regardless of whether they were male or female, had increased activity levels compared to juveniles with blank implants, due to increased rates of nearly every behavior monitored. These results are discussed in the context of the organization-activation theory of sexual differentiation and the particular life history of A. carolinensis.

Aging↗
PubMed2001

Developmental effects of estrogenic agents on mice, fish, and frogs: a mini-review.

Laboratory experiments have demonstrated that exposure of rodents to sex hormones during prenatal or early postnatal life can cause permanent and irreversible alterations of the endocrine and reproductive organs, such as ovary, fallopian tube, uterus, cervix, vagina, and mammary gland in females; and testis, epididymis, prostate, and seminal vesicle in males; as well as non reproductive organs including bones and muscle and immune and nervous systems in both sexes. Early development of Xenopus laevis into the tadpole and Fundulus heteroclitus goes through a rapid cell division, gastrulation, neurulation, and organogenesis within 1 week after fertilization. The developing embryo is very fragile and sensitive to estrogenic agents. Thus, these animals can be used as a suitable model for examining the effect of endocrine disruptors (hormonally active agents) on the development of aquatic living beings, which are most likely to be exposed to the compounds.

Animals↗
PubMed1994

Developmental effects of an environmental antiandrogen: the fungicide vinclozolin alters sex differentiation of the male rat.

In humans and rodents, exposure to hormonally active chemicals during sex differentiation can produce a wide range of abnormal sexual phenotypes including masculinized and defeminized females and feminized and demasculinized males. Although numerous "environmental estrogens," including pesticides, toxic substances (PCBs), and plant and fungal estrogens, have been shown to alter mammalian sex differentiation, similar information on environmental androgens is lacking. Recently, the fungicide vinclozolin (V) was found to inhibit sexual differentiation in male rats in an antiandrogenic manner. In the present study, V was administered to pregnant rats (p.o.) at 0, 100, or 200 mg/kg/day in corn oil during the period of sex differentiation (Gestational Day 14 to Postnatal Day 3) to examine the demasculinizing effect of this fungicide more closely. In both groups of V-treated male offspring, anogenital distance was female like at birth, and nipple development was prominent at 2 weeks of age. After puberty, most of the V-treated male offspring were unable to attain intromission even though they all mounted sexually receptive females. The V-treated male offspring that appeared to achieve intromission, failed to ejaculate normally, as no sperm were found in the uterus after overnight matings. A factor in the abnormal ejaculation was that all V-treated male offspring had cleft phallus with hypospadias. In addition, a number of unusual reproductive malformations were noted when the males were necropsied at 1 year. Many V-treated male offspring had suprainguinal ectopic scrota/testes, a vaginal pouch, epididymal granulomas, and small to absent sex accessory glands. During the study, about 25% of the V-treated males died as a result of bladder stones, hydroureter, or hydronephrosis, while other males displayed these lesions at necropsy. While some of the above malformations in male offspring can also be produced by perinatal administration of a potent estrogen, like DES, V-treated female offspring did not display any estrogen-like alterations of reproductive development or fecundity. The only change seen in the female offspring was a reduced anogenital distance during neonatal life. Our observation of perinatal-induced agenesis of the prostate and blocked testicular descent, a pattern of malformations nearly identical to that reported for the antiandrogen flutamide, is consistent with other recent evidence that this fungicide is an androgen-receptor antagonist.

Administration, Oral↗
PubMed1998

Adverse reproductive and developmental effects in Xenopus from insufficient boron.

Frog embryo teratogenesis assay--Xenopus (FETAX) was utilized as a model system to evaluate the effects on embryo-larval development at various low boron (B) exposure levels in the culture media. Concentrations tested ranged from < 1 to 5000 microg B/L. A statistically significant (P < 0.05) increase in malformations was observed at < or = 3 microg B/L, but not at the greater concentrations. Abnormal development of the gut, craniofacial region and eye, visceral edema, and kinking of the tail musculature (abnormal myotome development) and notochord were observed. In subsequent studies, adult frogs were maintained for 28 d on two diets: (1) low B (LB, 62 microg B/kg) or (2) boric acid supplemented (BA, 1851 microg B/kg); the frogs were subsequently mated, and their offspring were cultured in media containing various levels of B. Results of the 28-d depletion studies indicated that frogs maintained under LB conditions produced a greater proportion of (1) necrotic eggs and (2) fertilized embryos, which abnormally gastrulated at a greater rate and were substantially less viable than embryos from frogs fed the BA diet. Malformations similar to those seen in the initial study were observed in embryos from the B-depleted adults maintained in an LB environment; 28 d on the LB diet enhanced the incidence of malformations associated with the LB culture media. These abnormalities were not observed in embryos cultured in > or = 4 microg B/L from adults cultured on the BA diet. These studies showed that insufficient B reproducibly interfered with normal Xenopus laevis development during organogenesis, substantially impaired normal reproductive function in adult frogs, and thus represent the first studies demonstrating the nutritional essentiality of B in an amphibian species.

Animals↗
PubMed1993

Developmental effect of testosterone on estrogen sensitivity of the rat preoptic neurons with axons to the ventral tegmental area.

The neonatal effect of testosterone on neuronal sensitivity to estrogen was examined in the medial preoptic area of the rat when adult. Electrical stimulation of the ventral tegmental area induced antidromic action potentials in 683 neurons in 106 urethane-anesthetized animals which consisted of 38 males castrated on the day of birth (day 1), 30 females androgenized by testosterone injection on day 5, and 38 normal females. All females were used after ovariectomy when adult. Histological localization of the antidromically activated neurons was similar in all the animal groups. The latency jump in 40% of the potentials indicated that activated preoptic axons terminate in the stimulation site. The latency for activation was in the range 1.6-43.7 ms and the threshold was as low as 60 microA. The absolute refractory period did not exceed 1700 microseconds. Estrogen increased the threshold among 278 cells in the normal females and 181 cells in the neonatally castrated males. Preoptic neurons in the androgenized females (n = 224) differ from those in others in that their threshold, regardless of estrogen treatment, was at the ceiling values seen in the other groups in the presence of estrogen. Estrogen also prolonged the absolute refractory period in the females but not in the androgenized females. The reduced excitability and the lack of estrogen sensitivity may be responsible for the insensitivity of the androgenized females to feminine actions of estrogen, that may presumably underlie a sex difference in certain behavioral functions.

Action Potentials↗