bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced visualization of soft tissues in the study of aborted fetuses through the use of xeroradiography
Authors: Graham John M. , Crow Harte C. , Rawnsley Eileen F. , Simmons G. Millard , Hoefnagel Dick 
Published: June 2005

AbstractAs part of the diagnostic workup following an episode of fetal loss, it is generally recommended that fetal tissue be submitted for chromosome analysis and that the fetus be photographed and radiographed. Our recent clinical experience has suggested that, in those fetuses where size is compatible, xeroradiography may be superior to standard radiography. Xeroradiography utilizes principles similar to those in film radiology, with low‐energy photon beams and relatively long exposure times. The physical characteristics of the beam and imaging system provide optimal soft tissue visualization. We have found this technique to be of use in studying a broad variety of abortuses with abnormalities. Examples of fetal abnormalies in which we have used this technique include acardia, neural tube defects, nuchal cystic hygroma, and arthrogryposis. In fetuses weighing 500–1,000 gm, the exposure settings are 25 MA, 1 second, 40 KVP. For larger fetuses the KVP should be increased by 1 or 2. This technique has not been useful for a complete body view of large fetuses due to the size limitations of the xeroradioraphic cassette itself.
Decreased placental monooxygenase activities associated with birth defects
Authors: Manchester David , Jacoby Elizabeth 
Published: June 2005

AbstractWe have measured monooxygenase activities in placentas from 82 women who smoked throughout their pregnancies and correlated these with the presence or absence of major somatic anomalies. Monooxygenase activities toward benzo(a)pyrene and ethoxyresorufin in placentas from 18 abnormal infants were compared with activities in placentas from 64 concurrently studied normal infants. Placentas from normal infants were found to have high levels of monooxygenase activities and low apparent Kms toward ethoxyresorufin (10−7 M), reflecting induction of cytochrome P‐450 enzymes usually associated with maternal cigarette smoking. Placentas from the abnormal infants, however, had significantly lower monooxygenase activities and higher apparent Kms toward ethoxyresorufin (10−5 M), indicating that induction of specific cytochrome P‐450 systems occured less frequently among placentas from abnormal infants. The reasons for this association are unclear. Apparent lack of induction of monooxygenase activity occurred most frequently in placentas from anencephalic infants but was neither exclusively nor consistently found with this defect. No specific maternal condition or environmental exposure associated with lack of monooxygenase induction was identified.
Glucocorticoid teratogenesis in mouse whole embryo culture
Authors: Pratt Robert M. , Perry Everett L. , Chapman Lisa M. , Goulding Eugenia H. 
Published: June 2005

AbstractGlucocorticoids, such as triamcinolone acetonide (TAC‐A) and triamcinolone hexacetonide (TAC‐HA), are potent inducers of cleft palate in vivo in various mouse strains when administered on day 11 of gestation, whereas they are poor or ineffective inducers of cleft lip when given on day 7. The purpose of the present study was to determine whether glucocorticoids are capable of interfering with early embryonic development in culture. CD‐1 mouse embryos were cultured for 48 hours starting either on day 8 (plug day 0) with the embryo inside the yolk sac, or on day 10 with the embryo exteriorized from its functional yolk sac. At the end of the culture period, embryos were examined grossly for malformations and biochemically for altered DNA and protein levels. With the day 8 cultures, TAC‐A produced a dose‐dependent inhibition of growth along with malformations consisting of cardiac irregularities, abnormal rotation, and irregular neural tube closure. With the day 10 cultures, these malformations were not observed, presumably due to the advanced stage of development when the embryos were exposed to TAC‐A; however, TAC‐A did produce growth inhibition along with cleft lip. When TAC‐HA was administered in vivo to pregnant donor females on day 7, in combination with TAC‐A added on day 10 to the culture medium, there was a dramatic increase in the frequency of cleft lip along with other alterations in craniofacial appearance. Our results demonstrate that glucocorticoids are capable of directly affecting embryonic growth and development during the early stages of organogenesis.
Humoral immune dysfunction as a result of prenatal exposure to diphenylhydantion: Correlation with the occurrence of physical defects
Authors: Chapman John R. , Roberts Dean W. 
Published: June 2005

AbstractThe effect of prenatal exposure to diphenylhydantoin (DPH) on postnatal immune function of offspring was studied using a longitudinal experimental design and in vivo immunoassays. Maternal Balb/c mice were dosed by gavage on gestation days 9 through 18 with 0, 20, 40, or 60 mg/kg DPH. Humoral immune function was assessed by measuring the serum antibody levels to type III pneumococcal polysaccharide 5 days after immunization by radioimmunoassay. Cell‐mediated immune function was assessed by measuring the delayed‐type hypersensitivity response to the contact allergen oxazolone using a micrometer method. A dose‐related suppression of humoral immune function was observed in male and female offspring at 25 days but not at 15 weeks of age. Cell‐mediated immunity was not affected by prenatal DPH exposure at 25 days or 15 weeks of age. Offspring developed purulent eye exudates at 12 days of age; the incidence and persistence was related to DPH dose. The immunosuppressive effect of DPH on humoral immune function was significantly greater in offspring born with open eye defect than in similarly treated but physically normal offspring. The results suggest that prenatal exposure to DPH may adversely affect the normal development and expression of humoral immune function, particularly in those offspring with other manifestations of DPH's developmental toxicology.
Gene‐teratogen interaction and its morphological basis in retinoic acid‐induced mouse spina bifida
Authors: Kapron‐Brás Carolyn M. , Trasler Daphne G. 
Published: June 2005

AbstractHomozygotes for the splotch (SP) mutation in the mouse have spina bifida, whereas the heterozygotes have a white belly spot but otherwise appear normal. Spina bifida can be induced by maternal treatment with retinoic acid. Female SWV strain mice were treated intraperitoneally with retinoic acid suspended in peanut oil 8 days/12 hours after they had been mated to either Sp/+ or +/+ males. Probit analysis of the dose‐response data suggests that the presence of the SP gene causes an increased susceptibility of the embryo to the spina bifida‐causing effects of retinoic acid. To study the nature of this increase litters were obtained on gestation day 9 from untreated SWV females mated as above. The mean length of the posterior neuropore (the length of the posterior neural tube that has not yet closed) was determined for each somite number between 14 and 26 and was found to be significantly greater in embryos from the Sp/ + cross. This delay of closure of the neural tube in Sp/ + cross. embryos could explain the observed increase in their susceptibility to retinoic acid.
Acentric craniofacial cleft in a newborn female prenatally exposed to a high dose of diazepam
Authors: Rivas Fernando , Hernandez Alejandro , Cantu Jose Maria 
Published: June 2005

AbstractA newborn female with craniofacial clefts, including cleft lip and palate, was studied. The mother had ingested 580 mg of diazepam in a single dose at about the 43rd day of gestation. The synchronism of the drug intake and the embryological development of the affected structures suggests an etiopathogenic relationship.
Vascular abnormalities due to hyperthermia in chick embros
Authors: Nilsen Nils Øhre 
Published: June 2005

AbstractIntraembryonic vascular abnormalities were studied in chick embryos exposed to temperatures 3°C and 4°C above normal temperature (38°C) from the beginning of incubation. The average duration of hyperthermia was 54 and 53 hours, respectively. Immediately after exposure, the embryos were examined with FITC‐Dextran microangiography in vivo. Following hyperthermia various abnormalities in the heart, ventral aortae, aortic arches, omphalomesenteric arteries, and the distal dorsal aortae frequently occured. There were also significant microvascular changes in the head, in the lateral and caudal parts of the embryos, and in the pellucid area of the yolk sac. In another series incubation at 41°C, hyperthermia of 3°C during the first 3 days of development produced several extraembryonic vascular abnormalities. These included duplication and abnormal branching of the cranial vitelline vein, absence or abnormal course of the omphalomesenteric vessels, aneurysmatic dilatation or abnormal course of the caudal vitelline vein, and aneurysmatic dilatation or occlusion of the abdominal venous sinus. Most frequent findings were blind, congested, and dilated microvascular segments in the pellucid area, commonly associated with an irregular microvascular pattern and perivascular swelling.The abnormalities described are assumed to be caused by the direct effects of hyperthermia upon the developing vessels resulting in microvascular insufficiencies, pathological leakage, and perivascular oedema. Such disturbances may have serious consequences for embryonic vascular development and microcirculation, which in turn may have adverse effects on further embryonic growth and development.
Threshold for carbon monoxide induced fetotoxicity
Authors: Singh Jarnail , Scott Lou H. 
Published: June 2005

AbstractCarbon monoxide (CO) is said to be the most widely encountered occupational and environmental contaminant. Threshold for CO‐induced fetotoxicity was studied using mouse as an experimental animal. Pregnant animals of CD‐1 strain were exposed to 0, 65, 125, 250, or 500 ppm CO from gestation day 7 to 18. The animals were sacrificed on gestation day 18, and their uterine horns were examined for live or resorbed fetuses. The data suggest that maternal CO exposure to as low as 125 ppm affects fetal growth and higher levels affect viability. The data also suggest that the developing organism is sensitive to chronic CO exposure, and this sensitivity is dose dependent. The fetal mouse is influenced at levels of exposure below those found transiently for human cigarette smokers and ambient CO concentrations associated with various occupations.
Muscle abnormalities associated with the twin reversed‐arterial‐perfusion (TRAP) sequence (acardia)
Authors: Stephens Trent D. 
Published: June 2005

AbstractEven though over 400 acardia (twin reversed‐arterial‐perfusion, TRAP) specimens have been reported in the literature since 1533, few attempts have been made to provide detailed evaluation of anything other than the circulation. The purpose of this study was to evaluate the various limb defects in nine TRAP specimens in light of the presumed etiology and pathogenesis, reversed arterial perfusion, and subsequent degenerative changes in the fetus. Two hypotheses were tested: (1) degeneration of formed tissues should not result in tissue rearrangement and (2) one tissue type should be lost in preference to the others. Neither of these hypotheses were supported by the data. Alternative explanations are discussed as well as the implications of these observations on the concept of reversed arterial perfusion.
Immediate and delayed effects of oligohydramnios on limb development in the rat: Chronology and specificity
Authors: Houben J. J. 
Published: June 2005

AbstractExperimental oligohydramnios has been induced in pregnant rats on the 15th gestational day. Characteristic features of the amniocentesis syndrome can be observed in the posterior limbs and tail early after the amniotic puncture. Histological studies of the affected limb buds reveal immediate endothelial rupture of the marginal vein in the interdigital areas. General and nonspecific effects of the syndrome appear after 30 minutes: venous congestion, blebs, and periendothelial oedema. Such vascular disturbances can does not occur. Growth and differentiation of the condensed digital rays are often unimpaired. Since the condensed preskeletal rudiments are spared by the haemorrhage, resorption of the hematoma results in limb at the time of experiment. Current hypotheses formulated to explain the amniocentesis syndrome are reviewed on the basis of the new descriptive data. Congenital constriction band syndrome and amniotic ruptures have been observed in rare cases.
Injection of diethylstilbestrol on the first day of incubation affects morphology of sex glands and reproductive behavior of Japanese quail
Authors: Gildersleeve R. P. , Tilson Hugh A. , Mitchell Clifford L. 
Published: June 2005

AbstractJapanese quail eggs were injected with DES (0.9–1,000 μg) dissolved in 50‐μl of Corn oil on day 1 of incubation. Higher doses of DES (250–1,000 μg) reduced hatchability to 37–33% compared to 61% for corn oil–injected controls. Lower doses of DES (0.9–125 μg) had no effects on hatchability. In a second study, eggs were injected with 0.9 or 1.9μg of DES and the survivors were assessed up to 12 weeks posthatch. DES did not affect hatchability, but did increase mortality during the first 4 weeks posthatch. Females were affected more than males. At 10 days of age, open‐field activity of some birds was examined. The acquisition and reversal of a visual discrimination task was studied at 6 weeks of age. DES had no effect on these measurements. Ten females from each group were chosen randomly to determine egg production over a single 28‐day period beginning at 6 weeks of age. Exposure to DES blocked egg production in these birds. The oviduct weights of 12‐week‐old females were decreased by 50%, but ovarian weights were not affected. Testicular weights were not affected. In a third study reproductive behaviors and social‐dominance behaviors of males were markedly attenuated in birds exposed to 0.48 or 1.9 μg DES in ovo.
Pathologic features of the CHARGE association: Support for involvement of the neural crest
Authors: Siebert Joseph R. , Graham John M. , MacDonald Constance 
Published: June 2005

AbstractDefects associated with choanal atresia include coloboma, cardiac anomalies (usually involving the conotruncal region), physical or mental retardation, genital hypoplasia, and abnormalities of the ear. This constellation of defects is known as the “CHARGE” association and may be accompanied by other anomalies. Many of these defects seem to result from abnormalities in the development, migration, or interaction of cells of the cephalic neural crest. The range of variation in neural crest development is substantial, as indicated by the rather large number of malformation complexes and syndromes that are related phenotypically to the CHARGE association. The increasingly unwieldy nature of this collection of malformations demonstrates the need for an expanded classification of the “neurocristopathies”.
Critical periods during development as assessed by thalliu‐induced inhibition of growth of embryonic chick tibiae in vitro
Authors: Hall B. K. 
Published: June 2005

AbstractIn ovo application of thallium sulfate has been shown to produce a characteristic shortening and angulation of the tibia of the embryonic chick. The critical period for susceptibility to thallium‐induced inhibition of tibial growth ends at 8⅔ days of incubation, a time when the growth rate of the embryo declines by 55%. The aim of the present study was to expose tibiae to thallium in vitro to determine whether this response was intrinsic to the tibia. A 4‐hour exposure to 400 μg thallium was found to be most effective. Growth of tibiae from 8‐day‐old embryos was inhibited, growth of tibiae from 9‐day‐old embryos was not, and the response of tibiae isolated from embryos of 8⅔ days of incubation was intermediate. Therefore, the response of the tibia to thallium represents an intrinsic property and is not secondary to inhibited nerve growth as has been suggested. The critical period and its termination is also an intrinsic property of the tibia. Tibiae were exposed to thallium for 4 hours at various times after the tibiae had been established in vitro. Susceptibility to growth inhibition was shown to decline as tibiae developed beyond the critical period, a decline that could be correlated with a declining growth rate. Emphasis is placed upon critical events during development as a more useful concept than critical periods for explaining susceptibility to teratogens.
Goldenhar syndrome, anterior encephalocele, and aqueductal stenosis following fetal primidone exposure
Authors: Gustavson Edward E. , Chen Harold 
Published: June 2005

AbstractFetal exposure to primidone was associated with Goldenhar syndrome, hemifacial microsomia, tetralogy of Fallot, aqueductal stenosis, and anterior encephalocele in this male infant. No similar cases in anticonvulsantexposed pregnancies were found on literature review, despite the increased incidence of other anomalies following such exposure.Goldenhar syndrome, especially related to rare central nervous system anomalies, is reviewed. Experimental production of hemifacial microsomia by a folic acid antagonist, triaxene, is mediated via hemorrhage in the fetus. Intraventricular hemorrhage was noted in this infant as were dilated lateral and third ventricles. The hemorrhagic diathesis and/or the folic acid depletion of newborns following fetal anticonvulsant exposure may have been the underlying mechanism.
Developmental toxicity of ethylene glycol monopropyl ether in the rat
Authors: Krasavage Walter J. , Katz Gary V. 
Published: June 2005

AbstractIn order to determine the potential developmental toxicity of ethylene glycol monopropyl ether (EGPE), pregnant rats were exposed to vapor concentrations of 100, 200, 300, or 400 ppm of the compound for 6 hours per day on days 6–15 of gestation. Maternal effects included a slight reduction in red blood cell count and increased mean corpuscular volume and mean corpuscular hemoglobin at the 200‐, 300‐, and 400‐ppm concentrations. Reticulocyte counts and polychromasia of the red blood cells were increased at all exposure levels, while anisocytosis was increased at 300 and 400 ppm and macrocytosis was increased at 200, 300, and 400 ppm. Hematocrit, hemoglobin concentration, platelet, and total and differential white blood cell counts were comparable to those of the controls. Red urine was seen in the females after the first and second exposures to 200, 300, and 400 ppm of EGPE, but not after subsequent exposures. Absolute and relative spleen weights were increased by 200, 300, and 400 ppm EGPE. Histologic changes were seen in the maternal spleen, liver, and thymus, particularly after exposure to 300 and 400 ppm. Kidneys, bone marrow, and mesenteric lymph nodes were normal. Pregnancy rate, number of corpora lutea, implantation sites and viable fetuses per dam, the incidence of resorptions per litter, and the mean fetal body weights were comparable to those of the controls. Gross external, internal soft tissue, and skeletal examinations of the fetuses revealed that EGPE did not produce teratogenicity or significant embryo/fetotoxicity in the rat at vapor concentrations as high as 400 ppm. Variations in the ossification of certain skeletal elements and the incidence of 14th thoracolumbar rudimentary ribs were increased by exposure to 200, 300, and 400 ppm EGPE.
Two massive congenital intracranial immature teratomas with neck extension
Authors: Rostad Steven , Kleinschmidt‐DeMasters B. K. , Manchester David K. 
Published: June 2005

AbstractIn this report we detail two congenital intracranial immature teratomas, noteworthy for their massive intracranial growth and extension through the skull with compromise of neck structures. Cytogenetic studies were done in both cases on the fetuses and their tumors and are the first in the literature. Few previously reported congenital intracranial teratomas have been described with neck extension. In both cases, polyhydramnios was detected by prenatal ultrasonography and was possibly caused by the laryngoesophageal and/or brainstem distortion by neoplasm. Possible reasons for such excessive, unchecked growth of teratomas in the fetal period are discussed.
Gonadal dysgenesis induced by prenatal exposure to ethinyl estradiol in mice
Authors: Yasuda Yoshiko , Kihara Takahide , Tanimura Takashi , Nishimura Hideo 
Published: June 2005

AbstractDaily oral administration of ethinyl estradiol (0.02, 0.2, or 2.0 mg/kg of body weight) to pregnant Jc1:ICR mice resulted in ovotestis and intra‐abdominal testis with persistent Müllerian duct and Wolffian duct in male fetuses and ovarian hypoplasia in female fetuses when it was given from day 11 through day 17 of gestation (before gonadal differentiation in the fetus). The ovotestis consisted of testicular and ovarian portions. In the testicular portion, a few solid seminiferous tubules containing spermatogonia, some with pachytene nuclei with Sertoli cells and compact interstitial tissue including Leydig cells, were seen. In the ovarian portion, pachytene nuclei were seen. The intra‐abdominal testis was smaller and contained more spermatogonia per tubule in cross section than the control testis. These findings suggest that in male fetuses ethinyl estradiol affects Sertoli cell differentiation resulting in suppression of Müllerian inhibiting factor. On the other hand, in the ovarian hypoplasia, the primordial follicles and follicular cells in a primordial follicle were significantly decreased in number, and the number of the degenerated primordial follicles was significantly increased. It seems likely that ethinyl estradiol affects the intimate contact between follicular cells and oocytes to cause degeneration of primordial follicles.
The effects of 5‐bromodeoxyuridine on fusion of the cranial neural folds in the mouse embryo
Authors: Bannigan John Gerard 
Published: June 2005

AbstractThe effects of 500 and 300 mg/kg bromodeoxyuridine (BUdR) on the process of fusion of the neural folds were tested after injection into pregnant mice on day 8 of gestation (192 hours postcoitum). Various doses of the natural nucleoside, thymidine (TdR), were also tested. Both doses of BUdR retarded growth to the same extent, but only the larger dose caused neural tube defects in 28.8% of embryos. Treatment with the larger dose also caused extensive cell necrosis to appear in the neuroepithelium of the neural folds between 12 and 15 hours after treatment. No changes were detectable with the light microscope up to this time. Measurement of the cell generation time in treated and control embryos indicated that the BUdR prolonged the cycle by about 2 hours and that the dying cells were in the second DNA synthetic phase following incorporation of the analog. Treatment with the smaller dose of BUdR caused minimal cell necrosis. This was taken as evidence for the importance of cell necrosis in the pathogenesis of BUdR‐induced neural tube defects. Treatment with excess TdR did not cause either neural tube defects or cell necrosis, and a dose of TdR equimolar with the large dose of BUdR (400 mg/kg TdR) did not retard growth. Doses of 800 and 1,200 mg/kg TdR retarded growth to the same extent as BUdR. The administration of an equimolar amount of TdR, along with the teratogenic dose of BUdR, prevented the occurrence of cell necrosis and neural tube defects. When treatments were given on day 9 of gestation, 500 mg/kg BUdR caused cell necrosis in the neuroepithelium about 15 hours after treatment but no neural tube defects were produced by day 9 after treatment. It is suggested that in this case cell necrosis occurred too late to interfere with neural fold fusion. It was concluded that the ability of BUdR to cause exencephaly in mouse embryos was due to cell necrosis in the neuroepithelium.