bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perinatal infections and epidemiology of anencephaly and spina bifida
Authors: Kurent Jerome E. , Sever John L. 
Published: June 2005

AbstractThe cases of anencephaly and spina bifida occurring in the Collaborative Perinatal Study were analyzed for maternal and pediatric indices of intrauterine infections. As an extension of these studies epidemiological and clinical data from the study population were also analyzed. Review of data from serially collected maternal serum specimens for specific antibody to selected viral antigens as well as cord serum determinations of IgM provided no evidehce to suggest that perinatal infection plays a prominent role in the etiology of these malformations. The raciai distributions of anencephaly and spina bifida differed significantly in that the rate of anencephaly was six times higher in whites than blacks. On the other hand whites and blacks had approximately the same rates of spina bifida. In view of this raciai disparity the Suggestion that a single common environmental agent is responsible for both defects, as included in Renwick's ('72) hypothesis must be modified.
Autonomic drug effects on the heart rate of early rat embryos
Authors: Robkin Maurice , Shepard Thomas H. , Baum David 
Published: June 2005

AbstractWe examined the effect of cardioactive drugs on the heart rate of intact rat embryos at day 11 (25 somites) of gestation, the stage of development prior to cardiac innervation. Tested were the autonomic drugs methoxamine and isoproterenol, the β‐adrenergic receptor blocker propranolol, and the phosphodiesterase inhibitor theophylline. Our observations indicated that (1) methoxamine had no effect; (2) isoproterenol and theophylline caused in creases in the heart rate; and (3) propranolol inhibited the effect of isoproterenol but did not affect the response to theophylline. We concluded that our results are consistent with (1) Ahlquist's ('48) original concept of α and β adrenergic receptors and the observation that the heart has no α receptors, (2) with the role of cyclic‐AMP in the model of the adrenergic receptor proposed by Sutherland ('68), and (3) with the observations that the embryonic heart at this stage of development is not yet innervated and so is without the vagal reflex arc (Hogg, '57; Gomez, '58).
The inheritance of susceptibility and resistance to the teratogenic effect of 1‐ethyl‐1‐nitrosourea in Inbred Strains of mice
Authors: Diwan Bhalchandra A. , Meier Hans 
Published: June 2005

AbstractBecause the teratogenic effects of 1‐ethyl‐l‐nitrosourea (ENU) were observed to be strain dependent, a hybridization experiment was made between the susceptible C57L/J amd the resistant AKR/J strains of mice. ENU induced mortality and malformations were found to be influenced by maternal, cytoplasmically transmitted, sensitivity and resistance factors. Apparently, the C57L/J strain contributes maternal traits enhancing fetal susceptibility, whereas the AKRsol;J strain contributes resistance factors. Their nature and function are unknown but several possibilities are proposed as to how they may lead to the genetic differences observed in ENU‐induced teratogenicity.
Congenital infections due to reovirus type 3 in hamsters
Authors: Kilham Lawrence , Margolis George 
Published: June 2005

AbstractReovirus type 3 was able to induce various effects in fetuses depending on the period of gestation pregnant hamsters were inoculated. Inoculations on gestation days 1–5 resulted in a high rate of fetal deaths. Fetuses of females inoculated on days 9–11 all became infected, but survived and developed normally. Reovirus proliferated to high liters in placentas and uteruses and was recovered from amniotic fluids in higher titer than from fetuses. Presence of phloxinophilic cytoplasmic inclusion bodies in pathologic studies revealed a spectrum of fetal infection ranging from mild involvement of the epidermis and ora mucosa to widespread systemic disease involving skin, visual organs, skeletal muscle, and neural tissues as well as voluntary muscles. These findings were substantiated by immunofluorescence studies. Throughout these experiments pregnant animals remained in good health in spite of having relatively high and sustained viremias. In view of the ubiquitous distribution of reoviruses in nature, and their lack of interspecies differences, observations of their ability to induce serious transplacental infections as well as hydrocephalus in laboratory animals point to the desirability of continued study of their potential role in the etiology of human disease.
A community of human malformation syndromes involving the müllerian ducts, distal extremities, urinary tract, and ears
Authors: Pinsky Leonard 
Published: June 2005

Abstract“Syndrome fever” is a term used to characterize the prolific publication of “new” human congenital malformation syndromes in the last decade. One way to manage syndrome fever, that is, to assimilate and utilize efficiently its valuable informational by‐product, is to create nosologic communities composed of member‐syndromes which have close general and specific phenotypic similarities. The phenotypic community approach to human mal‐formation syndrome taxonomy is applicable to rare, family‐specific syndromes, to well‐known syndromes that have achieved firm, independent identities, and to mixtures of the two. A community of six syndromes, four of them apparently rare, is proposed. All share uterovaginal malformation, but neither this type nor any other single type of malformation is essential for a syndrome to merit membership in the community. Five of the six syndromes have distinc‐tive and and/or foot malformations. Four of the six share malformations of the urinary tract; in a fifth urinary incontinence probably reflects a subtle dysmorphism. Three of the six syndromes have anomalies of the aural appa‐ratus; in two this involves an association between severe renal dysgenesis and middle ear ossicle defects. The sharing of similar malformations involving several systems suggests that the respective causes of the syndromes act on the same developmental pathway(S). All six syndromes have occurred in a familial distribution; four are probably determined by major mendelian genes. Malformations of the axial skeleton are rare, but those of the distal extremities are common, in the familial syndromes belonging to the group. The reciprocal tendency is found in sporadic occurrences of severe uterovaginal dysgenesis (Rokitansky‐Küster‐Hauser syndrome) and in those with so‐called nonspecific female pseudohermaphroditism.
Human symmelia: Determination of sex and other features
Authors: Monie I. W. 
Published: June 2005

AbstractA specimen of human symmelia was judged at first to be a male from the appearance and disposition of the pelvic viscera but histological study of the gonads later showed that it was a female. This raises the question of whether the preponderance of males with this abnormality might be explained, at least in part, by incorrect diagnosis of sex particularly where this has been based on gross appearances. The bladder, rectum, anus, and external genitalia were missing and the kidneys were replaced by a mass of renal tissue dorsal to the lower aorta. There was a single umbilical arrery which was identified as a persistent left primary umbilical artery. Within the lower limb were two femora, two tibiae, and one fibula. Secondary centers of ossification were present in the distal ends of the femora and the proximal ends of the tibiae.
Teratogenic effects of ochratoxin A in mice
Authors: Hayes A. Wallace , Hood Ronald D. , Lee Humphrey L. 
Published: June 2005

AbstractTreatment of pregnant mice ip with 5 mg/kg ochratoxin A on one of gestation days 7–12 resulted in increased prenatal mortality, decreased fetal weight (with the exception of those treated on day 9), and various fetal malformations. Exencephaly and anomalies of the eyes, face, digits, and tail were the most common defects. The most severe malformations were complete median facial clefts associated with exencephaly and eye defects. Skeletal defects also were noted involving the ribs, vertebrae, and skull.
Caudal mesoderm pattern of anomalies: From renal agenesis to sirenomelia
Authors: Källén Bengt , Winberg Jan 
Published: June 2005

AbstractThe use of 6168 unselected malformed infants, obtained from the Swedish Register of Congenital Malformations during the years 1965–1971, made possible an analysis of a complex of malformations that form a series from the Potter syndrome to sirenomelia. A total of 73 infants belonging to this group were identified among the approximately 550,000 births — an incidence of 1/7500 births. They formed a series from infants with the typical Potter syndrome to typical sirenomelia. Analysis of the association of various malformations indicated til at pulmonary hypoplasia and “Potter face” are not only an effect of oligohydram‐nios. A mesodermal damage is postulated as the cause of the complex of malformations. A variable craniocaudal extension of the damage can explain the different expressions of the syndrome. Closure defects of the central nervous system, facial clefts, and congenital heart defects were less common than expected when compared with other infants with multiple malformations. The incidence of these infants born in Sweden has apparently increased over the years. There was also an apparent preponderance of them in central Sweden. Pregnancies ending with the birth of infants with this malformation complex began during summertime more often than could be expected. No exogenous cause was identified.
Presence of contractile proteins in mouse fetal palate prior to shelf elevation
Authors: Lessard James L. , Wee Elizabeth L. , Zimmerman Ernest F. 
Published: June 2005

AbstractThe presence of the contractile proteins, actin and myosin, was sought in palates from day‐14.5 mouse fetuses in an effort to account for the mechanism of palate shelf elevation. Day‐14.5 tongues were carried through the same procedures as a positive control. The excised tissues were labeled with radioactive amino acids by culturing in vitro. After adding carrier actin and myosin it was possible to purify these components to constant specific activity using both palates and tongues. On this basis at least 2.1–3.3% of the radioactivity in the palates copurified with actin and about 3.6–4.7% copurified with myosin. Similarly, 1.8–3.9% and 2.5–3.3% of the radioactivity in the tongues purified with actin and myosin, respectively. About 70% of the radioactivly labeled component purified from both palates and tongues migrated with the carrier actin in SDS‐polyacrylamide gels indicating an identical molecular weight. In contrast the major radioactive component in the purified myosin from both tissues had a molecular weight (180,000) slightly lower than adult myosin. In addition it was possible to extract these proteins from the labeled palates in the form of ac to myosin. The possibility that the myosinlike component may represent an embryonic form and the role that these proteins might play in palate shelf movement is discussed.
Amniogenic bands as a cause of syndactyly in a young human fetus
Authors: Ornoy Asher , Sekeles Eliezer , Sadovsky Eliahu 
Published: June 2005

AbstractA fetus spontaneously aborted in the 4th month of gestation is described. The fetus displayed nonsymmetrical syndactyly of both hands and partial amputation of fingers in one hand caused by a dense tissue microscopically found to be composed of multiple folds of amnion. The placenta was examined, and showed severe pathology: multiple hematomas, infarctions, and fibrosis. The possible mode of formation of amniogenic bands is discussed and correlated with the clinical history and pathology of the placenta and membranes.
Antiheart antibody production of cardiovascular malformations in the mouse: A preliminary study
Authors: Nora James J. , Miles Vincent N. , Morriss Jill H. , Joy Weishuhn E. , Nihill Michael R. 
Published: June 2005

AbstractCardiovascular malformations were produced in 17% of A/J and C57BL/6 mice using isogeneic antiheart antibody (RAMHS) and in 22% of C57BL/6 mice using allogeneic RAMHS by injecting on four consecutive days of gestation (days 8–11 or 12–15). The antiheart antibody was raised in rabbits and adsorbed against mouse kidney and liver to yield an antiserum with high antiheart activity and low activity against other organs, demonstrably kidney. Cardiovascular maldevelopment occurred in 9% of mice injected with antikidney antibody (RAMKS), 7% receiving normal rabbit serum, and 1% receiving normal saline. A highly significant (P < .001) difference between all of the RAMHS and the normal saline groups demonstrated that antiheart antibody is teratogenic to the developing heart; and a significant difference (P < .05) between allogenic RAMHS and RAMKS antibody in the frequency of induction of cardiovascular anomalies suggests that there is organ‐specific activity to antiheart antibody. The type of cardiovascular anomalies caused in the mice studied were the same (VSD in C57BL and ASD in A/J) as those that occur spontaneously or are produced by other teratogens such as dextroamphetamine. Antiheart antibody thus did not appear to produce a specific type of maldevelopment but rather made manifest the malformation to which there appears to be a hereditary predisposition (genetic‐environmental interaction).
Inhibition of palatal fusion in vitro by hadacidin
Authors: Fairbanks Mary B. , Kollar Edward J. 
Published: June 2005

AbstractThis study examined the effects of hadacidin, an analogue of L‐aspartic acid, on epithelial fusion, breakdown, and mesenchymal contact in explants of fetal mouse palatal shelves. Shelves from 14‐day C57BL/6Js were explanted to agar‐solidified Eagle's basal medium. Control palates grown in this medium mimicked normal closure; i.e., an epithelial seam formed, broke down, and mesenchymal contact occurred in vitro. Experimental palates were grown in this medium supplemented with 1 or 2 mg/ml hadacidin or with concentrations of L‐aspartic acid equal to or in excess of that of hadacidin. Histological observations of explants exposed to 2 mg of hadacidin for 2 days indicated that cells of the marginal epithelia became adherent to form epithelial bands, but that subsequent epithelial breakdown and mesenchymal contact did not occur. The presence of mi to tic figures in the epithelial bands and in the mesenchyme of treated explants indicated that hadacidin inhibited breakdown, and, in addition, that it did not severely suppress or debilitate all cellular activity. This observation supports the fact that explants treated with hadacidin for 2 days, when moved to control medium for an additional 2 days, were able to undergo epithelial‐band breakdown and mesenchymal penetration. Preliminary data from explants treated with hadacidin and L‐aspartic acid indicated that competitive reversal by the amino acid did not occur consistently in vitro at concentrations of the amino acid 3 times that of hadacidin.
Thiadiazole‐induced myelodysplasia in rats
Authors: Beaudoin Allan R. 
Published: June 2005

AbstractPregnant Wistar rats were injected ip with a teratogenic dose (100 mg/kg) of 2‐amino‐l,3,4‐thiadiazole hydro‐chloride (ATDA) on day 11 of gestation (sperm day = day 0). Pregnancy was terminated at various intervals following drug injection. At autopsy some embryos were dead, some severely affected, and others only mildly affected by the treatment. The neural tube was more sensitive to ATDA than was any other tissue. The first histologically observable effect of maternal ATDA treatment was embryonic cell death in the caudal end of the neural tube, 12 h after treatment. During the next 24 h additional cells in the neural tube died, as well as cells in associated ganglia and in areas of condensing mesenchyme and somites. The tissues of the tail were especially sensitive to ATDA treatment. Forty‐eight hours after treatment repair and regeneration of neural tissue was evident. At day 20, spinal cords of affected fetuses had excrescences growing from the luminal wall, rosettes, duplication of the central canal, premature termination, and disruption of normal cellular patterns. Fetuses with myelodysplasia also had short or absent tails. It is postulated that malformations resulting from maternal ATDA treatment are due to cell death caused by ATDA acting directly on embryonic cells, with the ultimate outcome depending on the number of mitotically active cells that survive treatment to continue the process of organogenesis.
Relation of mandible growth to palate closure in mice
Authors: Shih Ling‐Yu , Trasler Daphne G. , Fraser F. Clarke 
Published: June 2005

AbstractThe role of mandible growth in normal palate closure and the effects on the mandible of three teratogens‐—cortisone, 6‐aminonicotinamide (6‐AN), and hypervitaminosis A — during palate closure in A/J (susceptible to cleft palate induction by these teratogens) and in C57BL (resistant) inbred strains of mice were investigated. The rate of mandible growth in the control embryos of the two strains was similar during the period of palate closure. Mandible length in A/Js was greater than that in C57BLs at the initial stage of palate closure and this remained true when it was adjusted for palate stage and for body weight. The mandibles were not shortened at the beginning of palate closure by any of the teratogens in either strain. In the cortisone‐treated groups the mandibles of C57BL embryos were consistently longer than those of controls whereas the mandibles of A/J embryos did not differ from those of control embryos at comparable body weights. It is concluded that cortisone, 6‐aminonicotinamide, and hypervitaminosis‐A do not cause cleft palate by reducing the length of the mandible at palate‐closure time.
Inheritance of branchial sinuses and preauricular fistulae
Authors: Hunter Alasdair G. W. 
Published: June 2005

AbstractOn the basis of two families in which branchial sinus and pre‐auricular fistulas occurred together, and a review of the literature, it is proposed that the two conditions can result from an autosomal dominant gene with some‐what reduced penetrance and variable expressivity. Embryo logical considerations suggest that the mutant gene may interfere with proper obliteration of the pharyngeal clefts, whichmay lead to either or both of the two lesions. Conductive deafness may also occur as part of the syndrome.
The distalmost palmar axial triradius in children with selected types of isolated congenital heart disease
Authors: Hook Ernest B. , Aldrich Margaret , Bonenfant Richard , Desmond Ellen , Reiss Naomi P. , Weiss Sophie C. , Wolff Grace 
Published: June 2005

AbstractNumerous previous reports have suggested an association of elevation of the distal axial triradius on the palm with congenital heart disease. Our investigation, however, in which the maximum atd angles of children with (isolated) congenital heart malformation were compared with the measurement in children with functional heart murmurs (controls), revealed no statistically significant difference in any of seven types of heart defects investigated. Only in males with tetralogy of Fallot was there even a suggestive (but nonsignificant) trend towards elevation of the atd angle. The fact that in our study the data were corrected for age of the subjects may account for the difference between these observations and those of some earlier reports. It appears unlikely that screening the position of the distalmost axial triradius in ostensibly normal newborn infants will be useful in predicting the subsequent appearance of signs of a congenital heart malformation, as has been suggested by other workers.
Resistance of rat fetuses to nicotine‐induced lipolysis
Authors: Mosier H. David , Capodanno Carmen C. , Li Ivy O. W. , Magruder Caroline Sue , Jansons Regina A. 
Published: June 2005

AbstractPregnant Long‐Evans rats were fed stock diets containing 50 or 100 mg/kg of added nicotine during days 10–20 or 0–20 of pregnancy. Control rats were given stock diet during days 0–20. The mean nicotine intake ranged up to 6.03 mg/kg/day. In fetuses bled on day 20 there were no differences in levels of fetal plasma triglycerides, phospholipids, and cholesterol between the experimental and control groups. In another experiment single doses of 1 mg/kg nicotine were injected ip on day 20 into pregnant rats. Plasma free fatty acids (FFA) and triglycerides were determined at time intervals up to 30 min in the fetuses and 60 min in the females. Maternal values showed significant increases after nicotine, but fetal values did not change. Fetal adrenal and fetal whole body concentrations of epincphrinc and norepinephrine were determined up to 60 min. Fetal adrenal epinephrine decreased slightly after nicotine injection then rose and remained slightly higher than the control value. After saline injection there was no decrease in fetal adrenal epinephrine but instead there was a rise to a peak value greater than after nicotine. Fetal whole catecholamine concentrations were not changed after injection. These results are compatible with an increase in adrenal epinephrine release after nicotine. The resistance to change of fetal FFA after nicotine is probably due to a resistance to epinephrine‐induced elevation of fetal FFA. The placenta may be responsible for maintaining the steady state in fetal plasma lipids.
Developmental defects in rats treated postnatally with 5‐lododeoxyuridine (IUDR)
Authors: Percy Dean H. , Albert Daniel M. 
Published: June 2005

AbstractSprague‐Dawley rats were treated sc with 100–400 mg/kg/day 5‐iododeoxyuridine (IUDR) for 5 days beginning at 1, 5, or 10 days of age. Hair and somatic growth were markedly reduced in rats given 400 mk/kg beginning at 1 day of age. Animals were examined histologically at 10 or 20 days of age. Cerebellar cortical lesions were evident after the highest dosage in animals killed at 10 days of age, but lesions were of lesser magnitude in all series killed at 20 days of age. Retinal dysplasia was observed in rats treated beginning at 1 day of age. Lesions were characterized by thinning of the retina, undulations, and rosette formation in outer retinal layers. Foci of renal dysplasia were evident in rats treated beginning at 1 day of age. Poorly differentiated glomeruli and tubules together with nests of primordial epithelial cells, indicative of impaired nephrogenesis, were located in the superficial cortex. It is known that developmental defects can occur in the cerebellum, retina, and kidney of animals infected perinatally with certain cytolytic viruses. However, these appear to be the first studies demonstrating that a halogenated uridine given to newborn animals may result in obvious renal cortical and retinal dysplasia.
Brain cavitation and micrencephaly in lambs exposed to prenatal hyperthermia
Authors: Hartley W. J. , Alexander G. , Edwards M. J. 
Published: June 2005

AbstractEwes were exposed to 44o C for 9 h daily during the last two‐thirds or last third of gestation. The body weights of lambs were significantly reduced and cavitations of the cerebral white matter were found in 75% and micrencephaly in 44% of lambs.
Teratologic effects of ethylnitrosourea on brain development in rats
Authors: Pfaffenroth Michael J. , Das Gopal D. , McAllister James P. 
Published: June 2005

AbstractWistar rats were injected iv with ethlnitrosourea (ENU) between days 14 and 21 of gestation and the offspring killed 0, 3, 6, 10, 15, 21, and 75 days after birth. The brains obtained from these animals, on macroscopic examination, revealed that ENU produced micrencephaly of variable degrees reflected predominantly in the reduced dimensions of the cerebrum and cerebellum, inversely proportional in severity to the gestational age at which ENU was administered. The degrees of micrencephaly were first evident in 15‐day‐old animals and persisted throughout adulthood.