bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of plasma proteins in the palate of fetal mice
Authors: Gustine David L. , Zimmerman Ernest F. 
Published: June 2005

AbstractInvestigations were undertaken to correlate changes in proteins with development and morphogenetic movement of palate shelves in the fetal mouse. Soluble palate proteins were analyzed by polyacrylamide disc gel electrophoresis. Three major groups of proteins were present: (1) three bands at Mx 0.35–0.48 designated αl–3, (2) five bands at Mx 0.70–0.85 designated β1‐5, and (3) one band at Mx 1.0 designated γ. Changes in the relative concentration of some of these proteins occurred during development: by day 15.5 of gestation α3, β4, and β5 had increased while α1, μL2, β1, β2, and β3 had decreased. Comparison of these palate proteins with other fetal and adult tissue proteins indicated that α and γ were probably present in both fetal and adult tissues, but β was present only in fetal tissues. The results showed that α, β, and γ were present in the palate extracellular matrix but β was not found in isolated palate cells. Furthermore, a different electrophoretic distribution of proteins was found for the cell proteins. Further evidence indicated that α and γ were transferrin and albumin, respectively, and that β was a fetal plasma glycoprotein analogous to calf fetuin. The presence of these plasma proteins in the matrix was thought to be due to their circulation throughout the extracellular space of fetal tissues; and the relative change in the proportion of these electrophoretically separable proteins during development to reflect comparable changes in the fetal plasma.
Action of some cardiovascular and neurohumoral agents on the formation of the chick embryo heart. I. Morphology
Authors: Butros Joseph 
Published: June 2005

AbstractA study of some cardiovascular drugs was made with early chick blastoderms (stages 5–6) cultured in vitro to determine their action on the initiation of heart primordia. Ouabain (16–22 μ/ml) completely prevented the appearance of heart primordia and caused slight cytolysis of the brain and somites. Quinidine (15 μg/ml) caused swelling of the formed hearts but they were noncontracting. Atropine (100 μg/ml) had a slight cytolytic effect on the heart and more so on the brain. Epinephrine (25 μg/ml) had a strong cytolytic action but no selective action on any system. Acetylcholine (up to 500 μg/ml) had no inhibitory effect on development.
Action of spermine on early chick development. I. Morphogenesis and histogenesis
Authors: Butros Joseph 
Published: June 2005

AbstractUnincubated eggs were injected with spermine (2.61–10 mg/egg) and incubated for 1–7 days. Morphogenetic and histogenetic study of the recovered embryos indicated a teratogenic action of the agent. Abnormalities consisted of lack of head flexures, asymmetry, and general arrest of development at about stage 17. A few bizarre conditions occurred: some specimens consisted of nothing but blood sacs; in a few the neural tube was thrown into highly convoluted folds. The histological picture also indicated a general arrest of development at about stage 17: cells of the neural tube were disaggregated at abrupt points and moved out of the wall, taking a more rounded, smaller form. The most striking change pertained to the blood cells. Whereas day‐7 control embryos had mature erythrocytes, the spermine‐treated ones showed a proliferation of immature erythrocytes in the vessels, heart, and head, which often completely filled these organs.
A case of thoracopagus: Conjoined twins
Authors: Gilbert Enid F. , Suzuki Hiroshi , Kimmel Donald L. , Klingberg William G. , Lancaster Joseph R. 
Published: June 2005

AbstractA detailed anatomical description of a thoracopagus is presented. The complex venous anomalies were unique in combining absence of the inferior vena cava of one twin with drainage into an atrium of the other twin of its inferior vena cava with all the hepatic veins from the common liver. The other atrium received the entire venous drainage from the upper extremities of both infants.
BAL alleviation of arsenate‐induced teratogenesis in mice
Authors: Hood Ronald D. , Pike Charles T. 
Published: June 2005

AbstractTreatment of pregnant mice ip with 40 mg/kg aqueous sodium arsenate on gestation day 9 resulted in a significant increase in fetal mortality and malformation, and in fetal weight reduction. Treatment sc with 50 mg/kg BAL 4 h before, concurrently with, or 4 h after arsenate reduced the frequency or severity of malformation compared with the effects of arsenate alone.
Paternal age and congenital cleft lip and cleft palate
Authors: Perry T. B. , Fraser F. C. 
Published: June 2005

AbstractIn an analysis of 679 families no evidence was found of a diference in paternal or meternal ages between complete and incomplete forms of cleft lip, with or without cleft palate, or between familial and nonfamilial cases, It would appear that parental‐age effects for clefts of the lip or palate either do not exist or are so complex that their biological significance is likely to remain obscure.
Independent effects of maternal age and birth order on the incidence of selected congenital malformations
Authors: Hay Sylvia , Barbano Helen 
Published: June 2005

AbstractIncidence rates, specific for maternal age and birth order, were calculated for 16 categories of congenital malformations reported on birth certificates from a population of more than 8 million registered white, single livebirths. With maternal age held constant none of the malformations showed increasing incidence as birth order increased. Hypospadias, esophageal defects, omphalocele, and Down syndrome showed evidence of decreasing incidence as birth order increased. Some of the other malformation categories showed an excess of first births in most age groups, while no relation to birth order was observed in the incidence of other malformations. By contrast, most of the malformations analyzed exhibited increasing incidence as maternal age increased. Especially high rates of several malformations were observed among first births to women over 40 years of age.
Distribution and fate of nicotine in the rat fetus
Authors: Mosier H. D. , Jansons R. A. 
Published: June 2005

Abstract[3H] (−)‐Nicotine was administered iv into pregnant Long‐Evans rats on day 19 of gestation or in three consecutive daily doses given on days 16 through 18 of gestation. The concentration of radioactivity and proportions of labeled compounds were determined at intervals from 5 min to 20 h after injection in maternal plasma and liver, decidua basalis, placenta, amniotic fluid, whole fetus, and fetal plasma, brain, lungs, heart, liver, adrenals, kidneys, gonads, and the stomach‐intestine‐spleen‐pancreas en bloc. Nicotine, cotinine, and other metabolites appeared in the fetus within 5 min of injection. The concentration of radioactivity in the fetal plasma exceeded that of the maternal plasma from 30 min through 20 h. Fetal liver had a greater proportion of radioactivity as nicotine than did maternal liver. Fetal plasma as well as most of the fetal tissues had a greater proportion of nicotine to metabolites than did the maternal plasma throughout the time period that was studied. By 60 min an equilibrium was established between maternal plasma and amniotic fluid with respect to concentration of radioactivity. This equilibrium was maintained through 20 h after single injections and also after the three daily injections. The proportions of nicotine to major metabolites were similar in maternal plasma and amniotic fluid at 4 h. The findings show that fetal rat tissues are exposed to levels of nicotine greater than those found in maternal plasma beginning within 30 min of the time nicotine enters the maternal circulation.
Prenatal growth of Wistar rats: Circadian periodicity of fetal growth late in gestation
Authors: Barr Mason 
Published: June 2005

AbstractPregnant CFN Wistar rats demonstrated marked fluctuations of body weight within 24‐h periods during late gestation. Maternal weight loss during the daytime phase of the daily cycle was accompanied by a slowdown in fetal growth. The period of rapid maternal weight gain that occurred during the night was paralleled by a period of rapid fetal growth. The periodicity of fetal growth was due to variation in accumulation of solids and not to diurnal fluctuations in relative water content.
Limb development in mouse embryos. I. Analysis of teratogenic effects of retinoic acid
Authors: Kochhar D. M. 
Published: June 2005

AbstractRetinoic (vitamin A) acid produced phocomelia and micromelia in DBA/2J fetuses when administered to pregnant mice on the 12th or 13th day of gestation. The incidence of forelimb defects was higher after 12th‐ (in embryos having 33–41 somite pairs) than 13th–day treatment (40–51 somite pairs); the reverse was true for hindlimb defects. Hindlimb digits continued to be highly susceptible on the 14th day. Limb defects were not accompanied by body growth retardation or other skeletal malformations except cleft palate. The type and severity of limb defects depended on the average developmental stage of the limb bud at the time of treatment. From the beginning of the period of limb susceptibility, the 12th day, the ontogenetic sequence in which the long bones were rendered abnormal was: radius–ulna, humerus, fibula, tibia, femur or tibia‐femur. The sequence in which the long bones lost their susceptibility to retinoic acid was: humerus, femur, ulna, radius, tibia‐fibula. The radius appeared to be susceptible in some embryos at a time when the other long bones had escaped injury. An analysis of the shape of the same bone affected at different periods of prenatal development led to the following proposal. At earlier stages retinoic acid disrupts cellular activities that normally lead to the spatial organization of the mesenchymal cell condensations, resulting in a modified shape of the cartilage models; at later stages it prevents the enlargement of the condensations that have already appeared, resulting in smaller than normal models.
Hemorrhages in the limbs of fetal rats after amniocentesis and their role in limb malformations
Authors: Singh Shamer , Singh Gajendra 
Published: June 2005

AbstractWistar rats were subjected to amniocentesis on the 15th day of gestation and fetuses collected at various intervals (5 min to 2½ h) after the operation; 0.04 ml amniotic fluid was withdrawn through a thin dental needle (0.45 mm diam.) or no. 19 hypodermic needle (1.06 mm diam.) and in some cases sacs were punctured with a pair of iridectomy scissors (about 3 mm diam.) to determine the effect of rate of evaculation of the amniotic fluid through different‐sized openings. Limbs of the fetuses were examined for evidence of hemorrhages and their incidence and severity correlated with the size of the puncture. Hemorrhages were more frequent and more severe in the lower limbs than in other areas; this is correlated with the higher incidence of lower limb malformations reported after amniocentesis by others. To exclude the influence of uterine muscular contractions, some fetuses (15‐day) were removed along with their placentas and intact amniotic sacs and similarly punctured, outside the uterine horns. None showed hemorrhage in any area. The mechanism of the limb malformation seems to be compression of the fetus by uterine muscular contractions, after evacuation of the amniotic fluid, causing hemorrhages, which in turn lead to necrosis and various degrees of limb degeneration.
Congenital pericardial defects
Authors: Chaurasia B. D. 
Published: June 2005

AbstractA congenital partial defect of the left pericardium associated with a left diaphragmatic hernia and total myeloschisis in a stillborn dicephalus dibrachius triotus female monster is described. It is pointed out that the generally accepted view, viz., that pericardial defects result from either a failure of closure or incomplete closure of the pleuropericardial foramen, holds good only for the partial forms of the pericardial defects. It is proposed that complete defects of the pericardium are due to imperfect development of the pleuropericardial membrane, resulting in a rent, either medial or lateral to the phrenic nerve, through which the lung bud grows into the pericardial cavity. The hypothesis that imperfect development of the pleuropericardial membrane is due to a primary defect in the septum transversum is discussed. Rotation of the heart is proposed as an additional possible factor responsible for preponderance of left‐sided defects.
Sensitivity of embryos and intraspecies differences in mice in response to prenatal administration of corticoids
Authors: Dostál M. , Jelínek R. 
Published: June 2005

AbstractThe susceptibility of different strains of mice to the teratogenic action of corticoids is determined by the sensitivity of the embryo and by the protective properties of the maternal‐embryonic complex. The sensitivity of embryos can be determined by direct injection of corticoids into the amniotic sac while the degree of protective properties can be determined by comparing the effects of corticoids administered intraamniotically (ia) and intramuscularly (im) to different strains of mice. Exploring these relations, we applied 0.1 mg hydrocortisone on day 13 of pregnancy ia and 5.0 mg corlisone acetate on day 12 im to A/J, C57BL/6, CBA, and C57BL/10 mice, and to some of their F1, F2 and F3 matings. The effect was evaluated on day 16 of pregnancy by recording dead fetuses and fetuses with cleft palate. We found (1) there are differences both in sensitivity of embryos and degree of protective properties of maternal‐embryonic complexes; (2) the main factor determining susceptibility of the maternal‐embryonic complex to the teratogenic action of corticoids is degree of protective properties; (3) the differing sensitivity of embryos can be the cause of interstrain differences in susceptibility to corticoids only if there is no substantial difference in protective properties of the maternal‐embryonic complex; (4) the sensitivity of F1 hybrid embryos is essentially influenced by hybrid vigor.
Mucopolysaccharide synthesis in the developing inner ear of manganese‐deficient and pallid mutant mice
Authors: Shrader Ruth E. , Erway Lawrence C. , Hurley Lucille S. 
Published: June 2005

AbstractHistological development of otoliths was examined in the ears of fetal Mn‐deficient and pallid mutant mice and controls. As judged by 35S incorporation, sulfomucopolysaccharides of the otolithic membrane were secreted by cells in the macular epithelium of the utriculus and sacculus. Normal development of otoliths occurred between days 15 and 16 of gestation and was indicated by the appearance of fine granules of calcium carbonate associated with a metachromatic, PAS‐positive material which specifically incorporated 35S. Manganese deficiency or the pallid gene caused reduced incorporation of 35S in the macular cells, the formation of a nonmetachromatic, variably PAS‐positive matrix which did not contain 35S, and failure of otolithic calcification. Rate‐limiting effects of manganese deficiency on sulfomucopolysaccharide synthesis by periotic chondrocytes were observed, but 35S metabolism in cartilage was unaffected by the pallid gene. The possible role of manganese production of the otolithic defect is discussed.
Median facial cleft syndrome in half‐sisters. Dilemmas in genetic counseling
Authors: Warkany Josef , Bofinger Mary K. , Benton Corning 
Published: June 2005

AbstractTwo infant gids with median facial cleft syndrome are described. The patients were the children of the same mother but of different fathers. None of the parents had the same or similar malformations. The occurrence of this rare syndrome in half‐sisters is difficult to explain; it poses questions about etiology, usually not considered if malformation syndromes are seen in sisters who are the offspring of the same mother and father, both unaffected.
Apert syndrome and palatal mucopolysaccharides
Authors: Solomon Lawrence M. , Medenica Maria , Pruzansky Samuel , Kreiborg Sven 
Published: June 2005

AbstractBy means of histochemical techniques, six of seven patients with Apert syndrome were found to have a heavy deposit of acid mucopolysaccharides in the soft tissue of their characteristic palatal deformity, whereas only six of 15 patients with other palatal deformities (unassociated with the Apert syndrome) were found to have some acid mucopolysaccharide deposited in their palatal soft tissue. The mucopolysaccharides found in both groups were predominantly hyaluronic acid and to a lesser degree sulfated mucopolysaccharides. Examination of sections of skin from both groups of patients and the internal organs, postmortem, from one of the Apert patients failed to reveal the presence of mucopolysaccharides in these tissues.
Teratogenic effects of methylmercury in the cat: Note on the use of this species as a model for teratogenicity studies
Authors: Khera K. S. 
Published: June 2005

AbstractPregnancy was induced in cats by coordinating gonadotropin‐induced behavioral estrus and ovulation with natural matings. Reproductive indices were comparable with those already known for pregnancies in normally cycling estrous cats. Cats were orally administered 0, 0.03, 0.83, 0.25, or 0.75 mg/kg Hg (as CH3HgCl) from day 10–58 of induced pregnancy and at near term fetuses were delivered by Cesarean section. 0.75 mg/kg caused vomiting, ataxia, and death within 32 days of commencement of treatment. At 0.25 mg/kg there was an increased incidence of abortion and fetal anomalies; in surviving fetuses a reduced neuronal population in the external granular layer of the cerebellum was noticed. Minimal or no embryopathic effects were noted at lower doses. Mercury concentrations were determined and were in the following decreasing order: fetal blood > maternal blood > fetal brain. The blood and the brain of the test dams had similar concentrations. The literature on congenital anomalies in cats is briefly reviewed.
Prevention of anencephaly and spina bifida in man
Authors: Renwick J. H. 
Published: June 2005

AbstractAnencephaly and spina bifida, for some purposes, can be regarded as a single entity (ASB). The seasonal peak incidence has pointed to an influence of potato quality, that quality being worst in May or June. The ASB incidence is highest among infants conceived in late April, the damage occurring predominantly in May or June. In addition to this seasonal relation, I have found two other relations with potato quality. These are a concordance geographically between potato‐blight severity and ASB incidence; and a year‐to‐year concordance between these two variables. Perhaps some metabolite of the infected potato (say a phytoalexin), or a metabolite of one of its pathogens, accumulates during winter storage and is maximal in May or June at the likely time of teratogenesis. The year‐to‐year correlation has been confirmed in previously published data. The claim of 95% preventability in the British Isles by complete potato avoidance, a claim based on these associations, has not yet been tested. However, recent anecdotal data has confirmed that preventability cannot quite reach 100% by this means alone, even in the British Isles. I believe that women of childbearing age in whom conception is a possibility should avoid imperfect potatoes.
Metabolites accumulating in potato tubers following infection and stress
Authors: Kuć Joseph A. 
Published: June 2005

AbstractA broad spectrum of secondary plant metabolites are found in healthy, infected, and stressed potato tuber tissue. These include: chlorogenic, caffeic, vanillic, p‐hydroxybenzoic, and salicylic acids, scopolin, scopoletin, α‐solanine, α‐chaconine, solanidine, α‐solarnarine, β‐solamarine, rishitin, rishitinol, phytuberin, and lubimin. Infection and stress qualitatively and quantitatively influence these constituents. Chlorogenic and caffeic acids, scopolin, scopoletin, α‐solanine, α‐chaconine, and solanidine rapidly accumulate in injured tubers at or close to the sites of injury. In the 22 cultivars of potato studied α‐ and β‐solamarine were only found to accumulate in foliage or injured tubers of the cultivar Kennebec. Infection of tubers with Phytophthora infestans, the incitant of late blight, or a number of other fungi and bacteria causes accumulation at the site of infection of chlorogenic and caffeic acids, scopolin and scopoletin, rishitin, rishitinol, phytuberin, and at times lubimin. These compounds accumulate at levels that are fungitoxic and they appear part of the mechanism of disease resistance of the potato tuber. Resistant tubers infected with P. infestans accumulate more than 200 times the rishitin and related terpenoids found in uninfected tubers. Chlorogenic acid and caffeic acid, scopolin, scopoletin, α‐solanine, α‐chaconine, and solanidine are normal constituents of potato peel, and their concentration in the peel can be equal to that in injured peeled tubers. Freshly peeled healthy tubers contain little or none of the compounds. The danger of introducing substances potentially toxic to humans into food crops is suggested by tne occurrence of α‐ and β‐solamarine in aged tuber slices of the cultivar Kennebec. These substances might arise from the use of mutants or crosses with wild inedible species in breeding programs.
Supernumerary distal limb elements induced by 5‐fluoro‐2′‐deoxycytidine in mice
Authors: Kleinebrecht J. , Fränz J. , Degenhardt K.‐H. 
Published: June 2005

AbstractPolydactyly (including triphalangy) in C57BL/10 mice inducedby various dosages of 5‐fluoro‐2′‐deoxycytidine given at gestation day IX or XI isdescribed. These data are compared with those on aplasias in order to elucidate whether polydactyly is truly supernumerary or is the result of malposition of limb elements.
Teratogenic effects of aldrin, dieldrin, and endrin in hamsters and mice
Authors: Ottolenghi Anna D. , Haseman Joseph K. , Suggs Fred 
Published: June 2005

AbstractSingle oral doses of aldrin, dieldrin, and endrin, 1/2 LD50 incorn oil, administered to pregnant golden hamsters on day 7, 8, or 9 of gestationcaused a high incidence of fetal death, congenital anomalies, and growthretardation. The most frequent defects were cleft palate, open eye, andwebbed foot, often occurring in combination. Pregnant CD1 mice given equivalent oral doses of each pesticide on day 9 of gestation showed similar anomalieswithout concurrent increase in fetal mortality or growth impairment.
Scalp‐hair patterning: Its origin and significance relative to early brain and upper facial development
Authors: Smith David W. , Gong Bradley T. 
Published: June 2005

AbstractStudies of hair‐follicle development and scalp‐hair patterning innormal fetuses and children and in those with disorders of early brain development were indicative of the following hypothesis: hair directional slope is secondary to the plane of stretch exerted on the skin by the growth of underlying tissues during the period of downgrowth of the hair follicles, around 10–12 gestational weeks. The posterior parietal hair whorl was interpreted as the focalpoint from which the growth stretch is exerted by the domelike outgrowth of thebrain during the time of hair follicle development. Anomalies such as encephalocele and dicephaly, which must have antedated hair follicle development, showed expected aberrations in scalp patterning. Among patients with primarymicrocephaly 85% had altered scalp hair patterning, indicating an early onsetof the problem in brain development. This included 25% with no parietal whorl, a finding previously noted only in nonhuman primates. Aberrant scalp patterning was also found to be a frequent finding in five established syndromes, included Down syndrome, in each case being compatible with a problem in early brain development. Thus, aberrant scalp‐hair patterning may be utilized as an indicator of altered size and/or shape of the brain prior to 12 weeks of gestation.