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At least 1,315 records · Page 73Linked to original sources
PubMed1999

Natural course of combined limb and palatal tremor caused by cerebellar-brain stem infarction.

After infarction of the left superior cerebellar peduncle and dentate nucleus, a patient developed tremor of the left upper limb beginning on the twelfth day followed by palatal tremor appearing 10 months after infarction. Surface electromyogram revealed a difference in the frequency of the tremor in the upper limb and soft palate. When the palatal tremor appeared, brain magnetic resonance T2-weighted images revealed high signal intensity of the contralateral, right inferior olivary nucleus. Subsequently, when the amplitude of palatal tremor became less severe, the high olivary signal intensity subsided whereas the hypertrophy of the nucleus remained. This patient provides useful information on the pathogenesis of skeletal and palatal tremor with brain stem or cerebellar lesions based on the differences in the onset and frequency of tremors and morphologic changes in the inferior olive.

Arm↗
PubMed1976

Light and electron microscopic observations on hydrocortisone-induced cleft palate in hamsters.

Palatal histogenesis in hydrocortisone-treated hamster fetuses was studied by both light and electron microscopy. At an early stage in the hydrocortisone-affected fetuses, when the palatal shelves hung vertically on either side of the tongue, necortic changes could be seen in some of the basal epithelial cells which lay adjacent to the fragmented basal lamina. The normal looking cells lay on an intact basal lamina and were attached to the contiguous necrotic cells by desmosomes. With horizontal reorientation of the palatal shelves and their approach to the midline, cellular necrosis and fragmentation of the basal lamina increased. When compared with normal cells, the hydrocortisone-affected ones were seen to be lighter, to contain fewer ribosomes and no lysosomes. At a later stage, when midline palatal fusion was lacking, the epithelium underwent stratification and keratinization while the necrotic debris was removed by mesenchymal macrophages. It appears that the normal process of protein synthesis is inhibited following hydrocortisone administration and that this, in turn, during palatogenesis, disrupts normal cellular differentiation and the integrity of the basal lamina, which are associated with the production of a cleft palate.

Animals↗
PubMed2007

Prevalence of duplications and deletions of the 22q11 DiGeorge syndrome region in a population-based sample of infants with cleft palate.

The prevalence of duplications and deletions of the 22q11.2 (DiGeorge syndrome) region was studied among babies born in Norway with open cleft palate without cleft lip (cleft palate only, CPO). During a 5-year period (1996-2001), there were 245 live births with CPO that were referred for surgery. DNA was available from 174 cases with overt cleft palate. DNA copy number was analyzed with the multiplex ligation-dependent probe amplification (MLPA) technique, and an unambiguous result was obtained in 169 (97%) of the samples. We found no 22q11.2 duplications, and one known, and two previously undiagnosed cases with 22q11.2 deletions. All three del22q11-syndrome cases also had heart malformations, which represent one-third of the 10 babies with heart malformations in our study population. The prevalence of del22q11-syndrome among babies with cleft palate with or without additional malformations was 1 of 57 (1.8%). Because the prevalence of CPO in the 35 22q11.2 duplication cases published was 20%, we also investigated if dup22q11-testing was warranted in this group. However, no 22q11.2 duplications were found, indicating that the duplication cases ascertained so far might not be representative of the dup22q11-group as a whole. We conclude that neither del22q11 nor dup22q11 testing is warranted in babies with overt cleft palate as the only finding.

Chromosome Deletion↗
PubMed2005

Ontogeny of craniofacial sexual dimorphism in the orangutan (Pongo pygmaeus). I: face and palate.

The orangutan is widely recognized as a highly dimorphic species. An ontogenetic approach to the study of sexual dimorphism can assist researchers in understanding both where and when these differences develop. In this study, 357 orangutans from Borneo were divided into five developmental stages representing infancy to mature adulthood. Three-dimensional (3D) coordinate data from 16 landmarks representing the face and palate were analyzed by means of a Euclidean distance matrix analysis (EDMA), a quantitative method for the comparison of forms. Three separate analyses (an age-specific static comparison of forms, a sex-specific analysis of growth trajectories, and an intersex comparison of patterns of relative growth) were carried out with the intent to describe the rate, timing, magnitude, and pattern of growth in the orangutan face and palate. The results indicate that generally males and females share a similar, but not identical, pattern of growth or local form change, but differ in growth rate, timing, and magnitude of difference. Dimorphism in the face and palate can be localized in infancy and traced throughout all age intervals. Orangutan females grow slightly faster than males from infancy to adolescence, at which time male growth exceeds female growth. Female growth ceases with the advent of adulthood, while male growth continues (i.e., both the number and magnitude of the dimorphic dimensions increase). Males and females are similar in facial dimensions and growth related to the orbits, upper face, and palate width. They maintain these similarities throughout development. However, they differ in facial and nasal height, palate length, snout projection, depth of the nasopharynx, and hafting of the face onto the skull. The face broadens and the zygomatic bone flares dramatically in adult males, corresponding to the development of cheek pads. While growth patterns are similar between the two sexes, they differ in the lateral orbit, snout projection, and hafting of the face onto the cranium. Adult dimorphism is the result of growth patterns experienced throughout life, and it is not equally expressed across the cranium. An understanding of patterns of dimorphism, along with the magnitude of difference, may be helpful for interpreting dimorphism in the fossil record.

Animals↗
PubMed1980

Differential changes in cartilage cell proliferation and cell density in the rat craniofacial complex during secondary palate development.

During mammalian secondary palate formation sagittal growth of the lower face has been shown to be more rapid than that of the upper face, and the tongue and mandible extend beneath the primary palate. In order to identify factors contributing to this differential growth pattern, cellular and morphologic growth of the major cartilages of the upper and lower facial regions were studied in radioautographic sections labeled with tritiated thymidine. Evaluation of cell-density recordings, labeling indices, and structural dimensions revealed significant differences between Meckel's cartilage in the lower face, and the nasal cartilage and anterior cranial base cartilage in the upper face. After formation of the precartilaginous blastema, labeling indices were high in Meckel's cartilage (20-30%), but very low in the nasal cartilage and the anterior cranial base (0-2%). During secondary palate formation the volume of Meckel's cartilage increased more rapidly than the other cartilages and its growth was primarily in the sagittal direction. Between days 15 and 17, the increase in the length of Meckel's cartilage (165%) was approximately twice as great as the increase in the combined length of the nasal cartilage and the anterior cranial base (77%). During this period induction of cleft palate with some teratogens has been shown to severely retard growth of Meckel's cartilage and produce mandibular retrognathia that contributes to delayed elevation of the palatal shelves. Therefore, extensive cell proliferation in Meckel's cartilage, during a period of limited proliferation in other craniofacial cartilages, appears to contribute to its rapid growth and its differential sensitivity to growth inhibition.

Animals↗
PubMed1986

Catecholamine modulation of embryonic palate mesenchymal cell DNA synthesis.

Development of the mammalian embryonic palate depends on the precise temporal and spatial regulation of growth. The factors and mechanisms underlying differential growth patterns in the palate remain elusive. Utilizing quiescent populations of murine embryonic palate mesenchymal (MEPM) cells in vitro, we have begun to investigate hormonal regulation of palatal cell proliferation. MEPM cells in culture were rendered quiescent by 48 hr serum deprivation and were subsequently released from growth arrest by readdition of medium containing 10% (v/v) serum. The progression of cells into S-phase of the cell cycle was monitored by autoradiographic analysis of tritiated thymidine incorporation. Palate mesenchymal cell entry into S-phase was preceded by a 6- to 8-hr prereplicative lag period, after which time DNA synthesis increased and cells reached a maximum labeling index by 22 hr. Addition of 10 microM isoproterenol to cell cultures at the time of release from growth arrest lengthened the prereplicative lag period and delayed cellular entry into S-phase by an additional 2 to 4 hr. The rate of cellular progression through S-phase remained unaltered. The inhibitory effect of isoproterenol on the initiation of MEPM cell DNA synthesis was abolished by pretreatment of cells with propranolol at a concentration (100 microM) that prevented isoproterenol-induced elevations of cAMP. Addition of PGE2 to cell cultures, at a concentration that markedly stimulates cAMP formation, mimicked the inhibitory effect of isoproterenol on cellular progression into S-phase. These findings demonstrate the ability of the beta-adrenergic catecholamine isoproterenol to modulate MEPM cell proliferation in vitro via a receptor-mediated mechanism and raise the possibility that the delayed initiation of DNA synthesis in these cells is a cAMP-dependent phenomenon.

Animals↗
PubMed1985

Potentiation of chemically induced cleft palate by ethanol ingestion during gestation in the mouse.

The influence of ethanol consumption on cleft palate induction by methylmercury, cortisone, and retinyl acetate was investigated in Swiss white mice. Consumption of 20% ethanol throughout gestation significantly increased the incidence of cleft palate compared to water-fed mice, when methylmercury was given on four consecutive days (days 9-12, 5 mg/kg of body weight). Ethanol also increased the incidence of cleft palate in mice given retinyl acetate (3,400 or 5,100 IU) on day 12, compared to retinol acetate-treated mice given water, but did not affect cleft palate induction by cortisone (2.5 mg/d, days 8-11). Ethanol significantly reduced fetal weight in the presence or absence of the three teratogens, but the results do not support a hypothesis that growth retardation is directly responsible for the potentiating action of ethanol. It may be that ethanol acts to increase cleft palate induction by some teratogens by retarding fetal developmental processes.

Alcohol Drinking↗
PubMed1975

Some aspects of corticosteroid-induced cleft palate: a review.

Since the discovery 25 years ago that cortisone can produce cleft palate in mouse embryos investigations into possible mechanisms of this corticosteroid-induced defect have been many and varied. However, the teratogenic mode of action remains not fully clarified. It is with this thought in mind that we have reflected upon what is known concerning corticosteroids and cleft palate. The major metabolic pathways upon which glucocorticoids act as well as their intracellular mode of action are well known. Differential sensitivity of various mouse strains to cortisone treatment as well as recent results from interstrain blastocyst transfer experiments demonstrate that corticosteroid action is influenced by both the fetal and maternal genomes. Labeling experiments indicate that corticosteroid-induced cleft palate is the result of direct action of the steroid molecule on the fetus, whose own sensitivity to insult, perhaps owing to differences in binding of corticosteroids to tissue proteins, determines the final effect. Possible mechanisms that have been proposed by which corticoids may produce cleft palate include: disruption of glycosaminoglycan or collagen synthesis or both, intracellular lysosomal membrane stabilization, myopathy, weakened midline fusion, and loss of amniotic fluid. Also discussed is the role of stress and stress-induced corticosteroids and their possible role in the production of cleft palate.

Adrenal Cortex Hormones↗
PubMed1975

The relation between maternal restraint and food deprivation, plasma corticosterone, and induction of cleft palate in the offspring of mice.

The blood level of corticosterone was measured in mice following the injection on day 14 of pregnancy of a dose of corticosterone sufficient to cause a low frequency of cleft palate in the fetuses. This was compared with the blood levels present during maternal restraint and food deprivation that produced a similar frequency of cleft palate. The mean blood level over the 24 h following injection of corticosterone was 660 mug/100 ml, and during a similar period of restraint was 485 mug/100 ml. Other mice were subjected either to restraint or food deprivation for 24 h beginning day 14 of pregnancy, the plasma corticosterone levels measured during that time, and the frequency of cleft palate in late fetuses compared with the individual plasma corticosterone levels during treatment. There was a significant (P less than 0.025) correlation between high maternal corticosteroid levels and the frequency of cleft palate in the offspring of the restrained mice but not in the food-deprived animals. It is suggested that in some stressed mice endogenous plasma corticosterone can reach levels sufficient to account for the development of cleft palate.

Animals↗
PubMed1979

Palate morphogenesis. III. Changes in cell shape and orientation during shelf elevation.

The process of palate shelf elevation has been analyzed by light microscopy in mouse embryos cultured in vitro. The observations presented correlate changes in cell shape and orientation in the palate with the morphogenetic movement of the shelf. These studies suggest that in addition to any physical-chemical force elevating the shelf an active contraction of specific palate cells could also aid the process. Contribution to elevation could be derived from masses of contracting cells from the previously described non-muscle contractile systems in posterior (region 2) and mid-anterior (region 3) palate as well as other peripheral mesenchymal cells. Finally, elongation and contraction of the tongue side epithelial cells may also play a role in palate elevation.

Animals↗
PubMed1982

Backcross test demonstrates the linkage of glucocorticoid-induced cleft palate susceptibility to H-2.

Data in this report demonstrate a linkage between glucocorticoid-induced cleft palate susceptibility and H-2. B10.A X C57BL/10F1 females were backcrossed to C57BL/10 males. Cleft palate was induced in the BC1 fetuses by giving pregnant females 80 mg/kg of dexamethasone intraperitoneally (IP) on day 12 of gestation. The H-2a/b haplotype was detected on day 18 BC1 fetal spleen cells with an indirect immunofluorescent labeling technique. Fetuses without antigen H-2Kk were H-2b/b . H-2a/b fetuses had a cleft palate frequency of 29%; 11% of the H-2b/b fetuses had cleft palate (P less than .01), demonstrating that the higher susceptibility to cleft palate segregates with the H-2a halotype.

Animals↗
PubMed2006

Prenatal detection of associated anomalies in fetuses diagnosed with cleft lip with or without cleft palate in utero.

OBJECTIVE: The aim of this study was to determine the prenatal detection rate of associated anomalies in fetuses with a suspected cleft lip with or without cleft palate. METHODS: Fetuses with a suspected cleft lip with or without cleft palate, determined by prenatal ultrasound, were prospectively enrolled. Additional anomalies suspected by ultrasound or genetic testing were recorded. Postnatal outcome was obtained. RESULTS: Forty-five fetuses with a cleft lip with or without cleft palate, diagnosed prenatally with either two-dimensional and/or three-dimensional ultrasound, were studied. Postnatal follow-up revealed that 16 (35.6%) of these 45 fetuses had an additional structural or syndromic abnormality. Of the 37 fetuses with prenatally determined 'isolated' cleft lip with or without cleft palate, eight (21.6%) had an additional malformation identified after delivery. CONCLUSION: In pregnancies complicated by a cleft lip with or without cleft palate, patients should be informed of the risks of associated anomalies, some of which may be undetected prenatally.

Abnormalities, Multiple↗
PubMed1994

Distribution patterns in glycoconjugate expression during the development of the rat palate.

The distribution of complex carbohydrate structures during the embryonic development of the rat palate was analysed by examining lectin-binding patterns in serial paraffin and cryostat sections. With few exceptions, the binding patterns showed a general increase in lectin receptors in the more developed stages of palatogenesis. High mannose oligosaccharides were especially amplified during development. Terminal fucose molecules were not expressed. In contrast, terminal sialic acid molecules were ubiquitously distributed in epithelial and mesenchymal tissues. Non-sialylated terminal N-acetylglucosamine was specifically restricted to evolving bone matrix. Before palatal fusion, quantitative but not qualitative differences were detected between oral, nasal, and medial-edge epithelial surfaces. The only exception was LCA, which specifically marked epithelial cells at the tip of palatal shelves. A very selective affinity for Jacalin was demonstrated in the oral epithelium of the palate after day 16, suggesting the presence of sialylated terminal galactose-(beta-1,3)-N-acetylgalactosamine. PNA specifically marked the basal lamina of the oral side of palatal processes. The binding patterns of DBA, GSL IA, SBA, and VVA indicated that the epithelium of the tongue is characterized by terminal alpha- and beta-galactose residues, whereas palatine cells possess only molecules with beta-anomery. During palatogenesis, glycosaminoglycans patterns were significantly modified. Our data suggest that alteration of complex carbohydrate structures may play a central role in modulating cell-cell and cell-matrix interactions. The significance of these findings, however, remains to be elucidated.

Acetylglucosamine↗
PubMed1996

Histological changes in elastic components of soft palate scars after CO2 and contact Nd:YAG laser incisions in the dog as an experimental model.

Soft palate stiffening operations--often with CO2 or contact Nd:YAG lasers--have been used recently to treat patients with pronounced snoring. Differences in soft palate scars formed after CO2 and contact Nd:YAG laser incisions were studied in an animal model to determine which of these lasers produces a more rigid scar and consequently might be more effective for a soft palate stiffening operation. Six mongrel dogs were placed in each laser group, after which either the CO2 or Nd:YAG laser was used to make a 1.5-cm-long soft palate incision. The scars produced were then excised and studied histologically 4 weeks postoperatively. Special attention was paid to collagen density and elastin fibers in the scar tissue. After contact Nd:YAG laser incisions scar tissue was found to contain densely aligned collagen fibers and practically no elastin fibers. CO2 laser incisions produced significantly different scars: irregularly arranged collagen fibers with some elastin fibers also inside the scar tissue. Differences in the shapes of the scars and wound contractions were also found that were only seen after contact laser incisions. These findings suggest that the contact Nd:YAG laser might be more effective for soft palate stiffening operations.

Animals↗
PubMed1992

Palatal taste buds in man: topographical arrangement in islands of keratinized epithelium.

In an attempt to find and reconstruct the exact anatomical correlate of taste sensitivity in the human soft palate, a novel approach was used to examine the mucosal surface in conjunction with serial tissue sectioning. Six human subjects, 15 to 29 years of age, 3 females and 3 males, served to take precision impressions of the hard and the anterior soft palate, using non-commercial trays and a self-curing resin. From these impressions, replicas were cast in Epon and subsequently sputter-coated with gold and examined in a scanning electron microscope. In addition, one biopsy was taken from one of the volunteers, in an area including taste bud-suspicious elements. It was found that the anterior soft palate mucosa included 10 to 30, oval to round, site-exotic islands, about 0.2-0.6 mm in diameter, which were covered by a thin, keratinizing stratified squamous epithelium. These islands occurred mainly in an area located in the central part of the soft palate, immediately posterior to the hard/soft palate boundary. The keratinizing epithelium of such islands carried four to seven taste buds which were lacking elsewhere. These islands were formed by a large, mushroom-like connective tissue papilla penetrating most of the site-specific mucosal epithelium, with its cover of keratinizing epithelium, forming sharp external and internal cell-to-cell borderlines with the surrounding, non-keratinizing stratified squamous epithelium. These findings are discussed in relation to induction phenomena necessary to form such islands, and to the variable taste sensitivity detected clinically in this region.

Adolescent↗
PubMed1981

Corticosteroid-induced cleft palate in mice and H-2 haplotype: maternal and embryonic effects.

This report confirms and expands on the original preliminary observations made by Bonner and Slavkin that corticosteroid-induced cleft palate in mice is associated with H-2 haplotype. Using three congenic strains, B10, B10.A, and B10.D2, our studies demonstrate that B10.A (H-2a) is most susceptible and B10.D2(H-2d) is least susceptible, B10(H-2b) being intermediate. Variation in fetal loss among strains accounts for less than 1 percent of the variation in cleft-palate frequency among strains; variation in H-2 haplotype, however, accounts for more than 60 percent of the variation in cleft-palate frequency. With regard to all possible reciprocal F1 hybrids, our results indicate that while there is a significant maternal effect, maternal haplotype can account for only 11 percent of the variation in cleft-palate frequency among crosses. Embryonic haplotype accounts for 17 percent of the variation, which is indicative of an important embryonic effect. Finally, our studies suggest that susceptibility to corticosteroid-induced cleft palate is associated with the K end of the H-2 complex.

Adrenal Cortex Hormones↗
PubMed1984

Glucocorticoid-induced cleft palate genes in chromosome 17: genetic linkage and mapping analyses.

Genes that influence susceptibility to dexamethasone-induced cleft palate and tentatively designated Dep are linked to the major histocompatibility complex H-2 in chromosome 17 of the mouse. Experiments presented refine the map of genes. The results show two or three Dep loci. The two-locus model maps Dep genes to the class II gene E beta and to the chromosomal region between the S and D genes. The three-locus model maps the Dep genes to the chromosomal regions from the centromere to E beta, from E beta to S, and from D to Pgk-2. Experiments were done by comparing the dexamethasone-induced cleft palate dose response of congenic strains with H-2 haplotypes that are recombinants of H-2a and H-2b. The analysis of genetic linkage between H-2 and Dep was expanded to include reciprocal backcrosses. A maternal factor was found to influence the frequency of dexamethasone-induced cleft palate in the backcross fetuses. The factor's origin is associated with the H-2 haplotype of the outcross mother, so the effect is actually a "grandmother effect" that probably is transmitted horizontally. Finally, the sexes were distributed unevenly between the fetuses with cleft palate in two of the congenic strains. This suggests interaction between the H-2-linked Dep genes and a Dep sex-associated gene that modulates susceptibility to dexamethasone-induced cleft palate.

Alleles↗
PubMed1985

GABA uptake in embryonic palate mesenchymal cells of two mouse strains.

To obtain further evidence that the inhibitory neurotransmitter GABA functions in palate development, the presence of an active GABA uptake mechanism was sought using primary cultures of embryonic palate mesenchymal cells. Uptake was compared from cells of two inbred mouse strains in which the SWV strain shows greater sensitivity than the AJ strain to effects of GABA on palate morphogenesis and of diazepam in producing cleft palate. Palate cells were capable of accumulating [3H]GABA by saturable uptake mechanisms characteristic of a high and low affinity active transport as indicated by temperature, Na+ ion and carrier dependence as well as Km and Vmax values that were comparable to other biological systems. The Vmax of the high-affinity uptake system from cells of the SWV strain was 1.8 fold higher than that of the AJ. GABA uptake was also observed in fibroblasts from various sources including embryonic mouse limb cells, human skin fibroblasts and 3T3 cells. When active GABA uptake was measured in skin fibroblasts from the mouse SWV and AJ strains, the rate of uptake from SWV cells under high affinity conditions was also 1.8 fold greater than in AJ cells. Thus active GABA uptake appears to be genetically regulated in non-neural cells which may contribute to differential responses to GABA.

Animals↗