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Biomedical subjects

R M Shah

Publications and source records attributed to R M Shah.

At least 55 records · Page 3Linked to original sources
PubMed1989

Palatal shelf reorientation in hamster embryos following treatment with 5-fluorouracil.

A study was undertaken to examine the issue of whether achieving a critical mass of cells and/or palatal shelf volume during vertical development of shelf is essential for reorientation to occur. In control and 5-fluorouracil (5FU)-treated hamster embryos' palatal shelves, at different times during gestation, the numbers of both epithelial and mesenchymal cells were counted and cross-sectional area was measured. DNA synthesis was measured by 3H-thymidine incorporation and was used as an index of growth by cell proliferation. The control data indicated that, unlike development during initial 24 hours, the later period of vertical palatal development was characterized by a steady level of mesenchymal and epithelial cell numbers and palatal shelf area. Following 5FU treatment all the measurements were reduced, and until they reached the equivalent of control values, the palatal shelves did not reorient. The density of mesenchymal cells in the developing palate did not seem to affect cell number. On the basis of the analysis of results of the present study, along with those reported in the literature, it is suggested that, in hamsters, acquisition and maintenance of both a specified number of mesenchymal cells and shelf area, at least 24 hours prior to reorientation, may be critical for ensuing mesenchymal differentiation to enforce palatal shelf reorientation on schedule. 5FU affected these features to delay reorientation of the palatal shelf.

Abnormalities, Drug-Induced↗
PubMed1989

Effects of cyclophosphamide on the secondary palate development in golden Syrian hamster: teratology, morphology, and morphometry.

Cyclophosphamide (CP), when injected in hamster mother between days 9 and 11 of pregnancy, was teratogenic in fetuses. On the basis of a morphological study it was deduced that CP delayed the reorientation of hamster palatal shelves by 16-20 h. In a subsequent experiment, in both control and CP-treated palatal shelves, the numbers of epithelial and mesenchymal cells were counted and cross-sectional area was measured. DNA synthesis, measured by 3H-thymidine incorporation, was used as an index of growth by cell proliferation. The results showed that during the vertical development of palatal shelves, the mesenchymal cells reached their peak number during the initial 24 hours, i.e., at the end of the second peak in DNA synthesis, and remained unchanged thereafter throughout reorientation. The shelf area also showed rapid increase during the initial 24 h followed by a spurt 2 h prior to reorientation. Cyclophosphamide prolonged the acquisition of these features by affecting the mesenchymal cells and consequently delayed the reorientation of the vertical shelves until such time that the number of healthy mesenchymal cells and shelf area were restored to the control values. The data lend further support to the hypothesis that the acquisition of a specific number of cells and shelf volume, during vertical palatal development, may be essential for palatal shelf reorientation.

Abnormalities, Drug-Induced↗
PubMed1988

Gross and cellular analysis of 6-mercaptopurine-induced cleft palate in hamster.

The present study analyzes the morphological, histochemical, and ultrastructural aspects of the pathogenesis of 6-mercaptopurine (6MP)-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that 6MP stunts the growth of vertical palatal shelves and thus induces cleft palate. Ultrastructural analysis showed that, in contrast to controls, 6MP-induced alterations were first seen in the mesenchymal cells 24 hr after drug administration. The initial alterations were characterized by swelling of the nuclear membrane. During the next 12 hr, lysosomes were seen first in the mesenchymal cells and then in the cells of the medial edge epithelium (MEE) of the developing palatal primordia. The appearance of lysosomes was temporally abnormal and was interpreted as a sublethal response to 6MP treatment. Subsequently, the nuclear alterations and the lysosomes diminished; and 48 hr after 6MP administration, they were absent from the palatal tissues. Ninety hours after 6MP administration, unlike the controls (in which the palatal shelves were already fused), changes were seen at the epithelial-mesenchymal interface in the developing cleft palatal shelves. These changes were characterized by breakdown of the basal lamina and epithelial-mesenchymal contacts. Eventually, at term, the MEE of the vertical shelf stratified. It was suggested that 6MP affected cytodifferentiation in the palatal tissues during the critical phase of early vertical shelf development and thereby induced cleft palate.

Acid Phosphatase↗
PubMed1988

Vertical development of the secondary palate in hamster embryos following exposure to 6-mercaptopurine.

Cellular aspects of vertical development of the secondary palate were examined in control and 6-mercaptopurine (6MP)-treated hamster embryos. Cross-sectional area of the palatal shelf was measured and the numbers of both epithelial and mesenchymal cells counted. Also, in 6MP-treated palates the damaged mesenchymal cells, characterized by the presence of dense bodies, were counted. DNA synthesis in both control and treated fetuses was measured by 3H-thymidine incorporation. The results indicated that both the shelf area and cell numbers increased with age in control and 6MP-treated palates. However, in controls the mesenchymal cell density and DNA synthesis showed two peaks that were absent following 6MP treatment. Unlike controls, in treated embryos the damage to mesenchymal cells became increasingly pronounced between days 10:00 and 10:12 but subsided by day 11:00 of gestation. It is suggested that a major force in the development of the initial primordia and early vertical development of the palatal shelf may be provided by a spurt of DNA synthesis in the mesenchymal cells resulting in their increased number. After 6MP treatment, depression of DNA synthesis and consequent reduction in the mesenchymal cell number and density followed by cell damage lead to retardation in the vertical development of the palatal shelves.

Animals↗
PubMed1988

Histological evidence of fusion between the posterior palatal shelves and the floor of the mouth in Alligator mississippiensis.

Unlike the anterior four-fifths of the secondary palatal shelves the posterior one-fifth grows vertically downward along the side of the tongue and unites with the floor of the mouth. This feature appears to be unique to alligators, and may be important in the development of the basihyal valve. The valve seals off the mouth from the nasal cavities, pharynx and larynx, and thus allows simultaneous breathing and capturing of prey while in the aquatic environment. This developmental feature may enhance the survival value of the species.

Alligators and Crocodiles↗
PubMed1988

Embryogenesis of the secondary palate in pigeons.

Embryogenesis of the secondary palate in pigeons was studied, using light and electron microscopy. The secondary palate of the pigeon develops between Days 7 to 11 of incubation. During this period the palatal processes grow toward one another, but unlike those in the mammals and alligator, they never fuse. In contrast to both the chick, wherein the medial edge epithelium (MEE) differentiates to orthokeratinization, and quail wherein the MEE becomes parakeratinized, the MEE of the pigeon, like that of the duck, differentiates to a nonkeratinized, stratified squamous type. It is suggested that although patterns of morphogenesis of the secondary palate in different bird species appear to be similar, the programming, and consequently, the pattern of subcellular differentiation of the MEE may reflect natural selection or adaptation to differences in diets and feeding habits.

Animals↗
PubMed1988

In vitro differentiation of the Japanese quail secondary palate.

Differentiation of the Japanese quail secondary palate was studied in vitro. Results indicated that the medial edge epithelia (MEE) of quail were capable of full differentiation in vitro from a very early age. In contrast to in vitro mammalian palatal development, the quail palatal processes never fused. The cells of the MEE in the quail continued to divide, and the cyclic adenosine monophosphate (AMP) levels in the quail palatal tissues remained constant during development. In contrast to in vitro differentiation of MEE in the chick palate, the quail palatal MEE differentiated to parakeratinized epithelium. The results suggest that: (1) the programming of events of MEE differentiation in birds is different from that in mammals, (2) intraspecies differences in the MEE biology of chick and quail palate are intrinsic to the palate, not the environment, and (3) an inverse relationship between the levels of cyclic AMP and the synthesis of DNA in the MEE may exist during secondary palate development, which in turn may regulate the fate of the MEE in birds and mammals.

Animals↗
PubMed1987

Allergic interstitial nephritis due to diazepam.

A 56-year-old man developed allergic interstitial nephritis and deterioration of preexisting chronic renal failure after receiving diazepam. On discontinuation of diazepam, kidney function returned to the baseline level and itching, eosinophilia, and eosinophiluria subsided. A causative correlation between allergic interstitial nephritis and diazepam is suggested.

Diazepam↗
PubMed1987

Secondary palate development in the domestic duck (Khaki Campbell). An electron microscopic, histochemical, autoradiographic and biochemical study.

Prenatal development of the secondary palate in duck was studied using light and electron microscopic, histochemical, autoradiographic and biochemical techniques. The secondary palate of duck develops between Days 7-12 of incubation (HH 25-37). During this period the palatal shelves grow horizontally toward one another but, unlike those in mammals and the alligator, they never fuse, and a physiological cleft persists between them. In contrast to both chick, where the MEE differentiates to orthokeratinisation, and quail, where the MEE becomes parakeratinised, the MEE of duck differentiates to a non-keratinised stratified type. A continuation of DNA synthesis in the MEE, unchanged levels of cyclic AMP in the palatal tissues and an absence of programmed cell death in the MEE during duck palatogenesis distinguish it from the mammalian palate morphogenesis. Also, although the morphogenesis of palate in duck, chick and quail is similar, the cytodifferentiation of their MEE is different.

Animals↗
PubMed1986

Cellular reactions during drug-induced cleft palate.

Responses of the epithelial and mesenchymal cells of the developing hamster secondary palate to hadacidin, 5-fluorouracil, and hydrocortisone were analysed. Correlation of data on cellular response with morphological and biochemical observations suggested that several aspects of differentiation of palatal cells needs to be analysed before pathogenesis of teratogen-induced cleft palate can be defined.

Acid Phosphatase↗
PubMed1985

An ultrastructural and histochemical study of the development of secondary palate in Japanese quail, Coturnix coturnix japonica.

Embryonic development of the secondary palate of the Japanese quail, Coturnix coturnix japonica, was studied. The palatal shelves appeared on day 5 of incubation in a horizontal direction over the dorsal surface of the tongue. Subsequently, unlike those in mammals, the opposing palatal shelves do not fuse, and a physiological cleft persists between them. In comparison with the chick, where the palatal shelves do not fuse and the medial edge epithelium (MEE) becomes orthokeratinized stratified squamous type, the quail MEE differentiates into a parakeratinized stratified squamous type. The basal cells of the quail MEE differentiated from cuboidal to columnar and showed reorganization of their cytoplasmic organelles. In contrast to both the chick and mammalian MEE, quail MEE showed very little ruthenium red (RR) binding at the plasma membrane of both the basal and superficial cells. Initial development in a horizontal direction, lack of fusion, and an absence of programmed cell death in MEE of developing quail palate distinguished it from the mammalian palatogenesis. Also, although the morphogenesis of palate in quail and chick was similar, the pattern of cytodifferentiation in their MEE was different, which may be attributed to their ontogenesis.

Animals↗
PubMed1985

In vitro development of the hamster and chick secondary palate.

A series of experiments were undertaken to compare the in vitro behaviour of the medial edge epithelium (MEE) of hamster, in which palatal shelves normally fuse, and chick, in which they do not fuse. Homotypic pairs of hamster and chick embryo palatal processes, single palatal processes, and heterotypic palatal shelves of both animals were grown in vitro. The results indicated that contact between palatal shelves may not be crucial for MEE differentiation in mammals. The ability to acquire pre-fusion characteristics may be present in mammalian palatal tissue from their early development and may be expressed by cessation of DNA synthesis in the MEE, elevation of cAMP, and MEE cell death. Isolated chick palatal shelf cultured under identical conditions did not express these mammalian pre-fusion characteristics. When MEE of hamster and chick palatal shelves were placed in contact with one another, the intervening epithelia underwent cytolysis. This could be due to either the destruction of chick MEE by lysosomal enzymes liberated from adjacent degenerating hamster MEE cells, or by induction of cell death in chick MEE by hamster mesenchyme. Heterotypic palatal tissue combinations also suggest that release of lysosomal enzymes in the hamster MEE, which leads to its dissolution, may be the terminal event in epithelial differentiation prior to the establishment of mesenchymal continuity. It is suggested that an inverse relationship exists between DNA synthesis and cAMP levels during palatogenesis: when palate closes (as in mammals) the MEE is eliminated by increasing cAMP levels, whereas when palate remains open (as in birds) low level of cAMP preserve the integrity of MEE by supporting DNA synthesis.

Animals↗