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Biomedical subjects

R M Shah

Publications and source records attributed to R M Shah.

At least 91 records · Page 5Linked to original sources
PubMed1978

Teratological evaluation of 5-fluorouracil and 5-bromo-2-deoxyuridine on hamster fetuses.

A single intraperitoneal injection of 5-bromo-2-deoxyuridine (BUDR) between days 9 and 11 and a single intramuscular injection of 5-fluorouracil (FU) between days 8 and 11 of gestation were teratogenic in hamster. The malformation frequencies were related to the dose and time of BUDR and FU treatment but the pattern and types of malformations and their frequencies were different. BUDR showed lower embryotoxic effect than FU. Both drugs impaired general fetal growth. It is suggested that the differences between FU and BUDR may be related to the chemical nature and metabolism of the drug and their eventual effect on the species-specific target tissue.

Animals↗
PubMed1977

Palatomandibular and maxillo-mandibular fusion, partial aglossia and cleft palate in a human embryo. Report of a case.

A 32-mm CRL male human embryo was examined for malformation. Histological observation showed fusion between the left vertical palatal shelf and mandible and the maxilla and mandible in the posterior part of the oronasal cavity. The right shelf was horizontal anteriorly, vertical posteriorly and changing its position from a vertical to a horizontal plane in the middle. The tongue was underdeveloped anteriorly and completely absent posteriorly. The mandibular tooth buds were not formed. Both clinical and experimental literature were analyzed to find the mechanism of statu nascendi defect observed in the present case. It was deduced that the tongue may not play an active role during normal palatal development and that it may not have played any role during the fusion between different intraoral structures observed in the present case. It was concluded that, had the embryo developed further, then at the birth a cleft palate, partial aglossia and associated intraoral malformation would have been expected.

Abnormalities, Multiple↗
PubMed1977

Bactericidal activity of amikacin and gentamicin.

Using the membrane filtration method bactericidal activity of amikacin and gentamicin as a function of time and concentrations was determined. Amikacin was bactericidal against all Pseudomonas aeruginosa (n = 7) and Klebsiella pneumoniae strains (n = 8) tested. In 5 of the 7 P. aeruginosa and 3 of the 8 K. pneumoniae strains we saw a secondary regrowth at 24h. There was no difference between amikacin and gentamicin. The experiments to determine the effect of concentration on bactericidal activity showed that higher concentrations lead to a faster kill rate.

Amikacin↗
PubMed1977

Effects of prenatal administration of hadacidin, a cancer chemotherapeutic agent, on the development of hamster fetuses.

A single intraperitoneal injection of 1-2-5 g/kg body weight of hadacidin was teratogenic when administered to pregnant hamsters between days 8 and 11 of gestation. Both the frequency of malformation and resorption were related to the dose and time of hadacidin administration. The drug produced both gross and microscopic malformation in the fetus and impaired its general growth. The malformation involved craniofacial structures, central nervous system, respiratory, digestive and urinary systems, limbs and tail. Morphologically different types of cleft lip and cleft palate were related to the dose and time of hadacidin treatment. An association was observed between cleft lip, cleft palate and micrognathia on one hand, and between cleft palate and micrognathia on the other. Significance of association between the lip, the palate and the mandibular malformation was discussed and the hypothesis that human cases of Pierre Robin syndrome may result from an environmental assault was supported. It was suggested that the fetal weight and the microscopic analysis should be included in the criteria for the teratological drug safety evaluation procedures.

Abnormalities, Drug-Induced↗
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↗
PubMed1976

Morphogenesis of the secondary palate in normal and hydrocortisone-treated hamsters.

Fetal palate morphogenesis was studied in normal and hydrocortisone-treated hamsters. Formation of the normal palate was completed between day 12:00 and 13:00 of gestation, and during this period 8 distinct developmental stages were recognized. Following hydrocortisone administration the early stages, during which vertical-to-horizontal shelf reorientation occurs, appeared to be unaffected, but subsequent fusion between opposing shelves was inhibited. Both chronological age and fetal weight provided reliable criteria for stages of normal palatal development. Following hydrocortisone administration, however, fetal weight was a poorer indicator of stage of palate organogenesis than chronological age.

Abnormalities, Drug-Induced↗
PubMed1976

The teratogenic effects of hydrocortisone on palatal development in the hamster.

The effect of different doses of hydrocortisone, administered at various times during gestation, on the fetal hamster and its palatal development was studied. Both the frequency of cleft palate and that of resorption depended upon the dose of hydrocortisone and the time of its administration. Two peaks in the incidence of cleft palate were observed, which appeared to be due to inhibition of different events. Incidence of morphologically different types of cleft palate was related to the doses and gestational time of hydrocortisone treatment. A close association was observed between the frequency of cleft palate and fetal growth retardation and between the latter and the dose and time of drug administration. It was suggested that maternal physiology and the placental barrier may play a crucial role in cleft palate induction.

Animals↗
PubMed1976

Cleft palate induction in hamster fetuses by glucocorticoid hormones and their synthetic analogues.

The effect of prenatal administration of different doses of cortisone, corticosterone, dexamethasone, triamcinolone and prednisolone on the fetus and its palatal development was studied. All the glucocorticoids, except cortisone, produced cleft palate in the fetuses. Both the total frequency and morphologically different types of cleft palate were related to the dose of the teratogen. Triamcinolone appeared to be more potent than other glucocorticoid in inducing cleft palate. An association was noted between fetal growth inhibition, the dose of the teratogen and the frequency and type of cleft palate.

Abnormalities, Drug-Induced↗