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V Maharajan

Publications and source records attributed to V Maharajan.

12 recordsLinked to original sources
PubMed1992

Cellular and molecular regulation of odontogenesis.

Developing mammalian tooth is one of the most interesting model systems to study the mechanism of morphogenetic process especially to understand problems associated with spatial organization and symmetry. In the present article we recapitulate the morphologic aspects of odontogenesis and discuss the cellular and molecular regulatory factors involved in this process. The importance of cellular aspects such as epithelial-mesenchymal interactions and the cell kinetics are described. Role of growth factors such as Transferrin, Epidermal Growth Factor and its receptor and Transforming Growth Factor is analyzed. In addition the studies on transcription factors such as c-fos and Egr-1 and on homeobox genes are discussed to understand the molecular mechanism of odontogenesis.

Animals↗
PubMed1991

Recent progress in vertebrate limb morphogenesis.

Morphogenesis of vertebrate limb, specifically that of the chick wing, has been recognized as a suitable model to study the cellular and molecular mechanisms of pattern formation. The importance of cellular inductive phenomena and the relevance of the processes such as cell division and cell death in the above model are discussed. These studies have revealed the retinoic acid (RA) and retinols as convincing candidates for vertebrate morphogens. The recent discovery that the RA receptors belong to the steroid hormone receptor superfamily might indicate the universality of the RA morphogen and might enlighten the possible mode of its action. Identification and characterization of the 1d locus genes associated with the mouse limb morphogenesis and the possible involvement of the homeobox proteins in chick wing development have opened new prospects in understanding the molecular mechanisms of vertebrate morphogenesis.

Animals↗
PubMed1990

Transplantation of Lewis lung carcinoma in mouse uterus.

Earlier studies have shown that pregnant and nonpregnant mammalian uteri respond differently to tumor cell invasion, colonization and metastasis, but the biological basis of such differential uterine response has not been clarified. In the present study we have investigated the role of the metastatic potential of the tumor in the differential response of different stages of mouse uteri, using a highly metastatic tumor. The results obtained were compared with earlier data obtained using low metastatic or nonmetastatic tumors. Lewis lung carcinoma (LLC) cells were infused nonsurgically into nonpregnant uteri of various estrus stages and into pregnant uteri on day 3 postcoitum. Response of the uteri and embryos was studied histologically on days 2, 5 and 18 posttreatment (p.t.). The embryonic development was severely inhibited resulting in extensive resorption. In the tumor cell-treated animals, despite an early and uniform invasion the patterns of tumor cell colonization and metastasis differed remarkably from the pregnant to nonpregnant uteri. On day 5 p.t. 66% of nonpregnant animals showed tumor cells in the endometrium and 40% had tumor metastasis in other organs. Though 40% of the pregnant animals had tumor cells in the uteri, none had metastasis in other organs. By day 18 p.t., despite the absence of tumor cells in the uteri, 75% of nonpregnant animals showed metastasis in lung and liver. In pregnant animals, tumor cells were seen neither in uteri nor in other organs studied. These results indicate the refractory nature of both the pregnant and nonpregnant mouse uteri to the survival and colonization of LLC cells, but the mechanisms by which the tumor cells are eliminated differ between these two types of uteri.

Animals↗
PubMed1989

Invasion and metastasis of Lewis lung carcinoma in the mouse uterus.

Patterns of Lewis lung carcinoma (LLC) cell invasion, colonization and metastasis were studied in C57 mouse uteri. LLC cells (5 X 10(4) in 0.05 ml) were infused nonsurgically into nonpregnant and pregnant uteri, 3 days postcoitum. The fate of cells was studied histologically on days 2, 5 and 18 posttreatment (PT). Despite a large degeneration of LLC cells in the lumina of both the pregnant and nonpregnant mice, in 38% of these uteri, tumor cells had invaded the endometrium by day 2 PT. However, subsequent distribution of tumor cells differed remarkably between the pregnant and the nonpregnant uteri. By day 5 PT, in 66% of the nonpregnant mice, tumor cells were common in the endometrium and metastases in other organs were seen in 40% of the animals. But in the pregnant mice only 40% uteri showed tumor cells and no metastasis was recorded. On day 18 PT tumor cells were rare in the nonpregnant uteri, but significantly, 75% of those animals showed lung and liver metastases. In pregnant mice, tumor cells neither survived in the uteri nor metastasized to other organs. LLC cells, infused into nonpregnant uteri, promptly metastasized to lungs without colonizing the uteri: this unique system may provide insight into the effects of organ-specific host factors on the growth and metastatic potential of tumor cells.

Animals↗
PubMed1988

Influence of mouse uterus on the metastatic patterns of tumour cells.

Metastatic patterns of fibrosarcoma (FS) and Lewis lung carcinoma (LLC) cells transplanted into mouse uteri of various reproductive stages, were investigated. Tumour cells were infused non-surgically into the lumen of 3-day post coitum pregnant uterus or into non-pregnant uterus of known estrus stage. The fate of these tumour cells was studied histologically on days 2, 5 and 10 post treatment. No significant difference in the metastatic patterns of the FS or the LLC cells was seen between the non-pregnant uteri of various estrus stages. FS cells in few cases of non-pregnant uteri displayed the tendency to migrate and grow outside the myometrium without colonizing in the endometrium, but in pregnant uteri they colonized within the endometrium. LLC cells in the non-pregnant uteri promptly metastasized to distant organs like liver and lung; but those in the pregnant uteri rarely metastasized to other organs. These observations imply that the metastatic patterns of uterine tumour might depend on both the physiological state of the uterus and the tumour cell type.

Animals↗
PubMed1987

Response of mouse embryos and uterus to tumour extract treatment.

The influence of cell-free extract of mouse fibrosarcoma and normal fibroblast on the early development and organogenesis of mouse embryos, and on the histology of non-pregnant and pregnant uteri was studied in vivo. Both normal and tumour cell extracts inhibited normal mouse embryogenesis. However, the effects of tumour extract on mouse embryogenesis was far more drastic and significant. Despite such changes, no basic alteration of the morphology of the embryonic cells was seen. Observations on the uterine histology indicated extensive deciduation. Pyknosis followed by degeneration of the endometrium was the main effect of tumour extract on the pregnant mouse uterus. Such inhibition of embryogenesis and degenerative effect on the mouse uterus by tumour cell extract might be due to general degradative effects of the tumour constituents.

Animals↗
PubMed1986

Effects of 5 azacytidine on DNA methylation and early development of sea urchins and ascidia.

5-azacytidine (5-azaCR), an analogue of cytidine, inhibits nuclear DNA methylation in early sea urchin embryos. This inhibition is specific and dose-dependent. Exposure of sea urchin embryos at any stage between one-cell and blastula, to micromolar quantities of 5-azaCR invariably inhibits development beyond the blastula stage. In a substantial number of embryos arrested at the blastula stage, spicule formation proceeds although other morphological differentiation is lacking. No significant effect on development is seen if sea urchin embryos are exposed to 5-azaCR at post-blastula stages. 5-azaCR also inhibits the development of a mosaic egg such as the ascidian Phallusia mammilata at the blastula stage, indicating that both regulative (sea urchin) and mosaic (ascidian) embryos respond more or less similarly to 5-azaCR treatment.

Animals↗
PubMed1986

Behavioural pattern of tumour cells in mouse uterus.

The behavioural pattern of transplantable mouse fibrosarcoma (MFS) cells infused into the pregnant, pseudopregnant and nonpregnant mouse uteri was studied histologically. In some nonpregnant and pseudopregnant uteri, the tumour cells, without colonizing inside the uterus, traverse the endometrium and within 5 days of treatment form tumour nodules outside the myometrium, indicating the presence of an initial and temporary tumour rejection mechanism in these uteri. In later stages MFS cells form large necrotic tumours in these uteri. In the pregnant uterus no tumour nodules are formed outside the myometrium even after 20 days of treatment. Furthermore, the size of the tumour formed in the endometrium of the pregnant uterus is quite small and the tumour cell growth rate is lower than that of the tumour cells in the nonpregnant and pseudopregnant uteri. These results indicate that, in the pregnant mouse uterus, fibrosarcoma cells display an altered pattern of invasion and decreased growth rate compared to those in nonpregnant and pseudopregnant uteri.

Animals↗
PubMed1986

Bud induction in decapitated Hydra attenuata by 5-azacytidine: a morphological study.

The effect of 5-azacytidine (5-azaCR) on head regeneration and budding in hydra are reported. Hydra attenuata were exposed to various doses of 5-azaCR for 48 h and then decapitated and cultured. Head regeneration and bud formation were observed for 12 days after decapitation. Untreated control hydra regenerated heads within 7 to 8 days of decapitation with a budding index of 0.2. Buds invariably arose in the normal budding zone (below the gastric region). In the group treated with 0.8 mM-5-azaCR, 9 days after decapitation head regeneration was seen in only 13% of animals, and an average of two buds per hydra were formed, most of which were in the vicinity of the distal end. Induction of budding was also seen in the animals that regenerated heads. In animals exposed to 1 mM-5-azaCR three main types of responses were observed 9 days after decapitation. 44% of the animals regenerated normal heads; about half of them developed at least one bud and these buds originated in the budding zone. 17.5% of the animals developed abnormal, long hypostome-like structures with single or bifurcated tentacles at their tips. There were at least two buds per animal and they were invariably at abnormal sites. 32% of the animals failed to regenerate heads, although they developed two buds. 87% of these buds originated in abnormal sites of the body column and a large number (72%) did not detach even by the 12th day after decapitation. Both 5 and 10 mM of 5-azaCR were toxic to the animals; the survivors formed large globe-shaped heads. Bud induction was seen in 60% and 28% of animals in the 5 and 10 mM groups, respectively. These observations demonstrate that 5-azaCR induces bud formation in hydra at doses that inhibit head regeneration. This bud induction might be due to a specific expression of gene products responsible for bud formation.

Animals↗
PubMed1985

Effects of 2-deoxy-D-glucose on glycolysis, proliferation kinetics and radiation response of human cancer cells.

The effects of 2-deoxy-D-glucose (2-DG) on energy metabolism, cell proliferation kinetics, radiation-induced DNA repair, and micronuclei formation in HeLa cells have been studied. Results show that the 2-DG induced modifications of the radiation effects are biphasic: at high 2-DG concentrations (greater than 2.5 mM), DNA repair is inhibited and manifestation of radiation damage is enhanced as observed by an increase in the radiation (X ray) induced micronuclei formation; lower concentrations of 2-DG (less than 2.5 mM) do not inhibit DNA repair and a decrease in the frequency of micronuclei formation is observed. These data, in correlation with the effects of 2-DG on glycolysis and cell proliferation kinetics, can be explained by the hypothesis that 2-DG induced modifications of radiation effects arise as a result of energy linked differential inhibitions of pathways of repair and fixation of DNA damage. Implications for cancer therapy are discussed.

Cell Division↗