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Biomedical subjects

A Monroy

Publications and source records attributed to A Monroy.

At least 37 records · Page 2Linked to original sources

A theoretical equation for diauxic growth and its application to the kinetics of the early development of the sea urchin embryo.

The equation for diauxic growth is derived as a linear combination of two functions describing a slow and a fast rate of cell multiplication. The growth curve displays the typical biphasic shape, containing two sigmoidal branches. The curve fits very satisfactorily experimental data describing the increase of cell number in developing sea urchin embryos as a function of time, thus suggesting the presence of diauxia in this system. The hypothesis is formulated that diauxia in sea urchin embryos is the expression of two distinct metabolic pathways that result in a slow and a fast division process.

Animals↗

Cell-cell recognition.

The earlier step of morphogenesis is the segregation of cell lines which are homogeneous cell populations each endowed with its own specific developmental program. In order for the program to unfold in each line cells must be endowed with specific surface properties whereby the cells belonging to the same line can recognize each other as such in addition to recognizing those belonging to other cell lines as different. Experiments supporting this view are described. The hypothesis is presented that the cell-cell recognition system is phylogenetically linked with the invention of sexuality.

Animals↗

Histological studies of the elimination of Leishmania enriettii from skin lesions in the guinea-pig.

Nineteen guinea-pigs were each inoculated intradermally with 10(6) amastigotes of Leishmania enriettii, and the development of the lesions was followed from Weeks 4 to 10 with a view to elucidating the histological mechanisms involved with the elimination of parasites. Electron microscopic observations were made in 1 animal. Extensive necrosis of the parasite-laden macrophages was observed in 7 out of 7 animals at 4 and 5 weeks. In the ulcerated core of the lesion at 4 weeks no intact macrophages could be identified. Very many amastigotes were extracellular. Others were present in the cytoplasm of residual macrophages the cell walls of which had disintegrated. Necrosis was less marked at 8 weeks and absent in the resolving lesions at 10 weeks. Signs of stimulation or maturation of macrophages were only apparent when parasites were few. At 4 weeks macrophages were almost all of the non-stimulated form, but cytological evidence of activation became progressively more definite and widespread from 5 to 8 weeks, starting at the periphery of the lesion. Ultrastructural observations of amastigotes suggested that there might be more than one mechanism of degradation. It appeared that the majority of parasites were released through necrosis and discharged through the ulcer, and that intracellular degradation of the remaining parasites was important mainly in the later phase before resolution. The first phase was associated mainly with plasma-cell production, the second mainly with lymphocytes.

Animals↗