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The effect of tunicamycin (TM) on Leishmania braziliensis promastigotes in culture has been studied. TM at different concentrations (2, 4, 6 micrograms/ml) inhibits promastigote growth as the mean generation time of control cells, 36 hr, is changed to 41, 46 and 55 hr, respectively. Cells remain viable after long exposure to 2 micrograms/ml of TM and can be cultured in the presence of the drug for several generations. Under these conditions cells tend to round up and many "ruffle"-like structures appear at the parasite cell surface. At the ultrastructural level, cell coat disappears and the rough endoplasmic reticulum appears distended. Other structures remain unaltered by the drug treatment. The changes in cell morphology are discussed in relation to changes in cell surface morphology. The possible use of these TM-transformed cells as experimental systems for host-parasite studies is also considered.

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Light and electron microscopic studies of frontal and sagittal sections of embryonic chick hearts (Stages 25, 28-29), reveal mesenchymal tissue in the cephalic portion of the interventricular septum. The endocardium of this cephalic portion contains reoriented and invaginated cells with pseudopodia; in addition there are cells immediately subjacent to the endocardium. Similar cellular events take place during the formation of mesenchymal tissue in the atrioventricular and conotruncal regions. In these regions the mesenchymal tissue originates by means of an endocardial activation process. The structural characteristics of the formation of the cephalic portion of the interventricular septum suggest that local mesenchymal tissue is contributed by the endocardium. However, based upon the close anatomic relationship observed by us between the mesenchymal tissues of the atrioventricular canal, conotruncal region and the cephalic portion of the interventricular septum; we do not discard a contribution by migration of cells from atrioventricular and conotruncal regions to the interventricular septum.

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Parasites of the Leishmania genus, which are the causative agents of leishmaniasis, display a complex life cycle, from a flagellated form (promastigotes) residing in the midgut of the phlebotomine vector to a non-flagellated form (amastigote) invading the mammalian host. The cellular process for the conversion between these forms is an interesting biological phenomenon involving modulation of the plasma membrane. In this study, we describe a selective autophagic-like process during the in vitro differentiation of Leishmania mexicana promastigote to amastigote-like cells. This process is responsible for size reduction and shape change of the promastigote (15-20 μm long) to the rounded amastigote-like form (4-5 μm long), identical to the one that infects host macrophages. This autophagic-like process is characterized by a profound folding of the plasma membrane and the presence of abundant cytoplasmic lipid droplets that may be the product of changes in the lipid metabolism. The key feature for the differentiation process at either pH 7.0 or pH 5.5 is the shift in temperature from 25 to 35 °C. Flagella shortening during the differentiation process appears as the product of continuous flagellar microtubular disassembly that is also accompanied by changes in mitochondrion localization. Drugs directed at blocking the parasite autophagic-like process could be important as new strategies to fight the disease.