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Biomedical subjects

J L Ojeda

Publications and source records attributed to J L Ojeda.

At least 55 records · Page 3Linked to original sources

Cell death during detachment of the lens rudiment from ectoderm in the chick embryo.

The distribution and cytological characters of physiological cell death associated with formation of the lens vesicle in the chick embryo was studied by means of vital staining, light and electron microscopy. We have established a constant pattern of cell death which differs in some aspects from that reported for mammals and amphibians. The necrotic process is observed initially in the dorsal part of the lens cup (stage 15). The necrotic area progressively surrounds the lens pore as invagination proceeds (stage 16) and at stage 17 is located in the zone of fusion of the invaginated lens. After detachment of the lens (stages 18, 19 and 20) dead cells appear in the ectoderm, in the superficial epithelium of the lens vesicle and in the space between both structures. Ultrastructurally we observe isolated dead cells in different stages of degeneration and in phagocytosed cells. Phagocytosis is carried out by the neighboring healthy epithelial cells. Phagocytic activity was detected concomitant with the beginning of the necrotic process. Cell fragments were occasionally detected within the lens cavity.

Animals↗

Cell death during the development of the truncus and conus of the chick embryo heart.

The presence of cell death in the walls of the truncus and conus of the developing chick heart was investigated by a variety of light and electron microscopic techniques. Necrotic areas were observed in the myocardial layer of the truncus and conus and within the mesenchymal cells of the truncoconal ridges and aortopulmonary septum. These necrotic zones appeared first at Stage 25-26 and reached their maximum extent at Stages 29-32 undergoing later progressive disappearance. The morphological changes of the degenerating cells detectable under both transmission and scanning electron microscopy are also reported. The possible role of cell death in the morphogenesis of the truncus and conus is discussed.

Animals↗

In vivo phagocytosis by developing myocardial cells: an ultrastructural study.

Phagocytosis of naturally degenerating cells, by healthy myocardial cells of the bulbus cordis of 5--7-day chick embryos, was studied by electron microscopy. Myocardial cells showed cell processes surrounding dead cell fragments. The cell fragments appeared to be internalized later and digested within phagosomes. Ruthenium red was employed to ascertain whether the cell fragments were in fact internalized or located in pockets of the cell membrane. The results are discussed in the light of present knowledge of phagocytosis.

Animals↗

Cell death during the postnatal morphogenesis of the normal rabbit kidney and in experimental renal polycystosis.

We have studied, by means of optic and electron microscopy, the normal and abnormal cell death that takes place during the postnatal morphogenesis of rabbit kidney, and in the experimental renal polycystosis produced by methylprednisolone acetate. In the normal kidney intertubular cell death can be observed during the first 20 days of the postnatal development. However, cell death in the normal metanephric blastema is a very rare event. In the polycystic kidney numerous dead cells can be seen between the third and forty eighth days after injection. The topography and morphology of the dead cells depend on the stage in the evolution of the disease. In the 'stage of renal immaturity', dying and dead cells are present in the nephrogenic tissue, in the dilating collecting tubules and in the intertubular spaces. In this stage the cellular pathology is essentially nuclear. In the stage of tubular cysts, the dead cells are mostly located in the walls of cysts, with some dead cells, but mostly cellular debris in their lumina. At this stage the cellular pathology is basically cytoplasmic. The dead cells are eventually digested by what appear to be phagocytes of tubular epithelial origin. It is suggested that cell death is an important factor in the evolution of the lesions of renal polycystosis induced by corticosteroids, and probably in the initiation of the pathological process as well.

Animals↗

Cardiac jelly arrangement during the formation of the tubular heart of the chick embryo.

The hearts of chick embryos from stages 9 to 11 according to Hamburger and Hamilton are studied by means of the electron microscopy, and the arrangement of the cardiac jelly (CJ) during the different steps of the fusion of the paired heart anlage is described. It is shown that two different areas can be distinguished in CJ: the CJ located between the endocardium and the myocardium (MECJ) and the CJ located between the endocardium and the ventral foregut endoderm (EECJ). MECJ is a zone poor on ultrastructural components most of which are unbanded filamentous material and low-density amorphous material, and its arrangement remains constant during the whole fusion process; EECJ, on the contrary, is very rich in ultrastructural components containing greater amounts of high-density amorphous material, collagen fibrils and cellular, detritus, and the arragement of this area of the CJ undergoes changes during the different fusion steps. Alcian blue staining does not show difference between both areas of CJ. It is suggested that the CJ can play a role during the fusion of the heart. In addition, some observations are reported which suggest that all the epithelial tissues surrounding the CJ can take part in the elaboration of that extracellular material.

Animals↗

Cytological and cytochemical studies of the necrotic area of the bulbus of the chick embryo heart: phagocytosis by developing myocardial cells.

The muscular wall of the bulbus cordis of the chick embryo was studied by electron microscopy during H. H. stages 27--31. Results show that the muscle cells of the bulbus undergo necrosis during these stages. The morphology of dead cells in this area is similar to that described in other embryonic myogenic tissues. Although dead myocytes appear acid-phosphatase-negative, lysosomes may well be involved in this necrotic process as there is a significant number of cells with autolytic lesions among the neighbouring healthy muscle cells. The phagocytosis of the cell detritus resulting from the degenerative process appears to be carried out by neighbouring myocytes and by macrophages. The significance of these results is discussed both from the cytological and from the morphogenetic point of view.

Acid Phosphatase↗

Cell death during the formation of tubular heart of the chick embryo.

Light and electron microscopical examination of the heart of the chick embryo between stages 9 and 11 (Hamburger & Hamilton) revealed degenerating and dead cells specifically localized in the midline of endocardial tubes. The morphology of cell death in this system does not differ from that described in other embryonic tissues and organs. Phagocytosing cells are rarely seen. The results of this study show that a destruction of midline cells of both endocardial tubes takes place during the fusion of heart anlages. The possible roles of this cell death in the morphogenesis of the tubular chick heart are discussed.

Animals↗

[Iniencephalus apertus. Report of a case (author's transl)].

A macro and microscopic study carried out on an iniencephalic fetus weighing 650 g. is reported. This fetus is especially interesting as it presents anencephaly, supporting the view of classifying together iniencephaly and anencephaly with retroflexion. The main malformations present were: supernumerary ectopical thymus, esophageal atresia with inferior T-E fistula (Type V of Ladd), pulmonary hypoplasia with accessory lung, transposition of the large vessels, rectal atresia, single kidney, persistence of the urogenital sinus and single umbilical artery. The possible etiopathogenic causes are discussed and an embryological interpretation of the principal malformations is given.

Abdomen↗

[Importance of the early intravenous administration of streptokinase in acute myocardial infarct].

To evaluate the importance of early initiation of fibrinolytic therapy with intravenous streptokinase (IVSK), we studied 34 consecutive patients, within less than six hours of the onset of acute myocardial infarction, who were treated with 1.5 million units of intravenous streptokinase. All the patients had coronary angiograms in the first seventy two hours. We correlated the angiograms with the time of onset of the IVSK. The patients were divided into 3 groups: Group num. 1: From zero to two hours (twelve patients); Group num. 2: From two to four hours (13 patients); and Group num. 3: From four to six hours (nine patients). We had angiographic reperfusion in twenty-four patients (70.2%) P less than 0.05. We observed reopening in the patients of group num. 1 (83.3%); in group 2, nine patients (69%) and in group num. 3, five patients, (55.5%), with statistical significance only in group num. 1 (p less than 0.05). We also demonstrated the utility of the electrocardiographic and enzymatic criteria to predict reperfusion. No mortality was related to the procedure. We concluded that a higher percentage of reperfusion is obtained the sooner intravenous streptokinase therapy is initiated.

Coronary Circulation↗

[Intravenous streptokinase in acute myocardial infarction. A Mexican multicentric study].

To evaluate the benefits of intravenous streptokinase (SQIV) in acute myocardial infarction (AMI), we joined a group of ten Mexican university hospitals, that were coordinated by the National Institute of Cardiology of Mexico. We included patients less than 70 years of age admitted to the hospital with less than 6 hours from the onset of chest pain during their first myocardial infarction. All patients had ST segment elevation of 1.5 mm or more, and none had contraindication for SQIV. They received 1.5 millions of SQIV in one hour. Reperfusion criteria included absence of pain, ST segment reduction and a rapid rise and fall of enzyme levels. Angiographic criterion for reperfusion was the permeability of the affected coronary vessel. Of 66 patients studied, 57 (86%) had clinical reperfusion; of the 24 available angiographic studies, 92% demonstrated reperfusion. Eight (12%) of the patients had minor complications and 7 (10%) had serious complications. There were 0 deaths. We concluded that SQIV is a useful therapeutic procedure, easy to perform in general hospitals.

Adult↗