The fine structure of the thyroid gland of the hagfish, Eptatretus burgeri was observed using the electron microscope.
The thyroid follicles are diffusely distributed and embedded in the connective tissue of the ventral region of the gill pouch arteries. Each follicle is very large in size and is recognizable by the naked eye. Though follicular epithelial cells show a few microvilli on their apical surfaces, cilia which are usually seen in the lamprey thyroid, are lacking in the follicular cell of the hagfish. The cytomembranes such as rough endoplasmic reticulum and Golgi apparatus are poor in development as compared with those of higher vertebrates. The elements of these cytoorganelles are not dilated but flattened. Injected TSH does not cause so marked alterations on the fine structure of the epithelial cells. By electron microscopic autoradiography it was shown that silver grains are chiefly localized over the follicular lumen and the apical cell membrane region one hour after the injection of ¹²⁵I. The main site of iodination of thyroglobulin is the luminal colloid, the same as that in higher vertebrates. The colloid might be reabsorbed into the cell by pinocytosis. Large dense bodies, 0.5-3.0μm in diameter, which might be secondary lysosomes or residual bodies produced by the reabsorbed colloid and primary lysosomes, are often seen in the cytoplasm.
Blood capillaries are relatively scarce in distribution. Though the endothelial fenestration is absent, numerous pinocytotic vesicles are characteristic in the cytoplasm.
In respect to their function the hagfish thyroid cells are considered to exhibit a relatively low degree of activity as compared with those of elasmobranchs, teleosts, and higher vertebrates.

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The origin of bursal lymphoid cells in Japanese quails was studied by means of a quantitative morphological method during a 6 to 12 day incubation period. The findings obtained in this study are summarized as follows.
At 6 to 7 days' incubation, no lymphoid cells were observed in the bursal primordium. In 8 day embryonic bursa, the first appearance of lymphoid cells was found in the tunica mucosa. In the epithelium, the first appearance of lymphoid cells was observed at 9.5 days' incubation. At 9.5 to 11 days' incubation, lymphoid cells were frequently observed to pass through the epithelial basement membrane. It may be concluded that the lymphoid cells found in the epithelial region had migrated from the bursal mesenchymal region. The formation of epithelial buds began at about 11 days' incubation, but were never found prior to penetration of lymphoid cells into the epithelium.
It may be concluded from the present results that bursal lymphoid cells derive from mesenchymal cells in Japanese quails.

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The endocardial surface in the rabbit and rat was observed by scanning electron microscopy.
In both animals the endothelial cells were polygonal or stellate in shape without being elongated in any certain direction and without reflecting the direction of the blood stream or the underlying muscular arrangement.
More or less numerous, long microvillous and short granule-like projections occurred on the endothelial cell, tending to be gathered on the nuclear swelling. Cells with only a few or no projections were also mingled. A single cilium was identified on each cell in the rabbit, though its occurrence in the rat was equivocal. Marginal folds were constantly found on the cell border. No essential differences in the endocardial surface structures specific to the site in the heart were found.
The shape and surface structures of the endothelial cells covering the valves are essentially the same as those in other places, though they are apt to be deformed by the tensile conditions of the basal tissue.

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L-DOPA-³H (50μCi/g.b.w.) was injected intraperitoneally in two mice. They were killed 1hr and 24hrs after the injection and pieces of the gut were processed for both light and electron microscope autoradiography after fixation in glutaraldehyde followed by post-fixation with osmium tetroxide. At 1hr, a greater number of specific silver grains were found on EC cells than on other types of basal-granulated cells including G, L (EG) and ECL cells. At 24hrs, a considerable number of labels were found on only a few EC cells. Subcellular localization of L-DOPA-³H and its metabolites was studied by electron microscope autoradiography. By 1hr after the injection, specific radioactivity accumulated in the cytoplasm rich in secretory granules. Labeling on the Golgi area was conspicuously lower than in the granule-rich cytoplasm.
To study the process of the synthesis of secretory proteins, L-leucine-³H (100μCi/g.b.w.) was injected into the peritoneal cavity of two mice which were killed at 30mins and 2.5hrs after the injection. It was apparent that all morphologic types of basal-granulated cells had an ability to uptake exogenous leucine to synthesize proteins/polypeptides. At 30mins, specific silver grains were found primarily on the Golgi area. By 2.5hrs, however, silver grains were mainly associated with the secretory granules and frequently conglomerated to form a cluster of them in the cytoplasmic area rich in secretory granules.
These results are consistent with the view that in all types of basal-granulated cells the secretory granules together with their protein contents are formed in the Golgi area, and then incorporate amines from the cytosol to become ready to be released by exocytosis.

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Air-dried spreads of human blood platelets were prepared by incubating a drop of fresh blood from finger tips on collodion membrane covered copper grid for 4min at 37°C. The blood was blotted with filter paper and dried in the air at room temperature. Under the electron microscope various substructures were observable in the attenuated cytoplasm of platelets without any treatment, i.e., fixation, embedding or staining. The granulomere of platelets revealed dense bodies of 200-300nm diameter and smaller dense granules (about 50nm). Larger ovoid bodies with dense granules presumably corresponded to mitochondria and lysosomes. In the hyalomere there were vacuoles partly connected with surface of the platelet by a canalicule.
Using an energy dispersive type X-ray microanalyzer attached to a scanning transmission electron microscope, electron probe analysis detected high levels of calcium and phosphorus and an appreciable amount of chlorine in the dense bodies of platelets. The three elements were also detected in the smaller dense granule.
This technique offers some advantages for microanalytic study of the chemical components of cell organelles including the simplicity of the procedure, disuse of liquids in specimen preparation which were possibly causing substance escape, and avoidance of cryosections usually causing ice crystal artifacts.

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In order to clarify the mechanism of the hemostatic plug formation from the morphologic standpoint, scanning electron microscope observation was made on the inner surface of the rabbit carotid arteries 1, 5, 15, 30 and 45sec after stabbing with a needle. The arteries were first fixed in situ by an infusion of glutaraldehyde and then, after being excised, by immersion in glutaraldehyde and in osmium tetroxide. The critical point-dried and gold-palladium covered specimens were examined in a field emission type scanning electron microscope.
Stabbing made a hole, about 0.25mm in diameter, in the arterial wall, and the ruptured endothelial cell shrank and retracted. Thus the subendothelial collagen fibers were exposed and hung on the wall of the holes. Some of the fibers were single and wavy and others were compactly packed in bundles, forming a network.
The first step of the hemostatic process was adhesion of discoid platelets which were attached, with their bodies or frequently with their pseudopods, to the collagen fibers especially at the marginal and hanging part.
On the adhered platelets other free platelets subsequently came to be attached. A thin layer of the platelet aggregates thus formed grew thicker, though somewhat distorted by the blood stream. At this second stage some erythrocytes were found hanging from the collagen fibers or undergoing collapse, suggesting its contribution to platelet aggregation by releasing ADP through hemolysis. The aggregate layer became so thick that it almost obliterated the hole and rose on the arterial lumen 45 sec after the stabbing.
Aspirin which has been shown to affect platelet aggregation in the second phase was demonstrated to lower the rate of aggregate formation to half to one-third.

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