As already described, potency is tremendous and its developmental change is delicate which is caused by direct or indirect relationships of chemical substances inside the embryo and in between the areas. In order to confirm the relationships, the inductive action in the normal development of the crystalline lens was observed by using the tadopole of the larva bulgaris japonica.
The following conclusions we re obtained.
1) The retina in amphibian is formed by the sustentacular cells and fibers of Willer, migration in the deep layer of the epithelial cells, and the expansion of the protoplast. The origin of glial tissues, excluding the sustentacular cells and fibers, could not be elucidated in our specimen. These glial tissues, however, appear t o be epithelial-cells derivatives, as Bonnet and Peter explained.
2) The lens is induced from the sense layer, or the outer surface in the deep layer, with the radial sustentacular fibers of Muller as its inductor, and with m elanin granules as its induction factor. This fact is also the case with the regenerat ion of the crystalline lens.
3) According to O. Hertwiz, the external limiting membrane of the retina is formed by secretion. We, however, maintain that this specific membrane is a part of the protoplast remaining of the visual-cavity surface of the epithelial cells, or thin bla ck plates.
4) Melanin granules always attach to the surface of the radial sustentacular cells and fibers of Mfillar and are given to the mother tissues by the entering of the fibers.
5) Melanin appears to develop in the form of yolk granules. We, however, were unsuccessful in proving that this pigment granule, melanin, develops from melanoblast.
6) In amphibian, the optic vesicles commence to develop first at the 19 th stage of the development, and from the optic vesicles which contacted the outer surface, th e radial sustentacular fibers migrate into the sensory-layer tissues at the 20th and 21 st stages of development. At the 22nd stage, the optic vesicles begin to develop into the optic cup.
7) O. Hertwig maintains that the internal limiting membrane is formed by secretion. Our observation, however, seem to indicate that a part of the sustentacula r fibers remaining on the lateral outer-surface of the eye cup composes, or is responsible for composing, the internal limiting membrane.
8) We were not successful in clarifying the gluey connection of the processes of Müller's fibers and the visual cells between the fiber baskets of Müller's fiber s enveloping the basement layers of rods and cones and the cubic or short colu mnar cells in the yellow-coloring epithlium layers, as mentioned by W. Kolmer (1936).
9) J. Mann, W. Kolmer et al. report that in vertebrate species and the human fetus the ganglion cell layers in the innermost cell layers of the retina appear first, and O. Hertwig reports that the layer of rods and cones appears last. In our amphibi an tadopole, the pigmented layer of the retina was formed first (2nd 5th stage of development), and the inner plexiform layer, the nuclear layer, and the ganglion ce ll layer appeared respectively (26th stage), and the nerve fiber layer became distingu ishable (27th and 28 th stage). The outer plexiform layer and Henle's fibe r layer, however, did not yet appear as late as at the 31st stage. We, therefore, coul d not distinguish the outer nuclear layer from the inner one.
10) The development of the crystalline lens varies from animal to animal, as many researchers have pointed out. In amphibian, the lens is formed from the sense layer of the outer surface in the deep layer in contact with the optic vesicle, by the induction of the sustentacular fibers of the optic vesicle.

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It was aimed in the present investigation to observe the fine structural changes in the myocardium of a 2 -hour period of the selective continuous coronary perfusion with cold blood of low flow rate after the cross-clamping of the aorta as compared with those of the selective continuous coronary perfusion with cold Ringer-lactate solution and of the topical cooling with cold physiological saline solution, using normal adult dogs as well as dogs with experimentally produced left ventricular hypertrophy.
Twenty adult mongrel dogs, weighing 12 to 15 kilograms, and 10 mongrel dogs with left ventricular hypertrophy produced by banding of the ascending aorta were subjected to total body perfusion.
In the group of cold blood coronary perfusion, the structural integrity was well preserved during the cooling and even after weaning from the bypass. At the end of a 2 -hour period of the coronary perfusion, the myocardium was essentially normal in all its inner and outer layers, although mitochondria were slightly swollen with a mild decrease in stainable glycogen. Mitochondria were sharply demarcated and the cristae within mitochondria were clear and distinct. Neither clumping nor margination of the nuclear chromatin was demonstrated.
These findings were almost the same as those in the group of cold Ringer-lactate coronary perfusion. The ultrastructure of myocardium at a 2 -hour period of the aortic cross-clampin g in the group of topical cooling, showed distinct abnomality. Particulary, in the inner layer of the myocardium, swelling, clearing and destruction of mitochondria with margination of nuclear chromatin were significant. These findings tended to aggravate at the rewarming period after the release of the aortic cross-clamping or during the recovery period. These morphological changes were more severe in dogs with left ventricular hypertrophy.
Peroxidase in dogs with left ventricular hypertrophy, was injected into the coronary artery immediately before releasing of aortic cross-clamping to evaluate its distribution in the myocardium and its uptake to the endothelium of capillary. In the group of cold blood coronary perfusion, peroxidase could be observed in the endothelium in all areas of the myocardium. On the contrary, in the group of topical cooling, peroxidase was hardly demonstrated in the endothelium of the endocardium, although it was observed in the outer layer of the myocardium. Moreover, peroxidase could be observed not only in the endothelia, but also in the intercellular space based on changes in permiability.
These results clearly show ed that the protection afforded by means of topical cooling for the ischemic myocardium was doubtful in dogs with normal heart, and more doubtful in the case of dogs with left ventricular hypertrophy.
It was the conclusion from the results obtained in the present investigation that the coronary perfusion with cold blood of low flow rate was the choice of the method of myocardial protection for open heart surgery.

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It has long been suggested, through Lee's and other investigators' light microscopical studies, that necrotic changes may play an important role in the ceroidogenesis. On the other hand, Maeda presumed that ceroid is composed of glycoprotein- and lipid-containing compound substances which may be derived from red cell stroma or necrotic tissue. Thereupon an attempt was made to verify the participation of hepatic necrotic lesion in the ceroidogenesis in Kupffer cells in mouse liver by carbon tetrachloride inhalation. Mice were forced to inhale carbon tetrachloride (CCl₄) vapor 5 to 103 times (at a rate of three times a week); specimens from the mice liver were used for an electron microscopy after completion of the CCl₄ inhalation.
The necrotic lesion at vario us stages at the hepatic acinar center was light and electron microscopically observed throughout the whole process of the experiment. The necrotic liver cells showed cytoplasmic concentration and an increased matrical density of the cytoplasm in which cellular organellae were relatively well preserved. These features are thought to correspond to those of “shrivelled necrosis” termed by Takagi (1964). The necrotic liver cells showed all stages of focal cytoplasmic degradation and contained several autophagic vacuoles in which denatured cellular organellae were visible. Part of these necrotic liver cells and their cellular debris were found to be phagocytized by Kupffer cell, which contained much ceroid consisting of the aggregation of numerous pigment bodies.
It was noteworthy, especially in the early stage of the experiment, that, in addition to moderately osmiophilic, round or oval bodies and highly osmiophilic granules, fragments of a membranous structure arranged haphazardly and sometimes remnants of denatured cellular organellae were found in many phagolysosomes constituting ceroid. These fragments were assumed to be derived from denatured cellular organellae of liver cells which have undergone severe injuries or “shrivelled necrosis”. During the experimental process the phagolysosomes containing these fragments in Kupffer cells were increased in size and fused each other, showing a very complex configuration characteristic of mature ceroid seen at the end of the long-term experiment.
The above findings are thought to suggest that the phagocytosis by Kupffer cells of necrotic liver cells and their cellular debris plays an important role in the ceroidogenesis in the Kupffer cells; accordingly they appear to support Maeda's supposition that origin of ceroid sho uld be sought into compound substances including glycoprotein.

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