On the basis of the facts found in the previous report that chlorine destroyed cell membrane and stalk of Caulobacter crescentus and that the damaged cells abonrmally differentiated to elongate their stalks when the chlorinated cells were reincubated in fresh medium, it was suggested that there might be some ecological correlations between the level of water pollution and morphology and phsiology of Caulobacter cells. In order to determine such correlations in this study, 18 isolates of caulobacters were isolated from three sites of Musimcheon River which were gradually polluted by domestic sewages and 6 species were identified. Four cell types of bacteroid, vibroid, subvibroid, and fusiform is were isolated from the least polluted water at the rate of 43%, whereas only two cell types of bacteroid and vibroid were isolated from the more polluted waters at the rates of 7 and 10%, respectively. There was no significant difference in each species of Caulobacter isolateed from the gradually polluted river waters, except that abnormally long filamentous cells were occasionally observed in C. crescentus isolated from the most polluted water. Each species showed various responces to chlorine. The resistances of C. crescentus isolates to chlorine were proportionally correlated with the level of water pollution. When they were compared to C. crescentus CB 13 which had been adapted to laboratory enviroment, the C. cresucentus isolated from the most polluted water was more resistant to chlorine.

[ $1-{\beta}-D-Arabinofuranosylcytosine$ ](ara-C), which is a pyrimidine nucleoside analog is cytotonic to mammalian cells in culture and is active in vitro and in vivo against a variety of DNA viruses. The precise mechanism of action of ara-C has not been determined, although ara-C is thought to act as an antimetabolite, interfering with the synthesis of deoxyribonucleic acid(DNA). Cytosine arabinoside originally seemed to act principally by inhibiting the conversion of cytidine to deoxytidine, thus inhibiting DNA synthesis. But recent data suggest that effects upon DNA polymerase and effects via incorporation into DNA and RNA may well be of equal importance. The author have demonstrated the effect of cytosine arabinoside on the hepatocytes of albino mice treated with ara-C, observing changes in the cytoplasmic organelles of the hepatocytes. A total of 120 healthy male albino mice were divided into the control and ara-C treated groups. The animals of the ara-C group were given 10mg. per kg of body weight of mouse ara-C in physiological saline solution and the animals of control group were given physiological saline solution, intraperitoneally. After an administration of ara-C or physiological saline solution, the animal were killed at. interval of 6, 12, and 24 hours. The specimens, which were obtained from the left anterier lobe of the liver, were stained with uranyl acetate and lead citrate and observed with JEM 100B electron microscope. The results were obtained as follow: A pronounced dilatation, sacculation and fragmentation of the cisterane of rough endoplasmic reticulum with dissociation of membrane bound-ribosomes, disaggregation of free ribosomes in the cytoplasm, proliferation of the smooth endoplasmic reticulum associated with depletion of glycogen paracles, atrophies of Golgi complex, production of numerous lipid droplets, and formation of antophagic vacuoles, multivesicular bodies and residual bodies are recognized in the hepatocytes of ara-C treated mice. Consequently it is suggested that cytosine arabinoside would induce a changes of the cytoplasmic organelles of the hepatocytes in albino mice.

Ultrathin sections of intact mycelia, released protoplast and fused protoplast of Micromonospora rosaria were observed by electron microscopy Intact mycelia showed a typical gram-positive bacterial cell wall structure and mesosomes. Released protoplasts had no cell wall components and fibrous nuclear region was distinguished from cytoplsmic region clearly. Protoplasts which treated with sucrose supplemented buffer were stable. But those treated with buffer without sucrose were extensively damaged, forming mom braneous vesicles. It was surmised that those vesicles originated from the damaged cytoplasmic membrane. High frequency of fusion was achieved by 50%(w/v). polyethylene-glycol 1,000 Fusion bodies in different stage of fusion were observed. Cell membrane barrier was stepwise relieved.

A Scanning electron microscope which can obtain additional information not readily available with either the light or transmission electron microscope was used to study the mast cell shape and its granules in normal mammal tissue(rat mesentery, stomach and mouse stomach) by fretting cut using liquid nitrogen. The results showed that rat mesentery and mouse stomach mast cell surfaces had no ridges and microvilli, but revealed several microvilli projecting into the surrounding connective tissue in the rat stomach mast cell. The shape of the mast cell varied from discoid(in the rat mesenteric mast cell) to ellipsoid (rat and mouse stomach), ranging from 7.5 to $10{\mu}m$ in diameter. The shape of the nucleus was ellipsoid and nucleic membrane was adherent to the outer surface of the granules. The granules, approximately 0.2 to $0.9{\mu}m$ in diameter, were various shapes. Frequently, rounded protrusions of cytoplasmic granules could be discerned under the cell membrane. Many small granules were seen in the cytoplasm.

Protoplast releasing mechanisms from Trichoderma koningii, fine structures of the released protoplsts, and their regeneration mode were studied by scanning and transmission electron microscopy. Two types of protoplast releasing mechanisms were observed. In one mechanism, cytoplasm emerged through a cell wall pore developed by cell lytic enzymes and formed a spherical protoplast. In the other mechanism, as the cell wall became progressively thinner, the inner cytoplasm partially rounded to form nonspherical bodies which became spherical protoplasts after being released into the enzyme solution. But, these two types of protoplast releasing mechanisms did not seem to be. mutually exclusive but could occur on the same mycelium simultaneously. And it appeared that cytoplasm which did not become a protoplast by the first mechanism could from a protoplast by the second mechanism. The preparations contained two types of protoplasts, released from different sites of the mycelia. Those released from younger mycelia had dense cytoplasm and small vesicles. Those released from the older mycelia had less dense cytoplasm and larger vacuoles. In the case of regeneration, before producing normal mycelia, most of the protoplasts assumed aberrant tube and yeast-like-forms. Normal mycelia were produced at the end of the yeastlike-forms and sometimes in the middle of the aberrant tube.

The cell division of Bacillus thuringiensis are studed by a electron microscope. It was observed that when the cell division was occurred, the bacterial transverse septeum was centripetally formed, and the bacterial spore was divided into two daughter cells. The fore spore septum was initiated by invagination from either sides of the cell membranes, and was easily distinguished it from the transverse septum of the vegetative cell division. The large vesicular mesosome was. observed at one end of the cell membrane. The nucleoids were of variously irregular shapes and had no a nuclear membrane. The morphology of the bacteria was visualizd by a scanning electron microscope. The surface of the cell was generally rough and had a single polar flagellum, which was appeared to be $0.2{\mu}$ in width and $13{\mu}$ in length.

This study was made to investigate the ultrastructural changes of the hepatocyte of the maternal liver, and fetal liver by Actinomycin D in Wistar rats at the stage of pregnancy. Peritoneal injection of Actinomycin D to rats carried out gestation day 7 to 9 at the level of $15{\mu}g(11.5{\mu}g/100g$ body wt.), $20{\mu}g(15.8{\mu}g/100g$ body wt.) on each day. Treated animals with saline only were used for controls. Animals were sacrificed on day 15 of gestation. On electron microscopic examination, the hepatocytes of maternal liver given Actinomycin D $15{\mu}g$/ml had evidence of serious cellular damage, for example, hypertrophy of rough endoplasmic reticulum, loss in nucleolar osmiophilia, swelling of Golgi apparatus and change of mitochondrial structure. Maternal liver given Actinomycin D $20{\mu}g/ml$ shown similar changes to that of the $15{\mu}g/ml$ treated animals. But mitochondria of this group were not changed than that of $15{\mu}g/ml$ treated group. In the hepatocytes of fetal liver, changes were more pronounced. The drug produced alteration in nuclei and cytoplasm. The rough endoplasmic reticulum was swollen and there were ribosomes detachement. In addition, damages of mitochondria, Golgi apparatus were detected.