Phenytoin is clinically used as an anti-epilepsy drug and also is known as an inducer of cleft palate in the craniofacial area. It may be suggested that phenytoin cause cleft palate through the glucocorticoid receptor in the same fashion as does steroid hormone in mouse embryonic palates.

In order to investigate the teratogenic mechanism of phenytoin on the cleft palate, the present study examined immunohistochemically with anti-glucocorticoid receptor antigen and the incorporation of ³H-thymidine into the embryonic palate in which phenytoin (75㎎/㎏) had been intraperitoneally injected twice:on the day 12th and 13th of pregnancy of ddY mice.

The results obtained are as follows: In the control group, palatine shelves were fused on the 14th day of pregnancy. On the other hand, in most of the phenytoin-treated animals, palatine shelves were fused on the 15 day pregnancy one day later than the control group. At this stage, the failure of the adhesion of the palatine shelves caused the cleft palate. Intense immunostaining of anti-glucocorticoid receptor was observed on the cleft palates of phenytoin-treated group. Also, incorporation of ³H-thymidine was completely inhibited in the cleft palates of the phenytoin-treated group. These results indicate that phenytoin can induce the cleft palates by inhibition of DNA synthesis initiated via glucocorticoid receptor.

Arbitrarily primed polymerase chain reaction (AP-PCR) was applied to genome DNA fingerprinting of twenty clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA), and this method was evaluated in comparison with phenotypes, such as coagulase typing and minimum inhibitory concentration of four β-lactam antimicrobial agents. Genomic DNA, obtained by mild cell lysis and treated with phenol / chloroform, was suitable for AP-PCR, and the addition of 3mM MgCl₂ and using PI primer (5’-TCTGTCTTGAAAAACTGATGCCTG-3’) provided four different patterns of DNA fingerprinting. Althought a strong correlation between the phenotypes and DNA fingerprinting patterns was not observed in 20 isolates investigated, AP-PCR can be applicable for genotyping as a time-saving method.

The present study examined the effects of lidocaine, a local anesthetic, on the central cholinergic system in mouse brain. The mice were killed 5,10,20 and 60 min after the intraperitoneal injection of a non-convulsive dose (40㎎/kg) or a convulsive dose (80㎎/㎏) of lidocaine. The acetylcholine (ACh) contents in the striatum, hippocampus, cerebral cortex and hypothalamus were measured by HPLC-ECD. The ACh contents in the striatum and hippocampus increased 60 min after the injection of the non-convulsive dose of lidocaine. Those in the cerebral cortex increased 20 and 60 min after the injection of the non-convulsive dose of lidocaine. On the other hand, the changes in ACh contents in the striatum, cerebral cortex and hypothalamus after the injection of the convulsive dose of lidocaine showed a time-dependent diphasic pattern: the ACh contents in these brain regions decreased 5 min after the injection of the convulsive dose of lidocaine, and increased 20-60 min after the injection. These findings suggest that lidocaine has an influence on the central cholinergic system.

The effects of phenol on the contents of monoaminergic and amino acidergic substances were examined in the striatum, hypothalamus, cerebral cortex and hippocampus of the mice. The former substances were norepinephrine (NE), dopamine (DA), serotonin (5-HT), 3-methoxy-4-hydroxyphenylglycol(MHPG), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and the latter were aspartic acid (Asp), glutamic acid (Glu), glutamine (Gln), glycine (Gly), taurine (Tau), and γ-aminobutyric acid (GABA). The contents of the substances were measured by high-performance liquid chromatography with electrochemical detection (HPLC-ECD). The time course of the change in the content of the target substances in the striatum after injection of phenol (200㎎/kg, s. c.) was examined. The contents of DOPAC, HVA and 5-HIAA showed a time-dependent diphasic pattern, and the similar time pattern was found in the Asp level. These findings were different from the previous ones, which had shown a monophasic pattern in acetylcholine level and tremor score. The target substance contents in each brain area were also examined 40 min after the injection of phenol (200㎎/kg, s. c.). Almost all monoaminergic substances increased in the striatum, hypothalamus and hippocampus. The contents of DA and DOPAC, however, decreased in the cerebral cortex. Almost all amino acidergic substances increased in each brain area. These findings suggest that phenol affects the monoaminergic and amino acidergic systems of mouse brain, but that it may be not directly related to phenol-induced tremor.

The effect of epidermal growth factor (EGF) on cell proliferation was studied in HSG-AZA3, a subclone of human salivary gland adenocarcinoma cell line (HSG). The treatment with EGF, which is involved in cell growth, increased cell numbers and [³H]thymidine incorporation into DNA. In addition, stimulation of EGF enhanced both EGF receptor protein and EGF receptor mRNA levels. On the other hand, the treatment of HSG-AZA3 cells with EGF resulted in EGF-dependent tyrosine phosphorylation of EGF receptor, autophosphorylation, 5min after stimulation, followed by activation of MAP kinase which is one of the kinases invloved in the phosphorylation cascade. These findings indicate that MAP kinase received the signal from the membrane-bound EGF receptor. Moreover, the protooncogene product Fos, which acts as a transcription factor in the nuclei, was rapidly induced by EGF 1-3hr after stimulation. These results suggest that activation of EGF receptor-associated tyrosine kinase and MAP kinase may play an important role in the EGF signaling pathway, and that rapid induction of Fos be prerequisite for cellular proliferation of HSG-AZA3 cells.

After eruption of the tooth crown, the growth of the tooth root has continued at least 2 or 3 years till the end of complete forlnation of the root apex. During this period, however, tooth is functioning as a part of masticatory organ. It is considered that masticatory pressures controlled by food texture influence the growth of the size and shape of tooth root. Especially, it is presumed that this effect has appeared on the young generation who tend to take very soft and nutritious food.

From this view point, the differences of the root size between the young generation, born in 1957 to 1972, and the old one, born before 1937, were examined. Materials were 269 premolars obtained from these generations and their identifications were recorded. Measurements were carried out on root length, bucco-lingual and mesio-distal diameter by using a pair of sliding calipers with 1/100㎜ scale. The results were as follows: The root length of the young generation tended to be short, compared with those of the old generation. The root diameters just at the cervical margin among the young generation were larger than those of the old one. The difference in root diameter between the two generations was not significant at region of root apex.