[Surgical orthodontics. The present situation of our team approach; and two treated cases of mandibular prognathism].
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Biomedical subjects
Publications and source records attributed to T Wada.
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During the past 4 years, a sequential study was conducted to compare the effect of tamoxifen (TAM) alone and TAM plus 1-(2-tetrahydrofuryl)-5-fluorouracil (FT) in the treatment of advanced breast cancer. The overall response rates were 28.9% in 45 patients treated with TAM, and 43.2% in 37 treated with TAM + FT. In regard to dominant site of lesions, 4 out of 9 patients (44.4%) with visceral involvement responded to TAM + FT, whereas none out of 10 responded to TAM alone. In a crossover study, 4 out of 5 failures to TAM responded favorably to TAM + FT. The median value of survival was 24 months in patients treated with TAM alone and 36 months with TAM + FT. Side effects such as gastrointestinal disorders and bone marrow suppression slightly increased in incidence when cytotoxic chemotherapy was combined with TAM. The present chemo-endocrine regimen with TAM + FT showed some advantages over TAM alone.
Our experience with choledochoscopic extraction of intrahepatic calculi in eleven cases is presented. In three cases, the intrahepatic bile duct containing multiple stones was punctured under the guidance of ultrasonography, and the stones were removed choledochoscopically through the percutaneous transhepatic cholangial drainage (PTCD) tract which was dilated with catheters of increasing diameter. In nine cases, the removal of intrahepatic stones was attempted choledochoscopically through the T-tube tract or the jejunostomy. This procedure was successful in six of the nine cases. The advantage of the choledochoscopic removal through the PTCD tract compared with that through the T-tube tract is discussed, and an illustrative case is presented.
Experimental hepatoma of the rats was induced by chronic administration of 3'-methyl-dimethylamino-azobenzene. The folate level of the hepatoma-bearing rats tended to be low as compared with that of normal controls, and the co-existence of folate deficiency and reduced motor nerve conduction velocity of the dorsal nerve trunks appeared not uncommon. The hepatoma-bearing rats revealed the disturbance of serine to glycine conversion in serum, and folate administration to them prevented electrophysiological neuropathy along with normalization of serine to glycine conversion. Therefore, the reduced motor nerve conduction velocity could be at least in part the result of a metabolic impairment due to folate deficiency.
To elucidate the metabolic abnormality of musclar dystrophy, 27 kinds of enzyme activity in various organs of control and dystrophic mice were examined. The organs examined included muscle, bone, heart, testis, uterus, spleen, thymus, submaxillary gland, stomach, pancreas, liver, kidney, brain, and lung. The activities of 14 different aminopeptidases, 5 endopeptidases, 4 glycosidases, phosphatase, esterase, and ribonuclease were measured. Most of the enzyme activities were significantly elevated in muscles and bones of dystrophic mice. These organs were similar in their patterns of enzyme abnormality. Among the 14 kinds of aminopeptidase activity studied, the degree of increased activity was greater for the aminopeptidases (AP):Ala-AP, Leu-AP, Met-AP, Phe-AP, Trp-AP, Gly-Pro-Leu-AP. In addition to aminopeptidases, there were significant increases in activities of chymotrypsinlike enzyme, cathepsin C, cathepsin D, several glycosidases and neutral ribonuclease in the muscles of dystrophic mice. Similarly increased enzyme activity was also observed in organs other than muscle and bone. Furthermore, protein content in most organs was higher in dystrophic mice than in those of control mice. These abnormalities were seen in both males and females. The present results suggest that there are extensive abnormalities in the protein metabolism in dystrophic mice. It seems therefore that the therapeutic approach to muscular dystrophy should be studies not only from the well-known abnormality of intramuscular endopeptidases, but from other aspects as well.
The present study was performed to investigate the enzymatic changes in dystrophic chickens compared to those of dystrophic mice. The activities of 14 kinds of aminopeptidases, 5 kinds of endopeptidase, 4 kinds of glycosidases, phosphatase, esterase, and ribonuclease were measured in muscles of control and dystrophic chickens. When the enzyme activities were expressed as specific activity per unit weight of organs, only some of them were found to be significantly elevated in dystrophic chickens; e.g., alanine aminopeptidase (Ala-AP), Gly-AP and cathepsin D. On the contrary, the activities of alpha-D-glycosidase, alpha-D-galactosidase and alpha-D-mannosidase were significantly decreased. Muscular protein contents of dystrophic chickens also tended to be lower than those of controls. These observations offer a striking contrast with the one obtained in the study on dystrophic mice. However, when expressed as specific activity per mg protein, many enzyme activities were found to be significantly elevated suggesting an extensive abnormality of metabolism in dystrophic chickens. Among 14 kinds of aminopeptidase activities, highly significant elevations were seen especially in AP-A, AP-B, Gly-AP, Ala-AP, Ser-AP, Pro-AP, Leu-AP, Met-AP and Trp-AP. Interestingly enough, a statistical approach suggested a significant correlation between the aminopeptidase changes of dystrophic chickens with those of dystrophic mice. In addition to aminopeptidases, there were highly significant increases in the activities of cathepsin D, alpha-D-glucosidase, beta-D-galactosidase, alpha-D-mannosidase, esterase and RNase. These results indicate that the intramuscular metabolic abnormality of dystrophic chickens are generally different from but partly resembled with those of dystrophic mice.
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