[A case of glycogen storage disease type VIII found at the age of 62].
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Biomedical subjects
Publications and source records attributed to K Akagi.
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The effect of therapeutic irradiation upon the lymphocyte subpopulation has been investigated in patients with cervical uterine cancer. The influence of radiotherapy was studied on lymphocyte subpopulations analyzed by monoclonal antibodies such as anti-Leu 2a, anti-Leu 3a, anti-Leu 4, anti-Leu 12, and anti-Leu 11a by a FACS analyzer, and by the PHA (phytohemagglutinin) response in 29 patients with cervical uterine cancer. The absolute counts of the various lymphocyte subpopulations were seen to remarkably decrease during radiation therapy, however, their percentages remained unchanged. As for 17 patients with cervical uterine cancer who each received a radical operation, the Th/Ts (T helper T/suppressor) ratio was seen to slightly decrease during radiation therapy. In contrast, in the remaining 12 patients with cervical uterine cancer who each received radiotherapy alone, the Th/Ts ratio was found to be higher than the former cases. This suggests that this phenomenon might be caused by the presence or absence of a tumor.
In order to investigate changes in FHR when a fetus suffers acidemia, we produced progressively advanced acidemia in lamb fetus by intermittently repeated cord compression. FHR was monitored throughout the study. FHR patterns were classified into five characteristic types as fetal arterial pH fell from around 7.35 to below 6.90. It was confirmed by studies involving catecholamine release and the administration of drugs such as atropine sulfate, alpha or beta adrenergic antagonists that sympathetic and parasympathetic regulation was deeply involved in the changes. Among the patterns, type 4, in which decreased amplitude of the initial drop and hypoxia-induced deceleration was followed by overshoot acceleration, took place during acidemia at arterial pH below 7.15. In conclusion, the appearance of type 4 FHR indicates a deteriorating state in human fetus as well, induced by repeated cord compression, and obliges us to deliver the fetus as soon as possible.
A Comparative study of preoperative intra-arterial infusion chemotherapy (I.A.) and transcatheter arterial chemo-embolization (TAC-E) was carried out on thirty-eight patients with locally advanced breast cancer. The results were as follows. (1) In the primary lesions, there was no difference in response rate between these two treatment modalities. (2) As for side effects, moderate myelosuppression and gastrointestinal disorders were frequently observed in I.A. group. (3) Considerably lower recurrence rate of visceral metastasis was noted in I.A. group, in comparison with the TAC-E group. After TAC-E, however, there was no local recurrence. (4) Five-year cumulative survival rate of I.A. and TAC-E group were 52.3% and 60.7% respectively, without any significant difference between the two groups. These results indicated that both I.A. and TAC-E were effective preoperative treatment for locally advanced breast cancer. Therefore, we should select each treatment modality considering the patient's characteristics.
Adenovirus 2 (Ad2)- and simian virus 40 (SV40)-transformed hamster embryo cells differ markedly in a number of phenotypic properties including their potential for inducing tumors in hamsters. Both Ad2- and SV40-transformed cells are immortalized and readily induce tumors in immunoincompetent newborn syngeneic hamsters, but only SV40-transformed cells are highly oncogenic in both adult syngeneic and allogeneic immunocompetent hamsters. The reasons for the difference in the oncogenic potential of the Ad2- and SV40-transformed phenotypes remain elusive. However, recent studies with transforming growth factors (TGFs) indicate that these factors play an important role in determining many phenotypic characteristics of transformed cells. To determine whether TGFs secreted by Ad2- and SV40-transformed hamster embryo cells differ, we have examined the ability of media conditioned by these two transformed cell phenotypes to modulate thymidine uptake in quiescent, untransformed cells. We found that both transformed phenotypes secrete very similar TGF alpha-like mitogenic factors which inhibit binding of 125I-labeled epidermal growth factor to its receptor. Our results also show that SV40-transformed cells, but not Ad2-transformed cells, secrete a powerful mitogenic inhibitor (MI). The MI secreted by SV40-transformed cells is inhibitory for several transformed and untransformed cell types and exerts a cytostatic, not cytolytic, action on untransformed primary hamster embryo cells. MI elutes from size exclusion high-performance liquid chromatography columns with a molecular weight of 24,000. Although MI has about the same molecular weight as TGF beta, it differs from TGF beta in two important respects: it is heat labile and it has a different target specificity for antimitogenic activity. The MI secreted by SV40-transformed cells also inhibits thymidine uptake by concanavalin A-stimulated spleen lymphocytes. This finding suggests that MI might contribute to the extreme oncogenicity of SV40-transformed cells by inhibiting mobilization of immune effector cells at the site of tumor cell proliferation.
Thyroid function was investigated in 123 yusho patients who were exposed to toxic levels of polychlorinated biphenyls (PCBs) 16 years ago. In yusho patients, compared with the patients without evidence of yusho or normal controls, the serum triiodothyronine (T3) and thyroxine (T4) levels were significantly higher, while thyroid stimulating hormone (TSH) levels measured by sensitive assay were normal. There was no difference in serum levels of albumin, alkaline phosphatase, total cholesterol, and thyroxine binding globulin (TBG) between the two groups and the prevalence of positive antithyroid autoantibodies was almost the same, suggesting that hyperthyroxinemia in yusho patients was not due to increased TBG binding or abnormal autoimmune mechanism. Serum free T4 levels, however, were not elevated, although T4/TBG ratio was significantly higher. The thyroid hormone levels were higher than normal value in 4 of 123 yusho patients but only 1 case had clinical symptoms such as excessive perspiration. Despite higher serum PCBs in yusho patients, there was no correlation between PCB levels and levels of T3, T4, or TSH. The present results suggest hyperthyroxinemia without obvious clinical symptoms in yusho patients long after exposure to PCBs.
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Protein and RNA synthesis of the brain is affected by focal transient ischemia. Protein synthesis is depressed by the depletion of energy metabolism during ischemia, and its recovery following recirculation is slower than restoration of energy metabolism. On the other hand, RNA synthesis is more tolerable to ischemia than protein synthesis. Present study has designed to evaluate changes of protein and RNA synthesis of the brain after ischemia. We used a hindbrain ischemia model of gerbils, and quantitative autoradiography was applied for estimation of regional protein and RNA synthesis. The model was made by occluding the basilar artery for 15 minutes and recirculating afterwards. 14C-valine was used as a tracer for protein synthesis. In the ischemic group, protein synthesis was inhibited extremely in the medial thalamus, inferior colliculus, gray matter of the pons and midbrain, and cerebellum, RNA synthesis by salvage pathway was evaluated using tracer doses of 14C-uridine. It increased 1.6-2.4 folds of sham controls in the thalamus, and gray matter of the pons and midbrain. De novo synthesis of RNA was evaluated using 14C-carbamoylphosphate and 14C-NaHCO3. 14C-NaHCO3 antoradiogram showed inhibition of tracer incorporation into RNA and protein fraction in the ischemic lesions. 14C-carbamoylphosphate autoradiogram showed no significant change. These results indicate that protein synthesis is inhibited after ischemia but response of RNA synthesis to ischemia is not uniform. De novo synthesis of RNA is inhibited following ischemia, but RNA synthesis by salvage pathway increases in the ischemic lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
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The purpose of combined chemotherapy (CT) and radiotherapy (RT) is to improve the therapeutic ratio. The increase of the Therapeutic Gain Factor in combination of the two modalities may be obtained by the following methods; 1) the use of CT and RT under consideration of the difference of the sensitivities of cell cycle 2) the development of the effective drugs to the resting cells such as PLDR inhibitors 3) optimal time sequence between drug and radiation administration 4) the use of drugs by their selective toxicities toward oxygenated and hypoxic tumor cells. 5) the use of hyperthermia 6) increased drug delivery and uptake.