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EFFECT OF RADIATION ON THE NAIL TISSUE
Get PDF1. This article is concerned with the radiation effects on nail based upon macroscopic as well as histological investigations, and composes a series of studies on “Radiation Effect on Hard Tissues” in our Department of Radiology6-11). 2. The nail plate is produced by the nail mat1ix and classified into two layers, the outer and the inner, of different stratification. The outer layer originates from the posterior half of the nail matrix and, on the other hand, the inner layer from the anterior half. The growth of nail plate is influenced by two factors, i.e., formation of nail plate at matrix and forward march of the plate induced by hyponychium. 3. The length of nail plate on mid longitudinal section is 4.5 mm and length of nail bed is 2 to 3 mm on the same section. 4. Among the nail tissues the radiosensitivity is nail matrix, hyponychium and nail plate in order. In nail matrix, the posterior half is more sensitive than the anterior half. 5. The histological changes produced by a single 1000 R irradiation are slight, but ones in a single 3000 R irradiation are so severe that no recovery from the damage are observed. In a single 2000 R irradiation, the changes are severe but reversible. 6. The effect of irradiation to nail is lowered by fractionation. 7. The shedding of the nail due to irradiation, same as the histological change, is also more prominent in the higher dose and in less frequent fractionation. 8. The shedding of the nail is induced by combined processes such as the isolation of the nail plate from matrix, the separation of nail plate from the nail bed and the forward movement of the nail plate. 9. The recovery factor in nail is about same as one in the skin. 10. The growth of human nail is delayed by irradiation. 11. The radiosensitivity of nail is slightly lower than one of skin
STUDIES ON THE PREVENTION OF OUTBREAKS OF FOOD POISONING CAUSED BY VIBRIO PARAHAEMOLYTICUS
Get PDFAs far as our present knowledge regarding food poisoning in Japan it appears probably that Vibrio parahaemolyticus was the etiological agent in many of the outbreaks in which no definite evidence was available. However full information on the preventive measures against food poisoning is still lacking. This is because it is closely related to the peculiar etiology of Vibrio parahaemolyticus. Various experiments on this work have shown the following results: Vibrio parahaemolyticus could be killed if heated in peptone solution at 55°C for 10 minutes or at 60°C for 5 minutes. Further, resistance of the bacteria to other physical environmental factors in relative low temperature, freezing and drying condition was ascertained to be generally weak, although influenced by the bacterial counts, the length of time during which the bacteria were exposed to them and so on. The organisms of Vibrio parahaemolyticus were also killed in distilled water in a short period of time. Consequently, outbreaks can be prevented by washing seafish sufficiently in fresh water, or in boiling water if possible. It is likewise effective for this purpose to keep seafish and fish products cold, as well as to cook them by heating. Drying of utensils as sources of secondary contamination is recommended
PAI-1 inhibitor TM5614 leads osteosarcoma cells to G2 arrest
Get PDFOsteosarcoma is a malignant tumor that histologi- cally forms a tumor-like osteoid or bone. Plasmino- gen activator inhibitor 1 (PAI-1) is highly expressed in the blood of patients with various malignant tumors or in the tumors themselves, and its expres- sion is positively correlated with tumor grade. Therefore, PAI-1 is a potential target for cancer therapy. In this study, a small-molecule PAI-1 inhib- itor, TM5614, was tested on U2OS cells, which are osteosarcoma cell-like cells, to examine its effect on cell metabolism. The MTT assays and cell count analysis showed that TM5614 inhibited U2OS cell proliferation. We also tested the apoptotic activity of U2OS cells by multiple assays, and no induction of apoptosis by TM5614 was observed. In contrast, cell cycle analysis revealed that TM5614 induced U2OS cells in G2-M arrest. This study revealed that TM5614 treatment increased p53 and p21 Waf1/Cip1 expression in U2OS cells. In conclusion, we showed that the PAI-1 inhibitor TM5614 induced G2-M arrest in U2OS cells
