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Biomedical subjects

S Tsubouchi

Publications and source records attributed to S Tsubouchi.

12 recordsLinked to original sources

[Radiosensitization of mouse intestinal epithelial cells with BudR].

For the radiosensitization of the repair rich epithelial cells of small intestine, BudR (B.U.) was continuously infused into mice. Its uptake into the DNA, as shown by the substitution rate (S.R.) of thymine to B.U., was dose-dependent in low dose, but above the 4 mg/d/head it did not increased. The radiosensitization effect was assayed by the clonogenecity of the cells, and (1) the repair capacity (recovery factor, RF.) of the cells and (2) the isoeffect dose (I.D) were obtained. From these data, their enhancement ratios (E.R) were estimated. E.R. by R.F. increased remarkably both in low dose and in low S.R., but showed the plateau at about 10 level after 4 mg/d/h of dose or 10% of S.R. Whereas E.R. by I.D. increased linearly in dose or it did quadratically in S.R. From these results, it was discussed that radiosensitization by debromozation of B.U. was seen in low dose, and the direct cytocidal effect of B.U. became dominant with the dose-increase. Also the clinical application of B.U. was discussed in cell kinetical aspect of B.U. labelling as well as the progress of infusion techniques.

Animals

Whole-body hyperthermia-induced renal atrophy of mice as evinced by obstruction and degeneration of renal tubules caused by acute ischemia.

Effects of microwave-induced whole-body hyperthermia (WBH) on the mouse kidney were examined histologically for acute and late effects up to 150 days after WBH treatment at 43.5 degrees C (rectal temperature) for 20 min or 42 degrees C for 40 min. As a whole the damage could be divided into two types. One was the damage to distorted epithelial cells in the subcapsular region. This lesion was common in most animals, possibly caused by direct hyperthermic effect of microwave. The other was general renal atrophy accompanied with aqueous or protein-rich cysts due to a chain of physiological reactions of the whole body to WBH. The first reaction was characterized by general stasis of the blood stream in all parts of the kidney, which resulted in acute ischemia of some tissues. This was seen immediately by dilatation of the renal and interlobular veins as well as the bundles of capillaries in the medulla region. The subsequent event was rather specific cell necrosis of distal and collecting tubular epithelium as compared to proximal tubules. The cell destruction induced cell proliferation of the proximal tubular epithelia after two days. Later on, in accord with the recovery of the blood circulation, the proliferated cells were carried away into the lumen, these processes then resulting in obstruction of tubules through formation of protein casts in the lumen. The block incidentally led to the destruction of nephrons. The degenerated area sometimes consisted of aqueous or protein-rich cysts of various sizes after 7 to 30 days. Thereafter these cysts degenerated, decreasing in both number and size. Thus irreversible atrophy of the kidney developed after WBH.

Acute Disease

[Cellular thermosensitivity].

(1) modes of expression of thermosensitivity and theoretical interpretation of thermal dose, (2) differential thermosensitivities between strains of cells and the possible correlation to heat shock proteins and their syntheses, (3) cell phase responses to hyperthermia, (4) low hyperthermia and the induction of thermotolerance, (5) comparative thermosensitivities at the temperatures between below and above 42.5 degrees C -43 degrees C, (6) Arrhenius plot and mean cellular lethal heating periods, (7) step-up heating and the thermotolerance induction, (8) step-down heating and the thermoenhancement, (9) fractionated high hyperthermia and the thermotolerance induction and (10) modification of thermosensitivity by chemical substance including anticancer drugs; are compactly reviewed mainly on cell level.

Cell Cycle

[Segmental (L4-S1) motor and sensory innervation of the lower extremity determined by electrical potentials].

Reliable knowledge of the segmental innervation of the muscles and skin of the lower extremity is required to evaluate the anatomical localization of the lumbosacral nerve root involvement. There exist a number of reports on the segmental innervation of the muscles and the area of skin supplied by the lumbosacral plexus. However, no universal acceptance on the lumbosacral nerve root innervation exists. In order to confirm the reliability of the information on myotomes and dermatomes that has been reported, muscle action potentials were recorded from 11 lower limb muscles of 10 subjects by electrical stimulation of the L4, L5 and S1 nerve roots. Sensory nerve potentials were also recorded from roots by stimulations of the sural nerve, superficial and deep peroneal nerve, and the 1st toe of 8 subjects. Under an image intensifier, the electrodes were inserted near the nerve root in the intervertebral foramen or the first sacral foramen. The medial and lateral head of gastrocnemius and the soleus were confirmed to be S1 innervation, but tibialis anterior had a dual innervation at L4 and L5. Extensor hallucis longus, extensor digitorum longus and brevis, and peroneus longus were supplied predominantly by L5. Abductor hallucis and the long head of biceps femoris were supplied by S1, and rectus femoris was supplied by the L4 root. The sural nerve and superficial peroneal nerve were supplied by S1 and L5 nerve root, respectively. The deep peroneal nerve was supplied by either L4 or L5. The 1st toe was supplied by L5.

Action Potentials

Demonstration of expanding cell populations in mouse pancreatic acini and islets.

The acinar and islet cells of the adult mouse pancreas were examined by radioautography after continuous infusion of 3H-thymidine, for periods varying from 1 to 60 days, to determine whether they behaved like renewing or expanding cell populations. The labeling of both cell types increased with the duration of the continuous infusion and reached 2.22% and 12.0%, respectively, after 60 days. The rate of acinar and islet cell labeling was estimated from the regression line of the labeling index versus time and given as 0.039% and 0.20% cells per day, respectively. The rate of cell labeling was relatively low in these acinar and islet cells in comparison to the relatively high rate in duct cells. Occasionally, acinar cell labeling was not uniform, showing high labeling in the outer peripheral region of a lobe and at the periphery of the islets. Both acinar and islet cells increased in number in the adult, and at a rate indicating they are expanding cell populations. Their doubling times were estimated as 2,564 days (7.0 years) and 500 days (1.3 years), respectively. Duct epithelial cell populations were dividing at a rate indicating that they are renewing cell populations.

Animals

Dynamic features of duct epithelial cells in the mouse pancreas as shown by radioautography following continuous 3H-thymidine infusion.

The possibility of turnover of the epithelial duct cells was examined in the adult mouse pancreas by radioautography following continuous administration of 3H-thymidine for periods varying from 1 h to 60 days. One hour after an injection of 3H-thymidine, the label observed in small and large ducts was low but increased with the duration of the continuous infusion of 3H-thymidine and reached a level of about 67% cells labeled after 60 days. The rate of duct cell labeling was estimated from the regression line of the labeling index vs. time in four types of ducts classified according to their inner diameter and the presence of the adventitia and was given as 0.60% cells per day in small (adventitia-free) ducts (phi 4-12 micron), 0.89%, 1.02%, and 1.23% cells per day in large (adventitia-including) ducts (phi 15-29, 30-49, and 50-160 micron respectively). In contrast, the labeling index of aciner cells after a 60-day infusion indicated an addition of only 0.02-0.07% per day, and that of islet cells 0.14-0.22% per day. It is known that most parenchymal cells belong to either expanding or renewing cell populations. The acinar cells of the pancreas have been shown to constitute an expanding population, a conclusion confirmed by the low addition of cells observed in the present work. However, the relatively high rate of cell addition in the duct epithelia indicates that they may turn over in a period of 2.7 months in the case of large ducts and 5.6 months in the case of small ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Device of anoxic chamber system and repair of potentially lethal damage of anoxic cells in vitro.

In order to study radiation responses of anoxic plateau phase cells in vitro, an air-tight anoxic chamber was devised in which Chinese hamster V-79 or Swiss mouse NIH3T3 cells were deoxygenated by replacing the air with saturatedly humidified N2 gas. The cells as adhered on the culture plate, which was contained in the anoxic chamber, were x-irradiated. The deoxygenated condition in the anoxic chamber was maintained as long as necessary. Oxygen enhancement ratio obtained by the anoxic chamber was about 2.6. Repair of potentially lethal damage of the anoxic plateau phase cells was observed to the same extent of that of the oxic cells.

Animals

Recruitment of cells in the small intestine into rapid cell cycle by small doses of external gamma or internal beta-radiation.

Epithelial cell recruitment was examined in mouse ileum after external gamma-irradiation (50 cGy) or internal beta-irradiation (0.148 MBq/g of [3H]thymidine), using the per cent-labelled-mitoses method and by analysing the distribution of mitotic cells in the crypts. In the presumptive stem cell zone at the lower cell positions of the crypt, the slowly cycling cells decreased their cell cycle 6 or 12 hours after a dose of 50 cGy. In the higher cell positions, a slight shortening of the cell cycle was also observed. After administration of a high dose of [3H]thymidine, dormant (G0) cells also entered the cell cycle in the lower cell positions. The results suggest that stem cells in the crypt may react to irradiation in two ways: first, by shortening the cell cycle in cycling cells; secondly, by an entry into the cell cycle by other dormant cells. There was destruction of some cycling stem cells before any recruitment. The data support the idea that the stem cell population in the crypt is heterogeneous.

Animals

Migration and turnover of entero-endocrine and caveolated cells in the epithelium of the descending colon, as shown by radioautography after continuous infusion of 3H-thymidine into mice.

Adult male mice were given a continuous infusion of about 0.5 muCi of 3H-thymidine per gram body weight per day for periods varying from 1 to 60 days. Semithin sections of descending colon were cut from/plastic-embedded blocks and stained by a method combining silver impregnation and iron hematoxylin, by which argentaffin entero-endocrine cells and caveolated cells could be identified. From radioautographs, the labeling index of these cells was determined. One to three days after the beginning of 3H-thymidine infusion, label is observed in some of the stained entero-endocrine cells in the bottom of the crypts; the apices of these cells reach the crypt lumen and are joined to neighboring cells by terminal bars (junctional complexes). After five to seven days, labeled entero-endocrine cells are seen on the sides of the crypts, where their base stretches along the basement membrane and their apex has lost its terminal bar connections to neighboring cells. Finally, by 13 and 24 days, labeled cells are observed within the epithelium at the mucosal surface. The turnover time, which is taken to be equal to the mean time required for migration from site of origin to site of loss on the mucosal surface, has been estimated at 23.3 days. This is much longer than the 4.6 days required by the two main cell types of the epithelium -- vacuolated-columnar and mucous cells -- to travel the same route. It is likely that, after entero-endocrine cells lose their terminal bar attachment to other epithelial cells, they migrate independently and very slowly. Labeled caveolated cells are first seen in the crypt bottom one day after the beginning of 3H-thymidine infusion. By three to five days, they are on the sides of the crypts; their base is stretched along the basement membrane, but their apex retains its attachment to neighboring cells by terminal bars. By seven days, labeled caveolated cells are on the mucosal surface. Their turnover time has been assessed at 8.2 days. This is, again, longer than for the two main types to which they are bound by terminal bars throughout migration. The discrepancy is explained by the caveolated cells arising deeper in the crypts than most vacuolated-columnar and mucous cells.

Animals