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Biomedical subjects

Y Takeoka

Publications and source records attributed to Y Takeoka.

28 records · Page 2Linked to original sources

Suppression of acute experimental allergic encephalomyelitis by neurotropin: clinical, histopathologic, immunologic and immunohistochemical studies.

The effect of neurotropin, an extract isolated from the inflamed skin of rabbits inoculated with Vaccinia virus was examined on acute experimental allergic encephalomyelitis (EAE) in Lewis rats. A dose of 40 mg per kg body weight of neurotropin was administered intraperitoneally for 7 days post-inoculation. The severity of clinical signs of acute EAE was decreased by the administration of neurotropin. Histopathologic evaluation showed that lesion severity of EAE in neurotropin-treated rats was less than that seen in untreated rats. Blood lymphocyte subset analysis revealed that in comparison to untreated EAE rats, in neurotropin-treated rats, the percentage of OX6+ (Ia antigen) cells was lower and the W3/25+ (helper T cell): OX8+ (suppressor/cytotoxic T cell) cell ratio was greater during the period of peak inflammation. Immunohistochemical examination of neurotropin-treated rats demonstrated that OX6+ and W3/25+ cells within EAE lesions were fewer and that OX8+ cells in lesions occurred in greater numbers than those in untreated rats. These findings suggest that the OX8+ cells in the inflammatory lesions may have been induced by neurotropin treatment and that the suppressive effects on the disease may have been causally related to their presence.

Acute Disease↗

Neurotropin inhibits experimental allergic encephalomyelitis (EAE) in Lewis rats.

The effects of Neurotropin, a substance extracted from the inflammatory dermis of rabbits inoculated with Vaccinia virus, for experimental allergic encephalomyelitis (EAE) in Lewis rats, a model for human multiple sclerosis (MS), was studied. The peptide defined by residues 68-84 (MB 68-84) which corresponds to the encephalitogenic portion of the guinea pig myelin basic protein (MBP) in complete adjuvant H37Ra (CFA) was injected into the hind foot pad of each rat. Neurotropin significantly suppressed the clinical and histological expression of actively induced EAE when administered i.p. daily from day 0 to day 6 after immunization. In addition, passive EAE induced by precultured spleen cells from rats immunized with MB 68-84 in CFA was also suppressed by daily administration of Neurotropin after cell transfer. Neurotropin treatment significantly suppressed the delayed-type hypersensitivity (DTH) response to MB 68-84. Furthermore, the ability of spleen cells from Neurotropin-treated rats to transfer EAE was significantly lower than that of saline-treated rats. It seemed that the suppression may be due to the inhibition of the activation by MB 68-84 of sensitized spleen cells, as demonstrated by proliferative response to MB 68-84. However, no difference was observed in Con A-induced proliferative response of the spleen cells between Neurotropin- and saline-treated rats. These findings indicate that Neurotropin inhibits EAE by suppressing the immune responses to encephalitogenic MBP with little non-specific suppression.

Animals↗

Immunocytochemical study of pepsinogen 1-producing cells in the fundic mucosa of the stomach in developing mice.

Development and maturation of pepsinogen 1-producing cells were studied in the gastric fundic mucosa of the mouse by means of light- and electron-microscopic immunocytochemistry using rabbit anti-rat pepsinogen 1-serum. In the adult mouse, secretory granules in mucous neck cells, transitional mucous neck/chief cells and chief cells are immunolabeled. The numerical density of gold particles on zymogen granules is not significantly altered among different stages of maturation of chief cells. In addition, rough endoplasmic reticulum and Golgi complex of these cell types show a weak labeling. In mice from day 16 of gestation to postnatal day 14, mucous neck cells and chief cells cannot be distinguished, but only one type of pepsinogen 1-producing cell, called 'primitive chief cell', is identified in the fundic gland. The intensity of immunoreactivity of secretory granules in primitive chief cells is uniform within an individual cells but varies greatly among different cells. The majority of primitive chief cells contains weakly labeled granules regardless of the maturation stage of cells or of animals. On postnatal day 21, mucous neck, transitional and chief cells are distinguishable, and secretory granules in these cells are intensely immunolabeled as in the adult. These results suggest that pepsinogen 1-production rapidly increases with differentiation of mucous neck and chief cells.

Animals↗

Differential action of nerve growth factor, cyclic AMP and neurotropin on PC12h cells.

Nerve growth factor (NGF) induced the activities of acetylcholinesterase (AChE) and Na+,K+-ATPase concomitant with neurite outgrowth in PC12h cells, while dibutyryl cyclic AMP (DBcAMP) caused the induction of AChE activity and neurite outgrowth but not Na+,K+-ATPase activity. A nonproteinaceous extract isolated from the inflamed skin of rabbits inoculated with vaccinia virus (Neurotropin) induced neurite outgrowth and cell surface change similar to NGF without affecting AChE activity. The results suggest that NGF, DBcAMP and Neurotropin act on PC12h cells through different mechanisms.

Acetylcholinesterase↗

Electron microscopic observations on immature chief and parietal cells in the mouse gastric mucosa.

Panoramic and conventional electron microscopic examinations were conducted on the mouse gastric mucosa with special reference to the distribution of immature forms of chief and parietal cells. Immature chief cells were occasionally present as high as the transitional region between the isthmus and neck of the gland, although their main localization was at the uppermost part of the base. Immature parietal cells were found in the lower part of the isthmus and throughout the neck. Cells at the same stage of maturation were often present side by side. Some cells in the neck, showing the characteristic morphology of immature parietal cells, also contained mucous granules resembling those in the mucous neck cells (intermediate cell). These findings suggest that: a chief cell may be formed by direct differentiation from the stem cell in the isthmus as well as by possible maturation of the mucous neck cell and mitotic division of the immature chief cell itself; and a parietal cell can be formed in the lower part of the isthmus and throughout the neck by direct differentiation from the stem cell or by mitotic division of the cell already determined to be a parietal cell as well as maturation of the intermediate cell.

Animals↗

Histogenesis of the mouse pyloric mucosa with special reference to the development of surface mucous cells and pylorocytes, and the formation of the generative zone.

The distribution of proliferative cells and maturation of epithelial cells were studied in the pyloric mucosa of developing mice by 3H-thymidine autoradiography, carbohydrate histochemistry and electron microscopy. The formation of the gastric foveola and pyloric gland were seen to begin as an invagination in the epithelial surface and/or the formation of intraepithelial cavity on day 13 of gestation (day E13). Surface mucous cells and pylorocytes were first identified on day E16 by carbohydrate staining as well as by their fine structure. Both types of cells rapidly acquired abundant membranous organelles and secretory granules within the first postnatal day, maturing in fine structure by day 28. Proliferative cells were distributed over the epithelium by day E15, while they were rarely found at the mucosal surface after day E16. Concomitantly with the elongation of foveolae and glands during postnatal development, the proliferative capability of surface mucous cells diminished from the foveolae and that of pylorocytes from the glands, respectively; the generative zone was restricted to the isthmus by day 21, as in the adult animal. These results reveal that the histogenesis of the mouse pyloric mucosa is accomplished by the end of the weaning period.

Animals↗

Ontogenesis of gastrin cells in the pyloric antrum and duodenum of the mouse.

Ontogenesis of gastrin cells was studied in the pyloroduodenal mucosa of the mouse using anti-human G17 serum, R-1301, and anti-human G34(1-15) serum, R-2703. R-1301-immunostained cells first appeared in the pyloric mucosa of 14-day-old fetuses. Cells stained with both R-1301 and R-2703 appeared immediately after birth, and gradually increased in number to the adult level. Most R-1301-reactive cells were also reactive to R-2703, whereas some cells that reacted with R-1301 exhibited very weak or no reaction with R-2703. The discrepancy between these two immunoreactivities is discussed. In the duodenum, a considerable number of R-1301-reactive cells were present from the perinatal stage and through out adult development. A few R-2703-reactive cells were seen in the duodenum of young mice but not of the adult.

Age Factors↗

Electron microscopic observations of surface mucous cells in the mouse gastric mucosa during physiological degeneration and extrusion.

The gastric mucosa of adult mice was observed by electron microscopy, and the following findings were obtained. Surface mucous cells mostly undergo degeneration in situ before extrusion from the mucosal surface. Degenerating cells exhibit low electron density of the cytoplasmic matrix and interchromatin region of the nucleus. Some vacuoles can be seen in the cytoplasm. The rough endoplasmic reticulum and Golgi complex retain their normal configurations. Mitochondria are condensed. Lysosomes increase in number, and acid phosphatase activity is restricted within them. Massive exocytotic release of mucus is seen at the cell apex. The basolateral plasmalemma seems intact until the latest stage of extrusion. At the tight and gap junctions, the outer leaflets of apposing plasmalemmas remain fused. On the other hand, microfilaments and tonofilaments are dissociated from the intermediate junctions and desmosomes, respectively, during degeneration. Massive discharge of mucus and well preserved basolateral plasmalemma of the degenerating cell may restrict the back-diffusion of gastric juice into the mucosa to a minimum level during the degeneration and extrusion processes.

Animals↗

A case of 21q-syndrome with half normal SOD-1 activity.

A male Japanese infant was found to have a chromosomal aberration of del(21)(qter leads to q22.1-2) and decreased superoxide dismutase (SOD) activity in erythrocytes and polymorphonuclear and mononuclear leukocytes. The cuprozinc enzyme (SOD-1) level was 40-50% of normal, while the cyanide-insensitive manganese enzyme (SOD-2) activity was within the normal range. Determination of SOD activity in blood cells is a valuable method of classification of the syndrome.

Chromosome Aberrations↗