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Biomedical subjects

Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 667 records · Page 37Linked to original sources
PubMed1986

Effect of sulpiride on plasma prolactin in healthy volunteers and depressed patients.

Plasma prolactin (PRL) levels were measured before and 1, 2 and 4 h after oral administration of sulpiride (SPR) (2 mg/kg) in 91 healthy individuals (56 males and 35 females) and 36 patients with mental depression (15 males and 21 females). The identical measurements were conducted during remission in 16 available patients (9 males and 7 females) for comparison of the values during the depression and remission. During remission, the PRL values (lower in males and higher in females than the normal values), were closer to those of healthy subjects than they were during depression.

Adult↗
PubMed1986

Homotypic pair formation during conjugation in Tetrahymena thermophila.

In the ciliate Tetrahymena thermophila, conjugation has been believed to occur only between cells of different mating types. We found the formation of homotypic pairs during normal conjugation by using micronuclear morphological markers. Homotypic pairs formed preferentially during the first 10 min following the first pair formation and comprised about half of the pairs. These results suggest the involvement of mating-type non-specific adhesion of cells in the initial step of conjugation. Homotypic pairs apparently persist for at least 30 min and then separate into single cells. Homotypic pairs are also formed when conjugant pairs re-form after mechanical separation of heterotypic pairs. Five kinds of glycosidases, three kinds of proteases and phospholipase C showed no effect on either the formation of homotypic pairs of their separation. The relation between the mating-type substances and the molecules responsible for mating-type non-specific adhesion of cells is discussed.

Animals↗
PubMed1986

Enhancement of [3H]clonidine binding to rat cerebral synaptic membranes by treatment with arachidonic acid, prostaglandin (PG) D2, PGE2 and PGF2 alpha.

Pretreatment of cerebral synaptic membranes with arachidonic acid (10 nM-1 microM) at 37 degrees C for 40 min caused a significant increase in [3H]clonidine binding but pretreatment at 4 degrees C did not. Scatchard analysis showed that 100 nM arachidonic acid pretreatment resulted in a significant elevation of the Bmax value of the low affinity site. PGD2, PGE2 and PGF2 alpha (10-100 microM) pretreatment also enhanced binding. These polyunsaturated fatty acids could be involved in regulation of the alpha 2-adrenoceptor binding in rat cerebral cortical membranes.

Animals↗
PubMed1986

Ultrastructural changes in the ovaries of Sl/Slt mutant mice, showing developmental deficiency of follicles and tubular adenomas.

Structural changes in the ovaries of WBB6F1-Sl/Slt mutant mice aged 10, 25, 35, and 60 days and 7 months were studied light and electron microscopically. Neither secondary nor Graafian follicles could be found in any of the animals studied, and only primary follicles were usually seen until 35 days. In most follicles, the oocyte was lost. The hyperplastic proliferation of follicle epithelial cells, forming large round or oval cell clusters, occurred in 60-day-old mice. In 7-month-old animals, the ovaries were mostly occupied with invasive peritoneal epithelial tubules and masses of epitheloid cells which are apparently derived from the follicle epithelial cells. Although the ultrastructure of the oocyte and the follicle epithelial cell of the primary follicle is not different from that of +/+ control animals, the lack of gap junctions between the oocytes and the surrounding follicle epithelial cells may cause these abnormalities. The epitheloid cells that appeared in the 60-day-old animals are suggested to produce some steroid hormones, since they have cell organelles characteristic for steroid biosynthesis, such as well-developed smooth endoplasmic reticulum, oval mitochondria with tubulovesicular cristae, and numerous lipid droplets.

Adenoma↗
PubMed1986

[A case of heterotopic bone formation in the kidney].

A case of heterotopic bone formation in the right kidney is presented. The case was a 58-year-old woman who complained of right flank pain. Excretory pyelography revealed that the kidney was nonfunctioning and had a few calcification shadows. The right kidney was removed. By histological examination of the surgical specimen, the heterotopic bone formation with bone marrow was found beneath the renal pelvic mucous membrane.

Female↗
PubMed1986

Higher susceptibility of mast-cell-deficient W/WV mutant mice to brain thromboembolism and mortality caused by intravenous injection of India ink.

(WB X C57BL/6)F1-W/WV mice possess a genetic defect in multipotential hematopoietic stem cells; the mice are anemic and lack mast cells. The authors injected diluted India ink intravenously into W/WV mice and congenic normal +/+ mice and searched for genetically determined differences in the development of complications of the injection. In both W/WV and +/+ mice, intravenous ink resulted in thrombocytopenia and markedly prolonged bleeding times, as well as prolonged partial thromboplastin and prothrombin times and reduced fibrinogen concentrations. These effects were similar in W/WV and +/+ mice, although the reduction in platelet counts was greater in W/WV mice. In addition, the mortality associated with ink injection was significantly higher in W/WV mice than in congenic +/+ mice. Most W/WV mice which died first exhibited paralysis, and examination under the dissection microscope revealed that ink injection resulted in significantly more cerebral thromboemboli in W/WV mice than in +/+ controls. Bone marrow transplantation from +/+ mice corrected both the mast cell deficiency and the anemia of W/WV mice and protected the W/WV recipients from the adverse consequences of ink injection. By contrast, +/+ mice rendered as anemic as W/WV mice by breeding did not exhibit increased morbidity and mortality after ink injection. (WC X C57BL/6)F1-Sl/Sld mice, which are anemic and lack mast cells because of a genetic defect different from that of W/WV mice, also exhibited increased morbidity and mortality after intravenous ink. Finally, mixture of ink with commercial heparin prior to intravenous injection markedly reduced the incidence of cerebral thromboembolism and death in W/WV mice. Taken together, these findings suggest that the increased morbidity and mortality exhibited by W/WV and Sl/Sld mice that received injected ink might be related to their mast cell deficiency rather than to their anemia. But measurement of the histamine content of the blood and various tissues of WBB6F1-+/+ mice injected with ink, and examination of their tissues in 1-mu sections, indicated that intravenous ink did not cause substantial mast cell degranulation. As a result, the possibility that mast cells protect +/+ mice from the adverse effects of intravenous ink by a mechanism other than degranulation and release of heparin, or that the differences in the response of W/WV or Sl/Sld mice and their +/+ littermates are due to defects other than their lack of mast cells, cannot be excluded.

Animals↗