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Biomedical subjects

Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 703 records · Page 39Linked to original sources
PubMed1985

Heterogeneity in mouse seminal vesicle epithelial cells responding to androgen as evaluated by incorporation of [125I]iododeoxyuridine.

When the uptake of 5-[125I]iodo-2'-deoxyuridine ([125I]IdUrd) into the seminal vesicle of castrated mice was measured 3 days after starting injections of various doses of testosterone propionate (TP), logarithmic values of [125I]IdUrd uptake were proportional to the logarithmic doses of TP in the range of 0.04-2 micrograms/g BW. The [125I]IdUrd uptake values correlated well with the labeling and mitotic indices of epithelial cells. Since daily injections of 0.4 microgram TP/g BW did not increase significantly the weight or DNA content or protein content of the seminal vesicle, the [125I]IdUrd uptake is a sensitive index of androgen action. Moreover, this suggests that low doses of androgen induce division of epithelial cells without resulting in the increase in cell number. The [125I]IdUrd radioactivity in the seminal vesicle was measured 2-15 days after the injection of [125I]IdUrd, since the value represented the fraction of surviving cells synthesizing DNA at the time of [125I]IdUrd injection. When injections of 4 micrograms TP/g BW were continued, the incorporated radioactivity was retained. In contrast, continuous injections of 0.2 microgram TP/g BW did not maintain the radioactivity, of which incorporation was induced by the same dose of TP. Thus, the present result suggests the presence of heterogeneity in androgen-responsive epithelial cells of the seminal vesicle.

Animals↗
PubMed1985

Effects of steel mutation on spermatogenesis stimulated by fetuin.

The effect of the steel mutation on spermatogenesis was investigated using organ culture. Cultured cryptorchid testes from WB-+/+ mice showed an effective differentiation of type A spermatogonia in response to Pedersen type III fetuin. In contrast, the cryptorchid testes from WB-S1/+ showed neither differentiation nor division of type A spermatogonia. The findings reported here are the first demonstration of retarded response of steel mutation on a well-known agent, fetuin.

Alleles↗
PubMed1985

Extensive proliferation of subsequently injected marrow cells in parental-to-F1 hematopoietic chimeras that restored normal stem cell concentration after initial transplantation.

We investigated the fate of donor stem cells that were injected into hosts with a normal concentration of spleen colony-forming unit (CFU-S). Radiation chimeras were used as hosts. When CFU-S concentration in the marrow and spleen recovered to preirradiation levels after the initial bone marrow transplantation, the subsequent transplantation was done without reirradiation. Giant granules of beige C57B1/6 (bg) mice were used as a marker and proliferation and differentiation of the stem cells of the subsequent donor origin were evaluated by measuring the proportion of neutrophils with giant granules. No beige-type neutrophils were detectable at week 24 after transplantation of 5 X 10(7) marrow cells from bg mice to intact (WB X C57B1/6)F1 (F1) mice, which were used as control recipients. In contrast, transplantation of 5 X 10(7) marrow cells to radiation chimeras resulted in the appearance of neutrophils of second-donor origin. The proportion of beige-type neutrophils was 12% at week 24 after transplantation of bg marrow cells to F1-to-F1 (syngenic) or C57B1/6-+/+-to-bg (B6-to-bg) (congenic) chimeras; the proportion of beige-type neutrophils was 43% when bg marrow cells were transplanted to B6-to-F1 semiallogenic chimeras; the proportion of normal-type neutrophils was 82% when F1 marrow cells were injected to bg-to-F1 semiallogenic chimeras. Thus, the interaction of the host hematopoietic microenvironment with the stem cells of the initial donor as well as with the stem cells of the second donor seems to influence the proliferation and differentiation of the latter stem cells.

Animals↗
PubMed1985

[Fenestration of the internal carotid artery in the neck].

Fenestration or duplication of the internal carotid artery is extremely rare. A review of the literature revealed only two such cases by angiography. We present two further cases of internal carotid artery fenestration, incidentally disclosed by angiography. The embryological basis and the clinical significance of this anomalous condition were discussed. Case 1. A 47-year-old woman was admitted to hospital on May 13, 1982, after the first attack of subarachnoid hemorrhage. Four-vessel angiography showed a saccular aneurysm arising at the trifurcation of the right middle cerebral artery. In addition, a fenestration of the right internal carotid artery was demonstrated at the level of the atlas: the cervical portion of the vessel distal to the level of C-2 was markedly elongated and dilated in caliber. Moreover, the right external carotid artery occupied a dorso-lateral position relative to the internal carotid artery. Case 2. A 51-year-old man was admitted to hospital on April 20, 1983, for evaluation of grand mal seizures. CT scans and four-vessel angiograms showed a malignant glioma of the right temporal lobe. Additionally, a fenestration of the right internal carotid artery was identified at the level of the atlantoaxial joint, and the vessel was dilated in caliber at the level of C-1 to C-2.

Brain Neoplasms↗
PubMed1985

[Effect of recombinant alpha-interferon on advanced renal cell carcinoma].

The present study was undertaken to assess the efficacy of single agent chemotherapy with alpha A-interferon or alpha 2-interferon for metastatic renal cell carcinoma. alpha A and alpha 2-Interferon were administered i.m. at a primary dose of 3 X 10(6) units/day to 13 patients. Two patients (15%) showed partial response; 1 patient (8%), minor response; 5 patients (38%), no change; 6 patients (46%), progressive disease. These preliminary observations indicate that these interferons are active antitumor agents in patients with renal cell carcinoma.

Adenocarcinoma↗
PubMed1985

Fatal antral ulcer in conventionally fed W/Wv mutant mice given indomethacin by injection.

Antral ulcers develop spontaneously in (WB X C57BL/6)F1-W/Wv mice. Most W/Wv mice with severe ulcers die within 3 months after birth. When healthy-looking W/Wv mice were selected at 4 months of age, 80-90% of them were free from the ulcer. Even if the ulcer was present, it was small. The authors compared the susceptibility of such healthy-looking W/Wv mice to ulcerogenic treatments with that of the congenic +/+ mice. Stress caused development of fundic erosions in both W/Wv and +/+ mice. The susceptibility of the W/Wv mice to either cold or water-immersed stress was not higher than that of the +/+ mice. Topical administration of aspirin produced erosions in both fundus and antrum. The susceptibility of W/Wv mice to aspirin was comparable to that of the +/+ mice in either the starved or the fed condition. Subcutaneous injection of indomethacin produced both fundic erosions and antral ulcers in the starved condition, but it produced only antral ulcers in the conventionally fed condition. The susceptibility of the starved W/Wv mice to indomethacin was not higher than that of the starved +/+ mice. In contrast, the fed W/Wv mice were significantly more susceptible to indomethacin than the fed +/+ mice. A considerable proportion of the fed W/Wv mice died of blood loss from the ulcer within 24 hours. The size of the ulcer of the W/Wv mice was significantly larger than that of the +/+ mice. Both genetic and feeding conditions seem to determine the susceptibility to indomethacin.

Animals↗
PubMed1985

Inability of genetically mast cell-deficient W/Wv mice to acquire resistance against larval Haemaphysalis longicornis ticks.

Genetically mast cell-deficient (WB X C57BL/6)F1-W/Wv mice were used to investigate the role of mast cells for the acquisition of resistance against larval Haemaphysalis longicornis ticks. Resistance against ticks was evaluated by reduction in both number and weight of engorged ticks. Although (WB X C57BL/6)F1-+/+ mice with a normal number of mast cells acquired resistance after repeated infestation of ticks, the congenic W/Wv mice did not acquire it. Bone marrow transplantation from the +/+ mice were grafted onto the back of the W/Wv mice, resistance against the ticks was detectable in the grafted skin. In contrast, resistance was not detectable in the skin of the W/Wv mice which had been grafted onto the back of the syngenic W/Wv mice. Thus, we consider that the failure of the W/Wv mice to manifest resistance is attributable to the mast cell depletion.

Animals↗
PubMed1985

Uterotropic hormones produced by ovaries of Sl/Slt mutant mice before spontaneous development of tubular adenomas.

Tubular adenomas developed spontaneously in ovaries of (WB X C57BL/6)F1-Sl/Slt and -W/Wv mice after 150 days of age. The uteri of the W/Wv mice were hypoplastic before development of tubular adenomas, but the uteri of the Sl/Slt mice were not. Since oophorectomy significantly reduced the uterus weight in the Sl/Slt mice, we investigated the androgen- and estrogen-producing activity of Sl/Slt and W/Wv mice before development of tubular adenomas. Fragments of ovaries were cultured for 48 hr in serum-free medium containing either progesterone or 4-androstene-3,17-dione (androstenedione). The amount of androgens produced from progesterone by ovaries of Sl/Slt mice in the presence of human chorionic gonadotropin was comparable to that of W/Wv mice. In contrast, the amount of estrogens produced from androstenedione by ovaries of Sl/Slt mice in the presence of follicle stimulating hormone was much greater than that of W/Wv mice. Moreover, the amount of estrogens produced was much greater than the amount of androgens in the ovaries of Sl/Slt mice. Therefore, before development of tubular adenomas, estrogens rather than androgens seem to be a major uterotropic hormone produced by ovaries of Sl/Slt mice.

Adenoma↗
PubMed1985

Regression with secretory changes of ovary-independent rat mammary carcinoma by pharmacological doses of estrogen.

MT6 tumor is a transplantable ovary- and prolactin-independent rat mammary carcinoma containing estrogen and progesterone receptors. The effects of daily injections of 1 mg or 10 micrograms of 17 beta-estradiol for 28 days on the morphological changes and the proliferation and death of MT6 cells grown in male inbred Sprague-Dawley rats were investigated. Uptake values of 5-[125I]iodo-2'-deoxyuridine per g of living tumor, used as an index of cell proliferation, were not significantly reduced by treatment with 1 mg of 17 beta-estradiol. When tumor cell proliferation was evaluated by labeling with 5-[125I]iodo-2'-deoxyuridine just before the treatment, the radioactivity incorporated by the whole tumor remained almost unchanged in intact rats but was decreased slightly on day 21 and significantly on day 28 of the treatment in the rats treated with 1 mg of 17 beta-estradiol. Secretory changes characterized by the appearance of secretion in the lumina, vacuolation in the cytoplasm, marked increase in vesicular endoplasmic reticulum, accumulation of mature protein secretory granules and abundance of lipid droplets were observed in MT6 cells in rats treated with 1 mg of 17 beta-estradiol from the 14th day of treatment. On the 28th day, necrosis of MT6 cells with secretory changes was found. These changes were not found in intact rats or rats treated daily with 10 micrograms of 17 beta-estradiol. These findings suggest that the inhibitory effect of daily injections of 1 mg of 17 beta-estradiol on the growth of ovary- and prolactin-independent MT6 tumor is mainly due to secretory changes followed by loss of tumor cells induced by pharmacological doses of estrogens.

Animals↗
PubMed1985

Mechanism of estrogen enhancement in the growth of androgen-dependent Shionogi carcinoma 115.

The mechanism of estrogen enhancement in the growth of androgen-dependent Shionogi carcinoma 115 (SC115) maintained in castrated DS mice by low doses of androgen (10 micrograms of testosterone propionate or 4 micrograms of 5 alpha-dihydrotestosterone/mouse/day) is reported. Although the low androgen treatment slightly but significantly (P less than 0.05) stimulated tumor growth, concomitant estrogen (4 micrograms of 17 beta-estradiol/mouse/day) significantly (P less than 0.01) enhanced the tumor growth. The high growth rate, histological type (medullary carcinoma), androgen dependency, and high androgen receptor content of the tumor grown during estrogen plus low androgen treatment did not differ significantly from those of the original SC115 tumor grown in normal males or in castrated mice treated with high doses of androgen. On the other hand, the treatment with low doses of androgen alone induced the development of slowly growing spindle-shaped cells from the medullary SC115 cells. The spindle-shaped cells containing low levels of androgen receptor were shown to be androgen independent and were also induced from the SC115 cells in nontreated castrated mice. These findings demonstrated that low doses of androgen and estrogen synergize to maintain and increase the growth of SC115 cells, whereas low doses of androgen alone fail to maintain the SC115 cells.

Androgens↗
PubMed1985

Stimulative effect of physiological doses of androgen or pharmacological doses of estrogen on growth of Shionogi carcinoma 115 in mice.

It was generally accepted for 20 yr that the growth of Shionogi carcinoma 115 (SC115) is stimulated only by androgen. In the present study, the growth-stimulative effect of estrogen alone on SC115 tumors was examined in castrated mice. Daily injections of physiological doses of 17 beta-estradiol did not enhance the tumor growth. However, high doses of 17 beta-estradiol (10-100 micrograms/mouse/day) significantly stimulated the growth of tumors in a dose-dependent manner. Since high doses of diethylstilbestrol (10-50 micrograms/mouse/day), which does not bind to androgen receptor, could markedly stimulate the growth of tumors and since antiandrogen (cyproterone acetate) failed to inhibit the growth stimulation induced by high doses of 17 beta-estradiol, it is concluded that high doses of 17 beta-estradiol, which binds to androgen receptor with relatively low but significant affinity, enhance the tumor growth not via the androgen receptor system. The growth speed, histological type, content, and affinity of androgen, estrogen, and progesterone receptors and pattern of newly synthesized proteins labeled in vitro with [35S]methionine of tumors grown by high doses of estrogen were not significantly different from those of the original SC115 tumors grown in normal males. Furthermore, seed tumors from one to six generations grown by pharmacological doses of estrogen alone could rapidly grow only in normal males and not in castrated males. The present findings demonstrate that the growth of SC115 tumors in vivo is stimulated by physiological doses of androgen or pharmacological doses of estrogen.

Androgen Antagonists↗
PubMed1985

[A case of esophageal carcinoma with liver metastasis treated with cisplatin].

A patient with liver metastasis of esophageal carcinoma was treated with Cisplatin and showed complete response both in the esophageal region and liver metastasis. Combination chemotherapy using Cisplatin is now often employed against metastatic regions of epidermoid carcinoma of the esophagus, and shows certain degrees of response. Cisplatin is considered to be one of the most effective agents for the treatment of epidermoid carcinoma of the esophagus.

Carcinoma, Squamous Cell↗
PubMed1984

Proliferation of peritoneal mast cells in the skin of W/Wv mice that genetically lack mast cells.

Presence of mast cell precursors in the mouse peritoneal cavity was demonstrated, and the precursors were characterized. When a cell suspension, containing mast cell precursor(s), was directly injected into the skin of genetically mast cell-deficient WBB6F1 (WB X C57BL/6)-W/Wv mice, a cluster composed of approximately 2,000 mast cells appeared at the injection site. By determining the proportion of injection sites at which the mast cell cluster appeared, the concentration of mast cell precursors can be calculated by limiting dilution analysis. The concentration in the peritoneal cavity was about five times as great as the concentration in the bone marrow. Although peritoneal mast cell precursors were shown to originate from the bone marrow, physical characterization revealed that the peritoneal precursors differed from the marrow precursors. The peritoneal precursors were less susceptible to irradiation than the marrow precursors; the former were heavier than the latter. When a 95% pure mast cell suspension was prepared from the peritoneal cells by the removal of phagocytes and the density gradient centrifugation, 1 out of 16 cells had the potentiality to make a mast cell cluster in the skin of the W/Wv mice. Moreover, when a single mast cell was identified under the phase contrast microscope and picked up with the micromanipulator, 1 out of 17 mast cells made the cluster. This indicated that some peritoneal mast cells kept extensive proliferative potentiality even after morphological differentiation. In other words, some peritoneal mast cells themselves may function as the committed precursors.

Animals↗
PubMed1984

Isolation of HTLV derived from Japanese adult T-cell leukemia patients in human diploid fibroblast strain IMR90 and the biological characters of the infected cells.

HTLV was isolated in the human diploid fibroblast strain IMR90 directly from the leukemic cells of the Japanese ATL-patients. The infection was checked by the presence of virus-specific p24 and proviral DNA. The isolation was successful in three of four patients. The patient whose virus isolation was unsuccessful contained only a defective viral genome in his leukemic cells. The infected cells produced polykaryons when co-cultured with catS + L-cells. Human leukemia HL60 cells formed clusters adherent to the infected IMR90 cells but not to uninfected IMR90 cells. The former phenomenon was blocked by the ATLL patients' serum.

Cell Nucleus↗