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Biomedical subjects

N Uchida

Publications and source records attributed to N Uchida.

At least 217 records · Page 12Linked to original sources
PubMed1987

Development of cartilage-like tissue from androgen-dependent Shionogi carcinoma 115 in androgen-depleted hosts.

Androgen-dependent Shionogi carcinoma 115 (SC115) is an undifferentiated medullary carcinoma showing a compact cell pattern. When SC115 was inoculated into castrated DS mice, slowly growing tumors containing cartilage-like tissue developed. The cartilage-like tissue showed close similarities in electron microscopical and histochemical features to normal cartilage tissue. The origin of the cartilage-like cells was investigated by using the electrophoretic pattern of 3-phosphoglycerate kinase (PGK, EC 2.7.2.3) as a marker. The original DS strain had B-type PGK, but we developed a congenic strain with A-type PGK. The SC115 tumor, which had B-type PGK, was grafted into castrated congenic mice with A-type PGK. The cartilage-like tissue that developed was divided into two parts; one part was used for PGK analysis and the other for histological examination. All histologically confirmed cartilage-like tissues had only B-type PGK, suggesting that SC115 cells may change into cartilage-like cells in androgen-depleted conditions.

Androgens↗
PubMed1987

Both androgen and glucocorticoid induce identical secretory proteins in serum-free culture of Shionogi carcinoma 115 cells.

The effects of androgen or glucocorticoid on the induction of secretory proteins in SC-3 cells (a cloned cell line from Shionogi carcinoma 115) were examined in a serum-free medium [Ham's F-12: Eagle's minimum essential medium (1:1, v/v) containing 0.1% bovine serum albumin]. Through analysis of [35S]methionine-labeled proteins by one-dimensional (sodium dodecyl sulfate polyacrylamide) gel electrophoresis, we successfully demonstrated the production of a testosterone (10(-9)-10(-6) M)- or dexamethasone (10(-8) M)-induced secretory protein with a molecular weight of 24,000 in SC-3 cells. However, 17 beta-estradiol (10(-8) M) or progesterone (10(-8) M) had no such effect. The production of the secretory 24K protein increased slightly within 2 hr after the addition of 10(-8) M testosterone and increased further thereafter. The addition of tunicamycin to the incubation mixture with [35S]methionine resulted in the identification of a testosterone- or dexamethasone-induced secretory protein with a molecular weight of 20,000. By the use of two-dimensional gel electrophoresis, we could demonstrate that both testosterone (10(-8) M) and dexamethasone (10(-8) M) added to the serum-free medium stimulate the secretion from SC-3 cells of the same 5 proteins (30-40K, 39K, 30K, 27K proteins and the secretory 24K glycoprotein). The present findings show that physiological concentrations of both androgen and glucocorticoid induce the secretion of the same 5 proteins from SC-3 cells.

Animals↗
PubMed1987

[Absorption of 5-FU orally administered in a patient with postoperative gastric cancer under artificial dialysis].

A patient under artificial dialysis due to chronic renal failure suffered from gastric cancer concurrently. This patient underwent subtotal gastrectomy followed by consecutive oral administration of 5-FU (tablets) as a postoperative adjuvant chemotherapy. The 5-FU level in the peripheral blood on oral administration at 50 mg remained at 0.007-0.01 microgram/ml over 2 hours. This feature of 5-FU blood level is not seen in gastric cancer patients with normal renal functions on administration of 5-FU tablets, and it seems to approximate the features of a 5-FU prodrug level in the blood upon oral administration. Neither the influence of dialysis on the absorption of orally administered 5-FU nor side effects caused by 5-FU were observed. The above findings suggest that it may be possible to maintain a certain blood level of 5-FU and to perform adjuvant chemotherapy even in cancer patients under artificial dialysis, as long as the dose is controlled carefully.

Administration, Oral↗
PubMed1986

High efficiency gene transfer into murine T cell clones using a retroviral vector.

To establish a gene transfer and expression system for murine T cell clones, we have introduced the neomycin phosphotransferase gene encoding resistance to the neomycin analogue, G418, into non-neoplastic inducer T cell clones by using a replication-defective retroviral vector. This method allowed highly efficient gene transfer (20 to 40%) into two inducer T cell clones. The level of viral RNA expression in G418r T cells was 0.1% of poly(A)+ RNA. The infected G418r cells retained physiologic responsiveness to specific antigen as judged by antigen-specific proliferation and production of IL 3.

Animals↗
PubMed1985

Break of unresponsiveness of delayed-type hypersensitivity to sheep red blood cells by pertussis toxin.

Effects of pertussis toxin (PT) on the unresponsiveness of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) were examined in mice. DTH cannot be detected in mice injected iv with 1 X 10(9) SRBC. This unresponsive state was broken by 1 microgram of PT given iv to mice 1 or more days, even 21 days, after SRBC-injection and replaced by the development of high and persistent DTH responses with several days' lag after PT treatment. The restored DTH response was accompanied by the appearance of circulating DTH-mediating cells. In the non-PT-treated mice, DTH-mediating cells, which conferred DTH in syngeneic naive recipient mice by systemic transfer, were found in the spleen but not in the blood, whereas in the PT-treated mice, they were found both in the spleen and in the blood. On the other hand, the induction or the function of splenic suppressor T cells (Ts) for DTH in mice injected iv with 10(9) SRBC was inhibited by PT treatment. DTH-Ts, which appeared in the spleen around 4 days after SRBC injection and inhibited the induction of DTH response to SRBC in the syngeneic cyclophosphamide-pretreated recipient mice, failed to be induced in mice given PT 1 day after SRBC injection, and their ability was reduced when they were treated in vitro with PT immediately before transfer. These results demonstrate the possibilities that the reinforced migration of DTH-mediating cells from spleen to blood by PT is involved in the mechanisms by which PT break the unresponsiveness of DTH and that the interference with the induction or the function of DTH-Ts by PT may also be partly involved in the mechanisms.

Animals↗
PubMed1985

Urinary retention induced by estrogen injections in mice: an analytical model.

Daily subcutaneous injections of pharmacological doses of 17 beta-estradiol (E2, 0.4 micrograms./gm. body weight) resulted in significant urinary retention in the bladder of castrated mice. Although the urinary retention developed in both male and female mice, the increase in urethral resistance to urinary flow and the dilatation of posterior urethra were observed only in castrated male mice receiving E2. Histological changes common to male and female mice were cornification and stratification of urethral epithelium and fibrosis of connective tissues surrounding the urethra, suggesting that these changes may cause the urinary retention. Although the exact mechanism has not been defined, the urinary retention produced by the present method may be useful as a model of human disease.

Animals↗
PubMed1985

Gene structures of low-neurovirulent vaccinia virus LC16m0, LC16m8, and their Lister original (LO) strains.

Vaccinia viruses LC16m0 and LC16m8 are temperature-sensitive and low-neurovirulent variants derived from the Lister (Elstree) (LO) strain. Analyses of genome DNAs by digestion with restriction endonucleases and cross-hybridization of the digested fragments revealed that LC16m0 and LC16m8 possess a new XhoI site in addition to the 14 XhoI sites of LO. This new site is located at about 12 X 10(6) daltons from the right terminal end. There was no significant difference in the genome structures between the LC16 variants and LO except the new XhoI site and their terminal fragments which were not identified in LO owing to their heterogeneity. With HindIII digested fragments, there was no difference among the three viruses. This complete mapping raised the possibility that the putative gene responsible for temperature sensitivity and neurovirulence is located at the region of the XhoI site found in LC16m0 and LC16m8.

Cloning, Molecular↗
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↗
PubMed1984

Effects of pertussis toxin (PT) on T-cell populations sensitized for delayed-type hypersensitivity in mice.

Effects of pertussis toxin (PT) on sensitized T-cell populations for delayed-type hypersensitivity (DTH) were examined in mice. DTH was induced by sensitizing mice with ovalbumin (OA) and elicited by injecting OA into the footpad. DTH could be conferred on naive recipient mice by injecting sensitized spleen cells either intravenously into mice or locally into the footpad. When the sensitized mice were given PT at the time of DTH-elicitation, they did not express a high DTH reaction, with the maximum reaction 24 hr after elicitation. When the recipient mice were given PT just before intravenous injection of sensitized spleen cells, DTH was not conferred. In addition, when the sensitized spleen cells were treated with PT in vitro and then transferred intravenously, DTH was not conferred in recipient mice. However, DTH was conferred by local transfer of the sensitized spleen cells even after treatment with PT in vitro. Migration experiments using 51Cr-labeled, sensitized splenic T cells demonstrated that PT treatment of the T-cell population inhibited its accumulation in the DTH reaction site 24 hr after intravenous transfer. On the other hand, experiments on in vitro lymphokine production by the sensitized splenic T cells demonstrated that the PT treatment did not inhibit antigen-dependent production of a macrophage activating factor (MAF). These results suggest that PT suppresses the migration of the sensitized T-cell population from the circulation of the DTH reaction site but not their MAF production. Based on these findings, possible mechanisms by which PT affects DTH are discussed.

Adjuvants, Immunologic↗