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Biomedical subjects

K Hamada

Publications and source records attributed to K Hamada.

At least 487 records · Page 27Linked to original sources

In vitro studies of the mechanism of leukemogenesis. II. Characterization of endogenous murine leukemia viruses isolated from AKR thymic epithelial reticulum cell lines.

Thymic epithelial reticulum (TER) cell lines were established from thymuses of a young healthy AKR mouse (A2T), a preleukemic AKR mouse (A6T), and two lymphoma-bearing AKR/Ms mice (ASLT-1 and ASLT-2). Numerous type-C virus particles with occasional budding forms were observed in all cell lines. Expression of XC-detectable, N-tropic, ecotropic virus was observed in every cell line, whereas the presence of xenotropic and mink cell focus-inducing (MCF) viruses could be detected only in TER cells derived from preleukemic and leukemic mice. Expression of xenotropic virus in various cells of newborn and young AKR mice could readily be induced by IUdR treatment, whereas MCF virus was never detected in these cells, with the exception of the A2T cell line after more than 20 passages, in which MCF virus with dual-tropic infectivity emerged in addition to ecotropic and xenotropic viruses. These spontaneous and induced MCF viruses were purified, and their virological properties were characterized. The cloned MCF viruses (MCFs AT1, AT2, AT3, and AT4-IU) showed dual tropism and produced cytopathic effect-like foci in mink lung cells. Preinfection with either ecotropic or xenotropic virus interfered with the infectivity of MCF viruses. Spontaneous leukemogenesis in AKR mice was accelerated by the inoculation of MCF viruses. These findings indicate that TER cells could serve as the host cells for the genetic recombination of the endogenous MuLV; the recombinant MuLV, MCF virus, appears to be most closely associated with leukemogenesis in AKR mice.

AKR murine leukemia virus↗

Biological and immunological characterization of human luteinizing hormone discharged by the stimulation of synthetic luteinizing hormone-releasing hormone (LH-RH) in normal and anovulatory women.

Plasma samples were obtained by repeated venopunctures immediately before, and at 15, 30, 60, 120 and 180 min after intravenous bolus administration of 100 micrograms synthetic LH-RH in normal and various anovulatory women. Plasma hLH levels were determined by an in vitro bioassay and a radioimmunoassay with improved reagents. The LH-RH stimulation induced an abrupt elevation of both biological and immunological hLH activities in normal and anovulatory women, although the responsiveness to LH-RH differed from case to case. Both elevated biological and immunological hLH activities decreased gradually with a half disappearance time of 122.4 +/- 27.9 min and 112.5 +/- 25.4 min, respectively (Mean +/- S.D.). A transient and significant depression in the ratio of biological to immunological hLH activities (B/I ratio) was observed at 15 min after the LH-RH administration in normal subjects. This depression is attributable to the cross-contamination of an increased amount of hLH subunits induced by LH-RH stimulation. The B/I ratios were significantly elevated throughout the investigation period in the anovulatory patients when compared with those in the normal subjects. This elevation appears to indicate the increased discharge of special type(s) of hLH subpopulations of high biological potency in the anovulatory cases.

Adult↗

[Antitumor effects of aromatic retinoids (Ro 10-1670, Ro 10-9359) on the chemically-induced epithelial tumors].

Pathological and histochemical studies were made to clarify the response to an aromatic retinoids (Ro 10-1670, Ro 10-9359) of the papilloma and carcinoma in hamster cheek pouch and mouse dorsal skin. The sizes of papilloma and carcinoma were remarkably reduced or completely regressed following systemic and topical administration of the aromatic retinoids. The antitumor effects increased in proportion to the frequency of administration than doses and were showed no side effects. Tumor tissues responded remarkably to the aromatic retinoids indicated an irregular keratinization including loss of hornified cells, nuclear vacuolization and inflammatory infiltrates which located in the border layer between stromas and neoplastic epithelia. Histochemically, tumor tissues which intensely affected by drugs were characterized by the presence of abundant acid phosphatase active cells. Those acid phosphatase active cells may be consisted of tumor cells, histiocytes and fibroblasts. In the electrocytochemical study acid phosphatase (a lysosomal marker enzyme) activity was found in epithelial tumor cells and fibroblasts. These results were indicated that epithelial tumor regression by aromatic retinoids the might be due to the accelerated lysosomal activity in the tumor cells and fibroblasts.

9,10-Dimethyl-1,2-benzanthracene↗

Leukemogenicity and cell transformation mechanisms in vitro by Gross murine leukemia virus: analysis of virus subpopulations.

The leukemogenic activity of Gross murine leukemia virus adapted to rats was tested in W/Fu rats and NIH/Swiss mice. All animals infected with this virus developed thymic and nonthymic T-cell leukemia with a short latency period. It was observed that cell-free extracts from thymic lymphoma tissue of mice and rats, induced by either Gross murine leukemia virus or Gross murine leukemia virus adapted to rats, consisted of both small-plaque-forming and large-plaque-forming viruses, as determined by the XC plaque test. MCF-type virus was found in these virus complexes. Transformed cell foci were induced in SC-1 cell layers by double infection of the cloned MCF-type virus and an ecotropic virus. SC-1 cells containing transformed cell foci were shown to be tumorigenic upon inoculation into nude mice. The formation of transformed cell foci in mink lung cells was also observed after double infection with the cloned MCF-type virus and a xenotropic virus. The possible mechanism of leukemogenesis by endogenous viruses is discussed.

AKR murine leukemia virus↗

Mammary carcinogenic effect of low-dose fission radiation in Wistar/Furth rats and its dependency on prolactin.

The mammary carcinogenic effect in rats of low-dose fission radiation and its dependency on prolactin were studied. A total of 141 female W/Fu rats were exposed to 4.8, 8.9, or 19.5 rads of fission radiation that had both fision neutrons of 2.0 million electron volts (MeV) and gamma ray components similar to those produced by the Hiroshima bomb. Only 1 of 48 rats (2.0%) developed mammary tumor (MT) after irradiation alone, whereas 20 of 48 rats (41.6%) developed MT's if prolactin was supplied shortly after irradiation by means of grafting of the prolactin-secreting pituitary tumor. Furthermore, MT's occurred in 11 of 45 rats (24.4%) treated with prolactin as late as 12 months after irradiation, which suggested the long-term survival of radiation-induced dormant MT cells. A correlation was found between the development of MT and the elevation of serum prolactin level; most MT's appeared shortly after the grafted mammotropic pituitary tumor became palpable. The growth of MT's appeared to be promoted by prolactin in collaboration with ovarian hormones; the growth of adenocarcinomas was dependent on prolactin and ovarian hormones, whereas the growth of fibroadenomas appeared to be less hormone-dependent. Much higher biologic effectiveness, especially in the low-dose range, was found with 2.0-MeV fission neutrons compared with 14.1-MeV fast neutrons or 180-kilovolt peak X-rays in rat mammary carcinogenesis.

Adenocarcinoma↗

Sequential competitive enzyme immunoassay for human chorionic gonadotropin.

In the previous report, we had developed a simultaneous competitive enzyme immunoassay for hCG, using sheep red blood cells as the solid phase. The serum sample was not checked because of serum interference. In this report we have developed sequential competitive enzyme immunoassay. The sequential method is preferred because serum interference is removed and silicone rods are used as the solid phase instead of sheep red blood cells, which would be easily washed away in that procedure. The working range of this procedure is from 0.5 mIU/ml to 200 mIU/ml. That value for serum hCG correlates well with that by RIA (n = 0.904) Coefficients of variation are satisfied (14.2%: within assay and 15.2%: between assay).

Chorionic Gonadotropin↗