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K Usuki

Publications and source records attributed to K Usuki.

68 records · Page 4Linked to original sources
PubMed1987

Constitutive expression of the granulocyte-macrophage colony-stimulating factor gene in human solid tumors.

We detected constitutive expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) gene in 3 human solid tumors by Northern blot analysis. Two of them were also found to secrete the GM-CSF protein by colony forming unit-culture assay. Southern blot analysis of each tumor DNA showed no gross rearrangement of the GM-CSF gene. This is the first report that demonstrates expression of the GM-CSF gene in solid tumors at the mRNA level.

Colony-Forming Units Assay↗
PubMed1984

Relative contribution of antiproliferative and host immunity-associated activity of mouse interferon in murine tumor therapy.

Administration of mouse interferon (IFN; 0.5 to 1 X 10(7) reference units/mg protein) inhibited the growth of Meth A and Meth 1 fibrosarcomas, but to a lesser extent, if at all, the growth of Colon 26 adenocarcinoma in BALB/c mice. The in vitro IFN sensitivity of these three tumors was not consistent with the in vivo therapeutic response in mice bearing these tumors under the present experimental conditions; Colon 26, the most sensitive of the three tumors in the in vitro antiproliferation test, did not respond or responded most poorly to IFN therapy; furthermore, Meth A and Meth 1 tumors responded similarly well to IFN therapy, although there was about a 100-fold difference in their in vitro IFN sensitivity. These results as well as the kinetic analysis of IFN concentrations of the serum of Meth A- or Colon 26-bearing mice did not indicate that the antiproliferative activity of IFN was solely responsible for its in vivo therapeutic effect. In contrast, abrogation of T-cell immunity by alpha mouse thymocyte globulin completely nullified the IFN-dependent therapeutic effect in Meth A-bearing mice. Furthermore, the IFN-dependent therapeutic response in Meth A tumors was much weaker in T-cell-defective BALB/c (nu/nu) mice than that in immunologically competent BALB/c (+/+) mice and was marginal, if present at all, confirming that T-cell immunity was involved in the IFN-dependent therapeutic effect and suggesting that the antiproliferative activity of IFN may only be responsible to a small extent for the therapeutic effect.

Animals↗
PubMed1984

[Pharmacokinetics of human fibroblast interferon in rats].

Pharmacokinetic behaviors of human fibroblast interferon (HuIFN-beta) administered intravenously to rats were examined. After intravenous injection, plasma interferon level decreased in a biexponential fashion having the half-times of 15 min and 120 min respectively. Distribution levels of HuIFN-beta in the tissues at 30 min, though the actual concentrations were less than that of plasma, were observed according to the following order; kidney greater than adrenal greater than lung greater than spleen greater than liver greater than testis. Small amounts of HuIFN-beta were also detected in the thoracic lymph and bile but no HuIFN-beta was found in urine. The in vitro study indicated that the stability of HuIFN-beta was different in each tissue homogenates and body fluids. From the results obtained, we concluded that HuIFN-beta exhibited a low distributional character to the tissues when administered intravenously. It was also suggested that the kidney and the liver were the main catabolic sites of HuIFN-beta.

Animals↗
PubMed1983

Host-mediated antitumor effect of interferon in nude mice transplanted with human tumor.

Mouse interferon (MuIFN) strongly suppressed the growth of human nasopharynx carcinoma (KB) transplanted into nude mice when given by subcutaneous injection around the tumor, though KB cells were insensitive not only to the antiproliferative activity of MuIFN, but also to natural killer (NK) activity in vitro. Moreover, the antitumor effect of MuIFN was not influenced by treatment with anti-asialo GM1, which eliminates NK activity in vivo. These results indicate that NK activity is not essential to the antitumor effect of IFN mediated by the host. Subcutaneous injection of MuIFN was more efficacious than intraperitoneal injection, suggesting the existence of regional tumor resistance of the host induced by IFN. The sera of mice treated with MuIFN showed no inhibitory activity on the growth of KB cells in vitro, indicating that no antiproliferative agent secondarily induced by IFN treatment is present in the serum. There was no difference between control and MuIFN-treated group in terms of the histology of tumor tissues in nude mice. An undefined host-dependent antitumor mechanism distinct from the proposed immune modulatory effect of IFN might be present.

Animals↗
PubMed1978

Chronic hypertension induced by streptozotocin in rats.

An intravenous injection of 40 or 65 mg/kg streptozotocin induced not only diabetes but also severe hypertension in rats. Whereas the hyperglycemia developed fully within a few days after the injection of streptozotocin, the hypertension progessively advanced and reached maximum level several weeks after the treatment and lasted more than 20 weeks. Twenty mg/kg streptozotocin did not induce hyperglycemia but significantly increased blood pressure several weeks after the treatment. Arrest of growth, polyuria, glycosuria, hyperlipemia and lenticular cataracts developed in the animals treated with 40 or 65 mg/kg streptozotocin, but in none of the animals treated with 20 mg/kg. In histological examinations in the 24th week after the treatment, degranulation and necrosis in the pancreatic beta-cells, and vacuolization and deposition of PAS-positive materials in the renal proximal tubules were found in the animals treated with 40 or 65 mg/kg streptozotocin.

Animals↗