Search PubMed⌕ Search

Biomedical subjects

N Watanabe

Publications and source records attributed to N Watanabe.

At least 1,099 records · Page 61Linked to original sources
PubMed1986

[TNF induction in the serum and ascites of a gastric cancer patient treated with OK-432].

A 73-year-old female was diagnosed as having gastric cancer (undifferentiated adenocarcinoma), and received gastrojejunal anastomosis as an initial treatment. One year after the operation, she was readmitted to our hospital with the complaint of fullness in her stomach. Physical examination revealed a palpable mass in the epigastric region and ascites. An attempt to induce endogenous TNF was made using OK-432. Four doses of OK-432 (10 KE) were administered intraperitoneally every other day. Seven days after the last administration of OK-432 (10 KE), OK-432 (50 KE) was given at the same site to induce TNF. At 1.5h after the injection of OK-432 (50 KE), 20.8 U/ml and 8.1 U/ml of TNF activity could be detected respectively in the serum and ascites. This is the first report describing the induction of TNF in a cancer patient.

Adenocarcinoma↗
PubMed1985

Amperometric detection of reducing carbohydrates in high-performance liquid chromatography using an amino-bonded column and acetonitrile-water as the eluent.

Amperometric detection of reducing carbohydrates using copper bis(phenanthroline) as the mediator in the post-column reaction was applied to the partition mode of high-performance liquid chromatography using an amino-bonded column with acetonitrile-water as the eluent. The proposed method appears to be the most sensitive means of detection in the partition separation of carbohydrates. Glucose can be determined at levels down to 5 pmol (1 ng injection). Excellent selectivity was demonstrated in examples of chromatograms obtained with fruit juices and human urine.

Acetonitriles↗
PubMed1985

Adsorption and desorption of polydimethylsiloxane, PCBs, cadmium nitrate, copper sulfate, nickel sulfate and zinc nitrate by river surface sediments.

An investigation into the adsorption and desorption of polydimethylsiloxane, PCBs, cadmium nitrate, copper sulfate, nickel nitrate and zinc nitrate by river sediments was carried out using either a flow-through system or a semi-static system. The material balance in the sediment compartment could be explained by the equation, dCs/dT= K1Cw-K2Cs. The adsorption rate constants (K1), desorption rate constants (K2) and concentration factors (K1/K2) were calculated. For hydrophobic chemicals, the K1's were independent of water solubility, but the K2's were relatively related to water solubility. For both hydrophobic chemicals and heavy metals, the concentration factors per fraction organic carbon were similar to the soil sorption coefficients (Koc), expressed on a organic carbon basis.

Adsorption↗
PubMed1985

Production of cytotoxic factor into mouse peritoneal fluid by OK-432, a streptococcal preparation.

A cytotoxic factor was induced by the injection of LPS into the peritoneal fluids of mice which had been previously primed with a streptococcal antitumor preparation, OK-432. No cytotoxic effect on L-929 cells was observed in the peritoneal fluids of mice singly treated with OK-432 or LPS. Various mouse and human tumor cell lines were effectively killed by this peritoneal cytotoxic factor, though normal cell lines were insensitive, which indicates that this factor is not species-specific. The highest level of cytotoxic activity was obtained when LPS was given to mice 5 days after the injection of OK-432. The optimal time for collection of peritoneal fluids for the cytotoxic factor was 2 h following the LPS injection. Interferon activity was found to be negative by the plaque reduction test using L-929 cells with vesicular stomatitis virus. These results suggest that this cytotoxic factor is similar to the tumor necrosis factor (TNF) in the mouse serum.

Animals↗
PubMed1985

Inhibition of down regulation by chloroquine in cultured lymphocytes (RPMI-1788 line).

We studied the effect of chronic exposure to insulin on insulin receptors of cultured lymphocytes (RPMI-1788 line). The cells treated with insulin (2 micrograms/ml) at 37 degrees C for 12 h, showed a 36.5% decrease in the number of binding sites. Solubilized extract from the cells treated with insulin showed a 35.9% decrease of binding capacity, suggesting that insulin exposure induced the loss of total (cell surface and intracellular) receptors. Insulin-induced loss of receptors was blocked by chloroquine, suggesting that receptor loss is mediated by a chloroquine sensitive pathway. Bacitracin, which inhibited the insulin degradation, had no effect on insulin-induced receptor loss in this cell line. We also found that vitamin K5, one of the insulin mimickers, induced a 31.5% loss of insulin receptors. Therefore, the post-receptor process appeared to mediate down regulation. In cultured lymphocytes, insulin exposure caused a significant loss of total receptors, suggesting that insulin-induced receptor loss may be due to receptor degradation. Insulin-induced receptor loss is mediated by a chloroquine sensitive pathway, and is related to the post-binding process stimulated by vitamin K5.

Bacitracin↗
PubMed1985

The effects of Ba-wei-wan (hachimijiogan) on plasma levels of high density lipoprotein-cholesterol and lipoperoxide in aged individuals.

Ba-wei-wan was administered for 7 months to 24 aged, non-hospitalized subjects. Laboratory examinations showed an improvement in serum or plasma levels of total lipid, LPO and HDL-C. Other blood examinations were shown to be unaffected by the treatment. To reconfirm the effects of Ba-wei-wan on lipid metabolism, the three step administration of the drug was employed. The elevation of HDL-C levels and the decrease of LPO levels were obtained by this treatment. The discontinuation of this drug induced the converse effect on the plasma levels; decreased HDL-C and increased LPO. It could be concluded from these results that Ba-wei-wan administration improved the lipid metabolism in the aged subjects.

Aged↗
PubMed1985

Suppression of IgE antibody production after exposure to ozone in mice.

The effect of ozone exposure on IgE antibody production with aerosolized ovalbumin (OA) administration was investigated in Balb/c mice. Mice were continuously exposed to 0.8 ppm ozone for 1, 2, or 4 weeks, respectively, and subsequently aerosolized OA was administered through the respiratory tract for 6 min with a nebulizer. The mice were then immunized intraperitoneally 1 week later with OA. IgE antibody production was suppressed in ozone-exposed mice. However, no significant difference in the primary IgE antibody production by intraperitoneal immunization alone with OA was observed between ozone-exposed mice and nonexposed mice. In order to elucidate the suppressive mechanism of IgE antibody production, hapten-carrier antigenic system was used. It is shown that the induction of helper T cell function was suppressed if the aerosolized carrier protein was administered before intraperitoneal immunization in the mice exposed to ozone. These results suggest that ozone exposure has the effect on the stage of administration of inhaled antigen and the quite insignificant effect on the IgE antibody production after intraperitoneal immunization with OA.

Aerosols↗
PubMed1985

Preparation of antibodies to guinea pig IgE and its use for enzyme-linked immunosorbent assay of IgE antibodies.

Guinea pigs were infected with Trichinella spiralis. A pooled serum from the infected guinea pigs was fractionated by DEAE-cellulose column chromatography and Sephadex G-200 gel filtration. An IgE-rich fraction was injected into rabbits. The antiserum from the rabbits, after appropriate absorption with a normal guinea pig plasma, formed a precipitin line in immunoelectrophoresis and in immunodiffusion against a guinea pig serum containing IgE antibodies to ovalbumin. Uptake of 125I ovalbumin was observed in radioimmunoelectrophoresis. This anti IgE could be used in enzyme-linked immunosorbent assay of IgE antibodies to ovalbumin.

Animals↗
PubMed1985

Prolonged disappearance rate of a structurally abnormal mutant insulin from the circulation in humans.

The first mutant insulin, [LeuB25]insulin, was semisynthesized, and its disappearance rate from the circulation was measured. Three micrograms of normal human or [LeuB25] insulin per kg were administered to three normal subjects. The half-lives of normal insulin and the mutant insulin were 4.5 and 24 min, respectively. The decrement in blood glucose levels after injection of mutant insulin was 22.6% that after injection of normal insulin. The blood glucose-lowering effect of the mutant insulin, evaluated by the time required to reach the nadir, was slightly prolonged (30 vs. 45 min). These results indicate that hyperinsulinemia in patients with abnormal insulin is due to prolonged disappearance because of decreased receptor binding.

Adipose Tissue↗
PubMed1985

Estimation of antistreptococcal esterase in rheumatic fever and rheumatic heart disease.

In hemolytic streptococcal infection, a high ASE value in the absence of a rise in ASO has shown to occasionally occur. The relationship between ASO and ASE titers in rheumatic fever and rheumatic heart disease and the significance of these values was therefore studied. ASE values were measured by ASE Kit "Marupi" in 8 patients during the acute stage of rheumatic fever and in 9 patients with rheumatic heart disease, and then compared with the corresponding ASO values. Among the patients with rheumatic fever, a rise of ASO only was seen in 1 patient and a rise of ASE only was seen in another. In the remaining 6 patients, both ASE and ASO were elevated. Only in 1 patient with rheumatic heart disease was ASE found to be elevated.

Adolescent↗
PubMed1985

In vivo and in vitro effect of p-chlorophenoxyisobutyrate on insulin binding and glucose transport in isolated rat adipocytes.

We studied the in vivo and in vitro effect of p-chlorophenoxyisobutyrate (CPIB) on insulin binding and glucose transport in isolated rat adipocytes. In the in vitro study, adipocytes were incubated with 1mM of CPIB for 2 h at 37 degrees C, pH 7.4, and then insulin binding (37 degrees C, 60 min) and 3-0-methylglucose transport (37 degrees C, 2s) were measured. Incubation with CPIB did not affect either insulin binding or glucose transport in the cells. The addition of insulin (10 ng/ml) with CPIB to the incubation media also did not affect the following insulin binding and glucose transport. In the in vivo study, rats were fed a high sucrose-diet containing 0.25% CPIB for 7 days. Serum cholesterol, plasma free fatty acid, and insulin levels were significantly decreased in the CPIB-treated rats. The treated rats demonstrated an almost 2 fold increased maximal binding capacity for insulin (189,000 sites/cell for treated vs 123,000 sites/cell for control cells). Basal glucose transport (glucose transport in the absence of insulin) significantly decreased in the CPIB-treated rats, although insulin-stimulated glucose transport was comparable in treated and control cells. Thus, CPIB might have no direct effect on glucose transport and insulin binding, as determined by the in vitro studies. Furthermore, a relatively short-term in vivo treatment with CPIB, such as 7 days, did not stimulate glucose transport.

3-O-Methylglucose↗
PubMed1985

Characterization of a specific insulin-like growth factor-I/somatomedin-C receptor on high density, primary monolayer cultures of bovine articular chondrocytes: regulation of receptor concentration by somatomedin, insulin and growth hormone.

In order to obtain a phenotypically stable cell population of chondrocytes, high density primary monolayer cultures of bovine articular chondrocytes were established. Using these cultures, a specific insulin-like growth factor-I/somatomedin-C (IGF-I/SM-C) receptor was demonstrated and characterized. At 15 degrees C steady-state binding was attained by 5 h, and averaged 25% per 2.2 X 10(6) cells. Fifty per cent displacement of 125I-labelled IGF-I/SM-C by unlabelled IGF-I/SM-C occurred at concentrations of only 2.3 ng/ml, whereas IGF-II and porcine insulin were approximately 15- and 1000-fold less potent respectively. Scatchard analysis gave a linear plot, with a calculated association constant of 2.26 X 10(9) l/mol and a receptor number of 15 400 sites per cell. Preincubation of chondrocyte monolayers with either IGF-I SM-C or porcine insulin at 37 degrees C for 20 h resulted in reduction of 125I-labelled IGF-I/SM-C binding in a dose-dependent manner, although higher concentrations were required with insulin. More than 40% down-regulation of the receptor occurred with IGF-I/SM-C at concentrations of 10 nmol/l and nearly 70% reduction at 50 nmol/l. Interestingly, after preincubation with either human (h) or bovine (b) GH, 40% down-regulation of 125I-labelled IGF-I/SM-C binding was observed at concentrations of 10 mumol/l. Local production of IGF-I/SM-C by chondrocytes in response to GH stimulation may have occurred, but, because only 120 pmol IGF-I/SM-C and less than 30 pmol IGF-I/SM-C per litre were recovered from serum-free conditioned media preincubated with bGH and hGH respectively, this was not established.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Decreased biologic activity and degradation of human [SerB24]-insulin, a second mutant insulin.

A second mutant insulin, identified as [SerB24]-insulin, has a highly hydrophilic character. To determine the biologic activity and the degradation of this mutant insulin, human [SerB24]- and [SerB25]-insulin analogues were semisynthesized from porcine insulin by an enzyme-assisted coupling method. All of the following studies on isolated rat adipocytes were performed at 37 degrees C to directly correlate the binding potency and the biologic activity. The ability of these insulins to displace 125I-porcine insulin bound to adipocytes was 0.5-2% and 1-4%, respectively, of porcine insulin. When the ability of these insulins to stimulate glucose transport and glucose oxidation was measured, both analogues had full activity at high concentrations (250 ng/ml). However, ED50 of the porcine, [SerB24]-, and [SerB25]-insulins to stimulate glucose transport was 0.37 +/- 0.05, 46.3 +/- 5.4, and 23.3 +/- 5.5 ng/ml, respectively. Similarly, for glucose oxidation, ED50 was 0.38 +/- 0.06, 33.8 +/- 3.6, and 16.6 +/- 3.4 ng/ml, respectively. Thus, the biologic activity of [SerB24]- and [SerB25]-insulins was reduced to 0.5-2% and 1-4% of that of porcine insulin, which was compatible with our previous studies under different conditions. No antagonistic effects were observed for either analogue. Degradation of 125I-labeled [SerB24]- and [SerB25]-insulins was also decreased to 62.8% and 55.8%, respectively, of 125I-porcine insulin. These results confirm the importance of the hydrophobic residues at B24 and B25 in the biologic activity of insulin; the patient having this hydrophilic insulin was considered to be in an insulinopenic state despite the hyperinsulinemia due to decreased degradation of the mutant insulin.

Adipose Tissue↗