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S Kataoka

Publications and source records attributed to S Kataoka.

At least 91 records · Page 5Linked to original sources

High-molecular-weight hyaluronic acids inhibit chemotaxis and phagocytosis but not lysosomal enzyme release induced by receptor-mediated stimulations in guinea pig phagocytes.

The effects of high-molecular-weight (HMW) hyaluronic acids (HAs) of 1.9 x 10(6) Da, 8 x 10(5) Da and 3 x 10(5) Da on the receptor-mediated functions of guinea pig peritoneal phagocytes were studied. HMW-HAs of 1.9 x 10(6) Da (HA190) and 8 x 10(5) Da (HA80) effectively inhibited the chemotactic activity of polymorphonuclear leukocytes (PMNs) for formyl-Met-Leu-Phe (fMLP). The degree of inhibition was dose-dependent and the concentrations of HA190 and HA80 required for 50% inhibition were 0.5-1.5 mg/ml and 1.5-2.5 mg/ml, respectively. HMW-HA of 3 x 10(5) Da (HA30) hardly affected the chemotaxis within a concentration range of 0.5-5.0 mg/ml. The phagocytic activities of PMNs and macrophages (Mphis) for serum-opsonized zymosan (SOZ) and polystyrene latex particles were also inhibited by these HAs in a dose- and molecular-weight-dependent manner and HA190 was again the most inhibitory. By contrast, the release of lysosomal enzyme from Mphis stimulated with SOZ was not significantly affected by HMW-HAs at any concentration used. Furthermore, the binding of [3H]fMLP with PMNs and the rosette formation of Mphis with SOZ were not influenced by the presence of HMW-HAs. These findings suggested that the binding of HMW-HAs to the HA receptors on PMNs and M phi s might produce certain intracellular signals which would be responsible for the suppression of the chemotaxis and the phagocytosis but not for the release of lysosomal enzyme. For the generation of such signals, higher-molecular-weight HMW-HAs would be more effective than lower one.

Animals↗

A novel method for concentrating urinary type IV collagen based on precipitation with polyethylene glycol: application to its measurement by enzyme immunoassay.

We investigated the efficacy of polyethylene glycol (PEG) for effective and reproducible concentration of urinary type IV collagen prior to measurement by enzyme immunoassay (EIA). Human placental type IV collagen at low concentrations (5 and 10 micrograms/L) and urinary type IV collagen were readily precipitated by PEG-4000 added at a concentration of about 150 g/L in the presence of 0.5 g/L gamma-globulin. Type IV collagen measurement by EIA from PEG-concentrated urine samples showed complete recovery and good reproducibility. Analysis of size distribution by Sephacryl S-300HR gel chromatography and Western blotting following polyacrylamide gel electrophoresis confirmed that type IV collagen in PEG-concentrated urine samples was of high molecular weight comparable to that of human placental type IV collagen. After PEG concentration, type IV collagen was detectable by EIA even in the urine of healthy subjects. Significantly higher concentrations of urinary type IV collagen were found in 30 diabetic patients with nephropathy than in 20 healthy subjects [99.5 (8.9) micrograms/L, mean (SEM) versus 21.4 (2.6) micrograms/L, P < 0.0001]. Thus, urinary type IV collagen can be measured effectively by EIA following concentration with PEG. This method has potential for the assessment of the progression of diabetic nephropathy.

Adult↗

Antitumor activity of a spicamycin derivative, KRN5500, and its active metabolite in tumor cells.

KRN5500, (6-[4-Deoxy-4-(2E,4E)-tetradecadienoylglycyl]amino-L-glycero - beta-L-mannoheptopyranosyl]amino-9H-purine), was semi-synthesized in an attempt to increase the therapeutic effects of spicamycin analogues. The present study evaluated the antitumor activity of KRN5500 against murine tumors and human tumor xenografts. KRN5500 prolonged the survival of P388 leukemia- and B16 melanoma-bearing mice but was marginally effective on colon adenocarcinoma 26. The antitumor activity of KRN5500 (4 mg/kg/day x 5, IV) against xenografts of 10 human stomach, 14 colon and 2 esophageal cancers was evaluated with two parameters: the tumor growth inhibition rate (TGIR) and the tumor mass reduction by comparison with mitomycin C (MMC, 6.7 mg/kg/day x 1,IV). KRN5500 showed a marked efficacy in the human tumor xenograft model. The overall response rate of 26 cancers to KRN5500, evaluated by TGIR, was approximately equal to their response rate to MMC (72% vs. 73%). However, more tumors were reduced by KRN5500 than by MMC (52% vs. 39%). It is notable that the response rates of 14 colon cancers to KRN5500 were significantly higher than those to MMC, both in TGIR (69% vs. 58%) and in tumor mass reduction (46% vs. 23%). Among the tumors sensitive to KRN5500, COL-1 showed a marked response (TGIR 93%) and a significant reduction in tumor mass (0.22-fold the starting volume). In the mode of action, KRN5500 was found to show an inhibitory effect on protein synthesis in P388 cells (IC50 1.5 microM). However, KRN5500 was ineffective even at 170 microM in inhibition of protein synthesis in rabbit reticulocyte lysates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Simplified isoelectric focusing/immunoblotting determination of apoprotein E phenotype.

We developed a rapid, accurate method for phenotyping apoprotein E that can be used for large-scale population studies. In this method, adapted from the method of Kamboh et al. (J Lipid Res 1988;29:1535-43), 10-microL plasma samples are incubated with dithiothreitol and Tween-20 for 15 min and then applied to 5% polyacrylamide gels containing ampholyte (pH 4.5-8) and urea (3 mol/L). After 2 h of isoelectric focusing, the apoprotein E bands are made visible by immunoblotting. Utilizing whole plasma, this method does not require time-consuming ultracentrifugation, delipidation of samples, or dialysis. Small amounts of plasma are required, electrofocusing time is short, and as many as 160 samples can be processed per day. Identification of phenotype is easily accomplished by noting the location and number of protein bands instead of their intensity. Because identification of phenotype is not affected by sialylation, neuraminidase treatment is not necessary. Agreement in identification of 301 individuals from blinded duplicates was 96%, and there was 98% concordance of results for 431 samples that had undergone genetic typing. This method is thus well suited for large-scale population studies.

Apolipoproteins E↗

Apoptosis of T lymphoma cells and its inhibition by monoclonal antibodies against cell surface adhesion molecules.

We previously established the malignant T lymphoma CS-21 cell line from a spontaneously developed lymphoma in a BALB/c mouse. CS-21 cells produce lymph node metastasis with a high incidence following s.c. injection. CS-21 lymphoma cells grew continuously when the cells were co-cultured under the cell-cell attached conditions with stromal cells prepared from lymph nodes. However, they were unable to proliferate by themselves and underwent apoptosis when separated from the lymph node stromal cells. To identify the cell adhesion molecules of CS-21, we developed monoclonal antibodies (mAbs) directed against CS-21 cell-surface proteins. Fourteen mAbs partially inhibited the binding of CS-21 cells to a CA-12 stromal cell monolayer. MCS-5 (mAb against CS-21 No. 5) directed against a 168-kDa cell-membrane protein and MCS-19 against a 23-kDa protein were found to suppress apoptosis and stimulate CS-21 cell growth. Soluble factors secreted from CA-12 stromal cells enhanced CS-21 cell growth but were not sufficient to prevent apoptosis. In the presence of both stromal cell-secreted factors and mAbs MCS-5 or MCS-19, CS-21 lymphoma cells resisted apoptosis and grew as quickly as in the co-culture with CA-12 stromal cells. Based on these results, we conclude that CA-12 lymph node stromal cells support CS-21 lymphoma cell growth by secreting paracrine growth factors and presenting receptors for the 168-kDa and 23-kDa cell surface adhesion molecules of CS-21 cells that transmit signals to prevent CS-21 cell apoptosis.

Animals↗

Suppression of T-lymphoma cell apoptosis by monoclonal antibodies raised against cell surface adhesion molecules.

We have previously established a mouse malignant T-lymphoma CS-21 cell line that preferentially metastasizes to lymph nodes after s.c. inoculation into BALB/c mice. The CS-21 lymphoma cells were grown in vitro in the presence of CA-12 stromal cells isolated from lymph nodes. When CS-21 cells were cultured alone, they underwent apoptotic cell death with DNA fragmentation. In contrast, the culture of CS-21 cells attached to a monolayer of CA-12 stromal cells prevented CS-21 cell apoptosis and enhanced cell proliferation. To identify the cell adhesion molecules, we developed monoclonal antibodies (mAbs) directed against CS-21 cell surface proteins. Fourteen mAbs partially inhibited the binding of CS-21 cells to a CA-12 stromal cell monolayer. MCS-5 (mAb against CS-21 No. 5) directed against a M(r) 168,000 cell membrane protein and MCS-19 against a M(r) 23,000 protein were found to suppress apoptosis and to stimulate CS-21 cell growth. Soluble factors secreted from CA-12 stromal cells enhanced CS-21 cell growth but were not sufficient to prevent apoptosis. In the presence of both stromal cell-secreted factors and mAbs MCS-5 or MCS-19, CS-21 lymphoma cells evaded apoptosis and grew as fast as in the coculture with CA-12 stromal cells. Because of these results, we conclude that CA-12 lymph node stromal cells support CS-21 lymphoma cell growth by secreting paracrine growth factors and by presenting receptors for the M(r) 168,000 and M(r) 23,000 cell surface adhesion molecules of CS-21 cells that transmit signals to prevent CS-21 cell apoptosis.

Animals↗

Control of apoptosis and growth of malignant T lymphoma cells by lymph node stromal cells.

We have previously established the malignant T lymphoma CS-21 cell line from a spontaneous lymphoma in a BALB/c mouse. CS-21 lymphoma cells grew continuously when they were cocultured with stromal CA-12 cells prepared from lymph nodes. CS-21 lymphoma cells, however, could not proliferate by themselves, and they underwent apoptosis when separated from the stromal CA-12 cells. Apoptosis of CS-21 lymphoma cells was determined by observation of morphological changes using a transmission electron microscope and also by detection of nuclear DNA degradative fragments of oligonucleosomal size. Stromal CA-12 cells secreted soluble factors that enhanced DNA synthesis in CS-21 lymphoma cells. The soluble factors, however, were not sufficient to prevent apoptosis of CS-21 cells. Apoptosis of CS-21 lymphoma cells was suppressed only when the CS-21 lymphoma cells were cocultured with substantial numbers of CA-12 cells. The results suggest that the lymph node stromal CA-12 cells played an important role in the growth of CS-21 lymphoma cells by providing at least two different signals. One signal prevented CS-21 cells from apoptotic cell death by direct cell-to-cell contact, and the other signal enhanced the CS-21 cell proliferation by secreted soluble factors.

Animals↗

The chemoluminescence response of human polymorphonuclear leukocytes to Escherichia coli O and K antigens.

The interactions between Escherichia coli O or K antigens and polymorphonuclear leukocyte function were studied. Five types of O antigen and three types of K antigen were extracted from E. coli. These included O1, O6, O75 and K1 antigens from pyelonephritopathogenic strains, O44 and K74 antigens from an enteropathogenic strain and O14 and K7 antigen from a standard strain. The antigens all reacted specifically to their specific antisera and no cross-reactions were observed. The O1 or O44 antigen stimulated a significantly greater chemoluminescence response in polymorphonuclear leukocytes obtained from normal volunteers than O75, O6 or O14 antigen. In addition, the K1 or K74 antigen stimulated polymorphonuclear leukocytes significantly more than K7 antigen. These results suggest that pyelonephritopathogenic or enteropathogenic E. coli may produce severe tissue damage as a result of the response to their O or K antigens, as well as via adhesive agents such as pyelonephritopathogenic P-pili or the enteroadhesive factor, and exotoxins such as hemolysin or verotoxin.

Antigens, Bacterial↗

[Clinical results of radical surgery for prostate cancer].

We reported the clinical results of radical surgeries for 44 patients with prostate cancer performed between November 1984 and December 1992. The patients were aged from 57 to 79-year-old (mean 67.2) and classified as clinical stage A2 (6 cases), B1 (7), B2 (12), C (16) and D1 (3) respectively. Radical prostatectomy was performed in 42 cases and radical cystoprostatectomy with urinary diversion in 2 patients, and thirty-nine of 44 cases underwent endocrine or chemoendocrine therapies prior to the surgeries. In all patients with stage A2-B1, the operations were curative, on the other hand, more than 80% of clinical stage B2 patients had pT3 tumors and 33.3% of them had lymph node involvements. With regard to stage C patients, the incidence of lymph node metastasis and positive margin was more frequent. Postoperative adjuvant therapies were added to the patients with pT3,4 tumors and nodal involvements. Patients without residual tumors (n = 20) remained disease-free for 8-89 months (mean 32.8). Of 24 patients who had incomplete resection of tumors, 2 died of other diseases, other 2 were alive recurrent and 20 were alive free from disease for 3-99 months (mean 33.8). The surgical indication for low-stage (A2-B2) prostate cancer has been widely accepted, however that for high-stage cancer (C,D1) has remained controversial. It was our belief that radical surgeries for high-stage cancer could become a potentially curative therapeutic modality in combination with pre- and post-operative adjuvant therapies.

Aged↗

[Lymphatic metastasis and cell adhesion, growth and growth inhibition].

Malignant tumor cells often metastasize to regional and distant lymph nodes. The mechanisms of lymphatic metastasis, however, have not been well understood. To investigate these mechanisms, we used mouse CS-21 malignant T lymphoma cells which form tumors at subcutaneous sites and metastasize to lymph nodes with a high incidence. In contrast, CS-21 cells do not metastasize to other organs following intravenous injection. CS-21 lymphoma cells continuously grew in vitro when the cells were cocultured with CA-12 stromal cells isolated from lymph nodes. However, when CS-21 cells were separated from the stromal cells, they underwent apoptosis which was characterized by nucleus condensation and DNA fragmentation. We have developed monoclonal antibodies against CS-21 cell surface molecules by intrasplenic injection of the cell membranes. Several clones of monoclonal antibodies were able to partially inhibit adhesion of CS-21 cells to a monolayer of CA-12 stromal cells. Treatment of CS-21 cells with the monoclonal antibodies which specifically bind to the cell surface components of M(r) -168K and -23K prevented the apoptosis of CS-21 cells after separation from the stromal cells. In the experiments using Transwell chambers we found that the growth of CS-21 cells was also supported by soluble factors secreted from CA-12 stromal cells. The secreted factors were, however, not sufficient to prevent CS-21 cell apoptosis. The result suggested that the stromal cells of lymph nodes play an important role in lymphatic metastasis of CS-21 lymphoma cells by cell-cell adhesion and secretion of soluble factors that prevent apoptosis of lymphoma cells and enhance their growth in concert.

Animals↗

Neutrophil priming by granulocyte colony stimulating factor and its modulation by protein kinase inhibitors.

Upon stimulation by various ligands, freshly isolated human peripheral neutrophils (PMN) respond in a variety of ways, such as superoxide (O2-.) generation, phagocytosis enzyme release, migration etc. Chemotactic peptide formylmethionyl-leucyl-phenylalanine (FMLP) and opsonized zymosan activate neutrophils by a receptor-mediated mechanism, while phorbol myristate acetate and dioctanoylglycerol activate the cells by a mechanism involving Ca(2+)-and phospholipid-dependent protein kinase (PKC). Receptor-mediated but not PKC-mediated O2-. generation in PMN was enhanced by the priming of recombinant human granulocyte colony stimulating factor (G-CSF). FMLP-dependent luminol chemiluminescence was also enhanced by G-CSF. However, no appreciable enhancement was observed in FMLP-induced intracellular calcium ion concentration ([Ca2+]i). Enhancement of FMLP-induced generation of O2-. by G-CSF was inhibited by genistein or alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamide (ST 638), inhibitors of tyrosine kinase (TK), and was stimulated by staurosporine and 1-(5-isoquinolinesulfonyl)-3-methyl-piperazine (H-7), inhibitors of PKC. The ED50 values of genistein and ST 638 for the inhibition of the FMLP-induced O2-. generation from G-CSF were 0.5 and 5 microM, respectively. In contrast, O2-. generation by PKC activation without G-CSF priming was inhibited by stauroporine and H-7, but was stimulated by genistein and ST 638. These results suggested that the enhancing effect of G-CSF on receptor-mediated generation of the O2-. might be regulated by protein kinases, such as TK and PKC, and that the TK inhibitor selectively inhibited the G-CSF-primed receptor-mediated O2-. generation of neutrophils.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Increased receptor binding of low-density lipoprotein from individuals consuming a high-carbohydrate, low-saturated-fat diet.

The substitution of saturated fat by complex carbohydrate, according to current dietary recommendations, results in a decrease of plasma and low-density lipoprotein (LDL) cholesterol levels. To determine whether this decrease might result from structural and thus functional changes in LDL particles, the binding internalization and degradation of 125I-LDL were measured using TR715-19 cells, a mutant CHO line into which has been transfected the human LDL receptor, and in which measurements of binding are highly reproducible. Eleven nondiabetic subjects (35 +/- 4 years, 27% +/- 3% body fat) were studied after they had 15% protein, and 560 mg cholesterol/d and the other containing 21% fat (6% saturated), 65% carbohydrate, 14% protein, and 524 mg cholesterol/d.LDL cholesterol levels decreased form 125 +/- 6 to 108 +/- 5 mg/dl (P < .01) on the high-carbohydrate diet. There was an increase in the binding affinity of LDL (Kd 6.6 +/- 2.6 v 7.3 +/- 2.7 micrograms/mL +/- SD; P < .02), and internalization (P < .10), and degradation (P < .05) were also higher. The data suggest that decreasing dietary saturated fat may cause alterations in LDL composition that result in increased receptor clearance; this may partially explain the LDL-decreasing effect of this dietary change.

Adult↗

Effect of adenosine 3',5'-cyclic monophosphate derivatives on acute liver injury induced by carbon tetrachloride.

The inhibitory effects of 12 synthetic N6-alkyl cAMPs, 8-substituted cAMPs and cAMP alkylphosphoramidate derivatives (50 or 100 mg/kg, bolus, i.p.) on serum GOT and GPT activities and hepatocyte cytoplasmic vacuolation were examined in male Fischer 344 rats, which were exposed to CCl4 (0.5 mg/kg, p.o.) 30 min prior to the administration of cAMP derivatives. In CCl4-treated rats 6 h later, serum GOT and GPT levels were elevated 10- and 12-fold higher than those of vehicle rats, respectively. Treating CCl4-exposed rats with all cAMP derivatives, except those of alkylphosphoramidate, significantly decreased the levels of serum enzymes. Based on the effects of both serum GOT and GPT elevation, N6-butyl- and N6-heptyl-cAMP were the most potent. It was also observed histopathologically, that both compounds inhibited the occurrence of cytoplasmic vacuolation in CCl4-treated liver cells. This is the first report that cAMP derivatives possess a protective effect in the liver injury model induced by CCl4.

Alanine Transaminase↗

Inhibition of salvage synthesis of nucleic acid by adenosine 3',5'-cyclic decylphosphoramidate in mastocytoma P-815 cells.

Constant exposure of mastocytoma P-815 cells to adenosine 3',5'-cyclic decylphosphoramidate (1), which is permeable to the cell membrane and resistant to the action of phosphodiesterase, caused a dose-dependent (1 to 50 microM) inhibition in the synthesis of DNA and cell proliferation. Pretreating the cells with compound 1 (20 microM, 4 h) caused considerable inhibition of the incorporation of [3H]thymidine ([3H]TdR) into [3H]deoxythymidine 5'-triphosphate ([3H]dTTP) and that of [14C]hypoxanthine into nucleic acid, but not the synthesis of [14C]dTTP from [U-14C]aspartate. These results indicate that compound 1 preferentially inhibits the salvage synthesis of intracellular nucleotides and nucleic acids. Thymidine kinase, a key enzyme in salvage synthesis of nucleotides, was almost undetectable in cells pretreated with compound 1 at 20 microM for 4 h or at 5 microM for 15 h. On the other hand, compound 1 activated partially purified cAMP-dependent protein kinase A from bovine heart. Judging from these observations, it is likely that compound 1 readily permeates the cell membrane, activates cAMP-dependent protein kinase, then inhibits the salvage synthesis of nucleotides and nucleic acids by inhibiting thymidine kinase, which results in the inhibition of cell growth.

Animals↗

[A case of endometrioid carcinoma arising from endometriosis of the rectum].

A very rare case with rectal endometriosis heterotopic transformed into carcinoma is reported. A 44-year-old female patient underwent colostomy due to ileus. Postoperative examinations revealed submucosal tumors all around the rectum. Low anterior resection and the closure of the colostomy were performed. Thickening in the muscular layer and serosa were observed in the resected specimen, but the mucosal surface was maintained. Histopathological observation revealed glands of the endometrium and connective fibers with glandular adenocarcinoma in the periphery. Transformation of the benign endometrial tissues into carcinoma and squamous metaplasia were observed. A diagnosis of endometrial carcinoma in the rectum was made.

Adenocarcinoma↗

Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies.

A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed low-density and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for gamma-aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.

Adolescent↗