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Biomedical subjects

T Satoh

Publications and source records attributed to T Satoh.

At least 703 records · Page 39Linked to original sources
PubMed1993

Clinical evaluation of new cancer-associated antigen CA125 II in epithelial ovarian cancers: comparison with CA125.

With use of monoclonal antibodies (moABs) M 11 and OC125, a sensitive sandwich immunoradiometric assay (IRMA) for CA125 II was developed. CA125 antigen was adsorbed by moAB OC125 and M 11, but horseradish peroxidase-labelled OC125 did not compete with M 11, indicating that although these two moABs recognized CA125 antigen, they reacted with separate antigenic determinants. We also demonstrate that the dual capture technique with OC125 and M 11 antibodies has a larger dynamic range than OC125 alone. This could potentially increase the sensitivity in terms of low CA125 levels. Forty-six patients with ovarian cancer before therapy and a further 20 cases during follow-up were evaluated for the presence of two serum tumor markers: CA125 II and CA125. The overall positive rate for CA125 II was 97.8%, compared with 91.3% with CA125. Serum CA125 II levels were closely correlated with serum CA125 levels (r = 0.918). The mean CA125 II levels before treatment, at response, and at recurrence were 194.3, 19.6, and 103.5 U/mL, respectively. Normalization of serum CA125 II levels at response does not imply absence of microscopic residual disease. CA125 II changes during follow-up suggest recurrence and can be used to monitor individual patients.

Adult↗
PubMed1993

Gonadotropin-induced ovarian carbonyl reductase in mice and hamsters: comparison with carbonyl reductase in rats.

We investigated the effects of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) on ovarian carbonyl reductase activities towards 13,14-dihydro-15-ketoprostaglandin F2 alpha (15KD-PGF2 alpha), p-nitroacetophenone (PNAP) and p-nitrobenzaldehyde (PNBA) in mice and hamsters, and compared with their effects on those we observed previously in rats. The treatment with PMSG and hCG caused a significant increase in ovarian weights and superovulation in both mice and hamsters. Hamster ovary possessed appreciable carbonyl reductase activities towards all three substrates, whereas the activities were lower than those in rat ovary. The reductase activities were not increased by the treatment with gonadotropins, differing from rat ovarian carbonyl reductase. In untreated mice, carbonyl reductase activity towards 15KD-PGF2 alpha was not detected, whereas the activities towards PNAP and PNBA were detected, which activities were lower than those in rats and hamsters. The PNAP and PNBA reductase activities in mouse ovary were significantly increased up to 7.1- and 1.7-fold, respectively, by the treatment with gonadotropins. These results show that there are species differences in ovarian carbonyl reductase and response of the enzyme to gonadotropins.

Alcohol Oxidoreductases↗
PubMed1993

A truncated isoform of the thyrotropin-releasing hormone receptor is expressed in the rat central nervous system as well as in the pituitary gland.

Using the reverse transcription-polymerase chain reaction (RT-PCR), a cDNA encoding the entire rat thyrotropin-releasing hormone receptor (TRH-R) was isolated from normal rat pituitary gland mRNA. In addition, a novel truncated isoform of TRH-R which lacks 52 base pairs (bp) in the carboxyl (C-) terminal tail was isolated. This truncation, probably generated by alternate splicing, causes a frame-shift and results in a truncated TRH-R 25 amino acids shorter and with a different C-terminal amino acid sequence than the longer type receptor. This truncated TRH-R mRNA, along with the longer receptor form, was found to be expressed throughout the rat pituitary gland and brain.

Amino Acid Sequence↗
PubMed1993

Identification of thyrotropin-releasing hormone receptor messenger RNA in the rat central nervous system and eye.

TRH exerts a wide variety of neuropharmacological actions by interacting with specific receptors in the central nervous system (CNS). Specific binding sites for TRH have been identified also in the mammalian retina. However, whether TRH receptors (TRH-R) in the brain and retina are identical in structure with those in the anterior pituitary gland is presently unknown. In this study, TRH-R gene expression was examined by Northern blot analysis in the CNS and eye using a cloned rat pituitary TRH-R cDNA. Northern analysis demonstrated a specific hybridization band of approximately 3.8 kb in hypothalamus, cerebrum, cerebellum, brain stem, spinal cord, and eye, indistinguishable from that characterized in pituitary gland. These data strongly support the hypothesis that a TRH receptor similar or identical to that cloned from the pituitary occurs in the retina and throughout the CNS.

Animals↗
PubMed1993

Studies of quality control of 99mTc-labelled macroaggregated albumin--Part 1. Aggregation of non-mercaptalbumin and its conformation.

The aggregative condition of albumin was investigated using bovine serum albumin (BSA) as a model for quality control of 99mTc-macroaggregated albumin (99mTc-MAA). Uniformalized aggregates were obtained from the oxidized non-mercapt-type of BSA by heating. The size of the aggregates was affected by the pH and the types of buffer solutions used as well as the concentrations of albumin and buffers. The beta form structure of the albumin was more stable on heating and this may contribute to its aggregation. Aggregation of oxidized non-mercaptalbumin afforded a portion of smaller sized particles in MAA, this being an inappropriate factor for scintiscanning of lungs. Our results suggest that it is necessary to remove oxidized type albumin from human serum albumin as the starting material, in order to prepare MAA with a uniform and larger particle size.

Albumins↗
PubMed1993

Pathogenesis of autoimmune hypothyroidism induced by lymphokine-activated killer (LAK) cell therapy: in vitro inhibition of human thyroid function by interleukin-2 in the presence of autologous intrathyroidal lymphocytes.

Lymphokine-activated killer (LAK) cell therapy frequently results in primary hypothyroidism. To elucidate the responsible mechanism, we investigated the effects of interleukin-2 (IL-2) on thyroid function of cultured human thyroid follicles in the presence or absence of autologous thyroid-derived lymphoid cells (TDLC). Human thyroid follicles, obtained by subtotal thyroidectomy from patients with Graves' disease, were cultured in serum-free medium containing bTSH and various concentrations of human IL-2, with or without TDLC. After 5 days of culture, 125I was added, and after an additional 3 days of culture, 125I incorporated into thyroid follicles and organic 125I (125I-T4 + 125I-T3) released into the culture medium were estimated. In the absence of TDLC, IL-2 did not affect bTSH-induced thyroid function. In the presence of TDLC, however, IL-2 inhibited the bTSH-stimulated thyroid function in a concentration-dependent manner. The minimum IL-2 concentration required to inhibit thyroid function was 1 U/ml. At 100 U/ml, IL-2 inhibited thyroid function completely. IL-2 increased the concentration of IFN-gamma in the culture medium conditioned by TDLC but not by thyroid follicles. When both were cocultured, IL-2 more significantly increased the concentration of IFN-gamma to an extent sufficient for inhibiting thyroid function per se. Furthermore, the addition of anti-IFN-gamma antibody to the medium partially restored the IL-2-inhibited thyroid function. In summary, by coculturing human thyroid follicles and autologous intrathyroidal lymphocytes with IL-2, it was possible to reproduce the thyroid dysfunction associated with LAK cell therapy. Our data indicate that IL-2 inhibits thyroid function, at least partly, by stimulating production of IFN-gamma, a potent inhibitory cytokine for thyroid cells.

Analysis of Variance↗
PubMed1993

2-Amino-3-methylimidazo[4,5-f]quinoline (IQ), a carcinogenic pyrolysate, induces chromosomal aberrations in Chinese hamster lung fibroblasts in vitro.

The ability of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) to induce chromosomal aberrations (CAs) in Chinese hamster lung fibroblast (CHL/IU) cells in vitro was examined. On incubation with rat S9 (2.5-10%, v/v) for 3 h, followed by a recovery culture period of 21 h, IQ caused significant induction of CAs at a concentration 20 micrograms/ml, but had less effect at 40 micrograms/ml. With longer recovery culture times such as 27-33 h, however, IQ was much more effective at 40 micrograms/ml. No significant induction was observed with 1 or 6 h treatments followed by 23 or 18 h recovery cultures, respectively. On incubation without S9, only weak CA induction by IQ was observed. These results show that IQ is a clastogen and that its clastogenic effect varied with the experimental conditions, such as the time of exposure and the time of recovery culture. The cell cycle perturbation effect is suggested to be one of the critical factors for the detection of the clastogenic potential of IQ.

Animals↗
PubMed1993

Evidence that cyclosporine causes both intracellular migration and inappropriate urinary excretion of magnesium in rats.

We determined the effects of cyclosporine on calcium, magnesium, and potassium metabolism in rats. Thirty Sprague-Dawley rats were randomized into three groups of ten animals each--control rats given olive oil, rats given cyclosporine at a dosage of 5 mg/kg daily, and rats given 15 mg/kg daily for four weeks. Urinary excretion of calcium, magnesium, and potassium was determined before and after 2 and 4 weeks of cyclosporine therapy. All rats were sacrificed after 4 weeks of therapy, and calcium, magnesium, and potassium concentrations in serum and tissues were determined. Serum magnesium levels were significantly lower in the cyclosporine-treated groups than in the control group, but there was no significant difference between the control and either of the cyclosporine-treated groups with regard to total urinary excretion of magnesium after four weeks of treatment. Magnesium content in the kidney, muscle, and liver was significantly higher in the 15 mg/kg group than in the control group. Calcium content in the kidney and liver was significantly higher as well. Potassium content in any type of tissue was similar in the three groups. We conclude that the intracellular migration of magnesium plays an important role--as does impaired renal conservation of magnesium--in the pathogenesis of cyclosporine-induced hypomagnesemia and that there is a discrepancy between magnesium and potassium metabolism in cyclosporine-treated rats.

Animals↗
PubMed1993

Inhibitory effect of melanin pigment on sensitization and elicitation of murine contact photosensitivity: mechanism of low responsiveness in C57BL/10 background mice.

We have shown that murine contact photosensitivity (CPS) to 3,3',4',5-tetrachlorosalicylanilide (TCSA) is genetically controlled mainly by the major histocompatibility complex. The H-2b,d haplotypes are closely associated with high responders, whereas mice with the H-2k are non-responders. Irrespective of their H-2 haplotypes, the C57BL/10 (B10) background strains, including B10, B10.D2, B10.A, and B10.BR, possessing black fur color, were low or nonresponders in CPS to TCSA. In B10 mice, however, high-sensitivity responses were induced when subcutaneous inoculation of epidermal cells (ECs) photomodified in vitro with TCSA was used for both immunization and challenge, suggesting that the epicutaneous route for induction and elicitation is defective in B10 background mice. F1 mice obtained by crossing high-responder BALB/c and low-responder B10 mice, possessing agouti fur color, were non-responders of CPS. The magnitude of CPS in the F2 mice derived from F1 (BALB/c X B10) siblings varied from low to high. When these F2 mice were divided into five groups with regard to fur color, the magnitude of reaction was correlated with the fur color and there was inverse relationship between the magnitude of CPS and the amount of melanin pigment in earlobe ECs. Furthermore, the in vivo formation of TCSA-EC photoadducts was negatively correlated to the melanin amount in earlobes. These observations suggested that the failure in CPS of the B10 background mice stems from inability of in vivo photocoupling of TCSA to ECs, presumably due to absorption of ultraviolet radiation by melanin pigment.

Animals↗
PubMed1993

Acral ichthyosiform mucinosis in association with Sjögren's syndrome: a peculiar form of pretibial myxedema?

Two Japanese women developed well-demarcated ichthyosiform plaques on the lateral aspect of their lower legs. Deposition of mucin was demonstrated throughout the papillary dermis, unlike the site of mucin deposition seen in pretibial myxedema. Their thyroid function was normal. The condition of both women was complicated by Sjögren's syndrome. One of them who presented with positive anti-microsomal and anti-thyroglobulin antibodies had goiter, suggesting that her malady was also complicated by Hashimoto's thyroiditis. Their skin manifestations differed from those described in cutaneous mucinosis including pretibial myxedema, specifically with regard to the well-demarcated ichthyosiform appearance, the mucin deposition in the papillary dermis, and the association with Sjögren's syndrome. To the best of our knowledge, our cases may thus be considered to be a previously undescribed form of cutaneous mucinosis associated with Sjögren's syndrome.

Adult↗
PubMed1993

Strong inhibition of 2-amino-6-methyldipyrido[1,2-a:3',2'-d] imidazole-induced mutagenesis and hepatocarcinogenesis by 1-O-hexyl-2,3,5-trimethylhydroquinone.

The effects of 3-O-dodecylcarbomethylascorbic acid (3-O-DAsA), 3-O-ethylascorbic acid (3-O-EAsA) and 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ) on 2-amino-6-methyldipyrido[1,2-a:3',2'-d]-imidazole (Glu-P-1)-induced mutagenesis and hepatocarcinogenesis were examined. In a Salmonella assay, addition of 2.5 to 20.0 mg of HTHQ to Salmonella TA 98 in the presence of S-9 mixture dose-dependently inhibited Glu-P-1-induced mutagenesis. The highest dose showed a 99% reduction in revertants. 3-O-DAsA and 3-O-EAsA were without effect. In an animal study using the medium-term bioassay system for the detection of hepatocarcinogens or hepatopromoters in F344 male rats, treatment with Glu-P-1 alone was associated with a significant increase in the number and area of GST-P-positive foci (47.5 +/- 8.9 and 11.1 +/- 4.7, respectively). Combined treatment with 1.0% HTHQ significantly reduced the number and area of GST-P-positive foci (to 8.1 +/- 2.1 and 0.6 +/- 0.2) while 3-O-DAsA exerted marginal inhibition and 3-O-EAsA had no effect. On the other hand, all three of these compounds slightly enhanced the numbers and areas of foci when given alone. The results indicate that HTHQ is a potent chemopreventer of Glu-P-1-induced hepatocarcinogenesis.

Animals↗
PubMed1993

A new variant of punctate acrokeratoderma associated with a pigmentary disorder.

We report a Japanese patient with skin-coloured keratotic papules on the hands and feet, and pronounced hyperkeratosis of the palms and soles. There was no evidence of fragmentation of dermal elastic tissue on histology. Freckle-like pigmentation was also present on the dorsa of the hands and feet, and this appeared to be closely related to the keratotic disorder. The mode of inheritance was autosomal dominant. We consider our case to be a new variant of familial punctate acrokeratoderma, associated with a pigmentary disorder.

Family↗
PubMed1993

Platelet-derived growth factor receptor mediates activation of ras through different signaling pathways in different cell types.

A series of pieces of evidence have shown that Ras protein acts as a transducer of the platelet-derived growth factor (PDGF) receptor-mediated signaling pathway: (i) formation of Ras.GTP is detected immediately on PDGF stimulation, and (ii) a dominant inhibitory mutant Ras, as well as a neutralizing anti-Ras antibody, can interfere with PDGF-induced responses. On the other hand, several signal transducing molecules including phosphatidylinositol 3-kinase (PI3-K), GTPase-activating protein (GAP), and phospholipase C gamma (PLC gamma) bind directly to the PDGF receptor and become tyrosine phosphorylated. Recently, it was shown that specific phosphorylated tyrosines of the PDGF receptor are responsible for interaction between the receptor and each signaling molecule. However, the roles of these signaling molecules have not been elucidated, and it remains unclear which molecules are implicated in the Ras pathway. In this study, we measured Ras activation in cell lines expressing mutant PDGF receptors that are deficient in coupling with specific molecules. In fibroblast CHO cells, a mutant receptor (Y708F/Y719F [PI3-K-binding sites]) was unable to stimulate Ras, whereas another mutant (Y739F [the GAP-binding site]) could do so, suggesting an indispensable role of PI3-K or a protein that binds to the same sites as PI3-K for PDGF-stimulated Ras activation. By contrast, both of the above mutants were capable of stimulating Ras protein in a pro-B-cell line, BaF3. Furthermore, a mutant receptor (Y977F/Y989F [PLC gamma-binding sites]) could fully activate Ras, and the direct activation of protein kinase C and calcium mobilization had almost no effect on the GDP/GTP state of Ras in this cell line. These results suggest that, in the pro-B-cell transfectants, each of the above pathways (PI3-K, GAP, and PLC gamma) can be eliminated without a loss of Ras activation. It remains unclear whether another unknown essential pathway which regulates Ras protein exists within BaF3 cells. Therefore, it is likely that several different PDGF receptor-mediated signaling pathways function upstream of Ras, and the extent of the contribution of each pathway for the regulation of Ras may differ among different cell types.

Animals↗
PubMed1993

Demonstration of the Epstein-Barr genome by the polymerase chain reaction and in situ hybridisation in a patient with viral pericarditis.

A 42 year old man admitted with effusive-constrictive pericarditis had diastolic dysfunction and pericardial thickening. Pericardiectomy was performed because of uncontrolled heart failure. The Epstein-Barr viral IgG antibody titre was exceptionally high. The EB viral genome was demonstrated in the resected pericardium by polymerase chain reaction and in situ hybridisation. EB viral pericarditis was diagnosed.

Adult↗
PubMed1993

Evaluation of delta-aminolaevulinic acid in blood of workers exposed to lead.

Exposure-effect and exposure-response relation between exposure to lead and delta-aminolaevulinic acid concentration in blood (ALA-B) were examined in 238 male workers exposed to lead. Concentrations of ALA-B ranged from 26 to 352 micrograms/l and lead concentrations in blood (Pb-B) from 7.1 to 86.0 micrograms/dl. Concentrations of ALA-B correlated closely with concentrations of Pb-B (r = 0.74), and increased ALA-B concentration occurred at Pb-B concentrations of around 30 micrograms/dl. Exposure-response curves indicated that the 50 percentile response doses were roughly 30, 40, and 50 micrograms/dl Pb-B when cut off points of ALA-B were set at 50, 60, and 70 micrograms/l respectively. The sensitivity and specificity of measurements of ALA-B concentrations for health screening were sufficiently high when the health based exposure limits of lead were set at 30-50 micrograms/dl. Moreover, a pronounced increase in ALA-B concentrations occurred when the inhibition rate of erythrocyte ALA dehydratase exceeded 85%. These findings suggest that ALA-B is a useful indicator for assessing the early effects of exposure to lead on haem biosynthesis.

Adult↗
PubMed1993

Different mechanisms of renal Na-K-ATPase regulation by protein kinases in proximal and distal nephron.

We recently reported a novel intracellular mechanism of Na-K-adenosinetriphosphatase (Na-K-ATPase) regulation in the cortical collecting duct (CCD) by agents that increase cell adenosine 3',5'-cyclic monophosphate (cAMP), which involves stimulation of protein kinase A (PKA) and phospholipase A2 (PLA2). We now determined whether this mechanism also operates in other nephron segments. In the medullary thick ascending limb (MTAL) dopamine, the DA1 agonist fenoldopam, forskolin, or dibutyryl-cAMP inhibited Na-K-ATPase activity, similar to results in CCD. In both segments this effect was blocked by 20-residue inhibitory peptide (IP20), a peptide inhibitor of PKA, but not by staurosporine, a protein kinase C (PKC) inhibitor. PKC activators phorbol 12-myristate 13-acetate, phorbol 12,13-dibutyrate, and 1,2-myristate 13-acetate, phorbol 12,13-dibutyrate, and 1,2-dioctanoylglycerol had no effect on Na-K pump activity in either CCD or MTAL. In contrast, all three PKC activators inhibited pump activity in the proximal convoluted tubule (PCT), an effect reproduced only by dopamine or by parathyroid hormone [PTH-(1-34)]. In PCT the pump inhibition by dopamine or PTH-(1-34) was abolished by staurosporine but not by IP20. The PLA2 inhibitor mepacrine prevented the effect of all agents, and arachidonic acid produced a dose-dependent pump inhibition in each of the three segments studied. We conclude that intracellular mechanisms of Na-K-ATPase regulation differ along the nephron, as they involve activation of PKA in CCD and MTAL and of PKC in PCT. These two pathways probably share a common mechanism in stimulating PLA2, arachidonic acid release, and production of eicosanoids in both the proximal and distal nephron.

Animals↗