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Biomedical subjects

T Noguchi

Publications and source records attributed to T Noguchi.

At least 451 records · Page 25Linked to original sources
PubMed1995

Production of insulin-like growth factors and their binding proteins in primary cultures of rat liver parenchymal and nonparenchymal cells.

Regulation of the production of insulin-like growth factor (IGF)-I, IGF-II, IGF binding proteins (IGFBPs), and their related proteins by various hormones was investigated in primary cultures of rat liver parenchymal and nonparenchymal cells. Freshly isolated parenchymal cells contained mRNAs of IGF-I, IGF-II, IGFBP-1, IGFBP-4, growth hormone (GH) receptor, and the acid-labile subunit (ALS), which forms a ternary complex with IGF-I and IGFBP-3; however, parenchymal cells did not express the IGFBP-3 gene. In contrast, nonparenchymal cells contained IGFBP-3 mRNA exclusively, as we reported previously [Takenaka et al. Agric. Biol. Chem., 55, 1191-1193 (1991)]. Cultured rat parenchymal cells produced IGF-I, IGFBP-1, and IGFBP-4 prominently. In these cells, secretion of IGF-I and the content of IGF-I mRNA was greatly increased in the presence of GH in the medium. Insulin also increased the production of IGF-I. Secretion of IGFBP-1 into the medium was enhanced by treatment with glucagon, dibutyrylcyclic AMP (Bu2cAMP), and dexamethasone (Dex) and these enhancements with glucagon and Dex reflected the increase in its mRNA content. Insulin depressed the secretion of IGFBP-1. The content of IGFBP-4 in the parenchymal cells was increased by insulin, Bu2cAMP, and triiodothyronine (T3), thereby enhancing the production of IGFBP-4 and secretion into the medium. Cultured liver nonparenchymal cells of rats produced IGFBP-1, IGFBP-3, and IGFBP-4. Secretion of IGFBP-1 was increased by Bu2cAMP in the medium, that of IGFBP-3 by IGF-I, and that of IGFBP-4 by both IGF-I and Bu2cAMP. Regulation of the production of IGFBP-3 by IGF-I was demonstrated in these investigations. These results suggest that GH increases production of IGF-I in the parenchymal cells and this IGF-I, in turn, increases the production of IGFBP-3 in nonparenchymal cells. As we found GH also increases ALS production in parenchymal cells, by these mechanisms, GH increases the formation of the ternary complex of IGF-I, IGFBP-3, and ALS. This study clearly demonstrates the interrelationship between parenchymal and nonparenchymal cells in the production of IGF-I and IGFBPs in the liver.

Animals↗
PubMed1995

Effect of cysteine on expression of cystathionine beta-synthase in the rat liver.

Hepatic cystathionine beta-synthase activity is decreased by the addition of cysteine to the diet. This effect of cysteine was slightly greater in diets containing 0.25% methionine than in those containing 1% methionine, and was reduced during aging. Similar changes were observed in the level of the mRNA of this enzyme, although the changes in the transcript levels were slightly greater than the changes in enzyme activity. Thus, we conclude that the addition of cysteine to a methionine-containing diet causes a decrease in cystathionine beta-synthase activity mainly by diminishing its mRNA level.

Aging↗
PubMed1995

[Neuron specific enolase-producing IgD multiple myeloma with high serum amylase activity].

A 68-year-old man who was admitted to our hospital because of general fatigue and anorexia. He was diagnosed as suffering from neuron specific enolase (NSE)-producing IgD-lambda type multiple myeloma with high activity of serum amylase, based on the detection of monoclonal IgD-lambda M-protein in the serum and urine, markedly high activities of salivary-type amylase and NSE in the serum, and immunohistochemical evidence of NSE and IgD in the myeloma cells. After two courses of alpha-IFN and VMCP chemotherapy, serum IgD, amylase and NSE decreased to normal levels. These observations indicate that NSE was ectopically produced by myeloma cells.

Aged↗
PubMed1995

[Alteration of isozyme gene expression during cell differentiation and oncogenesis].

Rat pyruvate kinase (PK) has four isozymes, called the M1-, M2-, L-, and R-types. The M1- and M2-type isozymes of PK are produced from the PKM gene by alternative splicing, whereas the L- and R-type isozymes of PK are produced from the PKL gene by use of different tissue-specific promoters. In early development, only M2-type PK expresses in all tissues. After late morphogenesis, M1-, L-, and R-type PK express tissue-specifically. In contrast, cell proliferation such as regenerating liver and oncogenesis lead to decrease or cessation of the expression of tissue-specific PK isozymes and to stimulation of the expression of M2-type PK. These phenomena from the point of view transcriptional regulatory apparatus of the PKM and PKL gene are discussed.

Animals↗
PubMed1995

[Hypoplastic leukemia achieved long-term remission with low-dose cytosine arabinoside].

A 74-year-old woman was admitted in October 1988 with anemia and leukocytopenia. Hematologic investigations established a diagnosis of hypoplastic acute leukemia. She received a low dose of cytosine arabinoside (LDAC: 10 mg/m2 every 12 hours) subcutaneously for 21 days and achieved complete remission (CR) one month later. After one course of LDAC of 14 days, she received LDAC of 21 days every 5 to 6 months as maintenance therapy till April 1993. She has been in remission for 6 years. Intensification therapy with LDAC every 5 to 6 months might be useful in maintaining remission for hypoplastic acute leukemia.

Aged↗
PubMed1995

[Therapy related leukemia].

Eleven therapy related leukemias (TRL) who were hospitalized in the Department of Hematology and Chemotherapy, Kanagawa Cancer Center between October 1983 and December 1993 were identified. Six of the patients were males and five were females. Their median age was 62 years (range from 14 to 75). Three patients had previously received treatment for breast cancer and two patients for malignant lymphoma. The other patients had received treatment for lung cancer, urinary bladder cancer, gastric cancer, brain tumor, maxillary sinus cancer and macroglobulinemia, respectively. Seven patients had been treated with chemotherapy and four patients had been treated with chemotherapy and irradiation for the primary tumor. The TRL cases consisted of 8 acute non-lymphoid leukemias, two acute lymphoid leukemias and one hypoplastic leukemia, respectively. The status of primary tumors at the development of TRL was complete remission in ten patients and partial remission in one patient. Three of the 10 patients who received anti-leukemic therapy entered complete remission and the median survival time was 36 days (from 7 days to 489 days). One patient expired of pneumonia before he received anti-leukemic therapy. TRL patients showed poor response to chemotherapy and had poor prognosis. These data suggest that the use of reduced doses of carcinogenic drugs for primary tumors might be required to prevent the development of TRL.

Adolescent↗
PubMed1995

[Effect of endogenous and inhaled nitric oxide on pulmonary microcirculation].

The sites of action of endogenous and inhaled nitric oxide (NO) were reassured during hypoxic pulmonary vasoconstriction. Lungs of 21 adult cats were perfused in situ with autologous blood in zone-3 conditions. Capillary pressures were measured by the double-occlusion techniques and pressures in arterioles and venules 70-100 microns in diameter were measured by the servo-null micropuncture technique, both during normoxia (FiO2 = 0.3) and during hypoxia (FiO2 = 0.02). The effects of NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg), an inhibitor of NO synthase, and of inhaled NO (5-100 ppm) were also measured. The PO2 of the prefusate decreased from 187.6 +/- 5.3 mmHg during normoxia to 25.7 +/- 1.3 mmHg during hypoxia, and further decreased to 20.8 +/- 2.2 mmHg during hypoxia with 50 ppm NO (p < 0.05, compared with hypoxia only). Increases in pulmonary vascular pressure drop in response to hypoxia were 4.8 +/- 1.0 cmH2O and 9.1 +/- 1.4 cmH2O in non-treated and L-NAME-treated lungs, respectively (p < 0.05). L-NAME significantly increased hypoxic construction in the venous segment. The concentration of exhaled NO increased from 13 +/- 4 ppb during normoxia to 18 +/- 4 ppb during hypoxia (p < 0.1). Inhaled NO lowered not only pulmonary artery pressure but also capillary pressure in a dose-dependent manner, which reduced hypoxic pulmonary vasoconstriction. Pulmonary veins were more sensitive to inhaled NO than were arteries. Inhaled NO (50 ppm) dilated vessels smaller than 70 to 100 microns in diameter, by 39% (p < 0.05), and dilated venules greater than 100 microns in diameter by 26% (p < 0.05), but did not significantly dilate arterioles greater than 100 microns in diameter (11%). Inhaled NO did not significantly change the ratio of wet weight to dry weight. We conclude that both endogenous and inhaled NO attenuate hypoxic pulmonary vasoconstriction, with significant pulmonary venous dilation. The main site of action of inhaled NO is vessels smaller than 100 microns in diameter and venules greater than 100 microns in diameter. Inhaled NO (5-100 ppm) does not cause interstitial edema.

Administration, Inhalation↗
PubMed1994

Fourier transform infrared spectrum of the radical cation of beta-carotene photoinduced in photosystem II.

A Fourier-transform infrared (FTIR) spectrum of the radical cation of beta-carotene photoinduced in photosystem II (PSII) membranes was obtained at 80K under oxidizing conditions, by utilizing the light-induced FTIR difference technique. Formation of the beta-carotene cation was monitored with the electronic absorption band at 993 nm. An FTIR spectrum of a chemically-generated beta-carotene cation in chloroform was also measured and compared with the spectrum of PSII. Since the FTIR bands of carotenoid cation have characteristic features with strong intensities, they can be useful markers in studying the reaction of carotenoid in PSII.

Carotenoids↗
PubMed1994

Hippocalcin expression in the brain of the Snell dwarf mutant mouse.

To determine factors contributing to the expression of the brain-derived protein, hippocalcin, we mapped its distribution in the brain of Snell pituitary dwarf mutant mice (dw) by immunohistochemical and immunoblot methods. Our findings are as follows. (1) In the hippocampus, hippocalcin immunoreactivity was found in the cell body and dendrites of pyramidal neurons of the normal controls and dw mice, although the intensity of immunoreactivity in the dw mice was lower. (2) In the cerebellum, hippocalcin immunoreactivity was strongly expressed in the Purkinje cell body of both the control and dw mice. However, the Purkinje cell dendrites were found to be more intensely stained in the dw mice than in the normal controls. (3) In the dw cerebral cortex, the pyramidal neurons of layers II to VI strongly expressed hippocalcin, whereas its expression in the controls was weak. (4) The amount of hippocalcin in the dw hippocampus was less than in the normal controls, whereas the amount in the dw cerebral cortex and cerebellum was greater. These results indicate that the developmental expression of hippocalcin in the dw brain is affected by the retarded maturation of the neuronal network due to the deficient hormonal state (the lack of growth and thyroid hormones).

Animals↗
PubMed1994

cDNA cloning of a cytosolic protein tyrosine phosphatase (RKPTP) from rat kidney.

A rat cDNA encoding a non-receptor type phosphotyrosine phosphatase (PTPase; EC 3.1.3.48) was identified. The 1608 bp cDNA contains a single open reading frame that predicts a 382 amino acid protein with M(r) 44,438. The predicted protein has no apparent signal or transmembrane sequences, suggesting that it is a cytosolic protein. The C-terminal region has a PTPase catalytic domain that has 40-50% nucleic acid homology to other known PTPases. The N-terminal region has little amino acid sequence homology to any other known sequences. The recombinant protein of the cloned cDNA expressed in Escherichia coli was shown to possess PTPase activity using myelin basic protein, tyrosine phosphorylated by p43v-abl tyrosine kinase, as a substrate.

Amino Acid Sequence↗
PubMed1994

Expression of mouse phosphofructokinase-M gene alternative transcripts: evidence for the conserved two-promoter system.

Molecular cloning of the 5' part of mouse phosphofructokinase-M cDNA was performed. In the 46 cDNA clones isolated, there were two classes of 5' untranslated sequences. One had an EcoRI site within its 5' untranslated sequence. This showed 83.0% similarity with human type B mRNA for phosphofructokinase-M. The other lacked an EcoRI site, showing 92.9% similarity with human type C mRNA. Using the reverse-transcription PCR technique, we found that the transcript with an EcoRI site was exclusively expressed in cardiac and skeletal muscles, while that without an EcoRI site was expressed in all the mouse tissues examined. The results suggested that the mouse phosphofructokinase-M gene was transcribed through alternative splicing by the multiple promoters. This transcription mechanism was considered to be evolutionarily conserved. The level of phosphofructokinase-M gene expression in mouse cardiac and skeletal muscles decreased in the ketotic diabetic state. Although the regulatory mechanism and the physiological significance are not fully known, this would indicate that phosphofructokinase-M gene transcripts are affected during the diabetic state.

Animals↗
PubMed1994

Molecular cloning of a novel calcium-binding protein structurally related to hippocalcin from human brain and chromosomal mapping of its gene.

A cDNA clone (hHLP2) encoding a novel calcium-binding protein structurally related to hippocalcin has been isolated from the human hippocampus cDNA library. The primary structure consists of 193 amino acids, and contains three EF-hand structures and a possible NH2-terminal myristoylation site. A single transcript at a position corresponding to 1.7 kilobases was detected only in the brain. The hHLP2 gene was mapped to human chromosome 2.

Amino Acid Sequence↗
PubMed1994

A new variant of muscle phosphofructokinase deficiency in a Japanese case with abnormal RNA splicing.

A genetic defect was investigated in a newly diagnosed Japanese case with muscle type phosphofructokinase (PFK-M) deficiency. Polymerase chain reaction (PCR) amplification of patient cDNA revealed an in-frame truncation of 165 bases. This was compatible to the complete deletion of exon 19. The rest of the sequence was identical to that of the normal PFK-M cDNA. Sequencing of PCR amplified genomic DNA of the patient revealed a point mutation from G to A at the 5' donor site of intron 19. This mutation resulted in the skipping of exon 19 in the patient mRNA. Homozygosity of this patient was confirmed by allele specific amplification of the genomic DNA. Donor mutations in intron 15 and intron 5 associated with different splicing errors were previously reported to cause this disease. Thus, the human PFK-M gene mutations are heterogeneous, however, the donor mutations and splicing errors would represent one of the frequent causes of this disease.

Adult↗
PubMed1994

Expression of hippocalcin in the developing rat brain.

Expression of hippocalcin in the developing rat brain was investigated by a combination of Northern blot, in situ hybridization, immunoblot and immunohistochemical methods. In the hippocampus, hippocalcin mRNA and immunoreactivity first appeared in the CA3 pyramidal cells on embryonic day 19 (E19) and postnatal day 1 (P1), respectively, and extended throughout Ammon's horn. After P14, the hippocampal pyramidal cells, especially in the CA1 region, maintained the highest expression level among the brain regions. The dentate granule cells expressed a small amount of hippocalcin mRNA and immunoreactivity from P7 and maintained a low level through the developmental stages. In the cerebral cortex, hippocalcin mRNA and immunoreactivity appeared in the pyramidal cells of the piriform cortex from P1 and P4, respectively. Their expression extended throughout the cerebral cortex and reached the maximum level on P14, and then declined gradually with age to half of the maximum level by adults. In the cerebellum, a few Purkinje cells expressed a small amount of hippocalcin mRNA and immunoreactivity on P7. Their expression became evident in most of the Purkinje cells on P14 and increased gradually by P28. Then, their expression declined with age; however, the immunoreactivity was concentrated in the cell bodies and proximal segments of the dendrites in adults. These results suggest that the expression of hippocalcin mRNA and protein is strictly controlled by both the cell type and the developmental process and that hippocalcin plays a role in neuronal differentiation in the early stages of development and may relate to other neuronal function in the adult brain.

Animals↗
PubMed1994

Identification of chicken liver mitochondrial alanine:2-oxoglutarate aminotransferase and its response to starvation.

In chicken liver, alanine:2-oxoglutarate aminotransferase was located only in the mitochondria. In 40-day-old chickens, starvation resulted in a dramatic increase of liver mitochondrial alanine:2-oxoglutarate aminotransferase activity, reaching about a 100-fold increase in the activity (units/g of liver) on Day 7 of starvation. The mitochondrial alanine:2-oxoglutarate aminotransferase was purified to homogeneity and characterized from the mitochondrial extract of 7-day-starved chicken liver. The enzyme possessed alanine:glyoxylate aminotransferase activity and was also present in control chicken liver. The enzyme was found in the present study for the first time and named alanine:2-oxoglutarate (glyoxylate) aminotransferase. Alanine:2-oxoglutarate aminotransferase specific for alanine and 2-oxoglutarate as substrates was not detected in both control and starved chicken livers. In contrast, liver mitochondrial alanine:2-oxoglutarate aminotransferase from mammals did not possess alanine:glyoxylate aminotransferase activity. The increase in mitochondrial alanine:2-oxoglutarate aminotransferase activity during starvation was found to be attributed to an increase in enzyme protein.

4-Aminobutyrate Transaminase↗
PubMed1994

Improved method for mutagenicity testing of gaseous compounds by using a gas sampling bag.

A simple and safety gas exposure method was developed using a gas sampling bag as an exposure vessel and a preparation vessel of diluted gas. The gas exposure conditions such as amount of S9 in the plate, volume of gas for the plate, amount of top agar, exposure period and exposure temperature were examined by mutagenicity testing of 1,3-butadiene using the gas sampling bag. Mutagenicity tests of 14 compounds and 1,3-butadiene on S. typhimurium TA98, TA100, TA1535 and TA1537, and E. coli WP2 uvrA were also examined by the developed gas exposure method. 1,3-Butadiene, propyne (methyl acetylene), monochlorodifluoromethane, ethylchloride, diborane and silane were mutagenic. 1-Butene, 2-butene, 2-methylpropene, methyl vinyl ether, trichlorofluoromethane, dichlorodifluoromethane, 1,2-dichloro-1,1,2,2-tetrafluoroethane, 1,1-difluoroethane and phosphine were not mutagenic on S. typhimurium TA98, TA100, TA1535 and TA1537, and E. coli WP2 uvrA with or without metabolic activation. These results were compatible with a previous report, and this developed method has the advantage that it can be tested easily and safely for combustible and self-combustible substances such as 1,3-butadiene and silane.

Animals↗
PubMed1994

Immunohistochemical localization of neural visinin-like Ca(2+)-binding protein 2 in adult rat brain.

The distribution of neural visinin-like Ca(2+)-binding protein 2 (NVP2) in adult rat brain was analyzed by immunoblot and immunohistochemical methods. NVP2 immunoreactivity was expressed intensely in the pyramidal cells of the CA1 and 2 regions of Ammon's horn, the granule cells of the dentate gyrus and the pyramidal cells of the cerebral cortex layers II to VI, moderately in the pyramidal-shaped cells of the anterior olfactory nucleus and large spindle-shaped cells of the globus pallidus, and weakly in neurons in the nucleus accumbens and the anterior and dorsomedial thalamus. In most cell types, NVP2 immunoreactivity was located in the cytoplasm and plasma membrane of the cell bodies and dendrites.

Animals↗