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T Matsuda

Publications and source records attributed to T Matsuda.

At least 829 records · Page 46Linked to original sources
PubMed1994

[Duplication of the inferior vena cava with left renal cell carcinoma].

A case of duplication of the inferior vena cava (IVC) with left renal cell carcinoma is presented, and the clinical and radiological significance is discussed. Although computed tomographic (CT) scanning, inferior venacavography and renal venography revealed a sufficient amount of anatomical information, an accidental rupture to the inferior vena cava occurred during the procedure. The patient subsequently required 7 units of blood, and suffered acute hepatitis two months following the blood transfusion. However, no recurrences of renal cell carcinoma and hepatitis have been observed four year after the procedure.

Carcinoma, Renal Cell↗
PubMed1993

Genomic characterization of the human DNA excision repair-controlling gene XPAC.

We have characterized the human DNA excision repair gene, XPAC (xeroderma pigmentosum group A complementing). This gene of approximately 25 kb consists of six exons. The 5'-flanking region of the gene has a CAAT box, but no TATA box. The region upstream from the coding sequence of exon 1 is G + C rich (73%), and has a GC box. Transcriptional mapping analysis suggested that there is one major transcription start point (tsp). The presence of two polyadenylation signals suggests that the two XPAC mRNAs with different 3' untranslated regions in normal human cells are due to alternative polyadenylations. The promoter activity, measured by transient expression of the cat gene with the 5' flanking regions, indicated the presence of a functional promoter.

Amino Acid Sequence↗
PubMed1993

Selective induction of alpha 1 isoform of (Na+ + K+)-ATPase by insulin/insulin-like growth factor-I in cultured rat astrocytes.

Treatment of cultured rat astrocytes with insulin increased (Na+ + K+)-ATPase activity expressed per protein or DNA by 1.6- to 2.1-fold, but did not affect Mg(2+)-ATPase and adenylate cyclase activities. Insulin treatment increased protein and DNA contents under the conditions, while it did not cause morphological differentiation as determined by a microscopic inspection. Insulin-like growth factor-I (IGF-I) had a similar effect on the enzyme activity in astrocytes: the effect of insulin was observed at supraphysiological concentrations, while that of IGF-I was observed at physiological concentrations. Insulin and IGF-I both stimulated DNA synthesis at the concentrations that caused an increase in enzyme activity. The effect was blocked by tyrosine kinase inhibitors such as genistein and herbimycin A and by cycloheximide. Western blot analysis showed that alpha 1 and alpha 2 isoforms of (Na+ + K+)-ATPase were present in cultured astrocytes and that insulin and IGF-I increased the content of the alpha 1 isoform but did not that of the alpha 2 isoform. Two components of ouabain inhibition were observed in the enzyme purified partially from cultured astrocytes, and treatment of the cells with IGF-I increased the ratio of the low-affinity component of the inhibition, indicating a selective increase in the activity of the alpha 1 isoform. These results indicate that insulin increases (Na+ + K+)-ATPase activity through an activation of IGF-I receptors and the increase is due to the selective induction of the alpha 1 isoform in cultured astrocytes.

Adenylyl Cyclases↗
PubMed1993

Increased resting Ca2+ maintains the myogenic tone and activates K+ channels in arteries from young spontaneously hypertensive rats.

We examined whether the Ca2+ channel function in the resting state alters the resting tone in femoral and carotid arteries from spontaneously hypertensive rats (SHR) at early hypertensive stages (6 and 4 weeks of age), and data were compared with findings in age-matched normotensive Wistar-Kyoto rats (WKY). Strips of femoral and carotid arteries from 6-week-old SHR, but not from WKY, maintained a myogenic tone, that is, the resting tone decreased when 10(-7) M nifedipine was added. A similar myogenic tone was maintained in 4-week-old SHR. In strips of carotid arteries preloaded with fura-2, a fluorescent Ca2+ indicator, the decrease in cytoplasmic Ca2+ concentration following 0-Ca2+ solution or 5 x 10(-7) M nicardipine was significantly greater in SHR than in WKY. The basal 45Ca influx in femoral and carotid arteries from 6-week-old SHR was significantly increased when compared with WKY, and this increase in SHR was abolished by 10(-7) M nifedipine. The addition of charybdotoxin (a blocker of large conductance Ca(2+)-activated K+ channels) or of Bay k 8644 (an agonist of L-type voltage-dependent Ca2+ channels; VDCs), caused a concentration-dependent contraction, which was significantly greater in 6- and 4-week-old SHR than in WKY. These results suggest that the Ca2+ influx via L-type VDCs was increased in the resting state of femoral and carotid arteries from SHR at the early hypertensive stages, and therefore the myogenic tone was maintained and charybdotoxin-sensitive K+ channels were highly activated.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

A change in soybean agglutinin binding patterns of bovine milk fat globule membrane glycoproteins during early lactation.

Milk fat globule membrane (MFGM) glycoproteins were prepared from bovine milk at different stages of early lactation. Western blot analyses using several lectins revealed that reactivity of MFGM glycoproteins, especially 47K and 80K bands, to soybean agglutinin (SBA) remarkably increased during the lactation, while no change was observed for Ricinus communis agglutinin-I (RCA-I) binding. Sialidase treatment of MFGM glycoproteins revealed that the number of SBA-positive bands and the amount of SBA-positive oligosaccharides in these bands are increased during the lactation. Since SBA binds N-acetylgalactosamine terminated oligosaccharides, the results indicated that N-acetylgalactosaminylation of bovine MFGM glycoproteins is stimulated during the lactation.

Animals↗
PubMed1993

Purification of four forms of the beta gamma subunit complex of G proteins containing different gamma subunits.

To investigate the physiological significance of the diversity of gamma subunits of G proteins, we purified four forms of beta gamma of G proteins from bovine brain (beta gamma-B1, beta gamma-B2, beta gamma-B3), and spleen (beta gamma-S1) by the sequential chromatography on columns of DEAE-Sephacel, Ultrogel AcA 34, heptylamine-Sepharose, phenyl-5PW, and DEAE-5PW. Electrophoretic analyses showed that each beta gamma mainly contained the 36-kDa beta and a distinct but homogeneous gamma. These beta gamma complexes were subjected directly to proteolytic digestion and subsequent amino acid sequence analyses of their fragments. It was revealed that beta gamma-B1, -B2, and -B3 were identical to beta 1 gamma 7 (with a low level of beta 2 gamma 7), beta 1 gamma 2 and beta 1 gamma 3, respectively, while beta gamma-S1 was composed of beta 1 and an unidentified form of gamma. Then we examined the functional differences among these beta gamma complexes and the beta gamma of transducin (beta gamma-T, beta 1 gamma 1). Few differences were observed among all beta gamma complexes to enhance pertussis toxin-catalyzed ADP-ribosylation of the alpha subunits of G(o) and Gt. The four forms of beta gamma complexes purified from brain and spleen showed indistinguishable inhibitory effects on the release of GDP from G(o) alpha, but beta gamma-T was much less effective. Brain and spleen beta gamma complexes were equally effective in inhibiting calmodulin-stimulated adenylyl-cyclase activity, but beta gamma-T had a very weak inhibitory effect. Five forms of beta gamma facilitated metarhodopsin II-catalyzed binding of GTP gamma S to Gt alpha in a concentration-dependent manner with the following rank order of effectiveness: beta gamma-S1 > beta gamma-T > beta gamma-B1 > beta gamma-B2 > beta gamma-B3. Because the beta gamma complexes used in this study mostly contained the same beta subunit, the functional differences must be dependent on the gamma subunits. Thus, it seems likely that the receptor, the alpha subunits, and the effector are able to distinguish between the various gamma subunits.

Adrenal Glands↗
PubMed1993

The regulation of gene expression by insulin is differentially impaired in the liver of the genetically obese-hyperglycemic Wistar fatty rat.

The regulation by insulin and carbohydrates of the gene expression of three key enzymes involved in glucose metabolism was studied in the liver of the Wistar fatty rat, a model of obese non-insulin-dependent diabetes mellitus. A high glucose or fructose diet, or insulin administration caused a similar magnitude of increase in the level of L-type pyruvate kinase mRNA in the liver of Wistar fatty rats and their lean littermates. However, the induction of glucokinase mRNA and repression of phosphoenolpyruvate carboxykinase mRNA by dietary glucose or insulin were impaired in the fatty rats, whereas fructose caused a similar decrease in phosphoenolpyruvate carboxykinase mRNA in both types of rats. These results indicate that the regulation of gene expression of glucokinase and phosphoenolpyruvate carboxykinase, but not of L-type pyruvate kinase, by insulin is impaired in the liver of the Wistar fatty rat.

Animals↗
PubMed1993

Excitatory and inhibitory effects of toluene on neural activity in guinea pig hippocampal slices.

To investigate the effect of toluene and its derivatives on neural activity, postsynaptic field potential (population spike, PS) of granule cells as well as antidromic potential (AP) and presynaptic fiber potential (FP) (perforant path) were recorded in the guinea pig hippocampal slices. Toluene at the concentration of 0.2 ng/ml to 20 micrograms/ml in the perfusion medium increased the amplitude of PS to 109-150%. Toluene also increased the amplitude of FP and AP, although the most remarkable enhancement was observed in the PS. However, toluene at the concentrations over 1000 micrograms/ml completely depressed the PS, whereas it increased the amplitude of AP to 130% of the original level. These results indicate that toluene has excitatory and inhibitory biphasic effects on neurotransmission in the hippocampal slices according to concentration applied.

Animals↗
PubMed1993

Two genetic defects in a patient with complete deficiency of the b-subunit for coagulation factor XIII.

A genomic DNA obtained from a female patient with complete b-subunit deficiency was examined by Southern blotting analysis and in vitro amplification. Nucleotide sequence analysis showed that adenosine-4161 at the acceptor splice junction of intron A/exon II was deleted in half of the amplified DNAs, resulting in a loss of the obligatory AG splicing sequence. The absence of adenosine-4161 was confirmed by cleavage with TaqI endonuclease of the amplified DNAs. Moreover, sequence analysis showed that guanosine-11499 coding for Cys 430 (TGC) in exon VIII was replaced by thymidine in half of the amplified DNAs, resulting in an amino acid change to Phe (TTC) and the destruction of a disulfide bond in the seventh Sushi domain. This mutation was also confirmed by cleavage with MboII endonuclease. Thus, the proband turned out to be a compound heterozygote of two separate defective alleles. Although half of the amplified DNAs for exon VIII of her daughter or son were cleaved by MboII, those for intron A were not cleaved by TaqI. The replacement of guanosine-11499 by thymidine in their exon VIII has also been confirmed by sequence analysis, indicating that they are heterozygous for one normal and one defective allele.

Alleles↗
PubMed1993

Hemolytic uremic syndrome developing during remission of acute myelomonocytic leukemia.

A 47-year-old woman was diagnosed with acute myelomonocytic leukemia (AMMoL) and was treated with combination chemotherapy. After one cycle of remission induction therapy, she entered into complete remission and then received three cycles of consolidation therapy. A month after the last consolidation therapy, she was diagnosed with having the complication of chemotherapy-related HUS (C-HUS). The C-HUS improved after initiation of plasma exchange and antiplatelet therapy. In the present case, it seems that the antileukemic agents might play an important role in the development of C-HUS.

Antineoplastic Combined Chemotherapy Protocols↗