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K Ueda

Publications and source records attributed to K Ueda.

At least 523 records · Page 29Linked to original sources
PubMed1996

[Evaluation of occult atherosclerosis in the left main coronary artery in patients with acute anterior myocardial infarction].

Intravascular ultrasound was performed in 30 patients with acute anterior myocardial infarction to evaluate occult atherosclerosis in the left main coronary artery which could not be detected by coronary angiography. The intravascular ultrasound catheter was positioned in the left main coronary artery after successful intracoronary thrombolysis, and cross-sectional coronary artery scanning was performed. Percentage area stenosis (%AS) was calculated as (plaque cross-sectional area/vessel cross-sectional area) x 100. Images of crescent-shaped eccentric plaque were obtained in all patients. The mean vessel cross-sectional area was 28.6 +/- 8.0 mm2, and mean plaque cross-sectional area was 7.7 +/- 4.2 mm2. Mean %AS was 27 +/- 15% (range from 6 to 58%). In five patients, intravascular ultrasound was repeated 3 months later, which showed increased %AS more than 15% in two patients. These findings indicate that occult atherosclerosis is present in the left main coronary artery in almost all the patients with acute anterior myocardial infarction and should be treated with caution when coronary intervention is performed.

Adult↗
PubMed1995

NF1 gene mutations in Japanese with neurofibromatosis 1 (NF1).

Neurofibromatosis 1 (NF1) is an autosomal dominant disease characterized by abnormalities in multiple tissues derived from the neural crest. We analysed 50 unrelated Japanese patients for NF1 mutations by using polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis for exons 28 to 36. Here, we demonstrate a single base pair (bp) insertional mutations in exon 31 in one patient (5843insA/5844insA/5845insA/5846insA) and a single adenine to guanine transitional mutation 4 bp upstream from the 3' end of intron 31 in two unrelated cases. The insertional mutation in exon 31 was novel and resulted in premature termination of the transcript. The other intron 31 mutations resulted in 4 bp insertions of cDNA between exon 31 and exon 32 with premature termination of the transcript, indicating that those transitions of intron 31 caused aberrant splice acceptor sites upstream from the 5' end of exon 32. However, as the same mutation of intron 31 has been reported previously in two cases of unrelated Caucasians, the splice junction mutation of intron 31 is thought to be common among different ethnic groups.

Adenine↗
PubMed1995

Enhanced expression of cyclin D1 in senescent human fibroblasts.

When human fibroblast, TIG-1, was growth-stimulated with fetal bovine serum, the induction level of cell cycle-dependent genes was generally much lower in senescent cells than in young counterparts. Exceptionally, the expression level of cyclin D1 in senescent cells was constitutively higher than in young cells and further increased after serum stimulation, which was confirmed by Northern and Western blots and immunoprecipitation. This was also true in other human diploid fibroblast lines, TIG-3 and MRC-5. However, cyclin D1-dependent kinase activity was not detected in senescent cells. When sense- or antisense-cyclin D1 cDNA driven by beta-actin promoter was transfected into young TIG-1 cells, the number of appeared colonies from sense-strand transfected cultures was lower than that from antisense-strand-transfected ones. However, clones expressing cyclin D1 at low or undetectable level which were isolated after transfection with antisense-cyclin D1 proliferated up to the same division limit as untransfected and sense-strand transfected cells. Four clones of SV40-transformed TIG-1 expressed cyclin D1 at moderate levels during their extended proliferative lifespan. It appears that, if the extremely overexpressed cyclin D1 could cause an inhibition of cell proliferation at senescent stage, cellular senescence occurs regardless of overexpression of cyclin D1.

Animals↗
PubMed1995

Clinical efficacy of fluvastatin in the long-term treatment of familial hypercholesterolemia.

The long-term clinical efficacy of fluvastatin was assessed in 24 patients with familial hypercholesterolemia over a total treatment period of 104 weeks. Patients received an initial fluvastatin dose of 20 mg/day for 8 weeks, which was increased to 30 mg/day for a further 16 weeks. From week 24, if serum total cholesterol remained > or = 230 mg/dL, the fluvastatin dose could be increased to 40 or 60 mg/day, as necessary. By the end of treatment, 4 patients were receiving 30 mg/day fluvastatin, 1 patient was receiving 40 mg/day, and 19 patients were receiving 60 mg/day. Serum total cholesterol and low density lipoprotein cholesterol (LDL-C) levels showed a significant decrease from baseline at week 104 (total cholesterol, -26.8 +/- 2.4%; LDL-C, -33.1 +/- 3.3%; p < 0.001). The reductions in total cholesterol and LDL-C were dose-related. Statistically significant (p < 0.05) increases in serum high density lipoprotein cholesterol (HDL-C) were observed at week 24 (12.1 +/- 5.0%) and at week 76 (11.0 +/- 3.3%), although the effect was variable. Nevertherless, at the end of treatment the LDL-C: HDL-C ratio showed a 35% reduction from baseline. Changes in triglyceride levels failed to achieve statistical significance, with a reduction from baseline of -13.9 +/- 7.3% at week 104. Changes in apolipoprotein A-I were variable, with statistically significant (p < 0.01) increases observed at week 24 (7.6 +/- 2.3%) and week 76 (8.4 +/- 2.7%). By contrast, a significant reduction from baseline in apolipoprotein B was achieved by week 12 (-15.0 +/- 2.3%; p < 0.001) and was maintained throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Ligand western blotting for specific detection of active forms of proteases.

We developed a non-radioactive method of ligand western blotting for specific detection of active forms of serine proteases. The method consists of three steps: (i) separation of proteins by electrophoresis in sodium dodecyl sulfate-polyacrylamide gel, followed by blotting of proteins to nitrocellulose membrane; (ii) binding of a specific ligand, such as soybean trypsin inhibitor labeled with biotin, to protease on the membrane; and (iii) detection of the protease-inhibitor complex by color reaction (or chemiluminescence) developed by streptavidin-conjugated peroxidase (or alkaline phosphatase). By using this method, plasmin and trypsin (serine proteases) were detected, but papain (thiol protease) or pepsin (acidic protease) was not. Plasmin was detectable up to less than 4 ng. Inactive precursors of serine protease, i.e. plasminogen and trypsinogen, did not exhibit visible bands until they were activated by treatment with streptokinase or trypsin, respectively. We applied this method to clinical samples, and succeeded in detecting plasminogen, after conversion to plasmin with streptokinase treatment, in as little as 5 microliters of serum or trypsin, as it was in 10 microliters of pancreatic juice.

Bacterial Proteins↗
PubMed1995

Mutations of the p53 and ras genes in childhood t(1;19)-acute lymphoblastic leukemia.

We have investigated the alterations of p53 and ras genes including H-, K-, and N-ras genes in 22 acute lymphoblastic leukemia (ALL) cases and five cell lines carrying t(1;19) by use of polymerase chain reaction (PCR)-single-strand conformation polymorphism (SSCP) analysis and direct sequencing. The mutations of the p53 gene were found in 2 of 20 t(1;19)-ALL cases at diagnosis (10%), all of 4 cases at relapse (100%), and 4 of the 5 cell lines (80%). Four of the five patients who died had missense mutations at codons 49, 177, 179, and 248. In cases examined sequentially, one had the same point mutation at codon 179 at both diagnosis and relapse, and another had the same p53 gene mutation at codon 240 both in leukemic cells at relapse and in a cell line derived at that time. The other case had no mutation at diagnosis but had the mutation at codon 177 at relapse and cell lines derived from blast cells at diagnosis, suggesting that a small number of leukemic cells with the p53 gene mutation at diagnosis might have escaped PCR-SSCP analysis. In cell lines, SCMC-L9 had three point mutations in the p53 gene at codons 175, 248, and 358, whereas SCMC-L10 had frame shift at codons 209-211. One case had a rare polymorphism at codon 11. We found only one mutation of the N-ras gene that was a 2-bp substitution of GGT(Gly) to GTC(Val) at codon 13 among 22 t(1;19)-ALL cases and five cell lines. This case showed no mutation of the p53 gene and has had a good course. These results suggest that in t(1;19)-ALL, mutations of the p53 and ras genes are infrequent at diagnosis and that p53 gene alterations may be associated with relapse phase or progression of t(1;19)-ALL.

Adolescent↗
PubMed1995

Overproduction of the bleomycin-binding proteins from bleomycin-producing Streptomyces verticillus and a methicillin-resistant Staphylococcus aureus in Escherichia coli and their immunological characterisation.

The bleomycin-binding proteins designated BLMA and BLMS, which confer resistance to bleomycin (Bm), from Bm-producing Streptomyces verticillus ATCC15003 and a methicillin-resistant Staphylococcus aureus B-26, respectively, were overexpressed in Escherichia coli. The present study showed that both BLMA and BLMS quench the antibacterial activity of Bm by the binding to the drug. To immuno-characterize the Bm-binding proteins, we constructed a monoclonal antibody against BLMA. The antibody, designated 893-12, did not cross react to BLMS and another Bm-binding protein from tallysomycin-producing Streptoalloteichus hindustanus. Although the ability of Bm to cleavage DNA was eliminated by a binding of BLMA to Bm, as shown by Sugiyama et al. [Gene 151 (1994) 11-15], the Bm-induced DNA degradation was restored by pre-incubation of BLMA with the anti-BLMA monoclonal antibody.

Acetyltransferases↗
PubMed1995

[Analysis of arterial pulse propagation time variability for studying wave transmitting properties of arteries].

Propagation time of arterial pulse waves was studied concerning intervals R-R and intervals of corresponding peaks of differential radial arterial pressure. These signals were detected by an ECG monitor LIFESCOPE 6 (NIHON KOHDEN) and a tonometric arterial pressure detector JENTOW 7700 (NIHON COLIN), and are simultaneously recorded by a data-recorder. The cyclic variations in arterial propagation time and heart rate fluctuations were analyzed by means of fast Fourier transform (FFT) using a personal computer PC-9801RX (NEC). Apparently, they resembled each other in their power spectra. Therefore, an index for assessment of wave transform characteristics was induced as follows: Magnitude of variation can be calculated by sigma(power x frequency) = sigma PF, where the power means a square root of amplitude of power spectrum by FFT. Then, sigma PFRR and sigma PFRP were defined as the variation in arterial pulse wave propagation time and variation in heart rate fluctuations, respectively. Furthermore, they were normalized by their mean values (mRR, mRP), respectively, as sigma PFRR was found proportionate to mRR. The components of low (0.05-0.075Hz) and mid (0.075-0.15Hz)-frequency bands of heart rate variability are considered from pressure-derived-fluctuation dependent on the vasomotor tone and the baroreceptor reflex of arteries. On the other hand, high frequency (0.15-0.45Hz) component of the heart rate fluctuation with respiratory cycle is decreased by arterial elasticity and is induced to propagation time variation directly. Therefore, (sigma PFRP.mRP-1)/(sigma PFRR.mRR-1) in high frequency band was proposed as an index for assessment of wave transform characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Cell proliferation and differentiation of cultured chondrocytes isolated from growth plate cartilage of rat rib.

The present study was undertaken to investigate the relationship among cell morphology, proliferation, and maturation of chondrocytes in primary cultures. Chondrocytes were isolated from the growth cartilages of the rat ribs and cultured for 6 days. In situ DNA cytofluorometry using an inverted epi-illumination cytofluorometer (Nikon P1-I) and 3H-thymidine autoradiography were carried out for the correlated analysis of cell morphology and proliferation. Cytoskeletal staining with fluorescent phalloidin and 35S-sulphate autoradiography were also performed. In addition, in situ hybridization to c-myc mRNA was carried out using DNA probe. According to the results obtained, the cultured chondrocytes were composed of mixed populations of large, polygonal cells and of small, round cells. The round cells showed a significantly higher 35S uptake than the polygonal cells. The cytoskeletal staining clearly revealed stress fibers in the cytoplasm of the polygonal cells, whereas only a fine filamentous structure was shown in the cytoplasm of the round cells. In situ DNA cytofluorometry clearly demonstrated that cell proliferative activity was high in the polygonal cells and low in the round cells. In addition, 3H-thymidine autoradiography with cumulative labeling method revealed that the polygonal cells were changing into the small, round cells. C-myc mRNA signals were detected in the cytoplasm of over a half of the round cells, whereas no evidence of c-myc expression were found in the polygonal cells. From these results, it appears that as the shape of the cultured chondrocytes shifts from polygonal to round, the cell proliferative activity decreases in association with cell differentiation. It was also suggested that c-myc mRNA is amplified in the well differentiated round chondrocytes, and not in the proliferative polygonal cells.

Animals↗
PubMed1995

Role of ultrasound in managing neuroblastoma detected by mass screening: a proposed ultrasonographic grading for children with neuroblastoma.

The ultrasonographic (US) findings of 25 infant cases detected by the Japanese mass screening program for neuroblastoma (NB) were reviewed. The following results were obtained: An identification of the primary site was possible in 96% of the cases with abdominal US. An estimation of the tumor weight was possible based on the mass volume, which was calculated from US measurements. With the combination of the estimated mass volume, local involvement, and distant metastasis, the US grading of NB was possible and closely corresponded to the surgical staging (84%). The NB cases of adrenal origin at U1a, with a mass volume of less than 16 mL, were all found to be stage I and presented the possibility for spontaneous regression.

Adrenal Gland Neoplasms↗
PubMed1995

Tumor necrosis factor-alpha and interferon-gamma inhibit synergistically viral replication in hepatitis B virus-replicating cells.

The effects of tumor necrosis factor-alpha and/or interferon-gamma on the replication of hepatitis B virus were examined using HB611 cells. These cells were derived from human hepatoblastoma cells, Huh6, by integrating hepatitis B virus DNA, and produce hepatitis B virus continuously. Each of the cytokines inhibited hepatitis B virus replication in the cells assessed as the amount of episomal hepatitis B virus DNA, without a decrease in cell viability. When the two cytokines were administered together, the inhibitory effect became greater. Incubation of the cells with 1,000 U/ml tumor necrosis factor-alpha decreased HBV DNA replicative intermediates by 55%, and that with 1,000 U/ml interferon-gamma decreased these by 51%. Furthermore, incubation with 1,000 U/ml tumor necrosis factor-alpha and 1,000 U/ml interferon-gamma in combination decreased HBV DNA replicative intermediates by 71%. In contrast, the amount of hepatitis B virus RNA and secretion of hepatitis B e antigen were not apparently reduced by the cytokines, and 2',5'-oligoadenylate synthetase activity was not detected in the supernatant. These results suggest that tumor necrosis factor-alpha and interferon-gamma inhibit hepatitis B virus replication by blocking some step in reverse transcription and that the 2',5'-oligoadenylate synthetase is not involved in the mechanism underlying the inhibition by these two cytokines.

2',5'-Oligoadenylate Synthetase↗