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A Uchiyama

Publications and source records attributed to A Uchiyama.

At least 73 records · Page 4Linked to original sources
PubMed1997

Nonlinear analysis of visual evoked potentials elicited by color stimulation.

The relationship between chromatically modulated stimuli and visual evoked potentials (VEPs) was considered. VEPs of normal subjects elicited by chromatically modulated stimuli were measured under several color adaptations, and their binary kernels were estimated. Up to the second-order, binary kernels obtained from VEPs were so characteristic that the VEP-chromatic modulation system showed second-order nonlinearity. First-order binary kernels depended on the color of the stimulus and adaptation, whereas second-order kernels showed almost no difference. This result indicates that the waveforms of first-order binary kernels reflect perceived color (hue). This supports the suggestion that kernels of VEPs include color responses, and could be used as a probe with which to examine the color visual system.

Adaptation, Ocular↗
PubMed1996

Molecular cloning of cDNA encoding rat very long-chain acyl-CoA synthetase.

The cDNA encoding rat very long-chain acyl-CoA synthetase (VLACS) was cloned, using degenerative primers synthesized according to the partial amino acid sequences of the peptide fragments of the purified rat liver enzyme. The longest cDNA insert was 2972 base pairs with a 1860-base pair open reading frame encoding 620 amino acids. The calculated molecular mass of 70,692 daltons was consistent with size of the purified enzyme. In Northern blot analysis, a single band was detected at the position of about 3 kilobases, corresponding to the size of the cloned cDNA. cDNA-directed expression in Escherichia coli resulted in accumulation of expressed protein, as an inclusion body. An antibody was raised using this expressed protein to characterize the cDNA and the enzyme. The subcellular localization of VLACS in peroxisomes and microsomes was demonstrated in Western blot analysis. The specific activity and the substrate specificity of the cDNA expressed enzyme in COS-1 cells were consistent with those of the purified rat enzyme. The predicted amino acid sequence of VLACS had a high sequence similarity to fatty acid transport protein (Schaffer, J. E., and Lodish, H. F. (1994) Cell 79, 427-436), and was considered to have domains for adenylation and thioester formation. The entire structure of VLACS was dissimilar to that of long-chain acyl-CoA synthetase (Suzuki, H., Kawarabayashi, Y., Kondo, Y., Abe, T., Nishikawa, K., Kimura, S., Hashimoto, T., and Yamamoto, T. (1990) J. Biol. Chem. 265, 8681-8685), except for the domains.

Amino Acid Sequence↗
PubMed1996

Interleukin 4 inhibits hepatocyte growth factor-induced invasion and migration of colon carcinomas.

Hepatocyte growth factor (HGF) is known to have a number of biological properties including promoting tumor progression of human carcinomas. Metastasis involves a number of events that are attributed to induction by paracrine factors such as HGF. Identification of natural inhibitors of these events would allow better control of tumor progression. Recently we demonstrated that interleukin 4 (IL-4) can regulate proliferation of various human carcinoma cell lines. In the present study, we used established human colon carcinoma cell lines and primary colon carcinoma cell cultures to determine if IL-4 could regulate HGF-induced cell proliferation and other events of tumor progression such as MMP (matrix metalloproteinases)-1, -2, and -9 production, cell migration and cell-matrix invasive activity. All colon carcinoma cell lines expressed HGF and IL-4 receptors. IL-4 significantly inhibited HGF-induced proliferation of one cell line. Cell-matrix invasion was significantly enhanced by HGF (0.1-10 ng/ml); IL-4 (1-10 U/ml) significantly inhibited HGF-induced invasion in a dose-dependent manner. IL-4 also inhibited HGF-induced cell-matrix invasion of metastatic colon carcinoma cells and HGF-induced cell migration. HGF enhanced MMP-1, -2, and -9 production by cell lines. This effect could be inhibited by IL-4. These findings indicate that IL-4 is a potent inhibitor of HGF-induced invasion and metastasis-related functions of human colon carcinoma cells.

Antigens, CD↗
PubMed1996

In vitro analysis of peritoneal adhesions in peritonitis.

Peritoneal adhesions due to peritonitis make surgery more difficult and may cause complications. Clarifying the formation mechanism of peritoneal adhesions could help identify methods useful for their prevention. We cultured mesothelial monolayers on plates and microcarriers to simulate the parietal and visceral peritoneum, respectively. We then investigated the effects of lipopolysacchride (LPS) and tumor necrosis factor (TNF) on the homologous adhesion of these mesothelial monolayers. There was no adhesion of mesothelial monolayers in the control medium. When monolayers were cultured with endotoxin (LPS), approximately 90% of the microcarriers adhered to the mesothelial microplate. Adhesions occurred at LPS concentrations of 10 ng/ml and increased linearly in a dose-dependent manner. Kinetic studies revealed that the mesothelial adhesion appeared at 12 hr, and that 90% of the microcarriers were adherent after 24 hr. Open intercellular spaces were observed after a 24-hr treatment with LPS. Scanning electron microscopy revealed that the mesothelial cells adhered to the naked glass. LPS also caused increased permeability of the mesothelial monolayer. TNF did not cause any significant adhesion. Through our experiments we were able to develop an in vitro model of peritoneal adhesion using peritoneal mesothelial cell culture. Endotoxin caused an increase in homologous adhesion of peritoneal mesothelial monolayers, which may correspond to the initial stage of peritoneal adhesion formation in peritonitis.

Dose-Response Relationship, Drug↗
PubMed1996

Diurnal variations in resting-active cycles in full-term fetal heart rate changes.

To elucidate the mechanism of the resting-active cycles (RAC) of fetal heart rates (FHR), in the resting and non-resting phases (RP and NRP), 24-h FHR recordings were made on 16 normal full-term pregnant women. RP, NRP, RAC-1 (NRP-NRP cycle), and RAC-2 (RP-RP cycle) were defined based on the criteria of Nijhuis et al. Frequency distributions were plotted separately for the entire 24-h period as well as for the day-time (07:00-21:00 h) and night-time (21:00-07:00 h), and were compared using Kolmogorov-Smirnov two-sample tests. The mean durations (+/- S.D.) (min) of RP, NRP, RAC-1, and RAC-2 were 22.7 +/- 11.2, 67.3 +/- 47.2, 90.0 +/- 47.6, and 89.9 +/- 48.6 during 24-h periods, 20.1 +/- 7.7, 68.3 +/- 52.3, 88.6 +/- 53.1, and 88.4 +/- 53.0 during the day-time, and 25.4 +/- 13.2, 66.2 +/- 41.2, 91.4 +/- 41.0, and 91.5 +/- 43.4 during the night-time. Length of RP was the only factor significantly different during the day and night (P < 0.05). We propose that there are different mechanisms controlling RP and NRP.

Activity Cycles↗
PubMed1996

Mucopolysaccharidosis type I: identification of common mutations that cause Hurler and Scheie syndromes in Japanese populations.

alpha-L-Iduronidase (IDUA) deficiency (mucopolysaccharidosis type I; MPS-I) is an inborn error of lysosomal degradation of glycosaminoglycans that results in storage of undegraded glycosaminoglycans in lysosomes. Previous studies in Caucasian populations showed that (1) homozygosity or compound heterozygosity for the W402X and Q70X mutations are the common causes of MPS-I with a severe form (Hurler syndrome), and (2) the presence of R89Q may lead to a milder phenotype. We studied mutations in the IDUA gene from 19 MPS-I patients, including two pairs of siblings, with various clinical phenotypes (Hurler, 6 cases; Hurler/Scheie, 7 cases; Scheie, 6 cases). We report the presence of two common mutations that account for 42% of the 38 alleles in these patients. One is a novel 5-bp insertion between the thymidine at nt 704 and a cytosine at nt 705 (704ins5), which is seen only in the Japanese population. The other is a missense mutation, R89Q, which is also seen in Caucasians, although uncommonly. In the 19 Japanese MPS-I patients, the 704ins5 mutation accounted for 7 of 38 alleles (18%), while the R89Q accounted for 9 of 38 (24%). No Japanese patient was found to carry the W402X or Q70X alleles, the two most common MPS-I mutations in Caucasians. Homozygosity for the 704ins5 mutation is associated with a severe phenotype, and for the R89Q mutation with a mild phenotype. Compound heterozygosity for these two mutations produced an intermediate phenotype. Haplotype analysis using polymorphisms linked to the IDUA locus demonstrated that each mutation occurs on a different specific haplotype, suggesting that individuals with each of these common mutations derive from common founders. These data continue to document the molecular heterogeneity and racial differences in mutations in MPS-I.

Adult↗
PubMed1996

Vascular endothelial growth factor and platelet-derived growth factor are potential angiogenic and metastatic factors in human breast cancer.

BACKGROUND: Angiogenesis is a prerequisite for tumor growth and metastasis. Tumor angiogenesis may be mediated by several angiogenic factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), transforming growth factor-alpha, and basic fibroblast growth factor. METHODS: Differential mRNA expressions of VEGF, PDGF (A chain), transforming growth factor-alpha and basic fibroblast growth factor in 32 primary invasive breast tumors were examined by reverse transcriptase-polymerase chain reaction. We analyzed relationships between mRNA expressions of these angiogenic factors and the degree of angiogenesis, tumor size, and metastasis. Quantification of angiogenesis was achieved by the immunohistochemical staining of endothelial cells with antibody to CD31. RESULTS: VEGF and PDGF-A mRNAs were expressed more frequently in breast tumors than in nontumor breast tissues, whereas no difference was found in expression frequency of either transforming growth factor-alpha or basic fibroblast growth factor mRNA. Vascular counts in tumors correlated with each expression frequency of VEGF and PDGF-A mRNA. PDGF-A mRNA was expressed more frequently in tumors with lymph node metastasis than in those without metastasis. CONCLUSIONS: Expression of VEGF and PDGF mRNAs detected by reverse transcriptase-polymerase chain reaction in breast tumors correlates with tumor-related characteristics of angiogenesis and metastatic potential. Analysis of these mRNAs by reverse transcriptase-polymerase chain reaction may be useful for assessing the biologic behavior of a breast tumor before surgical treatment.

Angiogenesis Inducing Agents↗
PubMed1995

Mucopolysaccharidosis type IVA: common double deletion in the N-acetylgalactosamine-6-sulfatase gene (GALNS).

Mucopolysaccharidosis IVA (MPS IVA) is an autosomal recessive disorder caused by a deficiency in N-acetylgalactosamine-6-sulfatase (GALNS). We found two separate deletions of nearly 8.0 and 6.0 kb in the GALNS gene, including some exons. There are Alu repetitive elements near the breakpoints of the 8.0-kb deletion, and this deletion resulted from an Alu-Alu recombination. The other 6.0-kb deletion involved illegitimate recombinational events between incomplete short direct repeats of 8 bp at deletion breakpoints. The same rearrangement has been observed in a heteroallelic state in four unrelated patients. This is the first documentation of a common double deletion a gene that is not a member of a gene cluster.

Base Sequence↗
PubMed1995

Mucopolysaccharidosis IVA: structural gene alterations identified by Southern blot analysis and identification of racial differences.

Ninety-six alleles (36 alleles of Japanese and 60 of Caucasian origin) from forty-eight patients with mucopolysaccharidosis IVA were investigated for structural gene alterations using Southern blot analysis. All patients had a previously demonstrated deficiency of N-acetyl-galactosamine-6-sulfate-sulfatase and exhibited a wide spectrum of clinical severity. Initially, using the full-length cDNA as a probe, five of 36 chromosomes from the Japanese patients revealed similar rearrangements with respect to DNA digested with BamHI, SacI, and XhoI. Subsequent analysis using seven genomic fragments, covering the entire gene, enhanced the detection of aberrant fragments produced by the above restriction enzymes. Conversely, the 60 chromosomes of Caucasian origin revealed no evidence of large structural rearrangements when analyzed by these methods. There was a statistically significant difference between the two populations (P < 0.01). A severely affected Japanese patient showed structural rearrangements on both chromosomes by means of BamHI blots. An 8.0-kb fragment and a highly polymorphic 7.0-kb to 11.0-kb fragment present in normal individuals disappeared and two aberrant fragments of 11.5 kb and 12.0 kb were observed. Three other Japanese patients also showed these two aberrant fragments, in addition to the normal fragment pattern, and were thus heterozygous for this rearrangement. Interpretation of Southern blots was difficult because of the complexity of polymorphic bands resulting from variable number of tandem repeat elements. However, by utilizing these aberrant fragments or polymorphic bands, carrier detection was effective, even in families with poorly characterized mutations. Hybridization with probe MG-A (5'-end genomic probe in intron 1) showed a 8.4-kb fragment in BamHI blots of one Japanese and one Caucasian patient; XhoI, SacI, and EcoRI blots were normal. Since this BamHI alteration was also observed in one normal control, it appears to be a rare nonpathological polymorphism.

Alleles↗
PubMed1995

Mucopolysaccharidosis IVA: polymorphic haplotypes and informative RFLPs in the Japanese population.

Seven different restriction fragment length polymorphisms (RFLPs) at the N-acetylgalactosamine-6-sulfate sulfatase (GALNS) locus were analyzed using Southern blotting and polymerase chain reaction based techniques to search for the frequency of each RFLP produced by StyI, SphI, HaeIII, StuI, HapII, XhoI, and BamHI restriction endonucleases, respectively, in 36 mutant alleles, including two sibling cases and 100 normal alleles. Calculation of heterozygosity indexes showed that these RFLPs were polymorphic, ranging from 0.31 to 0.69 in mucopolysaccharidosis IVA (MPS IVA) patients compared with 0.21 to 0.65 in normal individuals. There was some significant difference in several RFLPs and in the combination with four kinds of RFLPs (SphI, StuI, HapII, XhoI polymorphisms). The normal alleles were composed of 13 different RFLPs haplotypes; the most common among the Japanese population carrying normal alleles was haplotype 8 (bDEF1) (31.3%), the others being dispersed. The same haplotype 8 was the most frequent in the mutant alleles (44.4%), with seven further haplotypes. These findings revealed the striking variety of polymorphic haplotypes in the MPS IVA gene. By using these five kinds of RFLPs, we examined the theoretical informativity of haplotype analysis in heterozygote detection in nine unrelated MPS IVA families and ten unrelated normal families. All the members of the MPS IVA families studied were diagnosed as a patient, carrier, or non-carrier. We propose that prenatal diagnosis or family analysis in cases in which mutations have not been characterized is now feasible.

Base Sequence↗
PubMed1995

Pulmonary resistance in dogs: a comparison of xenon with nitrous oxide.

Xenon (Xe) may cause an increase in airway resistance due to its high density and viscosity. The object of this study was to examine the effects of Xe on pulmonary resistance using dog models with normal and methacholine-treated airways. During anaesthesia 22 mongrel dogs' tracheas were intubated and the lungs were mechanically ventilated with 70% N2/30% O2 as a control gas. The gases 70% nitrous oxide (N2O), 50% N2O, 70% Xe and 50% Xe were administered in a random order for 25 min. Bronchoconstriction was produced by a continuous infusion of methacholine, 0.22 mg.kg-1.hr-1. Pulmonary resistance (RL) was calculated by the isovolume method using flow at the airway opening, volume and transpulmonary pressure. In normal dogs, RL breathing 70% Xe (mean +/- SEM, 0.84 +/- 0.12 cm H2O.L-1.sec-1) was greater (P < 0.05) than with 70% N2O, 50% N2O or control gas (0.61 +/- 0.08, 0.59 +/- 0.06 and 0.62 +/- 0.06 cmH2O.L-1.sec-1). Breathing 50% Xe the RL (0.77 +/- 0.10 cmH2O.L-1.sec-1) was not different from 50% N2O or control. Methacholine infusion increased RL 3.92 +/- 1.98 (mean +/- SD) times. The RL breathing 50% Xe (2.55 +/- 0.44 cmH2O.L-1.sec-1) was not greater than during 50% N2O or control (2.08 +/- 0.33 and 2.13 +/- 0.33 cmH2O.L-1.sec-1) in methacholine-treated dogs. The data suggest that inhalation of high concentrations of Xe increases airway resistance, but only to a modest extent in dogs with normal or methacholine-treated airways.

Airway Resistance↗
PubMed1995

A possible role of TGF-beta in the formation of malignant effusions.

The detailed mechanisms underlying the formation of malignant effusions are incompletely defined. In order to determine whether transforming growth factor-beta (TGF-beta) would contribute to the formation of malignant effusions, we investigated the effect of TGF-beta on the morphology, growth, and permeability of human mesothelial cells, which are thought to serve as a permeability barrier in the pleuroperitoneal cavities. Treatment of the mesothelial cells with a TGF-beta dose ranging from 0.1 to 10 ng/ml for 96 hr induced distinct morphologic changes in the cells. Each cell increased in size as did the volume of the intercellular spaces. TGF-beta also significantly inhibited the growth of mesothelial cells at a concentration ranging from 0.1 to 10 ng/ml. This growth inhibition was blocked completely by the addition of anti-TGF-beta antibody. Treatment of the mesothelial cells with 2.0 ng/ml TGF-beta significantly increased the permeability of a mesothelial cell monolayer as assessed by a FITC-albumin permeability assay. In our clinical analysis using 10 effusion samples obtained from patients with various types of carcinoma cells, considerable level of TGF-beta could be detected by ELISA, ranged from 0.90 to 8.75 ng/ml. Our data suggest that TGF-beta plays an important role in the formation of malignant effusions through structural and functional damage to the mesothelial cells. Malignant effusions may accumulate in the pleuroperitoneal cavity as a result of the mesothelial cell damage caused by this cytokine which is released from disseminated cancer cells.

Adult↗
PubMed1995

A comparative evaluation of pressure-triggering and flow-triggering in pressure support ventilation (PSV) for neonates using an animal model.

The triggering system in pressure support ventilation needs to respond rapidly, especially in neonates. The aim of this study was to compare the effects of flow-triggered and pressure-triggered pressure support ventilation on neonatal mechanical ventilation using an animal model. Respiratory flow, airway pressure, oesophageal pressure, and diaphragmatic electromyogram were measured during pressure support ventilation in five anaesthetized rabbits. The animals were connected to a VIPBIRD (Bird, U.S.A.) (CPAP mode, pressure support ventilation, 5 cm H2O and PEEP 0 cm H2O). Flow-triggering sensitivity was set at 0.2l/min, 0.5l/min, 1.01l/min, or 1.5l/min. Pressure-triggering sensitivity was set at -1.0 cm H2O. Shorter trigger delay and longer pressure support time were observed in flow-triggering. There was also less diaphragmatic activity in flow-triggering as evidenced by the amplitude of integrated diaphragmatic electromyogram and negative deflection of oesophageal pressure. The findings suggest that flow-triggering will prove superior to pressure-triggering in pressure support ventilation for neonates.

Animals↗
PubMed1994

Interleukin 4 regulates G1 cell cycle progression in gastric carcinoma cells.

We have previously reported that interleukin 4 (IL-4) inhibits the growth of human gastric carcinoma cells. To investigate the mechanism for this inhibition we analyzed the effect of IL-4 on cell cycle progression of the IL-4-sensitive gastric carcinoma cell line, HTB-135. IL-4 significantly inhibited cell cycle G1-S-phase progression. To assess the postreceptor molecular events that transduced the negative-growth signals by IL-4, we analyzed the expression of cell cycle nuclear-regulating factors such as retinoblastoma gene product (Rbp), c-myc, c-myc protein (c-mycp), and cyclin D1 expression which are known to be regulators of G1-S-phase transition. IL-4 was found to induce an unphosphorylated form of Rbp within 24 h and significantly reduce the phosphorylated form at 48 h. The transition of Rbp to a hypophosphorylated form concurs with the decrease in c-myc gene expression and c-mycp. In addition, we demonstrated that IL-4 down-regulated p34cdc2, a kinase associated with Rbp phosphorylation and cyclin D1. Cyclin D1, considered as a critical nuclear regulatory factor of G0-G1 to S-phase transition was down-regulated 24 and 48 h post-IL-4 treatment as well. These studies suggest that IL-4 inhibits gastric cell proliferation by blocking cell cycle progression by down-regulating several key G0-G1 cell cycle nuclear-regulating factors.

Adenocarcinoma↗
PubMed1994

Identification of a nonsense mutation in ALD protein cDNA from a patient with adrenoleukodystrophy.

The molecular basis of X-linked adrenoleukodystrophy (ALD) was investigated. Six (A to 50) fragments of cDNA for ALD protein (Mosser et al. Nature 361: 726-730, 1993) from an adult patient with adrenomyeloneuropathy were amplified by PCR and mutations were screened by Mutation Detection Enhancement gel electrophoresis. A single base substitution (2154 C-->T, which resulted in the formation of a termination codon for glutamine (Q590STOP) and deletes Pst I site (CTGCAG-->CTGTAG), was detected. Eight other ALD patients did not have this mutation. A family study revealed the presence of both the mutant and normal alleles in the mother, a sister and a niece, indicating that these individuals were carriers. A nephew with childhood ALD who died 10 years earlier had the same mutant allele as detected by Pst I restriction assay. This report is the first description of a mutant allele for ALD, at the cDNA level, and presents confirmatory evidence of ALD protein as the primary etiology of ALD.

ATP Binding Cassette Transporter, Subfamily D, Mem↗
PubMed1994

Quantitative analysis of crosslinks pyridinoline and pentosidine in articular cartilage of patients with bone and joint disorders.

OBJECTIVE: To determine the content of two crosslinks, pyridinoline (a mature crosslink) and pentosidine (a senescent crosslink), in human articular cartilage, and to examine the effect of bone and joint disorders on the content of those crosslinks in articular cartilage. METHODS: After pretreatment with SP-Sephadex C-25, high-performance liquid chromatography was conducted on a hydrolysate of human articular cartilage from 53 patients with one of the following diseases: osteoarthritis (OA), rheumatoid arthritis (RA), osteoporosis, femoral head necrosis, and renal osteodystrophy (ROD). RESULTS: Pyridinoline levels were either unchanged with age or were slightly decreased in elderly patients. Pentosidine levels increased with age in the entire patient population. There was no significant difference in the pyridinoline content among the study groups, but there was a significant difference in pentosidine content (P < 0.001). ROD patients had the highest mean level of pentosidine (407 mumoles/mole of hydroxyproline), and RA patients had a higher mean level than age-matched OA patients (214 versus 103 mumoles/mole of hydroxyproline). CONCLUSION: Bone and joint disorders do not affect the pyridinoline content in articular cartilage, but they do not affect the pentosidine content.

Adult↗