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Biomedical subjects

S Tsuji

Publications and source records attributed to S Tsuji.

At least 163 records · Page 9Linked to original sources
PubMed2000

Probability of hepatocellular carcinoma of small hepatocellular nodules undetectable by computed tomography during arterial portography.

Recent advances in imaging modalities enable the identification of small hepatocellular nodules. Among the imaging techniques currently used for detecting hepatocellular carcinomas (HCC), computed tomography (CT) during arterial portography (CTAP) is one of the most sensitive techniques available for detecting hemodynamic change. Even so, well-differentiated HCCs that display only limited hemodynamic change, a feature shared with nonmalignant hepatocellular nodules, are not always detectable by CTAP. To improve our ability to distinguish well-differentiated HCCs from nonmalignant hepatocellular nodules, we have attempted to clarify how the characteristics of the nodules are shown by each imaging technique. We studied the imaging and pathological characteristics of 31 nodules (in 22 patients) detected by ultrasonography (US), but not by CTAP. Histological diagnoses were as follows: HCC, 17 of 31 nodules (55%); high-grade dysplastic nodules, 1 of 31 (3%); and nonmalignant nodules, 13 of 31 (42%). Neither digital substraction angiography (DSA) nor CT arteriography (CTA) were able to detect any of the nodules. Detection rates for plain CT were: 5 of 17 (29%) HCC, 1 of 1 (100%) high-grade dysplastic nodules, and 1 of 13 (8%) nonmalignant nodules. Detection rates for T1/T2-weighted magnetic resonance imaging (MRI) were: 4 of 17 (24%) HCC, 1 of 1 (100%) high-grade dysplastic nodules, and 3 of 13 (23%) nonmalignant nodules. Dynamic CT and dynamic MRI provided no additional information. In conclusion, there is some probability that hepatocellular nodules detected by US, but not by CTAP, are HCC. Presently, it is difficult to distinguish between benign nodules and malignant ones with these imaging techniques, and our findings indicate that biopsy may be advisable for nodules detected under these conditions.

Adult↗
PubMed2000

Expression of cyclooxygenase-2 and nitrotyrosine in human gastric mucosa before and after Helicobacter pylori eradication.

To determine whether cure of Helicobacter pylori infection influences the expression of COX-2 and nitrotyrosine in the distal stomach of humans, biopsy specimens were examined immunohistochemically. H. pylori infection was determined using a rapid urease test, culture and histology. Positive staining of COX-2/nitrotyrosine in the epithelium was expressed as the percentage of stained cells to the total epithelial cells. There was a significant increase in COX-2/nitrotyrosine staining in H. pylori -positive subjects compared with H. pylori -negative subjects. Cure of the infection resulted in a significant decrease in both COX-2/nitrotyrosine staining in all patients (52.1+/-12.1% vs 15. 4+/-7.2%, P<0.001; and 57.3+/-13.6% vs 36.1+/-18.0%, P<0.01, respectively). However, immunoreactivity of COX-2/nitrotyrosine was observed in all cases with intestinal metaplasia even after the cure of H. pylori infection.Thus, cure of H. pylori infection may decrease the risk of gastric carcinogenesis due to COX-2 and NO-related compounds in gastric mucosa but not in those patients with intestinal metaplasia.

Adult↗
PubMed2000

A comparative analysis of the antigenic, structural, and functional properties of three different preparations of recombinant human interleukin-18.

We compared the structural and functional properties of three recombinant human interleukin-18 (rIL-18) preparations, commercially available (Pep rIL-18) and prepared in our laboratory (active and inactive, according to their ability to potentiate IL-12-mediated interferon-gamma [IFN-gamma] induction in lymphocytes). All three preparations showed multimer formation on SDS-PAGE/immunoblotting using monoclonal antibodies (mAb) against the inactive form of rIL-18. In contrast, only the 18-kDa bands were recognized in each sample by mAb against the active form of rIL-18. The amounts of multimers and the 18-kDa moiety of Pep rIL-18 resembled those of the inactive rather than the active form. Likewise, the reaction profile of Pep rIL-18 toward mAb was very similar to that of inactive but not active rIL-18 on sandwich ELISA. Pep rIL-18 potentiated IFN-gamma-inducing activity together with IL-12, but its potency was 100-fold less than that of the active rIL-18, and excess doses were required for its activity. The inactive rIL-18 showed virtually no IFN-gamma-inducing ability, but when reduced and reconstituted, it inhibited the IFN-gamma-inducing activity of active rIL-18. These results suggest that there are two categories of recombinant IL-18 that are structurally, functionally, and antigenically different, and the mAb 125-2H and 21 can discriminate these two IL-18 populations by recognizing the epitopes specifically expressed on active and inactive IL-18, respectively.

Animals↗
PubMed2000

A novel viral alpha2,3-sialyltransferase (v-ST3Gal I): transfer of sialic acid to fucosylated acceptors.

The substrate specificity of an alpha2,3-sialyltransferase (v-ST3Gal I) obtained from myxoma virus infected RK13 cells has been determined. Like mammalian sialyltransferase enzymes, the viral enzyme contains the characteristic L- and S-sialyl motif sequences in its catalytic domain. Analysis of the deduced amino acid sequences of cloned sialyltransferases suggests that v-ST3Gal I is closely related to mammalian ST3Gal IV. v-ST3Gal I catalyzes the transfer of sialic acid from CMP-NeuAc to Type I (Galbeta1-3GlcNAcbeta) II (Galbeta1-4GlcNAcbeta) and III (Galbeta1-3GalNAcbeta) acceptors. In addition, the viral enzyme also transfers sialic acid to the fucosylated acceptors Lewis(x) and Lewis(a). This substrate specificity is unlike any sialyltransferases described to date, though it is most comparable with those of mammalian ST3Gal IV enzymes. The products from reactions with fucosylated acceptors were characterized by capillary zone electrophoresis, (1)H-NMR spectroscopy and mass spectrometry. They were shown to be 2,3-sialylated Lewis(x) and 2,3-sialylated Lewis(a), respectively.

Animals↗
PubMed2000

Reduction of the major xenoantigen on glycosphingolipids of swine endothelial cells by various glycosyltransferases.

The effect of the various glycosyltransferases on glycosphingolipids was examined, using transfected swine endothelial cell (SEC) lines. The reactivity of parental SEC to normal human serum (NHS) and Griffonia simplicifolia IB(4) (GSIB4) lectin, which binds to the Gal alpha1-3 Gal beta 1-4 GlcNAc-R (alpha-galactosyl epitope), was reduced by approximately 20% by the treatment with D-PDMP (D-threo-1-phenyl-2-decan- oylamino-3-morpholino-1-propanol), suggesting that glycosphingolipids contained by SEC have a considerable amount of the alpha-galactosyl epitope. The overexpression of two different types of glycosyltransferase, N-acetylglucosaminyl transferase III (GnT-III), as well as alpha2, 6-sialyltransferase (ST6Gal I), alpha2,3-sialyltransferase (ST3Gal III), and alpha1,2-fucosyltransferase (alpha1,2FT), suppresses the total antigenicity of SEC significantly. However, the reduction in reactivities toward NHS and GSIB4 lectin in the case of GnT-III transfectants was milder than those in other transfectants. Western blot analysis indicated that the glycoproteins in all transfectants had diminished reactivity to NHS and GSIB4 lectin to approximately the same extent. Therefore, the neutral glycosphingolipids of these transfectants were separated by thin layer chromatography, followed by immunostaining with NHS and GSIB4 lectin. The levels of the alpha-galactosyl epitope in glycosphingolipids were not decreased in the GnT-III transfectants but were in the ST6Gal I, ST3Gal III, and alpha1,2FT transfectants. These data indicate that ST6Gal I, ST3Gal III, and alpha1,2FT reduced the alpha-galactosyl epitope in both glycoproteins and glycosphingolipids, while GnT-III reduced them only in glycoproteins.

Animals↗
PubMed2000

Comparative analysis of the genomic structures and promoter activities of mouse Siaalpha2,3Galbeta1,3GalNAc GalNAcalpha2, 6-sialyltransferase genes (ST6GalNAc III and IV): characterization of their Sp1 binding sites.

The genomic organization of the genes encoding the mouse N-acetylgalactosamine alpha2,6-sialyltransferase specific for Siaalpha2,3Galbeta1,3GalNAc (ST6GalNAc III and IV) has been determined. The ST6GalNAc III gene spans over 120 kilobases of genomic DNA with 5 exons; on the other hand, the ST6GalNAc IV gene spans over 12 kilobases of genomic DNA with 6 exons. But the exon-intron boundaries of these genes are very similar. The 5'-flanking regions of these genes do not contain a TATA- or CAAT-box but have three putative Sp1 binding sites for each promoter. Transient transfection experiments demonstrated functional promoter activity in an ST6GalNAc III-expressing cell line, P19, for the ST6GalNAc III promoter, and in an ST6GalNAc IV-expressing cell line, NIH3T3, for the ST6GalNAc IV promoter. Mobility shift assaying and mutational analysis of the promoter region indicated that two of the three Sp1 binding sites are involved in the transcriptional regulation of the ST6GalNAc III gene in P19 cells, while all three Sp1 binding sites are involved in the transcriptional regulation of the ST6GalNAc IV gene in NIH3T3 cells.

3T3 Cells↗
PubMed2000

Molecular cloning and genomic analysis of mouse GalNAc alpha2, 6-sialyltransferase (ST6GalNAc I).

cDNA clones encoding mouse GalNAc alpha2,6-sialyltransferase (ST6GalNAc I) were isolated from a mouse submaxillary gland cDNA library. The deduced amino acid sequence of cDNA clones is 526 amino acids in length and has highly conserved motifs among sialyl transferases, sialyl motifs L, S, and VS. The expressed recombinant enzyme exhibited similar substrate specificity to chicken ST6GalNAc I. The mouse ST6GalNAc I gene was expressed in submaxillary gland, mammary gland, colon, and spleen. The mouse ST6GalNAc I gene was also cloned from a mouse genomic library, which was divided into 9 exons spanning over 8 kilobases of genomic DNA. The genomic structure of the mouse ST6GalNAc I gene was similar to that of the mouse ST6GalNAc II gene. Unlike the ST6GalNAc II gene, however, which has a housekeeping gene-like promoter with GC-rich sequences, the ST6GalNAc I gene has two promoters and they do not contain GC-rich sequences but contain putative binding sites for tumor-associated transcription factors such as c-Myb, c-Myc/Max, and c-Ets. Analysis of the 5'-RACE PCR products suggested that the mouse ST6GalNAc I gene expression is regulated by these two promoters in tissue-specific manners.

Amino Acid Sequence↗
PubMed2000

Genomic organization and transcriptional regulation of the mouse GD3 synthase gene (ST8Sia I): comparison of genomic organization of the mouse sialyltransferase genes.

The genomic organization of the gene encoding the mouse GD3 synthase (ST8Sia I) has been determined. The mouse ST8Sia I gene spans over 100 kilobases of genomic DNA with a unique genomic structure of 5 exons. Analysis of the sequence immediately upstream of the transcription initiation site revealed that the ST8Sia I promoter contained no canonical TATA- or CCAAT-box, but contained a putative Sp1 binding site. Transient transfection experiments demonstrated functional promoter activity of the ST8Sia I promoter in an ST8Sia I-expressing cell line, P19, but not in an ST8Sia I-nonexpressing cell line, NIH3T3. Mobility shift assay and mutation analysis of the promoter region indicated that the Sp1 binding site is involved in the transcriptional regulation of the ST8Sia I gene in P19 cells. Here, the genomic structural analyses of mouse sialyltransferase genes are summarized and the genomic structures of these genes are compared.

Animals↗
PubMed2000

Effect of inhaled nitric oxide on cardiovascular response to catecholamine in heart failure.

We examined the dose responses to continuous infusion of isoproterenol (ISO) and norepinephrine (NE) in normal (control) and procainamide-induced heart failure dogs with or without inhalation of 70 ppm nitric oxide (NO). Inhaled NO affected neither left ventricular (LV) function nor hemodynamics at baseline in both control and heart failure dogs. There were no significant differences in the responses to ISO and NE with or without inhaled NO in the control. The responses of LV dP/dt to ISO and NE were significantly enhanced in heart failure; however, they were not affected by inhaled NO. In contrast, LV pressure and dimension at end diastole were significantly increased, and pulmonary vascular resistance (PVR) was significantly decreased by inhaled NO during infusion of both ISO and NE in heart failure. In conclusion, the positive inotropic response to cathecholamine is not affected by inhaled NO even in heart failure. Inhaled NO decreases PVR, but potentially increases LV preload in the presence of additional stress of cathecholamine in heart failure.

Administration, Inhalation↗
PubMed2000

Maturation of human dendritic cells by cell wall skeleton of Mycobacterium bovis bacillus Calmette-Guérin: involvement of toll-like receptors.

The constituents of mycobacteria are an effective immune adjuvant, as observed with complete Freund's adjuvant. In this study, we demonstrated that the cell wall skeleton of Mycobacterium bovis bacillus Calmette-Guérin (BCG-CWS), a purified noninfectious material consisting of peptidoglycan, arabinogalactan, and mycolic acids, induces maturation of human dendritic cells (DC). Surface expression of CD40, CD80, CD83, and CD86 was increased by BCG-CWS on human immature DC, and the effect was similar to those of interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), heat-killed BCG, and viable BCG. BCG-CWS induced the secretion of TNF-alpha, IL-6, and IL-12 p40. CD83 expression was increased by a soluble factor secreted from BCG-CWS-treated DC and was completely inhibited by monoclonal antibodies against TNF-alpha. BCG-CWS-treated DC stimulated extensive allogeneic mixed lymphocyte reactions. The level of TNF-alpha secreted through BCG-CWS was partially suppressed in murine macrophages with no Toll-like receptor 2 (TLR 2) or TLR4 and was completely lost in TLR2 and TLR4 double-deficient macrophages. These results suggest that the BCG-CWS induces TNF-alpha secretion from DC via TLR2 and TLR4 and that the secreted TNF-alpha induces the maturation of DC per se.

Antigen Presentation↗
PubMed2000

Comparison of genomic structures of four members of beta-galactoside alpha2,3-sialyltransferase genes in the mouse.

The mouse genes encoding beta-galactoside alpha2, 3-sialyltransferases-Siat4 (ST3Gal I), Siat5 (ST3Gal II), Siat3 (ST3Gal III), and Siat4c (ST3Gal IV)-were isolated and characterized. Siat4 and Siat5 comprise 8.4 and 14 kb, respectively, and are composed of six exons each. The genomic structures of the two genes were similar. Siat3 and Siat4c comprise over 100 and 9.7 kb, respectively, and are composed of 12 and 10 exons, respectively. Although the genomic sizes of these genes differ, some of their exon structures are significantly similar. These results suggest that the gene pair Siat4 and Siat5 arose from a common ancestral gene, as did the two genes Siat3 and Siat4c.

Amino Acid Motifs↗
PubMed2000

Model dependence in quantification of spike interdependence by joint peri-stimulus time histogram.

Multineuronal recordings have enabled us to examine context-dependent changes in the relationship between the activities of multiple cells. The joint peri-stimulus time histogram (JPSTH) is a much-used method for investigating the dynamics of the interdependence of spike events between pairs of cells. Its results are often taken as an estimate of interaction strength between cells, independent of modulations in the cells' firing rates. We evaluate the adequacy of this estimate by examining the mathematical structure of how the JPSTH quantifies an interaction strength after excluding the contribution of firing rates. We introduce a simple probabilistic model of interacting point processes to generate simulated spike data and show that the normalized JPSTH incorrectly infers the temporal structure of variations in the interaction parameter strength. This occurs because, in our model, the correct normalization of firing-rate contributions is different than that used in Aertsen, Gerstein, Habib, and Palm's (1989) effective connectivity model. This demonstrates that firing-rate modulations cannot be corrected for in a model-independent manner, and therefore the effective connectivity does not represent a universal characteristic that is independent of modulation of the firing rates. Aertsen et al.'s (1989) effective connectivity may still be used in the analysis of experimental data, provided we are aware that this is simply one of many ways of describing the structure of interdependence. We also discuss some measure-independent characteristics of the structure of interdependence.

Brain↗
PubMed2000

[Development and evaluation of a local area network system to make drug information paper for inpatient--adaptation to characteristics of diseases, and expansibility to other hospitals and the Internet].

We developed and evaluated a local area network system to make drug information papers. Because pharmacists should explain drug information both orally and using papers to patients in response to their understanding and characteristics of their diseases. The merit of this system is as follows: pharmacists can use it without any education for its operation; most data can be inputted by selection from the lists and automatic reference; the data are adjustable for individuals; different contents are available for different wards; multiple users can access the same data file. Input data in this system are available for making explanation papers on the medical examination of outpatients, and making a plan for pharmaceutical care and guidance services. This system is also available in other hospitals, and on the internet. First, we surveyed the time required for preparing drug information papers. Making a hand written paper for typical patient takes 395 sec. for manuscript, 160 sec. with the system using text data only, and 178 sec. with the system using text and picture data. Next, we surveyed 27 patients' views on the addition of drug pictures to drug information papers, and with the result that 19 patients thought it very good. Last, we surveyed 13 ward pharmacists about their usage of this system. We found that 8 pharmacists used frequently this system, and 3 pharmacists used the same file in the same hours at the maximum.

Aged↗
PubMed2000

A novel minisatellite repeat expansion identified at FRA16B in a Japanese carrier.

Previously, the allelic expansion of a 33-bp AT-rich minisatellite repeat has been reported to cause FRA16B, a distamycin A-inducible fragile site. Here, we identified a novel 35-bp minisatellite repeat at FRA16B in a Japanese carrier. The nucleotide sequence of the 35-bp minisatellite was highly AT-rich and nearly identical to the 33-bp one but with insertion of two nucleotides, thymine and adenine. The copy number of the AT-rich minisatellite was 21 in total in the carrier, while only a few copies of the 33-bp minisatellite were present in a non-carrier Japanese subject. These results suggest that the molecular mechanism involved in the allelic expansion of the minisatellite repeat in FRA16B recognizes both minisatellites, the 33-bp one and the 35-bp one, as an amplicon. These observations were different from the ones at folate-sensitive fragile sites, where the CCG triplet repeat was commonly involved in the allelic expansion. Although a slight reduction in AT content (95% > 90%) in the region of minisatellite expansion in the carrier subject was observed, both AT-content and length of the highly AT-rich region seem to play important roles in the cytogenetic expression of the distamycin A-inducible fragile site. In another normal subject, without fragile site expression, allelic expansion involving the 33-bp minisatellite was observed, and the length of the AT-rich DNA region was increased up to approximately 1000 bp. Since the length of the AT-rich minisatellite region was increased up to approximately 1,100-bp in the carrier subject, the threshold length for the cytogenetic expression of the AT-rich DNA region may be between about 1,000-bp and 1,100-bp.

Asian People↗
PubMed2000

Mutational analysis of X-linked adrenoleukodystrophy gene.

X-linked adrenoleukodystrophy (ALD) is an inherited peroxisomal disorder characterized by progressive neurological dysfunction, occasionally associated with adrenal insufficiency. The clinical phenotypes of ALD are quite variable, and include childhood ALD, adult-onset ALD, adrenomyeloneuropathy, and Addison's disease only. Although the causative gene for ALD has been identified, the physiological role of the gene product remains to be clarified. Despite many mutations having been identified in patients with these clinical phenotypes, the genotype-phenotype correlations have not been clarified. The authors investigated genotype-phenotype correlations in ALD by analyses on 29 unrelated Japanese patients with ALD and by a review of the literature. All the phenotypes were associated with mutations leading to protein truncation, as well as those resulting in subtle amino acid changes. Furthermore, there were no differences in phenotypic expression among the natures of the subtle amino acid changes. All these data indicate that no obvious correlations exist between the phenotypes of ALD patients and their genotypes, suggesting that other genetic or environmental factors may also be involved in determining phenotypic expression in ALD.

Adrenoleukodystrophy↗
PubMed2000

Immunohistochemical analysis of apoptosis-related proteins in human embryonic and fetal pancreatic tissues.

BACKGROUND: The growth of both cancer cells and fetal tissue is rapid; however, cancer cells de-differentiate and proliferate in a disorderly manner, whereas fetal tissues differentiate and proliferate in an orderly manner. Thus, there may be both common and different factors that are involved in the process of the uncontrolled cell growth of pancreatic cancers and the development of the fetal pancreas. The common part of the mechanisms should be in the regulation of the cell cycle, resulting in rapid proliferation via such mechanisms as growth stimulation and avoidance of apoptosis. Therefore, in the current study we investigated the expression of apoptosis-related proteins in fetal pancreatic tissues. METHODS: Sixteen human embryonic and fetal pancreatic tissues obtained between 6 and 32 wk of gestation were used. We immunohistochemically examined the protein expression of Bcl-2, Bcl-XL, Mcl-1, and Bax. Further, the expression of insulin, glucagon, and proliferting cell nuclear antigen (PCNA), and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining were examined. RESULTS: In embryonic and fetal pancreatic tissues, Bcl-2 was not detected in any type of pancreatic cell (acinar, ductal, or islet). Bcl-XL was expressed in all types of pancreatic cells throughout the gestation. Mcl-1 was expressed in all types of pancreatic components, and strongly expressed in the margin of the islets. Bax, a pro-apoptotic protein, was expressed in all components. PCNA was strongly expressed in the embryonic and fetal pancreas, especially in early stages of gestation; however, TUNEL staining was negative in all samples. At least one antiapoptotic protein was expressed in all types of pancreatic cells. CONCLUSION: The results of the current study indicate that active proliferation and avoidance of apoptosis take place in embryonic and fetal pancreatic tissues, which may be controlled by particular combinations of apoptosis-related proteins. Among these proteins, Bcl-XL and Mcl-1 may play an important role in the proliferation and differentiation of the embryonic and fetal pancreas.

Apoptosis↗
PubMed2000

Left atrial systolic function assessed by left atrial ejection force in patients with sick sinus syndrome and paroxysmal atrial fibrillation.

We evaluated left atrial systolic function using left atrial ejection force (LAEF) in 19 patients with sick sinus syndrome (SSS) and in 20 with paroxysmal atrial fibrillation (Paf) whose ages ranged from 48 to 80 years. We also evaluated 35 normal individuals for comparison. The LAEF was calculated as 1/3 x mitral valve area x (peak velocity of A wave)2 using two-dimensional and pulsed-Doppler echocardiography according to Newton's law of motion and hydrodynamics. In normal individuals, LAEF positively correlated with age (r = 0.82, p < 0.01). Normal LAEF was calculated as 0.098 x age - 0.74 (kdynes) from the regression line. Because of this correlation, we used age-corrected LAEF (%LAEF) that was calculated as (measured LAEF / normal LAEF) x 100. The results showed that this value was 53+/-26% in patients with SSS and 54+/-26% in patients with Paf. Both were significantly lower than normal individuals (p < 0.001). Among SSS subtypes, %LAEF was lower in types II and III than in type I (51+/-14%, 37+/-19%, and 81+/-35%, respectively). In conclusion, left atrial systolic function is depressed in patients with Paf and SSS, in particular, types II and III. These results suggest that the pathological abnormalities extend not only to the sinus node but also to the left atrial muscle in patients with SSS and Paf.

Aged↗