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Biomedical subjects

H Fujita

Publications and source records attributed to H Fujita.

At least 19 recordsLinked to original sources
PubMed1992

Production of matrix metalloproteinase-2 and metalloproteinase-3 related to malignant behavior of esophageal carcinoma. A clinicopathologic study.

BACKGROUND: Matrix metalloproteinases (MMP) are a gene family of zinc enzymes capable of degrading almost all of the extracellular matrix macromolecules in vivo. Their enzymic activities are believed to be responsible for tumor invasion and metastasis. METHODS: In this study, using peroxidase-antiperoxidase method, monospecific antisera against MMP-1 (tissue collagenase), MMP-2 (type IV collagenase/72-kilodalton [KD] gelatinase), and MMP-3 (stromelysin) were applied to 29 squamous cell carcinomas and normal epithelium of the esophagus to identify cells synthesizing and secreting these enzymes. RESULTS: Immunoreactivity of MMP-1, -2, and -3 was observed in small cancer nests of the deeply invasive or marginal portion of the tumor. Among the 29 patients studied, the presence of at least one MMP was observed in 17 (58.6%). All three enzymes were observed in six (20.6%) patients, MMP-2 and -3 in five (17.2%) patients, only MMP-2 in three (10.3%) patients, and MMP-3 alone in three (10.3%) patients. There was a good correlation among histologic stage and tumor invasion, lymph node metastasis, and MMP expression. In particular, expression of MMP-2 and -3 was closely related to lymph node metastasis and vascular invasion. CONCLUSIONS: These results suggest that MMP, especially MMP-2 and -3, play an important role in tumor invasion and metastasis and that analysis of MMP-2 and -3 production is useful for evaluation of malignant potential in esophageal carcinoma.

Aged↗
PubMed1992

Boy with a chromosome del (3)(q12q23) and blepharophimosis syndrome.

We report on a 6-year-old boy with de novo 46,XY,del(3)(q12q23) and bilateral blepharophimosis, ptosis, epicanthus inversus, in addition to multiple other anomalies. Since 4 previously reported cases of interstitial deletion of 3q involving 3q23 band are clinically similar, we propose this blepharophimosis sequence due to 3q23 deletion as a further "contiguous gene syndrome."

Adult↗
PubMed1992

Two patients with chromosome 6q terminal deletions with breakpoints at q24.3 and q25.3.

We report on 2 patients with de novo terminal deletion of 6q. The first was a 4-month-old boy whose karyotype was 46,XY,del(6)(q24.3); the second a 2-year-old girl whose karyotype was 46, XX, del(6)(q25.3). The main anomalies in both patients included mental retardation, minor craniofacial and cerebral anomalies, and cardiac defects. The characteristic manifestations were imperforate anus in the first patient, and retinitis proliferans and a triatrial heart in the other. Comparison of clinical findings of our 2 patients with those of 18 previously reported patients with similar phenotypes suggests that terminal deletion of the 6q23 or 6q25 band is critical in producing the main anomalies of del(6q) syndrome.

Abnormalities, Multiple↗
PubMed1992

Isolation and sequencing of a cDNA clone encoding the 85 kDa human lysosomal sialoglycoprotein (hLGP85) in human metastatic pancreas islet tumor cells.

A full length cDNA for a human lysosomal membrane sialoglycoprotein (hLGP85) was isolated as a probe of the cDNA of rat LGP85 (rLGP85) from the cDNA library prepared from total mRNA of QGP-1NL cells, a human pancreatic islet tumor cell with a high metastatic activity. The deduced amino acid sequence shows that hLGP85 consists of 478 amino acid residues (MW. 54,289). The protein has 10 putative N-glycosylation sites and 2 hydrophobic regions at the NH2- and near the COOH-termini, respectively. Thus, both domains probably constitute putative transmembrane domains. It exhibits 86% and 79% sequence similarities in amino acids and nucleic acids to rat lysosomal membrane sialoglycoprotein (rLGP85), respectively. The protein contained the short cytoplasmic tail at the COOH-terminus which does not form the glycine-tyrosine sequence (GY motif), the so-called lysosomal targetting signal.

Adenoma, Islet Cell↗
PubMed1992

Heme oxygenase is a positive acute-phase reactant in human Hep3B hepatoma cells.

The effects of human interleukin-6 (hIL-6), the major acute-phase inducer, on the level of the transcript of microsomal heme oxygenase (HO) were examined in a human hepatoma cell line, Hep3B. Messenger RNAs (mRNAs) encoding HO and haptoglobin (Hpt) increased after hIL-6 treatment in a time- and dose-dependent manner. hIL-6 had no effect on the induction of heat-shock protein 70 (hsp70) mRNA, suggesting that the induction of HO by hIL-6 is regulated by a different mechanism from that which mediates the heat-shock induction of this enzyme. The hIL-6-mediated induction of HO mRNA was completely abrogated by simultaneous treatment of cells with actinomycin D, but not with cycloheximide, suggesting that the induction occurs at the level of transcription. A nuclear factor was shown both in untreated, and in the hIL-6-treated Hep3B cells that binds specifically to the IL-6-responsive element (IL6-RE) of the human HO gene. These findings suggest that HO is a positive acute-phase reactant in this human liver-derived cell line, and that the nuclear factor specific to the IL6-RE may be involved in the activation of the HO gene after hIL-6 treatment.

Acute-Phase Proteins↗
PubMed1992

The molecular defect of ferrochelatase in a patient with erythropoietic protoporphyria.

The molecular basis of an inherited defect of ferrochelatase in a patient with erythropoietic protoporphyria (EPP) was investigated. Ferrochelatase is the terminal enzyme in the heme biosynthetic pathway and catalyzes the insertion of ferrous iron into protoporphyrin IX to form heme. In Epstein-Barr virus-transformed lymphoblastoid cells from a proband with EPP, enzyme activity, an immunochemically quantifiable protein, and mRNA content of ferrochelatase were about one-half the normal level. In contrast, the rate of transcription of ferrochelatase mRNA in the proband's cells was normal, suggesting that decreased ferrochelatase mRNA is due to an unstable transcript. cDNA clones encoding ferrochelatase in the proband, isolated by amplification using the polymerase chain reaction, were found to be classified either into those encoding the normal protein or into those encoding an abnormal protein that lacked exon 2 of the ferrochelatase gene, indicating that the proband is heterozygous for the ferrochelatase defect. Genomic DNA analysis revealed that the abnormal allele had a point mutation, C----T, near the acceptor site of intron 1. This point mutation appears to be responsible for the post-transcriptional splicing abnormality resulting in an aberrant transcript of ferrochelatase in this patient.

Amino Acid Sequence↗
PubMed1992

Differential induction responses of delta-aminolevulinate synthase mRNAs during erythroid differentiation: use of nonradioactive in situ hybridization.

Expression of mRNAs encoding the erythroid-specific delta-aminolevulinate synthase (ALAS-E) and the nonspecific delta-aminolevulinate synthase (ALAS-N) were examined in murine Friend virus-transformed erythroleukemia (MEL) cells using nonradioactive in situ hybridization. Following dimethyl sulfoxide (DMSO) treatment, ALAS-E mRNA increased markedly, while ALAS-N mRNA did not increase in wild-type MEL cells. In contrast, in a DMSO-resistant clone of MEL cells, ALAS-E was not detectable before and after DMSO treatment. These findings suggest that ALAS-E and ALAS-N mRNAs are under separate controls and that the expression of ALAS-E mRNA is a critical event in erythroid differentiation.

5-Aminolevulinate Synthetase↗
PubMed1992

Immunohistochemical, autoradiographic and electron microscopic studies on the transformation of fibroblasts into chondrocytes in the mouse subfascia induced by bone morphogenetic protein.

Functional morphology on the transformation of fibroblasts into chondrocytes induced by bone morphogenetic protein (BMP) was studied by light and electron microscopy using 35S autoradiography and immunohistochemistry for S-100 protein and type-II collagen. A pellet containing BMP obtained from a murine osteosarcoma was transplanted into the mouse subfascia. By 3 days after implantation, many typical fibroblasts, which were free of the silver grains for 35S and devoid of both S-100 protein and type-II collagen, entered the pellet region. By 5 days, the fibroblasts in the pellet region became polygonal in shape, and cytoplasmic vesicles and vacuoles appeared, both containing a homogeneous substance of low electron density. At 5 days, autoradiography revealed many silver grains for 35S over the Golgi apparatus and vesicles and vacuoles of the cells in the pellet region as well as over the surrounding extracellular matrix. Moreover, the cells at 5 days displayed immunoreactivity to both proteins. The extracellular matrix around the cell began to show clear metachromasia and increased in amount with time. At 9 days all the cells in the pellet region were round or oval in shape and surrounded by an abundant cartilaginous matrix. The rough endoplasmic reticulum and Golgi apparatus were extremely well developed, and a large number of vacuoles and vesicles were seen in the cytoplasm. These cells showed intense immunoreactivity to both proteins, and strong accumulation of sulfur was visualized in the extracellular matrix by autoradiography. These results suggest that the fibroblasts in the pellet region change into chondroblasts by 5 days, and become typical chondrocytes by 9 days.

Animals↗
PubMed1992

Immuno-electron-microscopic localization of basic fibroblast growth factor in the dystrophic mdx mouse masseter muscle.

The localization of basic fibroblast growth factor (bFGF)-like immunoreactivity in the masseter muscle of dystrophic mdx mice on postnatal day 28 was investigated by immunoblot analysis and electron microscopy. Crude homogenate of the masseter muscle, when subjected to immunoblotting with a bFGF antiserum, exhibited a main band with the same molecular weight (18 kDa) as bovine bFGF. By electron microscopy, bFGF immunoreactivity was detected in small regenerating myocytes; the smaller cells were the premature myocytes, the most intense staining was the immunoreactivity within the cytoplasm. Putative precursors of the muscle cells with a few myofilaments, which were most intensely labeled with anti-bFGF, contacted each other and possibly developed into multinucleated myocytes through cell fusion. Mature myocytes with densely packed myofilaments and peripherally located nuclei did not exhibit bFGF immunoreactivity; they formed myoneural junctions with motor nerve endings immunoreactive for bFGF. Early differentiating myocytes with intense bFGF-like immunoreactivity did not make contact with immunoreactive nerve terminals. Degenerating large myocytes with a limited number of distorted and/or disrupted myofilaments exhibited electron-dense deposits in the cristae of mitochondria; these deposits were not abolished by immunoadsorption control experiments. Thus, the cell-size-dependent decrease in bFGF immunoreactivity in regenerating but not in degenerating myocytes provides a morphological basis for an autoregulatory role of bFGF in muscle regeneration. This study suggests that neuronal bFGF is not involved in initial muscle regeneration in the dystrophic mdx mouse.

Animals↗
PubMed1992

Correlation between the virulence of Francisella tularensis in experimental mice and its acriflavine reaction.

Correlation between the virulence of Francisella tularensis in experimental mice and its acriflavine reaction was studied. The cultures derived from all four strains (Ebina, CMB2, Schu, and N9) that had long been subcultured on agar media yielded two types of colonies, i.e., acriflavine reaction-positive (acf+) and acriflavine reaction-negative (acf-) colonies. All acf+ colonies, regardless of their parent strains, were shown to be low virulent in mice. Acf- colonies were shown to be either high (Ebina, CMB2) or low (Schu, N9) virulent. The low-virulent acf- colonies gained virulence during several passages in mice, whereas the acf+ colonies remained low virulent even after the animal passages.

Acriflavine↗
PubMed1992

Induction of avascular yolk sac due to reduction of basic fibroblast growth factor by retinoic acid in mice.

Vasculogenesis depends on autocrine secretion of basic fibroblast growth factor (bFGF) from capillary endothelial cells. Retinoic acid (RA) induced avascular yolk sac (AVY) of mouse embryos of dams given 60 mg/kg of RA orally on Day 8 of gestation and sacrificed 3 days later. We studied the localization and transcriptional expression of bFGF and FGF-receptor (flg), heparin-binding growth factor (HBGF) activity, localization of lysosomal enzymes and alpha 1-antitrypsin (AAT), and electron microscopy of the normal mouse visceral yolk sac (VYS) and AVY. bFGF, which is normally present in the endoderm of the VYS of 8-day-old embryos and in all components of the VYS by Day 11 of gestation, was reduced in the AVY. However, in the presence of bFGF in vitro capillary nets were restored in the AVY. The mRNA for bFGF was not detectable in either VYS or AVY, while flg mRNA was detected equally in both organs in Northern blotting. The characteristic distribution pattern of lysosomal enzymes, acid phosphatase, lysozyme, and cathepsin D, and AAT was altered in the AVY. The level of acid phosphatase and AAT was reduced to 10% in the AVY. Electron microscopy revealed a partial or total loss of lysosomal membranes where the contents of lysosomes fused with adjacent lysosomes and the external organelles. These results suggest that vitelline blood vessels are not developed by endogenous autocrine bFGF but by exogenous transcellular bFGF from absorptive endodermal cells. Retinoic acid does not affect the angiogenic capacity of the VYS mesenchyme but destroys lysosomes, which release hydrolytic enzymes, leading to degradation of AAT in the endodermal cells and then digestion of endocytosed bFGF.

Acid Phosphatase↗
PubMed1992

Prevalence of Lyme borreliosis spirochetes in ixodid ticks of Japan, with special reference to a new potential vector, Ixodes ovatus (Acari: Ixodidae).

To determine the vectors of Lyme borreliosis in Japan, the ixodid ticks taken in Hokkaido, Fukushima, Nagano, Ehime, and Kochi Prefectures were examined individually for spirochetal infections by culturing their midgut tissues in BSK medium. The cultivable spirochetes identified as Borrelia burgdorferi were detected in Ixodes persulcatus Schulze adults (15.5% of 634), nymph (6.7% of 15) and Ixodes ovatus Neumann adult (9.6% of 188) from Hokkaido, I. ovatus adults (25.5% of 47) from Fukushima, and I. persulcatus adults (21.7% of 143) and I. ovatus adults (27.1% of 85) from Nagano. However, 72 Haemaphysalis spp. from Ehime and Kochi were free from spirochetal infection. I. persulcatus is a vector of Lyme borreliosis in the Far East, but in Japan, I. ovatus may also transmit the spirochetes to human and feral animals.

Animals↗
PubMed1992

Gelatin particle agglutination test for early serodiagnosis of Japanese spotted fever.

A gelatin particle agglutination (PA) test for Japanese spotted fever has been developed. Gelatin particles were sensitized with a sonicated causative rickettsia and used as antigens. The antibodies by PA test were detected as early as days 4-7 after the onset, whereas those by indirect immunoperoxidase (IP) test were detected after days 8-11. In addition, PA titers were higher than IP titers before days 20-23. The agglutinins detected by PA test were proven to be IgM because they were all sensitive to dithiothreitol. PA test was, however, less specific than IP test, giving a little nonspecific reaction to the sera from patients with scrub typhus and from individuals unrelated to those two rickettsioses. Nevertheless, PA test, which is simple, rapid, and easy to interpret the results, is useful for the early serodiagnosis of Japanese spotted fever.

Agglutination Tests↗
PubMed1992

Cardiac rupture complicating hemorrhagic infarction after intracoronary thrombolysis.

An 80-year-old woman with acute myocardial infarct received intracoronary thrombolysis by a large dose of urokinase four hours after the onset of chest pain. Despite the patient having no chest pain after intracoronary thrombolysis and her general condition being stable, she died suddenly on the 4th hospital day. Autopsy revealed hemopericardium due to cardiac rupture, which occurred at the center of the transmural hemorrhagic infarction of the anteroseptal wall. The massive hemorrhagic infarction was promoted by reperfusion from thrombolytic therapy. She had also classic risk factors for cardiac rupture, such as hypertension, senility, female gender, and first acute myocardial infarct. Therefore, the present case demonstrated that hemorrhagic infarction increased the incidence of cardiac rupture.

Aged↗
PubMed1992

Expression pattern of SR alpha promoter in human embryonal carcinoma and transgenic tissues in mice.

Human embryonal carcinoma is thought to be a counterpart of mouse embryonal carcinoma, which has provided useful information for studying early molecular events in murine embryogenesis. A major practical problem in the use of human embryonal carcinoma for molecular pathological studies is the lack of an efficient expression system for foreign genes. The SR alpha promoter is a fusion promoter containing the SV 40 early promoter and the R segment and part of the U5 sequence of the long terminal repeat derived from human T-cell leukemia virus type I. We analyzed the expression pattern of the SR alpha promoter in human and mouse embryonal carcinoma lines and transgenic mouse tissues. Efficient and stable expression was detected in all cell lines tested, and tissues from all mice of four independent transgenic lines carrying the SR alpha-CAT vector showed a detectable level of CAT expression. These data suggest that the SR alpha promoter is useful for studies of both human embryonal carcinoma and transgenic mouse tissue. Using this expression system, we are now able to label human embryonal carcinomas with various genes, for example beta galactosidase, and follow their fate at the single-cell level in nude mice, where xenotransplanted human embryonal carcinoma expresses differentiation capability.

Animals↗
PubMed1992

[Vectors of Japanese spotted fever].

In the southeast coast of Shikoku, most of the Japanese spotted fever (JSF) patients were found to be infected with the rickettsial pathogen through bamboo plantation, and also the eschar was frequently noticed in skin inspection, so that it was clinically speculated to be caused by ticks. According to out field research, the tick fauna was very rich throughout that area, and it was permissible enough to determine ticks as the vectors, based on arising of anti-SF group rickettsiae (SFGR) antibody in mice inoculated with some tick emulsions, findings of rickettsiae reactive to patient sera or a species-specific monoclonal antibody to JSFR in the hemolymph cells of some ticks, and electron microscopical observations of SFGR in various internal organs including the salivary gland of ticks. Also the transovarial and transstadial transmission of SFGR in ticks were supposed. Our results suggest that common species (adult/nymph) of the genus Haemaphysalis may be the most related vectors to man, based on their dominances, SFGR-prevalences, behavior and incidences of infestation but also indicate that various genera and species should be kept as the potential vectors, in spite of JSFR isolation from a restricted species of ticks in the future.

Animals↗