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Biomedical subjects

M Hatanaka

Publications and source records attributed to M Hatanaka.

At least 127 records · Page 7Linked to original sources
PubMed1994

Immunohistochemical reactions for fibroblast growth factor receptor in arteries of patients with moyamoya disease.

The cause of moyamoya disease remains unknown, and pathophysiological mechanisms remain uncertain. Basic fibroblast growth factor (FGF) is a pluripotent polypeptide that has been shown to play roles in angiogenesis, tumorigenesis and many other processes. In a previous study, we demonstrated immunohistochemically that the amount of basic FGF was increased above normal in the superficial temporal artery (STA) of patients with moyamoya disease. To clarify the function of basic FGF in moyamoya disease, we have performed an immunohistochemical study of the STA using a polyclonal antihuman FGF receptor antibody and also have tested immunohistochemical reactions for basic FGF. Twelve surgical specimens of the STA from patients with moyamoya disease were studied. Twelve specimens of the STA from skin flaps of patients with other neurological diseases were also investigated for comparison. The sections of the STA from patients with moyamoya disease showed dense and strong FGF receptor and basic FGF immunoreactivity in endothelial cells, in cells scattered in the thickened intima, and in smooth muscle cells in the media. In contrast, the sections of the STA of control patients showed faint basic FGF immunoreactivity. The statistical analysis revealed a significant difference of basic FGF immunoreactivity between moyamoya disease and other neurological diseases (chi 2 = 23; P = 0.0001). Moderately intense FGF receptor immunoreactivity was observed in most control patients. However, the statistical analysis revealed a significant difference of FGF receptor immunoreactivity between moyamoya disease and other neurological diseases (chi 2 = 13.382; P = 0.0012).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Distribution of C3-step regulatory proteins of the complement system, CD35 (CR1), CD46 (MCP), and CD55 (DAF), in hematological malignancies.

The distribution and levels of three membrane proteins, CD35, CD46, and CD55, which serve as complement regulators, were examined in normal peripheral blood and hematologically malignant cells. CD35 was negative in most leukemia cells regardless of the type of leukemia, although granulocytes, monocytes, and some populations of lymphocytes were CD35+. CD46 was present in all blood cells except erythrocytes, and levels were 2-8 times higher in most leukemia cells than in their mature counterparts, particularly in CML and CLL cells, except for those of B cell lineage. CD55, a widely-distributed phosphatidyl inositol-anchored protein, was more frequently lost in NHL cells than in other types of hematological malignancies. In this review, we discuss the roles, mechanisms, and clinical applications of cell-associated complement regulatory proteins in hematological malignancies.

Antigens, CD↗
PubMed1993

Novel internal promoter/enhancer of HTLV-I for Tax expression.

The transcription initiation signals in retroviruses lie within the long terminal repeat (LTR) sequences. We have found a new transcriptional promoter in a central portion of the genome of human T-cell leukaemia virus type I (HTLV-I). The transcription start site is located just upstream to the ATG codon of the transcriptional trans-activator molecule, tax protein (Tax). The internal promoter may provide a new insight into gene expression of HTLV-I. The mechanism of leukaemogenesis by the defective HTLV-I is also discussed. Furthermore, we have identified two repeats of a novel enhancer sequence AGTTCT, which are located around the initiation site. We call the sequence HIRE (HTLV-I Internal Regulatory Element).

Animals↗
PubMed1993

Nucleolar targeting signal of Rex protein of human T-cell leukemia virus type I specifically binds to nucleolar shuttle protein B-23.

Rex protein, the post-transcriptional regulator of human T-cell leukemia virus type I, is located predominantly in the cell nucleolus and is associated with the cytoplasmic accumulation of unspliced and singly spliced viral mRNAs. The N-terminal 19-amino acid segment of Rex has been identified as the nucleolar targeting signal (NOS) and shown to be important for Rex function. To study the molecular interaction between the NOS region of Rex and its binding host protein(s) in the nucleolus, we chemically synthesized a functional NOS peptide (wild type) and mutant NOS peptides. Fluorescein isothiocyanate-conjugated functional NOS peptide was rapidly taken up by human cells and was transported to the nucleolus. Using affinity chromatography, we identified nucleolar protein B-23 as the major protein that binds to NOS. We also identified two highly acidic regions of B-23 (amino acids 120-132 and 161-188) as acceptor regions for NOS. Previous experiments have suggested that B-23 functions as a shuttle protein for the nucleolar transport of ribosomal components. Our results suggest that B-23 may also serve as a shuttle for the import of Rex from the cytoplasm to the nucleolus coupled to the export of viral mRNAs containing the Rex-responsive element.

Amino Acid Sequence↗
PubMed1993

[MR imaging during arteriography (MR arteriography) in the detection of hepatocellular carcinoma].

MR imaging during arteriography was performed to evaluate the clinical utility to patients with hepatocellular carcinoma. After a conventional hepatic arteriography, the patients were transferred to the MR unit and MR arteriography was obtained with the gradient echo technique synchronously starting manual injection of Gd-DTPA diluted with normal saline into the hepatic artery using 5-F Cobra angiographic catheter. The tumors showed high signal intensity relative to surrounding normal parenchyma and a clear liver-to-lesion contrast was obtained. Especially in one case, a conventional hepatic arteriography did not show the recurrent mass, however it was demonstrated as a high signal intensity area on MR arteriography. Therefore, this new technique seemed to be useful for the detection of hepatocellular carcinoma.

Carcinoma, Hepatocellular↗
PubMed1993

Improved enzyme immunoassay for human basic fibroblast growth factor using a new enhanced chemiluminescence system.

An enhanced chemiluminescence reaction has been incorporated into an enzyme immunoassay (EIA) for human basic fibroblast growth factor (hbFGF). We developed a new luminol derivative, designated L-012 and a new enhancer, 4-(4-hydroxyphenyl)thiazole. Using these compounds, the detection limit of hbFGF was improved to 0.1 pg/assay, which was 10-20 and 2 times better than the o-phenylenediamine colorimetric and luminol chemiluminescence assays, respectively. The average concentration of bFGF in sera from 25 normal volunteers was 5.9 pg/ml. On the other hand, serum bFGF levels were elevated in renal, lung and brain tumor patients. The data presented here indicate that the serum bFGF level could be a useful diagnostic marker for these tumors. Furthermore, these new compounds could easily be applied to any other EIA that uses horse radish peroxidase to improve sensitivity.

Antibodies, Monoclonal↗
PubMed1993

[Usefulness of 2D FLASH multislice dynamic MR imaging for evaluation of parametrial invasion in cervical carcinoma].

Twenty seconds and 3 minutes after starting rapid injection of Gd-DTPA, multislice dynamic (MD) images were obtained with the 2 dimension fast low-angle shot (2D FLASH) technique. Four of 5 cervical carcinomas showed high signal intensity in the early dynamic phase (20 seconds), so they were readily distinguished from the myometrium that were not enhanced in the same phase. For evaluation of parametrial invasion, MD study showed better contrast between the tumor and the parametrium than did T2-weighted images because the tumor demonstrated a high signal intensity similar to that of the parameterium on T2-weighted images. MD images were able to scan the entire tumor especially in progressive cases and to evaluate the hemodynamics of the tumor. Therefore, MD imaging seemed to be useful for evaluation of parametrial invasion in cervical carcinomas.

Carcinoma, Squamous Cell↗
PubMed1993

Developmental expression of trkB and low-affinity NGF receptor in the rat retina.

Brain-derived neurotrophic factor (BDNF) promotes the survival of retinal ganglion cells, but these effects are dependent on the developmental stages, and a number of retinal ganglion cells are eliminated during pre- and neonatal stages. We have examined the expression of BDNF receptors, trkB and low-affinity nerve growth factor receptor (LNGFR), in the rat retina during these period using Northern blot analysis. The expression of trkB and LNGFR displayed two peaks during embryonic day 17 (E17) through postnatal day 1 (P1), and during P14-P17, indicating that it may play an important role in neuronal development and neuronal cell death.

Animals↗
PubMed1993

[Evaluation of early MR imaging of the liver in rabbits after ethanol injection].

Seven days after ethanol injection, MR images of the liver in 5 rabbits were evaluated by T1, T2-weighted SE and TURBO-FLASH dynamic images. Necrotic area was visualized as low-intensity on T1-weighted images and high-intensity on T2-weighted images. These findings were similar to the tumor that was not treated, so it is necessary to be careful for evaluation of therapeutic efficacy. Necrotic area was not meanwhile enhanced on TURBO-FLASH dynamic images, therefore, dynamic study seemed to be useful for therapeutic efficacy after ethanol injection.

Animals↗
PubMed1993

Extension of optic nerve fibers on genetically modified cells producing brain-derived neurotrophic factor.

Since brain-derived neurotrophic factor (BDNF) promotes the survival of retinal ganglion cells (RGCs), we transfected a rat BDNF cDNA into rat fibroblasts, and retinal fragments of rat embryos were cultured on cell monolayers of these cells. Retinal fragments showed enhanced neurite extension on BDNF-transfected cells compared with that on control cells. The degree of the neurite extension, however, decreased depending upon the embryonic stages. These results suggest that fibroblasts genetically modified to produce BDNF might be a promoter of neurite extension by RGCs, but this does not apply to the RGCs of late embryonic stages.

Animals↗
PubMed1993

Molecular diversity of calpastatin in human erythroid cells.

According to differences in mobility on SDS-polyacrylamide gel electrophoresis, calpastatins (inhibitor proteins of the calcium-dependent proteinase calpain) are classified into the tissue type (100-120 kDa) and the erythrocyte type (70 kDa), which lacks the amino-terminal domains (domains L and 1). We investigated the molecular diversity of calpastatin in human hematopoietic cells by Western-blot analysis and by the reverse-transcription-polymerase-chain reaction method. While the mononuclear and polymorphonuclear cells in peripheral blood showed the tissue type (110 and 114 kDa), a cell line of erythroid cells (JK-1) showed both the tissue type (110 kDa) and the erythrocyte type (70 kDa) at approximately equal ratios. When the lysate of JK-1 cells was incubated in the presence of ATP, the 110-kDa form was degraded much faster than the 70-kDa form. In human erythrocytes, the 110-kDa form was identified as the tissue type by an antibody recognizing domain L, and this form was also present in addition to the predominant 70-kDA form. JK-1 cells, as well as nucleated cells in peripheral blood, contained calpastatin mRNA with exon-3-deleted. Glioblastoma and fibroblast cell lines expressed the nondeleted calpastatin mRNA in addition to the deletion type, and they showed bands corresponding to 117 kDa as well as 110 and 114 kDa. The 117-kDa band was detectable by an anti-exon 3 peptide antibody. These results suggest that diversity among the tissue type calpastatins is caused by both alternative splicing and post-translational processing whereas the apparent conversion from the tissue type to the erythrocyte type is caused by proteolytic processing.

Adenosine Triphosphate↗
PubMed1993

Implication of membrane factors other than DAF and CD59 in complement-mediated lysis of paroxysmal nocturnal hemoglobinuria erythrocytes.

Erythrocytes from two patients (F.K. and A.M.) with paroxysmal nocturnal hemoglobinuria, which were almost completely deficient in decay-accelerating factor and CD59, were found to differ in their susceptibility to homologous complement. Whereas 50-70% of F.K. erythrocytes were lysed, almost 100% of the erythrocytes from A.M. were lysed. These observations were seen under both acidified and nonacidified conditions, and regardless of whether or not the normal human serum was adsorbed with normal erythrocytes to remove natural antibodies. Erythrocytes from two other patients, J.S. and Y.K., about 85% of which did not express CD59, showed lytic profiles similar to those of patient F.K. The differences between patients were not related to levels of natural antibody or other membrane regulatory proteins such as complement receptor type I or membrane cofactor protein. Erythrocytes from F.K. and A.M. differed in their reconstitution with decay accelerating factor and CD59. While erythrocytes from F.K. were reconstituted with CD59 in a unimodal pattern, erythrocytes from A.M. showed a bimodal pattern of reconstitution assessed by flow cytometry. After reconstitution with CD59, erythrocytes from F.K. and A.M. differed in their protection against homologous complement. It is concluded that erythrocyte membrane constituents other than the known inhibitors differ in these patients.

Antigens, CD↗
PubMed1993

Acute promyelocytic leukemia with CD59 deficiency.

CD59 is a phosphatidyl inositol-anchored protein (which is lost in paroxysmal nocturnal hemoglobinuria (PNH) cells) with the capacity to block the formation of membrane attack complex, and protects host cells from autologous complement-mediated cytolysis. We found a patient with acute promyelocytic leukemia (APL) accompanied by disseminated intravascular coagulation (DIC), the cells of which were CD59-negative. Although the CD59 deficiency in the malignant cells was not related to PNH, we offered the possibility that DIC was induced by APL lysis secondary to the deficiency of CD59.

Aged↗
PubMed1993

A monoclonal antibody against human decay-accelerating factor (DAF, CD55), D17, which lacks reactivity with semen-DAF.

Human decay-accelerating factor (DAF, CD55) is a phosphatidyl inositol-anchored glycoprotein consisting, from the N-terminus, of 4 short consensus repeats (SCR), a Ser/Thr (ST)-rich region providing O-glycosylation sites, and the membrane-anchoring unit. A mAb, named D17, was raised against purified erythrocyte-DAF. This mAb recognized DAF on blood cells and most cell lines as determined by flow cytometry and immunoblotting. Its reactivity was similar to but weaker than that of two other well-characterized mAbs to DAF, IA10 (seeing an epitope within SCR1) and 1C6 (seeing an epitope within SCR3). The reactivity of D17 with erythrocyte DAF became increased by treatment with sialidase/O-glycanase, suggesting that its epitope is located close to the O-glycosylation sites, probably within the ST-rich region or SCR4. D17 barely blocked the decay-accelerating activity of DAF. Using the three mAbs, tissue-associated and soluble forms of DAF were identified by SDS-PAGE/immunoblotting and immunohistochemical staining. IA10 and 1C6 recognized a 50 kDa protein in spermatozoa lysate and two proteins of Mr 70 and 55 kDa, respectively, in seminal fluid. These represented membrane-associated and soluble forms of DAF, which were neither recognized by mAb against membrane cofactor protein (MCP, CD46) and C3b/C4b receptor (CR1, CD35) nor by non-immune IgG. In contrast to IA10 and 1C6, D17 did not recognize either spermatozoa-DAF or seminal plasma-DAF, or the deglycosylated or untreated forms of them. Immunohistochemical analysis showed that testis was stained with IA10 but not with D17.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

2-Amino-3-methylimidazo[4,5-f]quinoline (IQ), a carcinogenic pyrolysate, induces chromosomal aberrations in Chinese hamster lung fibroblasts in vitro.

The ability of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) to induce chromosomal aberrations (CAs) in Chinese hamster lung fibroblast (CHL/IU) cells in vitro was examined. On incubation with rat S9 (2.5-10%, v/v) for 3 h, followed by a recovery culture period of 21 h, IQ caused significant induction of CAs at a concentration 20 micrograms/ml, but had less effect at 40 micrograms/ml. With longer recovery culture times such as 27-33 h, however, IQ was much more effective at 40 micrograms/ml. No significant induction was observed with 1 or 6 h treatments followed by 23 or 18 h recovery cultures, respectively. On incubation without S9, only weak CA induction by IQ was observed. These results show that IQ is a clastogen and that its clastogenic effect varied with the experimental conditions, such as the time of exposure and the time of recovery culture. The cell cycle perturbation effect is suggested to be one of the critical factors for the detection of the clastogenic potential of IQ.

Animals↗
PubMed1993

Requirement of different subdomains of calpastatin for calpain inhibition and for binding to calmodulin-like domains.

Calpain requires Ca2+ for both proteolysis of its substrates and interaction with its endogenous inhibitor, calpastatin. The mechanism of inhibition of calpain by calpastatin has remained unsolved, although Nishimura and Goll [J. Biol. Chem. 266, 11842-11850 (1991)] reported that autolyzed calpain fragments containing calmodulin-like domains (CaMLDs) bound to an immobilized calpastatin column. We investigated the correlation between CaMLD-binding and calpain inhibition using immobilized columns of gene-engineered CaMLDs derived from the human mu-calpain large subunit and various recombinant calpastatin mutants. Among the four internally repetitive inhibitory domains of calpastatin, each having conserved regions A, B, and C, only domains 1 and 4 showed the binding activity. The region B deletion mutant of domain 1, retaining the CaMLD-binding ability, no longer had the calpain inhibition activity, and became susceptible to proteolysis. In contrast, a synthetic oligopeptide of region B with moderate calpain inhibition activity did not bind to the column. Domain 3 acquired the binding ability on substitution of region A with that of domain 1. These results suggest that calpain inhibition and binding to the CaMLDs are not correlated or mediated by different subdomains of calpastatin.

Amino Acid Sequence↗