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S Hirose

Publications and source records attributed to S Hirose.

At least 415 records · Page 23Linked to original sources
PubMed1991

DNA superhelicity affects the formation of transcription preinitiation complex on eukaryotic genes differently.

In vitro transcription was reconstituted with HeLa cell transcription factors and RNA polymerase II, which were essentially free from DNA topoisomerase activities. DNA templates with defined negative superhelical densities were tested for transcription activity. Transcription of the Bombyx mori fibroin gene increases and plateaus from templates of increasing superhelicity, and transcription from the adenovirus 2 major late promoter rises and then falls, while transcription of the Drosophila hsp70 gene remains unchanged. Dissection of transcription into pre and post-initiation steps by the use of Sarkosyl reveals that formation of a preinitiation complex on the fibroin gene or the adenovirus 2 major late promoter is slow on relaxed DNA and accelerated by DNA superhelicity. On the contrary, the preinitiation complex assembles rapidly on the hsp70 gene irrespective of DNA topology. As is the case with the fibroin gene promoter, DNA superhelicity appears to facilitate the interaction of transcription factor IID to the adenovirus 2 major late promoter.

Animals↗
PubMed1991

Cloning and sequence analysis of a cDNA encoding human non-selective type of endothelin receptor.

A cDNA encoding non-selective type (ETB) of endothelin receptor was isolated from a human liver cDNA library. The cDNA had an open reading frame encoding a protein of 442 amino acid residues with a relative Mr of 49,643. The deduced amino acid sequence of human ETB receptor was 88% and 64% identical to those of rat lung ETB receptor and bovine lung ET-1-specific (ETA) receptor, respectively, and contained a relatively long and proline-rich extracellular N-terminal region in addition to a significant similarity with the G protein-coupled receptor super-family with seven transmembrane segments.

Adult↗
PubMed1991

Assembly and deacetylation of N-acetylglucosaminyl-plasmanylinositol in normal and affected paroxysmal nocturnal hemoglobinuria cells.

Decay-accelerating factor (DAF) is anchored in cell membranes by a glycosyl-plasmanylinositol (GPI) moiety that is transferred to it en bloc in the rough endoplasmic reticulum. To analyze the biochemical reactions involved in preassembly of this structure, a human hematopoietic cell-free system was employed. Incubation of cell extracts with UDP-[3H]GlcNAc and butanol partitioning of reaction mixtures yielded two products similar in TLC mobility to intermediates described in Trypanosoma brucei. Both species were sensitive to Bacillus thuringiensis phosphatidylinositol-specific phospholipase C, indicative of association of [3H]GlcNAc label with a plasmanylinositol-containing acceptor. In contrast to trypanosome intermediates, which contain phosphatidylinositol (1,2-diacylglycerophosphoinositol), however, alkali treatment and phospholipase A2 digestion generated butanol-phase products characteristic of glycosylated plasmanylinositol (1-alkyl-2-acylglycerophosphoinositol). Kinetic and pulse-chase experiments indicated that the slower-migrating species was a product of the faster and that it, but not the faster, was sensitive to both GPI-specific phospholipase D and nitrous acid deamination, consistent with conversion of GlcNAc- to GlcN-plasmanylinositol. Accordingly, acetic anhydride acetylation retransformed the slower species back to the faster. Further incubation with cell extracts converted the slower species into more polar products. Lysates of normal and of affected blood leukocytes from two paroxysmal nocturnal hemoglobinuria (PNH) patients supported assembly of the two intermediates within 1 min. Thus, the initial enzymes mediating human GPI-anchor assembly are GlcNAc-plasmanylinositol transferase and GlcNAc-plasmanylinositol deacetylase, their substrates contain plasmanylinositols, and the products of their activities are normal in affected PNH cells.

Acetylglucosamine↗
PubMed1991

Identification of G protein-coupled endothelin receptors in cultured bovine endothelial cells.

Autocrine and paracrine regulation of vascular endothelial cells by endothelins has been postulated and has been the target of many recent investigations. In the present study, we demonstrated, by affinity labeling, the presence of endothelin-1- and endothelin-3-specific receptors on cultured bovine endothelial cells that secrete endothelin; the endothelin-3 receptor was the major form. Analysis using the GTP analogue guanosine 5'-O- (thiotriphosphate) indicated that these receptors are coupled to G proteins.

Animals↗
PubMed1991

Negative supercoiling of DNA facilitates an interaction between transcription factor IID and the fibroin gene promoter.

Transcription of the fibroin gene can be reconstituted with partially purified components from HeLa cells. Transcription factors IIB, IID, and IIE and RNA polymerase II are required for accurate initiation of transcription. Linear and relaxed closed circular DNA show a similar level of template activity. However, transcription of closed circular DNA is stimulated when negative supercoils are introduced by the addition of DNA topoisomerase II and supercoiling factor purified from the posterior silk gland of Bombyx mori. Dissection of transcription into pre- and postinitiation steps by the use of Sarkosyl reveals that DNA supercoiling promotes formation of a preinitiation complex. Furthermore, order of addition experiments suggest that DNA supercoiling facilitates a functional binding of transcription factor IID to the promoter.

Cell Nucleus↗
PubMed1991

Demonstration of extrinsic DNA from immune complexes in plasma of a patient with systemic lupus erythematosus.

Antigen DNA isolated from immune complexes present in plasma of three patients with active systemic lupus erythematosus using an affinity column was cloned and sequenced. One clone, designated pKS7, was found to have a region homologous with that of the E. coli metK gene, and another, designated pKS8, had a region homologous with a sequence including the replication origin of bacteriophage f1. Gel retardation assay revealed that pKS7 and pKS8 interacted with the patient's IgG fraction to form immune complexes, respectively. The affinity-purified antigen DNA was proved to be originated from bacteria or bacteriophage.

Antigen-Antibody Complex↗
PubMed1991

Suppression by IL-2 of IgE production by B cells stimulated by IL-4.

IgE production was obtained from B cells of BALB/c or nude mice when these cells were cultured with IL-4 plus LPS. IL-2 added to these cultures at the start (day 0), 1 or 2 days later completely suppressed the production of IgE. The production of IgG1 was also inhibited, but only if IL-2 was added on day 0. The production of other isotypes (IgM, IgG2a, IgG2b) was only slightly decreased by addition of IL-2. No suppression of IgE or IgG1 production was observed if monoclonal anti-IL-2 was added, whereas anti-IFN-gamma had no effect on the suppression of the production of these isotypes. The expression of CD23 on the third day of culture on B cells stimulated with LPS and IL-4 was markedly decreased when IL-2 was added to the cultures on day 0. Addition of monoclonal anti-IL-2 suppressed all effects produced by IL-2, whereas addition of anti-IFN-gamma had no effect. These results show that the suppression by IL-2, at least for the first signaling processes, are different from the suppression produced by IFN-gamma.

Animals↗
PubMed1991

Contribution of the gene linked to the T cell receptor beta chain gene complex of NZW mice to the autoimmunity of (NZB x NZW)F1 mice.

We have investigated the contribution to the autoimmune disease of (NZB x NZW)F1 (NZB/W) mice made by the T cell receptor beta (TcR beta) chain gene complex, or genes linked to it, that are derived from the NZW strain. For this we developed the NZW.TcR beta NZB strain, a NZW congenic line carrying the TcR beta of NZB type, and produced NZB x NZW.TcR beta NZB (NZB/W.TcR beta NZB)F1 mice. We compared the amounts of anti-DNA and anti-histone antibodies and also the severity of lupus nephritis in these mice with those in the original NZB/W F1 mice. We obtained evidence for significantly lower serum levels of autoantibodies to double-stranded and single-stranded DNA and histone, and a later onset and a lower incidence of proteinuria in the NZB/W.TcR beta NZB F1 mice than in the original NZB/W F1 mice. These findings clearly indicate that the gene(s) within or closely linked to the TcR beta chain gene complex on chromosome 6 of the NZW strain acts to intensify the feature of systemic lupus erythematosus in the NZB/W F1 strain. The significant relationship of this finding to the strict dependency of NZB/W F1 disease on the H-2d/H-2z heterozygosity is discussed.

Animals↗
PubMed1991

Major histocompatibility complex controls clonal proliferation of CD5+ B cells in H-2-congenic New Zealand mice: a model for B cell chronic lymphocytic leukemia and autoimmune disease.

By employing H-2-congenic NZB, NZW and (NZB x NZW)F1 mice with either the homozygous H-2d/H-2d, H-2z/H-2z or heterozygous H-2d/H-2z haplotype, we found that in the spleen of all the congenic strains homozygous for H-2z, there were extremely high frequencies of CD5+ B cells. These cells eventually proliferated in an oligoclonal or even monoclonal fashion, and B cell-chronic lymphocytic leukemia (B-CLL) developed in some cases. Because this feature was not observed in H-2d/H-2d homozygotes or H-2d/H-2z heterozygotes, the high CD5+ B cell frequencies are apparently controlled by the homozygosity of a locus or cluster of loci closely linked to H-2z complex of NZW strain. As the CD5+ B cell frequencies in the peritoneal cavity did not differ among the H-2-congenic strains, the frequencies of these cells in the peritoneal cavity and in the spleen appear to be at least in part under separate control. Flow cytometry and Southern blot analyses using an immunoglobulin gene JH probe revealed that the H-2z/H-2z homozygotes, there was a propagation of distinct clonal populations between the spleen and the peritoneal cavity, a finding which suggested that in the major histocompatibility complex (MHC)-related microenvironments for CD5+ B cell propagation differ between the two compartments. All our findings taken together imply that certain different but related MHC haplotypes may predispose either to B-CLL or to autoimmune disease, in close relatives.

Animals↗
PubMed1991

Clinical significance of IgG subclasses of Anti-Sm and U1 ribonucleoprotein antibodies in patients with systemic lupus erythematosus and mixed connective tissue disease.

IgG subclasses of anti-Sm and anti-U1 ribonucleoprotein (U1 RNP) antibodies were determined using a new clone of the anti-IgG2 antibody (HG2-56F). Although the predominance of IgG1 coincided with previous reports, IgG2 anti-Sm and U1 RNP antibodies were detected in numerous patients. IgG3 anti-Sm antibody significantly correlates with joint involvement and a high titer of anti-DNA antibody. On the other hand, IgG4 anti-U1 RNP antibody significantly correlated with esophageal dilation and muscular involvement. These results may suggest that some IgG subclasses are related to a specific clinical feature or manifestation.

Autoantibodies↗
PubMed1991

Klinefelter's syndrome associated with progressive systemic sclerosis: report of a case and review of the literature.

A case of Klinefelter's syndrome associated with progressive systemic sclerosis (PSS) is described. The patient had been infertile for 20 years after marriage and was diagnosed as PSS with Klinefelter's syndrome at the age of 43. In reviewing the literature, we observed that five cases with PSS within the range of 41 to 61 years of age, and seventeen cases with systemic lupus erythematosus (SLE), but only few cases with other connective tissue diseases were reported in association with Klinefelter's syndrome. Possible involvement of male hypogonadism in the pathogenesis of PSS was suggested.

Connective Tissue Diseases↗
PubMed1991

Preferential reactivity of autoantibodies in murine lupus NZB mice to neuraminidase-treated monosialogangliosides on B cells of mouse spleen.

When analyzed by flow cytometry, reactivity of IgM autoantibodies in sera from NZB mice to spleen B cells, but not to T cells, from BALB/c mice was remarkably increased after treatment of the cells with Vibrio cholerae neuraminidase. By TLC immunostaining with the antibodies, neither neutral nor acidic glycosphingolipids from both BALB/c and NZB mouse spleens were found to be reactive, but after neuraminidase treatment of the TLC plate, prior to the immunostaining, three components became reactive. All of the reactive glycosphingolipids were found to carry a single sialic acid residue and were at a concentration less than 1.3% of the total lipid-bound sialic acids. Their mobilities on TLC plate were close to those of IV3 NeuAcnLc4Cer, IV3 NeuAcII3 NeuAcGg4Cer, and IV3 NeuAcII3 NeuAc2Gg4Cer. In addition, the monosialogangliosides, which became reactive with the autoantibodies after neuraminidase treatment, were found to be predominantly distributed on B cells from BALB/c mice spleen, but not on T cells by TLC immunostaining. These studies demonstrate that the majority of IgM autoantibodies to spleen lymphocytes in sera from NZB mice might react preferentially to terminal sugar residues of three new glycosphingolipids masked by a single sialic acid on B cells, but not on T cells.

Animals↗
PubMed1991

CD5+ B cells in autoimmune disease and lymphoid malignancy.

Evidence is accumulating that CD5+ B cells belong to a developmental lineage distinct from that of conventional B cells and mainly participate in natural immunity. They have attracted attention because of their involvement in autoimmunity and lymphoid malignancy in both mice and humans. Patients with rheumatoid arthritis and Sjögren's syndrome were found to show a striking increase in the number of CD5+ B cells. B cell-chronic lymphocytic leukemia cells frequently express CD5. However, there are arguments against the role for CD5+ B cells in autoimmune disease, particularly in murine and human systemic lupus erythematosus (SLE). Whereas most IgM anti-DNA antibodies are produced by CD5+ B cells, high-affinity, pathogenic IgG antibodies are produced mainly by CD5- B cells. Either of two possibilities can explain the failure of CD5 expression of B cells responsible for producing IgG anti-DNA antibodies: either the cells are conventional B cells or the cells are CD5+ B cells that lack CD5 expression. In studies using SLE-prone NZB x NZW F1 mice and their H-2-congenic progeny, we discussed herein the possibility that CD5+ B lineage cells are also responsible for the pathogenic IgG autoantibody production by phenotypic switching from CD5+ to CD5-, probably under a particular genetic background. A line of H-2-congenic NZB x NZW F1 progeny failed to produce IgG anti-DNA antibodies, but in turn, showed a marked clonal proliferation of CD5+ B cells. Thus, it appears that genetically determined signals for either proliferation or differentiation would lead CD5+ B cells to cause distinct disease, i.e., autoimmune disease or lymphoid malignancy. Further studies using H-2-congenic New Zealand mice may provide insights into the correlation between autoimmunity and related lymphoid malignancy.

Animals↗
PubMed1991

Post-irradiation treatment with OK432 can prevent radiation-induced bone marrow death.

The radioprotective effect of OK432, a Streptococcus haemolyticus preparation, on bone marrow death was examined in mice. The LD50 value was increased from 7.55 Gy in controls to 8.45 Gy in mice treated once with OK432 immediately after irradiation. Multiple administrations of the agent further elevated the LD50 value to 9.56 Gy. The radioprotective effect was also apparent when multiple treatments were commenced as late as 72 h after irradiation.

Animals↗
PubMed1991

Plateau-wave phenomenon (I). Correlation between the appearance of plateau waves and CSF circulation in patients with intracranial hypertension.

Plateau waves, as described by Lundberg (1960), can often be observed in patients with increased intracranial pressure (ICP) resulting from brain tumours, benign intracranial hypertension and other causes. The clinical significance of the waves, however, is still debated. In this study, the ICP was recorded continuously, the size of the ventricular system was evaluated using computerized tomography (CT), the cerebrospinal fluid (CSF) flow was studied using isotope cisternography, and the absorptive capacity of the CSF was determined by measuring the conductance to CSF outflow, in 94 patients with increased ICP. All patients who received continuous ICP monitorings had a basic ICP level of more than 200 mmHg, and these patients were assigned to two groups on the basis of the presence or absence of the plateau waves in the ICP recordings: group I comprising 17 patients without plateau waves but with a high ICP resulting from subarachnoid haemorrhage or hypertensive intracerebral haemorrhage, within 5 days after the start of bleeding; and group II consisting of 77 patients with both plateau waves and a high ICP resulting from brain tumours, meningitis carcinomatosa, benign intracranial hypertension, superior sagittal sinus thrombosis and communicating hydrocephalus. The isotope cisternography and conductance to CSF outflow studies showed that there was neither a delay in CSF circulation nor an impairment of CSF absorption in the group 1 patients and these patients showed no ventricular dilatation on CT, whereas there was a marked sluggishness in the CSF flow and a severe defect in the CSF absorption capacities of the group II patients irrespective of the presence or absence of ventricular dilatation on CT. The present observations indicate that patients with a plateau-wave phenomenon have a marked impairment of CSF absorption and CSF flow. We suggest that the phenomenon is an important sign indicating an impairment of CSF absorption capacities.

Adult↗
PubMed1991

Plateau-wave phenomenon (II). Occurrence of brain herniation in patients with and without plateau waves.

From 1980 to 1989, during intracranial pressure (ICP) recording, brain herniation (central transtentorial herniation associated with uncal herniation) developed in 15 patients as a result of aneurysmal rebleeding, uncontrollable brain swelling and/or oedema in spite of attempts at treating increased ICP. The relationship between the ICP level at which herniation occurred and the ICP fluctuation patterns in continuous ICP recordings prior to the development of the herniation was studied retrospectively. As for the ICP fluctuation patterns, the patients were assigned to 2 groups on the basis of the presence or abscence of plateau waves of Lundberg: group I comprising 8 patients without plateau waves but with a high ICP, and group II comprising 7 patients with both plateau waves and a high ICP. In the group I patients the herniation occurred as a result of aneurysmal rebleeding or brain swelling after subarachnoid haemorrhage, and in the group II patients the herniation resulted from brain tumour, meningitis carcinomatosa and superior sagittal sinus thrombosis. In the group I patients the herniation developed at a mean ICP level of 70-98 mmHg, and in the group II patients it occurred at a mean ICP level of 120-150 mmHg, far higher than the ICP level causing herniation in the group I patients. It has been shown that patients with a plateau-wave phenomenon in continuous ICP recordings have a marked impairment of cerebrospinal fluid (CSF) absorption and a delayed CSF flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of acetylpolyamines on in vitro protein synthesis and on the growth of a polyamine-requiring mutant of Escherichia coli.

The functions of acetylpolyamines were examined with respect to stimulation of protein synthesis and cell growth. Unlike polyamines, acetylpolyamines could not lower the optimal Mg2+ concentration of protein synthesis, and the degree of stimulation of protein synthesis by acetylpolyamines was small. The addition of N1-acetylspermine did not stimulate cell growth of a polyamine-requiring mutant of Escherichia coli MA261, although acetylspermine was accumulated in the cells. Acetylspermine did not interfere with polyamine stimulation of protein synthesis and cell growth of E. coli MA261. The binding of acetylpolyamines to RNA was very weak, and the binding of polyamines to RNA was not disturbed significantly by the presence of acetylpolyamines. When the growth of E. coli MA261 was stimulated by addition of polyamines, significant amounts of acetylpolyamines were also formed in the cells. These results suggest that acetylation of polyamines, together with polyamine excretion, may regulate the intracellular level of the parent polyamines when excess amounts of polyamines accumulate intracellularly.

Acetylation↗