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S Morikawa

Publications and source records attributed to S Morikawa.

At least 145 records · Page 8Linked to original sources
PubMed1993

Induction of CD5 antigen on human CD5- B cells by stimulation with Staphylococcus aureus Cowan strain I.

We have examined whether the CD5 phenotype could be induced on human B cell surfaces by the polyclonal B cell stimulator, Staphylococcus aureus Cowan strain I (SAC). Fresh tonsillar B cells were prepared by Percoll density gradient from E- cells. The proportion of CD5+ B cells in the 50/60% and 60/70% interface high-density fractions varied between 1.2 and 10.2% depending on the tonsil preparations when they were placed on the in vitro culture 12-60 h prior to flow cytometric analysis. The expression of CD5 antigen obviously increased in the presence of SAC (1:10(5) v/v). The percentage of CD5+ B cells varied from tonsil to tonsil, from 25.1 to 65.9% in a series of experiments. The CD5+ B cells were found both among CD23+CD25+CD71+ and CD23-CD25-CD71- B cells. The level of CD5 expression was related to the cell size enlargement. The addition of anti-CD5 antibody in the culture blocked the CD5 induction by SAC without interfering with the expression of other activation markers. A time-course study showed that CD5 antigen appeared to be induced on the cell surface during the G0 to G1 phase transition in the cell cycle. When CD5+ and CD5- B cells were separated by magnetic isolation, the CD5- B cells showed DNA synthesis to the stimulation by SAC and expressed CD5 antigen on their cell surface. These results suggest that human CD5- B cells can express the CD5 phenotype by stimulation with the polyclonal B cell stimulator, SAC.

Antibodies, Monoclonal↗
PubMed1993

Zinc protease of Bacillus subtilis var. amylosacchariticus: construction of a three-dimensional model and comparison with thermolysin.

The active site structure of the Zn-containing neutral protease from Bacillus subtilis var. amylosacchariticus (BANP) was predicted by computer-aided modeling on the basis of the three-dimensional structure of thermolysin (TLN). As expected from the high homology in amino acid sequence of the two enzymes, the overall folding of BANP was very similar to that of TLN. Glu144, Tyr158, and His228 of BANP were located near the active site Zn ion, to which three amino acid residues, His143, His147, and Glu167, were coordinated. This model is supported by the previous results that chemical modifications of Tyr158 and photooxidation of His228 of BANP markedly affect the proteolytic activity of the enzyme. Interestingly, BANP was found to be significantly less sensitive to metalloprotease inhibitors such as phosphoramidon and talopeptin. From a comparison of the enzyme-inhibitor complex models between BANP and thermolysin, it is suggested that replacement of Thr129 in TLN by Phe130 in BANP is related to difference in inhibitor sensitivity between BANP and TLN.

Amino Acid Sequence↗
PubMed1993

Impaired G-CSF production at post-transcriptional level in a patient with chronic idiopathic neutropenia.

Chronic idiopathic neutropenia (CIN) is a disorder characterized by severe neutropenia and a maturational arrest of the neutrophil precursors in the bone marrow. The pathogenesis of this disorder has been obscure. We examined the production of endogenous G-CSF and the expression of G-CSFmRNA in a patient with adult type CIN. The G-CSF production by the patient's mononuclear cells was deficient in spite of the adequate accumulation of G-CSFmRNA. Our data suggests that the defect in the endogenous G-CSF production at the post-transcriptional level is likely to be an aetiological factor in CIN.

Aged↗
PubMed1993

Immunosuppressive property of bromocriptine on human B lymphocyte function in vitro.

Bromocriptine (BRC), a dopamine ergot alkaloid, inhibits the release of pituitary prolactin (PRL). Hypoprolactinaemia induced in rat by treatment with BRC produces a similar immunosuppressive effect as observed in hypophysectomized rats. The effect of immunosuppression by the administration of BRC has been interpreted as the result of hypoprolactinaemia produced by BRC. However, the direct effect of BRC on lymphocyte function has never been evaluated. The purpose of this study was to investigate the in vitro effect of BRC on human B cell functions. Highly purified B cells from tonsil samples were isolated by Percoll density gradient from non-rosetted cells, and were used as target cells. BRC significantly suppressed the proliferative response of resting and activated B cells in vitro. It suppressed immunoglobulin generation of activated B cells. The inhibition of BRC was manifested in the early stage of the proliferation and differentiation of B cells. The conditioned medium from the polyclonal B cell mitogen-stimulated B cell cultures did not contain PRL as detected by immunoradiometric assay. Treatment with low-dose cyclosporin A or FK506 in conjunction with BRC has proved more effective than either drug alone in suppression of B cell proliferation. Thus, the combined therapy of BRC and immunosuppressants may be effective with decreased toxicity for clinical use.

Antigens, CD↗
PubMed1993

G-CSF enhances the immunoglobulin generation rather than the proliferation of human B lymphocytes.

The effect of granulocyte-colony stimulating factor (G-CSF) on human B-cell function was studied in in vitro cultures. G-CSF alone had no effect on the proliferative response of resting B cells, but it slightly enhanced the proliferative response of these cells in the presence of polyclonal B-cell mitogen, Staphylococcus aureus Cowan strain I (SAC) at concentrations of 0.2 to 25 micrograms/ml (1.5-fold increase in the DNA synthesis). In contrast, immunoglobulin (Ig) secretion of activated B cells was increased approximately three-fold to four-fold by adding G-CSF to the cultures. The neutralization of G-CSF bioactivity with anti-G-CSF antibody abrogated this effect. Though cytoplasmic Ig-positive cells or plasma cell marker-positive cells did not change, the expression of IgM mRNA in antibody-producing B cells increased in the presence of G-CSF in the cultures. Interestingly, human B lymphocytes are shown to express the binding to biotin-conjugated G-CSF preparation, but not to biotin-conjugated GM-CSF preparation when examined by flow cytometry. These data suggest that G-CSF may influence B-cell function in special circumstances.

Antibodies↗
PubMed1993

Immunosuppressive activity of fosfomycin on human T-lymphocyte function in vitro.

Recent investigations have shown that some antibiotics also work as immunomodulators. We have recently reported that fosfomycin (FOM) has an immunomodulatory effect on human B-cell activation. FOM is a unique antibiotic which is chemically unrelated to any other known antibacterial agent. In the present study, we examined the effect of FOM on human T-cell function. FOM inhibited the proliferation of human lymphocytes induced by polyclonal T-cell mitogens in a dose-dependent manner. FOM also strongly suppressed mixed lymphocyte reaction and interleukin-2 (IL-2) production by T cells. Moreover, FOM inhibited the expressions of IL-2 receptor (CD25) and transferrin receptor (CD71) on the activated T-cell surfaces. These data suggest that FOM may block the T-cell division during the transition from G1 to S phase of the cell cycle. Combined treatment with FOM and low-dose cyclosporin A or FK506 caused additive or synergistic suppression of T-cell proliferation, but not on IL-2 receptor expression. It seems that the mode of action of FOM on T-cell function involves a specific suppression of IL-2 production.

Animals↗
PubMed1993

Immunomodulatory effect of fosfomycin on human B-lymphocyte function.

Fosfomycin (FOM) is an unique antibiotic which is chemically unrelated to any other known antimicrobial agent. Recent investigations have demonstrated that FOM inhibits histamine release from basophils. In this study, we examined the effect of FOM on human B-cell functions. FOM inhibited the proliferative response of resting B cells induced by Staphylococcus aureus Cowan 1 in a dose-dependent manner. FOM interfered with the transition from the G0 to the G1 phase of the cell cycle, leading to cell arrest. The proliferative response of in vivo-activated B cells and lymphokine-induced B-cell proliferation were also affected by FOM. In addition, FOM suppressed immunoglobulin secretion by antibody-producing B cells. Interestingly, FOM did not affect the expression of activation antigens such as the CD25 (interleukin-2 receptor) and CD71 (transferrin receptor) antigens. Moreover, FOM sustained the increased Ia expression on B-cell membranes induced by S. aureus Cowan 1 stimulation, which suggests that FOM may not block the role of B cells in antigen presentation in T-cell-B-cell interaction.

Adjuvants, Immunologic↗
PubMed1993

Hepatic blood flow and energy metabolism during hypotension induced by prostaglandin E1 and nicardipine in rabbits: an in vivo magnetic resonance spectroscopic study.

Hepatic blood flow (HBF) and energy metabolism during moderate hypotension induced by prostaglandin E1 (PGE1) and nicardipine were studied by in vivo magnetic resonance spectroscopy. HBF was determined by the deuterated water clearance method by using deuterium magnetic resonance spectroscopy, and energy metabolism was estimated from the changes in the levels of adenosine triphosphate and inorganic phosphate by using phosphorus (31P) magnetic resonance spectroscopy. Mean arterial blood pressure was intentionally reduced to 60% of control with PGE1 (n = 5) or nicardipine (n = 5). The HBF decreased by 38% and by 50% during the hypotension induced by PGE1 and nicardipine, respectively. The level of adenosine triphosphate decreased by 12% and that of inorganic phosphate increased by 80% during nicardipine-induced hypotension, whereas the corresponding levels showed no remarkable changes during PGE1-induced hypotension. After the cessation of drug administration, mean arterial blood pressure and HBF recovered to the control levels in the PGE1 group, but not completely in the nicardipine group. In the latter group, the level of inorganic phosphate did not recover either. These results indicate that during hypotension induced with PGE1 hepatic circulation and metabolism are conserved to a greater extent than during hypotension induced with nicardipine.

Adenosine Triphosphate↗
PubMed1993

Heterogeneous metabolic changes in the calf muscle of the rat during ischaemia-reperfusion: in vivo analysis by 31P nuclear magnetic resonance chemical shift imaging and 1H magnetic resonance imaging.

Non-localized and localized 31P nuclear magnetic resonance (NMR) spectra of rat calf muscle during arterial occlusion and after reperfusion were concurrently observed using chemical shift imaging and 1H magnetic resonance imaging (MRI). During ischaemia, the levels of high-energy phosphates (phosphocreatine and adenosine 5'-triphosphate) were depleted and that of inorganic phosphate was increased. In addition, the signal intensity on 1H MRI was increased. These changes were observed to be relatively homogeneous throughout the calf. In contrast, the changes during reperfusion were heterogeneous. In the central part of the calf, inorganic phosphate disappeared, phosphocreatine was restored immediately on reperfusion and the 1H signal was decreased. However, in the regions of the tibialis anterior muscle and the superficial part of the gastrocnemius muscle, inorganic phosphate persisted for several hours, phosphocreatine was not restored and the signal intensity on T2-weighted 1H MRI was increased further. The heterogeneous changes detected by 31P NMR spectroscopy and 1H MRI showed close agreement. The susceptibility of different calf muscles to ischaemia and reperfusion seems to depend on their predominant muscle fibre type (i.e. fast-twitch or slow-twitch fibres). Reversible and irreversible ischaemic changes could be non-invasively distinguished by in vivo 31P NMR spectroscopy and 1H MRI.

Adenosine Triphosphate↗
PubMed1993

[A case of prostatic carcinoma presenting as abdominal mass].

A 69-year-old man was admitted to the hospital on August 7, 1991 because of a lower abdominal mass. On physical examination, firm, rough-surfaced, unmovable masses of over fist size were palpable in the lower abdomen along with some small masses in the bilateral inguinal regions. On rectal examination the prostate was rough, hard and stony and larger than a chicken's egg in size. The serum prostatic acid phosphatase and prostatic specific antigen levels were elevated. A computerized tomography scan disclosed a large mass in the pelvis. Both a needle biopsy of the prostate and resection of an inguinal mass revealed moderately differentiated adenocarcinoma. Bone scintigram disclosed multiple metastases. Treatment with diethylstilbestrol diphosphate, etoposide, peplomycin and ifosfamide was effective, resulting in regressed intrapelvic masses and decreased serum prostatic acid phosphatase and prostatic specific antigen levels close to the normal limits. In November 1991, the patient was discharged and was surviving with the tumor as of August 1992.

Abdominal Neoplasms↗
PubMed1993

Two distinct types of cellular mechanisms in the development of delayed hypersensitivity in mice: requirement of either mast cells or macrophages for elicitation of the response.

Using mast cell-deficient mutant W/Wv mice and their normal counterpart we re-evaluated the significance of participation of mast cells in allergic inflammatory response. W/Wv mice developed immediate hypersensitivity (IH) footpad reaction (FPR) to a somewhat lesser degree than the normal mice, suggesting that the mast cell might amplify the response. To exert classical tuberculin (tbc) delayed-type hypersensitivity (DTH) mast cells were not an essential cellular component. Vasoactive amines were essential to develop the response, but it did not necessarily originate from mast cells. When mice were immunized with methylated human serum albumin (MHSA) emulsified in incomplete Freund's adjuvant (IFA), mast cells were required to elicit DTH FPR. This was confirmed by the lack of the response in W/Wv mice, and the restoration of FPR by local transplantation of mature mast cells into mutant mice. This mast cell-dependent (MD) DTH was different from tbc DTH as follows: mast cell dependency, macrophage dependency as revealed by ferritin sensitivity, kinetics of sensitization, effect of host's age and histopathology. Thus we concluded that there are two types of DTH in mice; one is macrophage-dependent tbc and the other is mast cell-dependent DTH. The correspondence of the DTH to the Jones-Mote (JM) DTH is discussed, although the dominance of mast cells in MD DTH lesion was not observed.

Animals↗
PubMed1992

Chemical assessment of phospholipid and phosphoenergetic metabolites in regenerating rat liver measured by in vivo and in vitro 31P-NMR.

For the assessment of 31P-NMR spectroscopic data, phospholipid precursors (phosphorylethanolamine (PE) and phosphocholine) and catabolites (glycerophosphorylethanolamine (GPE) and glycerophosphorylcholine (GPC)), as well as adenosine phosphates were chemically determined in regenerating rat liver. The data were compared with those obtained by in vivo and in vitro 31P-NMR spectroscopies. Chemical assay revealed a significant increase of PE and a decrease of GPE, GPC and ATP in hepatectomy group compared to sham operation group. The values obtained by in vitro NMR were in good agreements with those of chemical assay, but significant differences between the two groups were observed only in PE and inorganic phosphate (Pi). Noticeable increase in PME was not detected by in vivo 31P-NMR spectroscopy, although the increase of PE was about 2.5-times that of the control and its constitution ratio to the whole phosphomonoester (PME) was less than 15%. On the other hand, in vivo NMR showed a large phosphodiester (PDE) peak occupying approx. 40% of the total phosphorus signal, while the contribution of its constituents, GPE and GPC was about 5% found by both chemical assay and in vitro NMR. The PDE peak in in vivo NMR seemed to reflect the membrane phospholipid itself rather than its catabolites. A slight decrease of phosphoenergetic level in regenerating rat-liver was commonly suggested by all three analytical methods.

Animals↗
PubMed1992

The synthesis of cadystins, heavy metal chelating peptides, is induced in the fission yeast by wounds of the cell wall or by incubation with chitosan.

It has been shown that heavy metal administration induced the synthesis of cadystins, the small metal chelating peptide with the general structure of (gamma-glu-cys)n-gly, in the fission yeast and in plants. Besides heavy metals, wounds to the cell surface or the incubation with chitosan induced the cadystin synthesis in the fission yeast. Under these induction conditions, the membrane permeability of the fission yeast significantly increased suggesting the structural alteration of the membrane. In these induction, the synthesized cadystins formed complexes with the cellular zinc ions together with or without glutathione.

Amino Acid Sequence↗
PubMed1992

Identification and analysis of the gag-pol ribosomal frameshift site of feline immunodeficiency virus.

The pol genes of retroviruses are translated as gag-pol fusion proteins by ribosomal frameshifting within the gag-pol overlap region. During the ribosomal frameshift event, the gag open reading frame is shifted -1 nt to allow in-phase reading of the pol open reading frame. A consensus frameshift signal sequence of GGGAAAC within the gag-pol overlap region of feline immunodeficiency virus (FIV) has been identified followed by a sequence that has the potential for a pseudoknot tertiary structure. Using recombinant baculoviruses in which the frameshift occurs efficiently, the consensus sequence has been shown to be the site of the frameshift event. A mutation creating a termination codon just downstream of the putative frameshift signal sequence but upstream of the potential pseudoknot structure made a shorter gag product, but did not affect the efficiency of frameshifting. A mutation creating a termination codon just upstream of the putative frameshift signal made a shorter product and essentially abrogated frameshifting. Mutations in the first stem or the second stem in the potential pseudoknot structure severely reduced the frameshifting efficiency. Mutations which altered the length between the frameshift signal and the pseudoknot structure (the so-called spacer region) also reduced the frameshift efficiency. The insertion of a palindromic sequence, which could form a hairpin structure just upstream of the frameshift signal sequence, also affected the frameshifting. These results support the view that the ribosomal frameshift event in the FIV gag-pol region involves the identified signal sequence and appears to require the precisely positioned downstream sequence and indicated pseudoknot structure for efficient frameshifting.

Animals↗
PubMed1992

Analysis of a human immunodeficiency virus type 1 isolate carrying a truncated transmembrane glycoprotein.

We have recently reported the isolation of a human immunodeficiency virus type 1 (HIV-1), KB-1gp32 carrying a shorter size (32 kDa) of transmembrane glycoprotein (TMP) from TALL-1 cells persistently infected with KB-1gp41 virus strain (Shimizu et al., 1990a). Endoglycosidase treatments showed that the different size of the TMP between the two strains was due to a truncation of 9 kDa of polypeptide in the KB-1gp32 TMP coding region. Sequence analysis revealed the substitution of a CAG codon to a TAG stop codon just downstream of the putative membrane-spanning domain of the TMP of KB-1gp32. This resulted in a truncation of some 133 amino acids of the cytoplasmic domain of TMP. The data indicate that a premature stop codon in KB-1gp32 has been introduced during adaption of the parental virus to TALL-1 cells. We have constructed two chimeric clones between the env region of a clone pKB-1, derived from KB-1gp32, and an infectious molecular clone pNL-432. We have also constructed a site-directed mutant of pNL-432 carrying a premature stop codon at the same position as the env stop codon of pKB-1. Among the three clones carrying a premature stop codon in env, only one chimeric clone was infectious to TALL-1 but not MT-2 cells. This clone contained the entire tat, rev, vpu, and env genes of pKB-1. The pNL-432 mutant was not infectious. The results suggest that some sequences of pKB-1 might compensate for the truncation of the TMP during replication in TALL-1 cells.

Amino Acid Sequence↗
PubMed1992

Inhibition of proliferation and differentiation of human B-lymphocytes by a biscoclaurine alkaloid.

A biscoclaurine alkaloid, cepharanthine, is known to be a potent inhibitor of snake venom-induced hemolysis by interaction with the lipid bilayer of the membrane. The drug also interferes with the ion channel intracellularly. In this study, we examined the effect of cepharanthine on human B-cell functions. Small dense B-cells from tonsil samples were isolated using a Percoll density gradient from non-rosetted cells and were used as the target cells. Cepharanthine inhibited the proliferation of the lymphocytes and antibody production of human B-lymphocytes. The inhibitory effect of cepharanthine on the proliferation was caused by the arrest of the late G1 to S phase transition in the cell cycle. However, the mechanism of suppression of antibody formation remains unknown. These results suggest that cepharanthine acts on human B-cells as an immunomodulating agent.

Adjuvants, Immunologic↗
PubMed1992

Major core proteins, p24s, of human, simian, and feline immunodeficiency viruses are partly expressed on the surface of the virus-infected cells.

We have previously shown the expression of human immunodeficiency virus type 1 (HIV-1) major gag protein, p24, on the surface of persistently HIV-1-infected cells by using murine monoclonal antibodies (mAb). We now report that the cell surface gag p24 antigen expression is a universal phenomenon among HIV-1, simian immunodeficiency virus (SIV), and feline immunodeficiency virus (FIV). The mAbs prepared by immunization with purified HIV-1 particles were used as antibodies cross-reactive to HIV-1 and SIVagmp24 antigens. The mAbs to FIV p24 were raised against the gag precursor 50 kDa protein of FIV, which was expressed by Baculovirus vector. The p24 antigen expression on the cell surface was detectable in certain combinations of virus-host cell systems in all of these viruses. Since these p24 regions of the animal viruses seem to play as important a role in cell-mediated immunity as that of HIV-1, the p24 applicability as a candidate epitope for vaccine development could be evaluated in those animals.

Animals↗