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Biomedical subjects

H Yoshida

Publications and source records attributed to H Yoshida.

At least 739 records · Page 41Linked to original sources
PubMed1998

Induction of TSC-22 by treatment with a new anti-cancer drug, vesnarinone, in a human salivary gland cancer cell.

We undertook the present study to clarify the molecular mechanism of the effect of a new anti-cancer drug, vesnarinone, on a human salivary gland cancer cell line, TYS. We isolated TSC-22cDNA as avesnarinone-inducible gene from a cDNA library constructed from vesnarinone-treated TYS cells. TSC-22 was originally reported as a transforming growth factor (TGF)-beta-inducible gene. The expression of TSC-22 was up-regulated within a few hours after treatment with vesnarinone and was continued for 3 days. The level of TSC-22 mRNA in TYS cells was continuously increased until the cells reached confluency. Furthermore, the induction of TSC-22 by vesnarinone was inhibited by treatment with cycloheximide. When we treated the cells with an antisense oligonucleotide against TSC-22 mRNA under quiescent conditions, the antisense oligonucleotide stimulated the growth of TYS cells; however, under growing conditions the antisense oligonucleotide did not affect cell growth. Furthermore, the antisense oligonucleotide suppressed the antiproliferative effect of vesnarinone. These results suggest that TSC-22 may be a negative growth regulator and may play an important role in the antiproliferative effect of vesnarinone.

Antineoplastic Agents↗
PubMed1998

Effects of the antihypertensive agent, cicletanine, on noradrenaline release and vasoconstriction in perfused mesenteric artery of SHR.

1. The mechanism by which cicletanine (CIC) exerts its antihypertensive effects has not been fully elucidated. The present study was undertaken to examine the effects of in vivo and in vitro treatment with CIC on the pressor response and noradrenaline (NA) overflow during periarterial nerve stimulation (PNS) in perfused mesenteric arterial beds isolated from spontaneously hypertensive rats (SHR). 2. CIC at a dose of 50 mg kg(-1) day(-1) was administered orally to both SHR and normotensive Wistar-Kyoto rats (WKY) from the 6th to 10th week of age. At the 10th week, the isolated mesenteric arterial bed was perfused with Krebs-Henseleit buffer and changes in perfusion pressure and NA overflow during PNS were measured. 3. Chronic treatment with CIC suppressed the age-related elevation of systemic blood pressure in SHR but not in WKY. 4. The PNS (20 Hz)-induced mesenteric vasoconstrictor response and NA overflow were greater in SHR than in WKY. In the vasculature of SHR chronic treatment with CIC resulted in a significant attenuation of the vasoconstriction and the NA overflow during PNS, whereas it did not alter vasoconstrictor responses to bolus injections of KCl and phenylephrine. 5. Treatment with 30 microM CIC in vitro diminished the PNS-induced vasoconstriction and NA overflow but not the NA- and KCl-induced vasoconstriction in the vasculature of untreated SHR. 6. In the vasculature of SHR PNS-induced NA overflow was attenuated by prostaglandin E2 (0.05 microM), whereas it was augmented by the cyclo-oxygenase inhibitor diclofenac-Na (30 microM). In the presence of diclofenac, in vitro treatment with CIC did not attenuate the NA overflow during PNS. 7. The results suggest that the antihypertensive effect of CIC in SHR is partially due to the presynaptic inhibition of NA release during sympathetic nerve activation. Transjunctional inhibition of NA release by prostaglandins may contribute to the inhibitory action of CIC on NA release in the vasculature of SHR.

Animals↗
PubMed1998

Etoposide-related acute promyelocytic leukemia.

The development of therapy-related acute myeloid leukemia (t-AML) has become a growing concern over the past decade, because of the increase in the percentage of long-term survivors of primary malignancy. We reviewed 17 cases with etoposide-related acute promyelocytic leukemia (APL) reported in the literature. The close association between treatment with etoposide for Langerhans cell histiocytosis (LCH) and the development of etoposide-related APL was demonstrated among Japanese and Italians. Our data on the breakpoints (b/ps) of the PML and RARalpha genes are presented. It is suggested that chromatin structure might be more important than specific consensus sequence in the distribution of b/ps in etoposide-related APL.

Adult↗
PubMed1998

Effect of the interaction between fibronectin and VLA-4 on the proliferation of human B cells, especially a novel human B-cell line, OPM-3.

Very late antigen (VLA)-4 integrin has been suggested to play an important role in haemopoiesis. However, little is known concerning the roles of the fibronectin (FN)/VLA-4 interaction in the proliferation of human B cells. In this study we investigated the effect of immobilized FN on the proliferation of various B-cell lines, including a newly-established B-cell line, OPM-3, and human tonsillar B cells, that primarily express VLA-4 but not VLA-5. Immobilized FN significantly promoted the proliferation of OPM-3 cells and normal B cells via VLA-4. The cross-linking of beta1 integrins of OPM-3 cells resulted in the phosphorylation of the focal adhesion kinase (FAK) associated 90 kD protein, an increase in FAK-associated kinase activity, and the phosphorylation of Raf-1. Furthermore, the MEK1 inhibitor, PD98059, inhibited the FN-promoted proliferation of OPM-3 cells. These results demonstrate that the FN/VLA-4 interaction transmits the growth signal(s) which may be mediated by Ras pathway in OPM-3 cells, and suggest that OPM-3 cells may be of great value in studying the roles of the FN/VLA-4 interaction in human B-cell growth.

B-Lymphocytes↗
PubMed1998

Decreased nitric oxide-mediated natural killer cell activation in chronic fatigue syndrome.

BACKGROUND: L-Arginine (L-Arg), one of the essential amino acids, has been reported to have an immunomodulatory effect. The precise mechanism of the L-Arg-induced natural killer (NK) cell activation remains unresolved,and the effect of L-Arg on NK cells in chronic fatigue syndrome (CFS) patients has not been estimated. METHODS: NK cell function was evaluated in 20 subjects with CFS and compared with that in 21 healthy individuals. RESULTS: In healthy control subjects, NK activity was significantly increased after treatment with L-Arg, an NK function enhancer, for 24 h, whereas the same treatment failed to enhance NK activity in the CFS patients. We thus focused on L-Arg metabolism, which involves nitric oxide (NO) production through NO synthase (NOS). The expression of inducible NO synthase (iNOS) transcripts in peripheral blood mononuclear cells was not significantly different between healthy control subjects and CFS patients. The L-Arg-mediated NK cell activation was abolished by addition of NG-monomethyl-L-arginine, an inhibitor for iNOS. Furthermore, incubation with S-nitroso-N-acetyl-penicillamine, an NO donor, stimulated NK activity in healthy control subjects but not in CFS patients. CONCLUSION: These results demonstrate that the L-Arg-induced activation of NK activity is mediated by NO and that a possible dysfunction exists in the NO-mediated NK cell activation in CFS patients.

Adjuvants, Immunologic↗
PubMed1998

Gamma delta T cells in infection-induced and autoimmune-induced testicular inflammation.

In a previous report, we investigated inflammatory responses induced by injecting Listeria monocytogenes into one testis of a mouse. We demonstrated that the contralateral testis also developed an orchitis despite the absence of bacteria, indicating that the inflammation on the uninfected, contralateral side was of autoimmune character. In both infected and autoimmune testes, gammadelta and alphabeta T cells infiltrated during the inflammation. In this paper, we present the data of a comparison of the character of gammadelta T cells of the infected and autoimmune testes. In both testes, gammadelta T cells appeared to be activated, as assessed by high CD44 and low l-selectin expression. Analysis of T-cell receptor (TCR) usage in both inflammation types revealed the same gammadelta TCR repertoire. Finally, the semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) demonstrated that gammadelta T cells in both types of inflammation were capable of producing interleukin-2 (IL-2), IL-4, interferon-gamma (IFN-gamma), IL-10 and transforming growth factor-beta (TGF-beta). These results imply that gammadelta T cells present in infected-induced and autoimmunity-induced inflammation have the same characteristics and could work as immunoregulatory cells.

Animals↗
PubMed1998

Inducer exclusion in Escherichia coli by non-PTS substrates: the role of the PEP to pyruvate ratio in determining the phosphorylation state of enzyme IIAGlc.

The main mechanism causing catabolite repression in Escherichia coli is the dephosphorylation of enzyme IIAGlc, one of the enzymes of the phosphoenolpyruvate:carbohydrate phosphotransferase system (PTS). The PTS is involved in the uptake of a large number of carbohydrates that are phosphorylated during transport, phosphoenolpyruvate (PEP) being the phosphoryl donor. Dephosphorylation of enzyme IIAGlc causes inhibition of uptake of a number of non-PTS carbon sources, a process called inducer exclusion. In this paper, we show that dephosphorylation of enzyme IIAGlc is not only caused by the transport of PTS carbohydrates, as has always been thought, and that an additional mechanism causing dephosphorylation exists. Direct monitoring of the phosphorylation state of enzyme IIAGlc also showed that many carbohydrates that are not transported by the PTS caused dephosphorylation during growth. In the case of glucose 6-phosphate, it was shown that transport and the first metabolic step are not involved in the dephosphorylation of enzyme IIAGlc, but that later steps in the glycolysis are essential. Evidence is provided that the [PEP]-[pyruvate] ratio, the driving force for the phosphorylation of the PTS proteins, determines the phosphorylation state of enzyme IIAGlc. The implications of these new findings for our view on catabolite repression and inducer exclusion are discussed.

Bacterial Proteins↗
PubMed1998

Aortitis syndrome (Takayasu's arteritis) with cataract and elevated serum level of vascular endothelial growth factor.

The aortitis syndrome is a chronic inflammatory process that affects the aorta and its primary branches. Patients with aortitis syndrome exhibit various ocular changes. We present a patient in whom cataract was the initial objective finding. The serum concentration of vascular endothelial growth factor, a cytokine that affects neovascularization, and vasopermeability, was elevated before the initiation of prednisolone treatment. Cataract should be considered as a possible characteristic initial finding in patients with aortitis syndrome. Vascular endothelial growth factor may be involved in the progression of aortitis syndrome.

Adult↗
PubMed1998

Vascular endothelial growth factor in patients with rheumatoid arthritis.

To examine the role of vascular endothelial growth factor (VEGF), an endothelial cell specific growth factor, in rheumatoid arthritis (RA), serum concentration of VEGF was examined in patients with RA, osteoarthritis (OA), systemic lupus erythematosus (SLE), systemic sclerosis (SS) and control subjects. Serum C-reactive protein (CRP) level, erythrocyte sedimentation rate, white blood cell count and rheumatoid factor titer were also determined in patients with RA. The serum concentration of VEGF was significantly higher in patients with RA than in controls (p < 0.01), and patients with OA (p < 0.05), SLE (p < 0.05), and SS (p < 0.05). The serum concentration of VEGF correlated with serum levels of CRP (r = 0.698, p < 0.0001). The serum concentration of VEGF before treatment was significantly higher than that after treatment in patients with RA who experienced clinical remission (p < 0.05). Our data suggest that VEGF is involved in the pathogenesis of RA and that measurement of serum concentration of VEGF is a noninvasive, useful method for monitoring the disease activity of RA.

Adolescent↗
PubMed1998

Midkine induces histamine release from mast cells and the immediate cutaneous response.

Midkine is a product of a retinoic acid-responsive gene and exerts a variety of biological activities. The aim of our investigation is to determine whether human midkine have histamine-releasing effects on mast cells, and to show the evidence of the inflammation induced by midkine. Midkine induced histamine release from rat peritoneal mast cells with a rapid response in a dose-dependent manner. Extracellular calcium inhibited the histamine release induced by midkine in a dose-dependent manner. Pertussis toxin and benzalkonium chloride inhibited the histamine release induced by midkine. Gi-proteins exert an effect on the histamine release of midkine. The immediate cutaneous response induced by midkine was positive. These results suggest that midkine may take part in some inflammation via histamine release from mast cells.

Animals↗
PubMed1998

Cloning and sequencing of cDNA encoding ribonuclease F1 from Fusarium moniliforme.

Two cDNA clones encoding ribonuclease F1 (EC 3.1.27.3) have been isolated using a probe prepared by polymerase chain reaction with primers designed on the basis of amino acid sequence of the enzyme. They derived probably from the same gene and contained 393-base pair open reading frame encoding 131 amino acid residues (Mr 13,606) including a putative 25-residue signal peptide. The sequences of 43-base pair 5'-untranslated region and 125-base pair 3'-untranslated region including a poly(A) tail of 25 nucleotides were also elucidated. Homology analyses showed that cDNA for ribonuclease F1 has 65% homology to that for ribonuclease T1 in the coding region. At the preprotein level, they share 53% homology.

Amino Acid Sequence↗
PubMed1998

Neonatal hyperbilirubinemia and mutation of the bilirubin uridine diphosphate-glucuronosyltransferase gene: a common missense mutation among Japanese, Koreans and Chinese.

We analyzed the bilirubin uridine diphosphate-glucuronosyltransferase (B-UGT) gene in 42 Japanese newborns with hyperbilirubinemia and determined that 21 infants were heterozygous while 3 was homozygous for Gly71Arg. Allele frequency of Gly71Arg was 0.32 in newborns with hyperbilirubinemia, which was significantly higher than 0.13 in healthy Japanese controls. This mutant allele is also prevalent among Korean and Chinese healthy controls with a frequency of 0.23 in both populations. However, this mutation was not detected in 50 healthy German controls. These data suggest that the high frequency of the Gly71Arg mutation of the B-UGT gene is associated with high incidence of neonatal hyperbilirubinemia in Japanese, Korean and Chinese populations.

Alleles↗
PubMed1998

Essential role of IL-7 receptor alpha in the formation of Peyer's patch anlage.

We investigated the role of IL-7 receptor alpha (IL-7Ralpha) signal in the formation of Peyer's patch (PP) anlage. Although pan-lymphopenia is a common phenotype of rag2-/- and il7ralpha-/- mice, a close inspection revealed nodules corresponding to PP in the adult rag2-/- but not in the il7ralpha-/- mouse. In our previous study, three histologically distinct steps in the formation of PP were identified. The first is the appearance of VCAM-1 + spots in the intestine, which probably represents an initial stage of the formation of the PP anlage. Accumulation of cells bearing IL-7Ralpha, CD4 or Ia in this region then follows and eventually entry of mature lymphocytes expressing CD3 or B220 occurs just before birth. Based on this criterion, we next investigated which of these events is defective in mice with severe combined immunodeficiency. Formation of VCAM-1 + spots and cluster formation of IL-7Ralpha+ cells proceed normally in the rag2-/- mouse which completely lacks mature lymphocytes. In contrast, no VCAM-1+ spots were detected in the embryonic nor neonatal il7ralpha-/- mice, suggesting that IL-7Ralpha signal is involved in the early phase of PP anlage formation. The same defect was found in the jak3-/- mouse. In addition to the appearance of VCAM1+ spots, the clustering of IL-7Ralpha+ cells was absent in the jak3-/- mouse, though IL-7Ralpha+ cells are found to scatter over the intestine. These results indicate that IL-7Ralpha is an essential signal for an early step of PP anlage formation, without which the subsequent processes cannot be initiated.

Animals↗
PubMed1998

Essential role of platelet-derived growth factor receptor alpha in the development of the intraplacental yolk sac/sinus of Duval in mouse placenta.

Platelet-derived growth factor receptor alpha (PDGFRalpha) is expressed in multiple tissues and exerts its function throughout mouse embryogenesis. Upon screening the PDGFRalpha-expressing tissues in mouse embryos by immunohistochemistry using our established monoclonal antibody against murine PDGFRalpha, we found its expression in an epithelium lining a sinusoidal structure in placenta. This structure was proven to be the sinus of Duval, and the PDGFRalpha-positive epithelium to be the intraplacental yolk sac (IPY). The IPY has been postulated to be a derivative of primitive endoderm because of its morphology and its expression of vitamin D-dependent 9-kDa calcium-binding protein, and to play some roles in materno-fetal transport. In this study, we demonstrated that the IPY develops from primitive endoderm by its invagination into chorioallantoic placenta and continues to strongly express PDGFRalpha until the prenatal stage. Moreover, we found that the IPY is completely absent in PdgfraPh/PdgfraPh mutant embryos, which lack the Pdgfra gene, suggesting that the function of PDGFRalpha is essential to its formation. Hence, PDGFRalpha expressed in the IPY should be listed as a component of the cytokine network of murine placental development.

Animals↗
PubMed1998

Differences in responses to norepinephrine and adenosine triphosphate in isolated, perfused mesenteric vascular beds between normotensive and spontaneously hypertensive rats.

The responses to norepinephrine and adenosine 5' triphosphate (ATP) of isolated, perfused mesenteric vascular beds were compared between spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. Norepinephrine (0.01-100 nmol) dose-dependently increased perfusion pressure in the intact bed and the arteries, but not in the veins. The maximal responses in SHRs were larger than those in WKY rats. ATP (0.1-3,000 nmol) increased perfusion pressure in all preparations. The responses of the intact bed and the veins were larger in SHRs, whereas there was no strain difference in the arteries. Indomethacin (5 x 10(-6) M) enlarged the norepinephrine responses of both strains only in the intact beds and did not affect the ATP responses, except the veins in SHRs, where it was reduced. N(G)-nitro-L-arginine methyl ester (5 x 10(-6) M), in combination with indomethacin, potentiated the responses, except the arterial response to high doses of norepinephrine in SHRs, which was not affected. Endothelium denudation in the arteries produced similar changes to those after the combined treatment. UK14,304-induced and ADPbetaS-induced decreases in perfusion pressure at increased tone were similar between the strains. Thus neither the vasodilation induced by the stimulation of alpha2-adrenoceptors nor of P2y receptors seems to affect the response to norepinephrine or to ATP, respectively. These results demonstrate that the intact mesenteric vascular bed of SHRs shows potentiated responses not only to norepinephrine, but also to ATP, as compared with WKY rats, and that the critical regions for determining the strain differences for norepinephrine are overall arteries, and that for ATP are the vessels downstream from arterioles. In the intact beds, neither regulation by endogenous prostanoids nor that by endothelium-derived relaxing factors (EDRFs) is implicated in the strain difference. However, these two types of regulation differ markedly between different kinds of vessels.

Adenosine Triphosphate↗
PubMed1998

Oxidative stress and mitochondrial damage precedes gastric mucosal cell death induced by ethanol administration.

Although it has been speculated that active oxidants and mitochondrial membrane damages play roles in ethanol-induced gastric mucosal damages, its detail remains unknown. The present study was designed to investigate whether ethanol induces oxidative stress and mitochondrial permeability transition (MPT) before cell death of gastric mucosal cells. Rat gastric mucosal cells (RGM-1) were kept in serum-free Dulbecco's modified Eagle's medium before addition of various concentrations of ethanol. Nuclear morphological aftemations and membrane barrier dysfunction of RGM-1 cells were assessed by staining with Hoechst 33342 and propidium iodide, respectively. To assess the contribution of oxygen-derived free radicals and intracellular glutathione, scavenger of hydrogen peroxide and the hydroxyl radical, N,N-dimethylthiourea, glutathione precursor, N-acetyl-L-cysteine, and an inhibitor of alcohol dehydrogenase, 4-methylpyrazole were added before treatment with ethanol. To investigate MPT, calcein and tetramethylrhodamine methyl ester were loaded before addition of ethanol, and the changes of fluorescence intensity were monitored using a laser scanning confocal microscope. Ethanol (>5% v/v) dose-dependently increased the number of propidium iodide-positive cells, suggesting a diminished barrier function of cell membrane. After addition of ethanol, mitochondria were filled quickly with calcein indicating MPT, which was accompanied by mitochondrial depolarization, as shown by loss of tetramethylrodamine methyl ester before cell death. Ethanol-induced cell death was significantly attenuated by simultaneous incubation with either N,N-dimethylthiourea or N-acetyl-L-cysteine, suggesting the importance of intracellular redox states in inducing cellular damage, whereas such change was not attenuated by 4-methylpyrazole. Present results suggest that ethanol treatment induces intracellular oxidative stress and produces MPT and mitochondrial depolarization, which are preceding cell death in gastric mucosal cells. Intracellular antioxidants, such as glutathione, may have a significant protective action against ethanol in gastric mucosal cells.

Animals↗
PubMed1998

Differentiation of Chlamydia species by combined use of polymerase chain reaction and restriction endonuclease analysis.

To differentiate Chlamydia spp., a primer pair designed to generate a genus-specific region of the major outer membrane protein (MOMP) gene was used in a PCR to amplify a single DNA fragment of 245-259 bp. In the PCR, the expected single DNA fragment was amplified from strains of Chlamydia trachomatis, C. psittaci, C. pneumoniae and C. pecorum, respectively. By restriction endonuclease analysis with AluI and PvuII, the amplified products exhibited four distinct patterns, corresponding to the four species. It is, therefore, concluded that one-step PCR followed by restriction endonuclease analysis as described in this study could be a valuable method for the detection and differentiation of Chlamydia species.

Chlamydia↗