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Biomedical subjects

Y Nawata

Publications and source records attributed to Y Nawata.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Effects of fluconazole on onychomycosis in the patients with collagen diseases].

Thirty-four patients with collagen diseases suffering from onychomycosis were treated with fluconazole and showed remarkable improvement. Thirty-one patients showed improvement while only four patients showed adverse reactions. More than half of the cases with onychomycosis in their fingers showed improvement within four weeks and complete recovery within 20 weeks after the administration of fluconazole. Patients with collagen diseases are liable to have onychomycosis as an opportunistic infection which is recalcitrant and resistant disease from the previous therapy. In this trial it became obvious that fluconazole was not only effective on onychomycosis but also a safe drug for the patients with collagen diseases.

Adult↗
PubMed1994

HLA-DR alleles in patients with Sjögren's syndrome over-representing V beta 2 and V beta 13 genes in the labial salivary glands.

To identify genetic factors that play a role in the pathogenesis of patients with SS over-representing V beta 2 and V beta 13 genes in the lips, HLA-DR and -DQ alleles of 10 primary SS patients with predominant expression of V beta 2 and V beta 13 genes in the lips were analysed, using the polymerase chain reaction (PCR) and sequence specific oligonucleotide probes. The CDR3 amino acid sequences of cDNA clones encoding V beta 2 and V beta 13 genes were also determined by PCR. The results showed that the DRB4*0101 allele was significantly increased (80%) and that the frequency of DRB3 allele was decreased (0%) when compared to findings in healthy subjects (35.6 and 26%, respectively). Sequencing analyses demonstrated that 75% of V beta 2 cDNA clones and 87% of V beta 13 cDNA clones had a glutamine residue at position 106, in the CDR13 region. Moreover, the conserved sequences (Y*TLRNEQ) in the CDR3 of V beta 13-positive T cell were detected in two different clones (27%) from the two individual SS patients. These findings suggest that the decreased DRB3 and increased DRB4*0101 alleles may be associated with the antigens recognized by V beta 2- and V beta 13-positive T cells.

Alleles↗
PubMed1994

[Thrombotic thrombocytopenic purpura (TTP) observed in a patient with primary antiphospholipid antibody syndrome].

Thrombotic thrombocytopenic purpura (TTP) is a rare syndrome of unknown etiology and has a high mortality rate. TTP is characterized by a pentad of clinical findings, including microangiopathic hemolytic anemia, thrombocytopenia, renal abnormalities, neurologic signs and fever. The pathological feature of TTP consists of disseminated microvascular platelet thrombi. We describe a case of TTP with primary anti-phospholipid syndrome. A 27-year-old woman developed TTP in her second trimester of pregnancy. She presented with classical symptoms of TTP with compatible renal biopsy findings. Although four articles of SLE criteria (1982 ARA) were fulfilled, three of them were considered to be derived from multiple thrombosis except for a positive antinuclear antibody. Positive antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibody) with SLE-like findings suggested the diagnosis of antiphospholipid antibody syndrome rather than SLE. Although TTP has been described in patients with SLE and they can share common clinical and pathological features, the relationship between these two diseases is controversial. Many theories have been proposed to explain the nature and cause of intravascular platelet aggregation in TTP. But the pathogenesis of TTP is still unclear. This case suggests an important causal relationship between antiphospholipid antibodies and TTP during pregnancy. In TTP patients who also have SLE or SLE-like features, the antiphospholipid antibodies may have a role in the development of multiple microthrombosis.

Adult↗
PubMed1994

[Hemophagocytic syndrome observed in a patient with systemic lupus erythematosus].

A 52-year-old woman was admitted to our hospital because of a skin rash, high fever and myalgia. She had been diagnosed ten years ago by a dermatologist as having MCTD (mixed connective tissue disease). At the time of admission a diagnosis of active SLE was made by fulfilling four of the 1982 ARA criteria together with increasing levels of anti-DNA antibody and low levels of complements. Prednisolone (PSL) given orally in an initial dosage of 60 mg/day was effective during the first 6 weeks. Then a high fever, skin rash and pancytopenia appeared without active findings of SLE. Infection caused by bacteria, fungus or virus was suspected, but no infectious agent was present in cultures derived from blood or other sources. Antimicrobic drugs used were not effective at all. The clinical picture was suggestive of a drug allergy, but no causative drug was found. A diagnosis of hemophagocytic syndrome (HPS) was made because of the increased number of unusual hemophagocytic cells in the bone marrow. High levels of serum ferritin and neopterin, which are known to reflect macrophage activation, supported the diagnosis of HPS. HPS is characterized by activated phagocytosis presumably induced by hypersecretion of cytokines. Malignant lymphoma and infection are the two representative diseases which may cause HPS. Recently, an acute lupus HPS was reported in patients with active SLE. Here we reported a case of reactive HPS observed in a patient with SLE who had been receiving high dose PSL. Symptoms and findings of the patient gradually disappeared in several weeks after rapid reduction of the PSL dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Disseminated Intravascular Coagulation↗
PubMed1994

Chronic salicylate intoxication and rhabdomyolysis in a patient with scleroderma and Sjögren's syndrome.

A 44-year-old woman with scleroderma and Sjögren's syndrome developed altered consciousness, acute renal failure, and rhabdomyolysis. She had no history of trauma, seizures, alcohol abuse, hyperthermia, or other possible causative factors for rhabdomyolysis. A high serum salicylate level indicated a diagnosis of salicylate intoxication. Medical history after recovery revealed chronic salicylate ingestion for severe headaches. This is possibly the first reported case of rhabdomyolysis caused by chronic salicylate intoxication. Continuous hemodiafiltration early in hospitalization was an effective treatment.

Acute Kidney Injury↗
PubMed1990

Surface immunoglobulin ligands and cytokines differentially affect proliferation and antibody production by human CD5+ and CD5- B lymphocytes.

Normal human peripheral blood B lymphocytes were separated into CD19+ CD5+ and CD19+ CD5- subsets by dual-color FACS sorting. In most experiments the cells were activated with Staphylococcus aureus Cowan I (SAC) and cultured in the absence or presence of recombinant human IL-1 alpha, IL-2, or IL-6, or combinations of these cytokines. Unstimulated CD5+ and CD5- B cells showed a comparable, low level of incorporation of [3H]thymidine into DNA. SAC stimulated proliferation of CD5+ and CD5- B cells, and this proliferation was augmented by IL-2 in the case of CD5- B cells. Anti-mu beads stimulated some proliferation of the CD5- subset and augmented SAC-induced proliferation of these cells. In contrast, anti-mu beads did not stimulate proliferation of the CD5+ subset and had no effect on SAC-induced proliferation of these cells. CD5+ B cells activated by anti-mu beads were stimulated to proliferate in the presence of IL-4, but not in the presence of IL-2. These observations support the interpretation that two signals are required for proliferation of CD5+ B cells. Using a two-step culture system, SAC activation itself did not induce Ig production by either subset of purified B cells. However, it primed the cells for antibody production in the presence of IL-2. IL-1 and IL-6 by themselves augmented antibody formation by these cells slightly, if at all. However, IL-6, and to a lesser extent IL-1, augmented antibody production in the presence of IL-2. Under the culture conditions used CD5- B cells produced IgM, IgG, and IgA whereas the CD5+ B cells produced almost exclusively IgM. The expression on B cells of surface activation markers was analyzed after culture for 2 days with SAC or anti-mu beads. In both subsets expression of Leu-23 and Leu-21 was increased, with some differences in intensity (Leu-23 greater in CD5+ cells, Leu-21 greater in CD5- cells). SAC increased IL-2R expression to a greater extent than anti-mu beads. In neither subset was expression of CD23 increased. These observations are discussed in the context of the possible role of the CD5+ subset of B lymphocytes as components of a system of natural immunity.

Antibodies, Anti-Idiotypic↗
PubMed1989

Structure of thiolactomycin.

[4R,(2E,5E)]-3-Hydroxy-2,4,6-trimethyl-2,5,7-octatriene-4-thiol ide, C11H14O2S, Mr = 210.30, hexagonal, P6(5), a = b = 9.8514 (6), c = 19.954 (1) A, V = 1677.1 A3, Z = 6, Dx = 1.249 g cm-3, lambda(Cu K alpha) = 1.5418 A, u = 23.07 cm-1, F(000) = 672, T = 298 K, R = 0.028 for 1021 unique reflections [Fo2 greater than 2 sigma(Fo2)]. The absolute configuration was determined by the Bijvoet method. The thiolactone ring is planar with S-C bond distances of 1.774 (3) and 1.856 (3) A, and C-S-C angle of 93.3 (1) degrees. The angle between least-squares planes for the thiolactone and butadienyl groups is 101.7 degrees.

Anti-Bacterial Agents↗
PubMed1989

IL-6 is the principal factor produced by synovia of patients with rheumatoid arthritis that induces B-lymphocytes to secrete immunoglobulins.

First, IL-6 is produced by synovial tissue of patients with rheumatoid arthritis (RA) and is the principal mediator produced by that tissue inducing differentiation of B-lymphocytes into antibody-forming cells. The Leu-1+ subset of B-lymphocytes is induced by IL-6 to secrete rheumatoid factor (IgM with anti-Fc gamma specificity). Second, the main cell types producing IL-6 in cells dissociated from RA synovial tissue are mononuclear leukocytes. Connective tissue type cells (synoviocytes) cultured from RA synovial tissue produce IL-6 in response to IL-1 beta, and IL-6 formation is increased by TGF-beta. Glucocorticoids strongly inhibit and PGE2 slightly inhibits IL-1-induced IL-6 mRNA expression in synoviocytes. Production of IL-6 increases when undissociated RA synovial tissue is maintained in culture, thus suggesting release from inhibition by a factor or factors not yet identified. Third, the major known local effect of IL-6 in RA synovial tissue is the augmentation of antibody formation and the major known systemic effect is the induction of the synthesis by the liver of acute-phase proteins, especially C-reactive protein. Levels of circulating C-reactive protein are reported to decrease in RA patients receiving long-acting antirheumatic drugs, which would be consistent with the interpretation that immature monocyte-derived macrophages are major producers of IL-6 in these patients.

Antibody Formation↗
PubMed1989

Relationship between anti-IgE autoantibody and severity of bronchial asthma.

To determine whether anti-IgE autoantibody (aIgE) is involved in modulating allergic asthma, we examined the relationship between the titers of aIgE and severity of asthma in 63 allergic asthmatics. The titer of aIgE in patients' sera was 14.4 +/- 17.9 units (mean +/- SD). Thirty-one patients had aIgE greater than 5 units (26.4 +/- 22.1 units), whereas 32 patients had aIgE less than 5 units (2.0 +/- 0.9 units). Patients with high aIgE (greater than 5 units) were less severe than those with low aIgE (less than 5 units) (1.65 +/- 0.42 and 2.19 +/- 0.52 of severity score, respectively; p less than 0.01). There was an inverse correlation between the titers of aIgE and the severity scores (r = -0.328; p less than 0.01). Patients with high aIgE also had lower bronchial reactivity to methacholine than those with low aIgE (556 +/- 292 and 170 +/- 182 micrograms/ml of threshold dose of inhaled methacholine, respectively; p less than 0.005). There was a significant correlation between the titers of aIgE and the threshold dose of methacholine (r = 0.499; p less than 0.01). These findings suggest that aIgE plays a protective role in bronchial hyperreactivity in allergic asthma.

Antibodies, Anti-Idiotypic↗
PubMed1988

Monoclonal hybridoma anti-cardiolipin antibodies from SLE mice.

To determine whether the anti-cardiolipin antibodies are identical with the lupus anticoagulant and other antibodies to phospholipids and DNA, we prepared monoclonal hybridoma autoantibodies to cardiolipin from SLE-prone MRL/lpr mice and characterized their specificity. Using a somatic cell hybridization technique, we established three hybridoma clones which produce antibodies to cardiolipin (CAL-1: IgG2b, k, CAL-2: IgM, k and CAL-3: IgM, k). These hybridoma antibodies preferentially reacted with cardiolipin and phosphatidylserine, weakly reacted with phosphatidylinositol, but not with other phospholipids such as phosphatidylcholine, sphingomyelin, phosphatidylethanolamine and VDRL antigen. Two hybridoma anti-cardiolipin antibodies bound to ssDNA and were found to act as the lupus anticoagulant when mixing activated partial thromboplastin time with cephalin. These autoantibodies may prove to be good tools for elucidating mechanisms of thrombosis, thrombocytopenia, fetal loss and other related manifestations found in patients with systemic lupus erythematosus.

Animals↗
PubMed1985

Anti-IgE autoantibody in patients with atopic dermatitis.

The anti-IgE autoantibody in the IgG class was detected in 39/45 (86.7%) patients with atopic dermatitis by using a newly established solid-phase enzyme immunoassay. The epsilon-chain specificity of the anti-IgE autoantibody was confirmed by competitive inhibition by using human IgG, IgA, IgM, IgD, IgE, and heat-denatured IgE protein. Significant correlations were observed between the levels of the anti-IgE autoantibody and the serum IgE. Gel filtration studies indicated that the anti-IgE autoantibody in sera from atopic dermatitis was mainly present in the form of an immune complex with self IgE. The role of the IgE-anti-IgE immune complex and the role of the anti-IgE autoantibody in the modulation of the IgE-mediated immune system in atopic dermatitis are discussed.

Antibodies, Anti-Idiotypic↗
PubMed1984

Anti-IgE autoantibody in patients with bronchial asthma.

The anti-IgE autoantibody in the IgG class was detected in 95.5% of patients with atopic asthma, and in 72.2% of those with non-atopic asthma, using a newly established solid phase enzyme immunoassay (EIA). The specificity of anti-IgE autoantibody was confirmed by both competitive inhibition and absorption experiments, using human IgG, IgA, IgM, IgD, IgE and rabbit anti-human IgG. Significant correlations were observed between the levels of the anti-IgE autoantibody and the serum IgE. Gel filtration studies indicated that the anti-IgE autoantibody in sera from asthmatic patients was present in the immune complex form with self-IgE, in addition to the monomeric antibody. Furthermore, this anti-IgE autoantibody has the ability to induce the reversed type immediate skin reaction, in asthma free individuals. These observations strongly suggest the putative role of the anti-IgE autoantibody in the modulation of IgE-mediated immune systems and the pathogenesis of bronchial asthma.

Antibodies, Anti-Idiotypic↗