Biomedical subjects
Publications and source records attributed to S Takei.
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BACKGROUND: It is well known that many diseases may be associated with obesity resulting from an energy-rich diet, and that a westernized diet may increase the incidence of urinary stone formation. To evaluate degree of obesity, we investigated body mass index (BMI) in patients with calcium containing upper urinary stones and examined their blood with regard to lipid metabolism. METHODS: Between July 1994 and December 1995, we analyzed 332 fresh renal-stone formers (253 males and 79 females) who visited 7 hospitals located in Ehime prefecture. As a control, 949 residents older than 20 years (387 males and 562 females) of the same prefecture were also examined by the annual Ehime prefecture office report of 1994. Body mass index as degree of obesity, stone-recurrence, blood test and other complicated diseases were examined. RESULTS: In male stone formers the rate of obesity was significantly higher than that of control males (p < 0.001). The differences were seen only in their twenties and fifties. Furthermore, among male stone formers the rate of obesity was significantly higher in recurrent stone formers than in single stone formers (p < 0.05). On the other hand, in female, there was no significant difference in the rate of obesity between stone formers and controls. No difference was seen between recurrent stone formers and single stone formers. In the blood test, there was no differences in the level of calcium, phosphate and uric acid between stone formers and controls. The level of cholesterol and triglyceride in male were significantly higher in controls (p < 0.01) and there was no difference in the level of high density lipoprotein (HDL) between stone formers and controls. Among the stone formers, 48 males (20.0%) and 17 females (21.5%) had other diseases. The rate of complicated diseases was similar to that of controls and no specific diseases in the stone formers were identified. CONCLUSION: Our report suggested that obesity in male should be considered as a risk factor for calcium containing stone formation.
We showed that i.v. IgG contains Abs against a major group of bacterial superantigens, and that they can inhibit superantigen-elicited T cell activation. The B cell epitope region of the superantigen and the inhibitory mechanism have remained unknown. To analyze the dominant B cell epitopes on the bacterial superantigen SEB (staphylococcal enterotoxin B), we constructed fusion proteins of SEB deletion mutants, and the reactivities of these recombinant proteins to i.v. IgG and healthy human sera were evaluated by means of immunoblotting. Intravenous IgG and healthy human sera mostly recognized the C-terminal fragment (amino acid (aa) 133-239). The C-terminally truncated protein (aa 1-228) and the truncated mutant delta 225-234 lost reactivity, while the truncated protein (aa 1-234) did not, suggesting that the region (aa 225-234) is the dominant B cell epitope. The mutant, in which residues 226-229 of SEB were exchanged for residues 209-212 of streptococcal pyrogenic exotoxin A, reduced the reactivity with the C-terminal region-specific IgG purified by affinity chromatography. The C-terminal region-specific IgG inhibited SEB-elicited T cell activation, suggesting that this Ab that recognizes the epitope functions as the humoral defensive factor against SEB in humans. Furthermore, the assumed epitope region was homology to the residues (aa 32-41) of human thymopoietin, containing the biologic active site.
BACKGROUND: Histamine has a particular role in the pathogenesis of bronchial asthma, and many antiallergic drugs have been developed with antihistaminic action in mind. Recently, a sensitive and specific assay for measuring histamine and its metabolites has been developed. There are, however, no reports of the effect of antiallergic drugs on histamine levels in asthmatic patients. OBJECTIVES: To determine the relationship between clinical symptoms and histamine levels in asthmatic patients receiving an antiallergic agent. METHODS: A prospective study was designed in asthmatic children treated with azelastine hydrochloride. The evaluation of clinical symptoms was based on scores of the severity of exacerbations, activities of daily living, quality of sleep, and required therapy. Urinary excretion of N-methylhistamine, a major metabolite of histamine, was measured by double antibody radioimmunoassay. RESULTS: In the patients treated with azelastine, the improvement in clinical symptoms of bronchial asthma correlated significantly with a decrease in urinary N-methylhistamine excretion (r2 = 0.434, P < .001), while no such relationship was noted in patients receiving no antiallergic agent. Urinary N-methylhistamine excretion showed no diurnal change or influence of meals. CONCLUSIONS: Decreased urinary N-methylhistamine excretion may be a direct reflection of the antihistaminic action of azelastine in vivo. Measurement of urinary N-methylhistamine excretion can be used to evaluate the efficacy of agents with antihistaminic action in the treatment of bronchial asthma.
Marked advances have been made in the past decade in the management of adults with systemic lupus erythematosus (SLE). Therefore, a nationwide retrospective survey was conducted between 1980 and 1994 to investigate the clinical manifestations of SLE in Japanese children and adolescents. Questionnaires were sent to 340 hospitals. Of 405 patients reported by 176 hospitals, 373 patients, diagnosed by the criteria established by the Pediatric Study Group of the Japanese Ministry of Health and Welfare in 1985, were enrolled in the study. Forty-nine of the 354 patients (13.8%) had relatives with a connective tissue disease within the third degree of consanguinity. The frequent manifestations in 373 patients were the presence of antinuclear antibody (98.9%), immunologic disorders (93.0%), hypocomplementemia (87.1%), malar rash (79.6%) and fever (74.0%). Lupus nephritis was present in 148 of the 309 patients (47.9%) at their first visit to a clinic, and 261 of the 373 patients (70.0%) developed renal involvement during the observation period. Of 370 patients, 92 patients (24.9%) exhibited central nervous system lupus. Of 368 patients, 192 patients (52.2%) were treated by methylprednisolone pulse therapy and 148 patients (40.2%) received immunosuppressants in combination with steroid therapy at some stage during the observation period, Survival rate at 5 years from onset was 95.9%. Management of infection, coagulopathies, and central nervous system involvement is essential to improve the prognosis of SLE in Japanese children and adolescents.
Although the shortest (class I) minisatellite (i.e., variable number of tandem repeats [VNTR]) alleles in the 5' region of the insulin gene are positively associated with IDDM in Caucasians, the majority of Japanese are homozygous for class I alleles. Here, we determined the exact length, in number of repeat units (RUs), of class I alleles in Japanese subjects. The distribution of class I alleles in Japanese was trimodal, with peaks located at 32/33, 41, and 44 RUs. The shortest component (i.e., 1S [25-38 RUs]) alleles were significantly increased in the IDDM group compared with the control group (54 vs. 46%; P = 0.040). The 1S/1S genotype was significantly increased in the IDDM patients (34 vs. 20%; P = 0.005; relative risk 2.1). Furthermore, the transmission disequilibrium test of Japanese families with 1S/1M or 1S/1L heterozygous parents confirmed the association of 1S alleles; 17 alleles of 1S and 6 alleles of 1M (39-41 RUs) or 1L (42-44 RUs) were transmitted to affected offspring (P = 0.022). In addition, we found tight linkage of 1S with allele 9 of the tyrosine hydroxylase gene microsatellite and allele (-) of the IGF-II gene Apa I polymorphism, but neither 9 nor (-) alleles were significantly associated with IDDM. The present study suggests that a class I subset may have a role in IDDM susceptibility in Japan. It was revealed that the difference between 1S alleles and 1M or 1L alleles is almost consistently characterized by a sequence variation generated by deletion of two copies of an ACAGGGGTCC CGGGG repeat element, implying that sequence variation of class I alleles may influence disease susceptibility.
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In order to discuss the diversity of clinical features and the difficulty in diagnosis of children with juvenile rheumatoid arthritis (JRA), we present two cases who have documented the development of systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD) after a long period of disease characterized only by arthritis that was initially diagnosed as JRA. The first case was a girl diagnosed for her arthritic joints as polyarticular JRA at 15 years of age. At onset, she had Raynaud phenomenon but autoantibodies such as anti-nuclear antibody (ANA), anti-DNA antibody, and rheumatoid factor were negative. Five years after onset, she became ANA positive and 3 years later she became pregnant. During her pregnancy, she became positive for anti-DNA antibody without any signs of nephritis. One month after the delivery, however, she developed butterfly rash, carditis, nephritis, and was diagnosed as SLE. No destructive changes were observed in her joints though arthritis continued for 8 years form onset to pregnancy. The second case was a 3 years old girl who was diagnosed as polyarticular JRA. Treatment by aspirin induced complate remission after one year from the onset. However, 10 years after that remission, she developed Raynaud phenomenon and arthralgia in her knees and hip joints. Her laboratory findings showed hypergammaglobulinemia, positive ANA, positive anti-DNA antibody, positive anti-RNP antibody. She was eventually diagnosed as MCTD when she was found to have polymyositis by EMG and serum CK. In the present paper, two cases imply the difficulty in diagnosing JRA and diversity of rheumatic diseases such as JRA, SLE and MCTD. Closer and longer period of observation is essential for the JRA patients with nondestructive arthritis.
The DNA methylation status of the 5'-regulatory region of human tumor necrosis factor-alpha (TNF-alpha) gene was examined using two human monocytic cell lines representing different differentiation stages: one cell line, THP-1, represents the most differentiated macrophage-like phenotypes and the other, HL-60, represents a least differentiated phenotype. Two restriction enzymes were used to detect methylated sites in the 5'-regulatory region of the TNF-alpha gene. The restriction enzyme Msp I, which recognizes both CCGG (unmethylated) and C(me)CGG (methylated) sequences, whereas Hpa II recognizes only the unmethylated CCGG sequence. Two Msp I sites located at -600 and +200 nucleotides, respectively, from the transcriptional initiation site were unmethylated in DNA from the THP-1, whereas these sites were methylated in the one from the HL-60. Treating the HL-60 cells with 1,25-vitamin D3, ( 1,25-(OH)2D3), which is known to induce monocytic cell differentiation, induce demethylation of the sites, suggesting the methylation status was correlated with the differentiation stages of monocytes.
The human red blood cells with phenotype En(a-) were characterized by the lack of MN antigens. The red blood cells with phenotype En(a-) which were found in a Japanese family were tested to clarify the changes in membrane surfaces of the red blood cells during in vivo ageing. The contents of sialic acid, glucose, mannose, galactose, fucose, N-acetylglucosamine and N-acetylgalactosamine of the red blood cell membranes obtained from the old red blood cells with phenotype En(a-) were significantly lower than those of the young red blood cell membranes. Neither the young nor the old red blood cells with phenotype En(a-) showed the agglutination with Arachis hypogaea (PNA) which was capable of binding to T agglutinogen. It is presumed that En(a-) red blood cells are not exposed to sialidase in vivo. In comparison with the young En(a-) red blood cell membranes, the number and the distribution density of lectin receptor sites on the old ones for Limulus polyphemus (LPA), Canavalia ensiformis (Con A), Triticum vulgaris (WGA) and Bauhinia purpurea (BPA) were significantly lower. It is thought that En(a-) red blood cell ageing is accompanied by elimination of some sialoglycoconjugates which have affinity for LPA, Con A, WGA and BPA, whereas En(a-) red blood cells lack glycophorin A.
UNLABELLED: We measured anti M protein antibody (AMPA) titres in children with idiopathic mitral regurgitation (MR), streptococcal infection, rheumatic fever (RF), post-streptococcal acute glomerulonephritis (AGN) and normal healthy children. We investigated the association of MR with streptococcal infection and whether high AMPA titres can be used as persisting evidence of previous streptococcal infection. AMPA titres were measured with an enzyme-linked immunosorbent assay. We found significantly higher antibody titres in patients with MR and in streptococcal infection, RF, and AGN than in healthy controls. In the MR group (n = 15), 54% patients had AMPA titres above the 90th percentile value that was found in normal controls. An elevated AMPA titre persisted for a long period even when the anti-streptolysin O titres had declined to normal in RF patients. Our data suggest that the high AMPA titres in MR should be further investigated to clarify the probable association with previous streptococcal infection. CONCLUSION: High AMPA titre is a risk factor for developing complications after streptococcal infection. Our serological evidence suggests that in some patients, MR may be related to previous streptococcal infection.
Several bacteria, such as staphylococci and streptococci, can produce superantigens (SA) that induce the activation of T cells in humans. Although these organisms are the major causes of infection in children, the evidence that T cells are vigorously activated by SA produced by such organisms has not been reported except for toxic shock syndrome. In a previous paper, we demonstrated that inhibitory IgG antibodies (Ab) to SA in humans may protect against SA stimulation. In the present study, we investigated the occurrence of these inhibitory Ab to SA in 94 healthy children by the enzyme linked immunosorbent assay technique and the suppressive effect on T cell stimulation by SA. The positivity of Ab to streptococcal pyrogenic exotoxin (SPE)-A, SPE-C and staphylococcal enterotoxin B (SEB) increased with age. The age at which more than 50% of children exhibited Ab to SA was 1 year for SEB, 6 years for SPE-C and 11 years for SPE-A. Sera from these children were inhibitory to T cell proliferation elicited by SA in proportion to the concentration of IgG Ab to each SA. Sera supplemented with IgG Ab to SA by gamma-globulin therapy became inhibitory to T cell proliferation by SA. We conclude that, as children grow, they can develop Ab to SA that may play a role in protecting them against vigorous T cell activation by SA.
Nonobese diabetic (NOD) mice develop type I diabetes spontaneously and have been utilized as a model for human autoimmune insulin-dependent diabetes. The disease is caused by the destruction of insulin-producing beta cells in the pancreatic islet of Langerhans by infiltrating inflammatory cells, which are primarily T lymphocytes. The incidence of diabetes in NOD mice is increased in females compared with males, suggesting that sex steroid hormones play an important role in the development of the disease. We therefore investigated the effect of a male steroid, 5-alpha-dihydrotestosterone (5DHT), on disease development, T-cell phenotype, T-cell proliferation, and cytokine profiles in this model. None of the mice that received 5DHT for 120 days (n = 7) developed insulitis, whereas all control mice (n = 8) developed the disease. The percentage of CD4+ T cells in peripheral blood mononuclear cells was markedly decreased in the 5DHT-treated females compared with those in controls (37.1 +/- 4.8 vs 51.3 +/- 9.3, P < 0.02), whereas no significant differences in the percentage of CD8+ T cells were observed between treated and control female mice. Results of a syngeneic mixed lymphocyte reaction (SMLR) also suggested that T cells are major target cells of 5DHT administration. An increased expression of IL-4 mRNA, representing T helper 2 (Th2) T cells, was observed in the SMLR. On the basis of these results, a systemic administration of 5DHT appears to have direct effects on the expansion of Th2 cell populations with subsequent restoration of normal immune responses.
OBJECTIVE: Elevated serum levels of hyaluronic acid (HA) correlate with joint inflammation in adult rheumatoid arthritis (RA). There are no laboratory indices for specifically assessing joint inflammation. Therefore, serial measurements of HA were assessed as a possible tool for measuring the severity of arthritic symptoms in children with juvenile rheumatoid arthritis (JRA). METHODS: Serum levels of HA, measured by a sandwich assay method using HA binding protein, were correlated with the severity of joint symptoms and with laboratory test values in 71 patients with JRA, 30 children with other rheumatic diseases, and 138 children without rheumatic disease. RESULTS: Serum levels of HA showed significant correlation with the severity of joint symptoms, but not with systemic symptoms, in patients with systemic and polyarticular JRA. No other laboratory tests, including C-reactive protein and erythrocyte sedimentation rate, reflected the severity of joint symptoms. This correlation of serum levels of HA with joint symptoms was observed in patients with systemic and polyarticular JRA, but not in pauciarticular JRA, other rheumatic diseases, or nonrheumatic diseases, even when signs of arthritis were present in the latter 3 groups. CONCLUSION: Serum levels of HA are useful in objectively evaluating arthritic symptoms in patients with systemic and polyarticular JRA, and may have diagnostic value in this disease.
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We present a rare case of a 10 year old Japanese boy with acute rheumatic fever accompanied with poststreptococcal acute glomerulonephritis. We isolated group A Streptococcus serotype T 12, a strain that was thought to be nephritogenic but not rheumatogenic, from throat culture. Although rare, physicians should be aware that acute renal disease may accompany rheumatic fever.
The present study was undertaken to examine the possible augmentation of clonidine on the control of renal sympathetic nerve activity by Bezold-Jarisch reflex in anesthetized cats. Veratrine (3-20 micrograms/kg) produced dose-dependent decreases in arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RNA). Clonidine (3 micrograms/kg) resulted in decreases in BP, HR and RNA. Clonidine significantly potentiated the influence of Bezold-Jarisch reflex on RNA, but did not potentiate the influence of Bezold-Jarisch reflex on BP and HR. Bezold-Jarisch reflex gain calculated as percent inhibition of renal sympathetic nerve activity divided by decreases in mean blood pressure was significantly higher after the administration of clonidine.