Concurrent development of BECCT in a pair of monozygotic twins.
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Child↗
Biomedical subjects
S Takei
Publications and source records attributed to S Takei.
Acute rheumatic fever and poststreptococcal acute glomerulonephritis caused by T serotype 12 Streptococcus.
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.
Acute Disease↗
[Augmentation of clonidine on Bezold-Jarisch reflex control of renal sympathetic nerve activity in cats].
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.
Animals↗
Glipizide-induced prevention of diabetes and autoimmune events in the BB rat.
To determine whether glipizide, a sulfonylurea, can prevent diabetes in the diabetic-prone BB rat model, rats were studied from 35 to 240 days of age. Treated animals received oral glipizide (10 or 100 mg/kg/day) from 35 to 200 days of age, and control rats received oral placebo. From 80 to 135 days of age at both drug doses, glipizide decreased the incidence of diabetes, thus delaying disease onset (P < 0.02). At the higher dose of glipizide, a diabetes preventive effect was observed (P < 0.025). There were no significant differences in body weights between the treated and control groups. At 240 days, i.e. 40 days after stopping glipizide and placebo treatments, diabetes incidence remained stable in the two groups; thus the effect of glipizide persisted after discontinuation of the drug. Serum glucose and insulin levels measured at 90 and 200 days did not reveal differences between the glipizide treated and control groups. To determine whether the sulfonylurea affected autoimmune events, the prevalence and severity of islet inflammation were examined. In glipizide-treated BB rats at 240 days, only 44% of rats had islet inflammation compared to 86% in the control group (P < 0.01). At both 90 and 240 days the severity of islet inflammation was decreased in the glipizide treatment groups compared with the control groups (P < 0.01). These data indicate that glipizide (a) prevents diabetes in the diabetic-prone BB rat strain, (b) decreases the prevalence and severity of islet inflammation even after drug withdrawal and (c) may dampen autoimmune events leading to diabetes onset.
Age Factors↗
In situ islet cytokine gene expression during development of type I diabetes in the non-obese diabetic mouse.
Expression of cytokine genes in the islets of non-obese diabetic (NOD) female mice was examined. RNA samples were prepared from the islets and spleens of NOD mice at different time points at prediabetic stages during the natural disease process. Cytofluorometric analyses showed that the majority of lymphocyte infiltrates in the islets at 14 weeks of age consisted of T cells (68%). Of these, 80% of Thy1.2+ cells were CD4+ T cells. Less than 1% of in situ islet immune cells expressed a cell surface marker specific for the macrophage (Mac-1). Results of polymerase chain reaction using RNA (RT-PCR) prepared from spleens, and isolated and purified islets demonstrated that IFN-gamma message was detectable in the islets at 7 weeks of age (an early stage of insulitis). No message for this gene was detected in the spleen at any stage studied (7, 14 and 16 weeks of age). In contrast, TNF-alpha message was detected in both spleen and the islets at all stages, although the level of expression of TNF-alpha in the islets was much higher than that in the spleen. These results suggest that both cytokines are produced by in situ islet T cells, possibly activated T cells, which may be responsible for initiating or perpetuating autoimmune reactions in the islets.
Animals↗
Isolation and function of human and pig islets.
This report confirms reproducible methods to isolate and assess viability and function of pig and human islets. We processed 10 pig and five human pancreata. The pancreata were digested by a modification of Ricordi's automated method for islet isolation. The number of islet equivalents (150 microns diameter islets) was 335,190 +/- 79,345 islets per pig pancreas (5,146 +/- 1,274 islets/g pig pancreas) and 323,630 +/- 147,810 per human pancreas (6,252 +/- 2,572 islets/g human pancreas). The majority of islets were in the range of 50-200 microns diameter, and 20% of the islet population had a size distribution of 200 microns diameter in both porcine and human models. The purity of the final preparations exceeded 90%. The secretory response of perifused islets showed a biphasic insulin release pattern in both species. Perifused fresh pig islets released 2.5 pmol/L islet-1 min-1 at 2.0 mM glucose and 6.2 pmol/L islet-1 min-1 at 16.7 mM glucose. After 7 days culture at 37 degrees C, human islets released 1.32 pmol/L islet-1 min-1 at 2.0 mM and 12.24 pmol/L islet-1 min-1 at 16.7 mM. These results indicate that this procedure is useful to obtain pure, large, and functional islets from pig and human pancreata.
Adult↗
[Clinical features of infantile patient with juvenile rheumatoid arthritis].
Little is known about clinical features of infantile juvenile rheumatoid arthritis (JRA) because it is very rare for the patients to develop JRA within one year of age. In the past 20 years, we experienced three JRA patients whose onset was under 1 year of age. The incidence of infantile JRA was 3.2% of all JRA patients in our facility. They are 9 month-old male with systemic onset, 6-month-old female with polyarticular onset and 8 month-old female with systemic onset. It was difficult to evaluate subjective symptoms such as arthralgia or morning stiffness since the patients could not complain precisely. Therefore, careful observation on their behaviors, such as the delayed development of their motor function and bad humor and/or loss of activity in the morning, was important for evaluating joint symptoms. In case 1, measuring the serum level of hyaluronic acid was specifically useful to evaluate the arthritis. Drug therapy was not successful especially in infantile JRA. One of the reason for this ineffectiveness of drug therapy might be explained by poor adsorption of drugs in infants; the serum acetyl salicylic acid level was lower in infantile patients than the other patients with JRA even though they received enough dose of aspirin. Infantile JRA was revealed to have specific difficulties in early diagnosis and adequate treatment. Therefore, accumulated case studies about clinical features of infantile JRA is essential for their better prognosis.
Arthritis, Juvenile↗
Transient negative effect of dithizone on dynamic insulin secretion of isolated islets in SA rats.
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Animals↗
Weak N activity of En(a-) human erythrocyte membranes.
The propositus's erythrocytes with phenotype En(a-), which was found for the first time in a Japanese family, reacted more weakly with anti-N serum than the ordinary phenotype N erythrocytes. The En(a-) erythrocytes lack the major membrane sialoglycoprotein (glycophorin A) as demonstrated by Bio-Gel 1.5m gel filtration from active sialoglycoproteins, which were isolated from En(a-) erythrocyte membranes by the method of lithium diiodosalicylate (LIS)-phenol extraction. It is suggested from observation via enzyme-linked immunosorbent assay (ELISA) that N activity is derived from the glycophorin B molecule on En(a-) erythrocyte membranes.
Antigens↗
Quantitative phenotypic and functional analyses of islet immune cells before and after diabetes onset in the BB rat.
Inflammatory cells invading islets are thought to be mediators of islet destruction in spontaneous autoimmune diabetes mellitus. Thus methods were developed to isolate and characterize in situ islet inflammatory cells from 75-95-day-old prediabetic and diabetic BB rats. Islet inflammatory cells were structurally examined using single- and double-colour flow cytometry. Functional studies consisted of cytolytic assays using normal rat islet target cells and in situ islet or spleen effector cells. Structural data reveal natural killer cells to be the major cell population (70%) of total immune cells present in inflamed islets during prediabetes. At diabetes onset, the natural killer cell population remained at a high level (47%), but an increasing population of T cells (40%) was noted also. Analyses of T-cell subsets before and after diabetes onset revealed CD4+ T cells as predominant (50-55% of total T cells) with double-negative (CD4-CD8-) T cells (25-30%) and CD8+ T cells (15-20%) also present in significant quantities. Activated T cells accounted only for a minority of T cells (< 3%). Functional studies indicate that in situ islet-derived cytolytic effector cells are more potent killers (ten-fold) of normal islet target cells than are splenic effector cells. These data suggest that in situ islet inflammatory cells (a) can be quantitatively studied both structurally and functionally; (b) express structural phenotypes differing substantially from splenic mononuclear cell populations; (c) are considerably more cytolytic than splenic effectors; and (d) should prove informative in determining the most significant autoimmune functional events prior to and during islet beta-cell destruction.
Animals↗
Quality of life and daily management of children with rheumatic disease.
Appropriate management of the daily life of patients with rheumatic diseases is an important part of therapy for favorable results and a high quality of life. At home, gymnastic exercise, night splints and appropriate fun activities will help to preserve the function of affected joints of patients with juvenile rheumatoid arthritis (JRA). Improvement of home fixtures according to patient disability will provide a higher quality of life for the patients. The patient should be helped to perform as many school activities as would normally be possible. Instructional charts for management of school life for patients with JRA and systemic lupus erythematosus is shown in this article. Cooperation with school personnel is also crucial to support the patient emotionally and physiologically. For the best long-term treatment and a good relationship between patient and physician, comprehensive management is essential. Not only physicians, but also psychiatrists, occupational therapists, physical therapists and social workers should be involved in the treatment of children with rheumatic diseases.
Activities of Daily Living↗
Intravenous immunoglobulin contains specific antibodies inhibitory to activation of T cells by staphylococcal toxin superantigens [see comment].
Superantigens are products of bacteria with dual affinity for HLA-DR and the variable region of the beta chain of the T cell receptor, leading to the stimulation of large numbers of T cells. Because there is evidence for the involvement of superantigens in various disease conditions in which intravenous IgG (IVIgG) is used as therapy, the purpose of the present study was to determine if IVIgG contains antibodies inhibitory to T cell stimulation by the superantigens. ELISA and Western assays revealed high concentrations of antibodies in the pooled IgG against eight different staphylococcal toxin (Staph-toxin) superantigens. The IVIgG inhibited in vitro stimulation of human peripheral blood T cells by the Staph-toxins, but did not inhibit responses elicited by phytohemagglutinin or anti-CD3. Inhibition was mediated by Staph-toxin-specific antibodies as shown by affinity adsorption depletion studies. The antibodies functioned by inhibiting the binding and/or presentation of Staph-toxins by DR+ accessory cells. In conclusion, this report is the first to show that normal pooled IgG contains antibodies against a major group of the superantigens, the Staph-toxins, and that the antibodies can inhibit Staph-toxin-elicited T cell activation, suggesting a possible immunoregulatory role for the antibodies in vivo.
Antibodies, Bacterial↗
Pancreatic islet function in nondiabetic and diabetic BB rats.
A decreased acute insulin response to glucose in islet cell antibody positive humans predicts diabetes. Because the dominant mechanism leading to decreased in vivo acute insulin response to glucose remains unclear, perifused islets were examined before and after diabetes onset in BB rats to assess the role of glucose sensitivity on insulin secretion in individual islets. Islets from normal WF rats, diabetes-prone rats without inflamed islets, diabetes-prone rats with inflamed islets, and diabetic rats were studied at 2.0, 8.3, and 16.7 mM glucose. Immunoreactive insulin from WF islets at 16.7 mM glucose was 0.15 +/- 0.02 ng.0-7 min-1 x islet-1 for the first phase and 1.00 +/- 0.05 ng.7-20 min-1 x islet-1 for the second phase of biphasic secretion, compared with basal secretion of 0.10 +/- 0.03 ng.20 min-1 x islet-1 at 2 mM glucose. Diabetes-prone noninflamed islets showed a 0.20 +/- 0.03 ng first-phase secretion, a 1.32 +/- 0.13 ng second-phase secretion after 16.7 mM glucose, and 0.093 +/- 0.02 ng.20 min-1 x islet-1 at 2 mM glucose, indicating no intrinsic BB rat strain secretion abnormality. Diabetes-prone inflamed islets had secretions of 0.35 +/- 0.02 ng during the first phase (P < 0.05 vs. WF) and 1.78 +/- 0.29 ng during the second phase (P < 0.05 vs. WF) after 16.7 mM glucose, with 0.24 +/- 0.08 ng.20 min-1 x islet-1 at 2 mM glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Quantitative and functional analyses of spleen and in situ islet immune cells before and after diabetes onset in the NOD mouse.
Cytofluorometric analysis using specific monoclonal antibodies directed against the T cell antigens Thy-1.2, CD4, CD8, CD4V beta(8.1 + 8.2 + 8.3), and the antigen Mac-1 expressed by mature macrophages and NK cells were used to characterize and quantify the phenotypes of (1) unfractionated and Percoll gradient fractionated in situ islet immune cells isolated from prediabetic and diabetic female NOD mouse spleens. We found in prediabetic female mice that the majority (approximately 70%) of the in situ islet immune cells were Thy-1.2 positive T cells. CD4 positive T cells (approximately 40%) were the most abundant phenotype together with double negative T cells (approximately 20%). The percentage of CD8 positive T cells were approximately 10%, and only approximately 4% of the immune cells were Mac-1 positive. The percentages of CD4V beta (8.1 + 8.2 + 8.3) positive and double negative T cells in diabetic spleens were significantly higher in comparison to prediabetic spleens. In C57B1/6J control nondiabetic mice the percentage of double negative T cells in the spleens was significantly 4-fold lower when compared to diabetic NOD spleens. The specific cytolytic activity mediated by in situ islet immune cells against 51Cr-labeled dispersed syngeneic single-cell islet cells at an effector to target ratio of 20 was twenty- to thirty-fold higher than that mediated by prediabetic splenic lymphoid cells. It is concluded that prediabetic NOD mouse in situ islet immune cells are mostly CD4 positive and double negative T cells, and that CD4 and CD8 positive T cells in the intra-islet infiltrate warrants further evaluation as potential effector T cells in target beta-cell destruction.
Animals↗
Serological and biochemical studies on En(a-) human erythrocytes in a Japanese family.
The propositus erythrocytes with phenotype En(a-), which was found in the first example of a Japanese family, reacted with anti-N serum weaker than the ordinary phenotype N erythrocytes. When the erythrocyte membranes of the propositus were subjected to SDS-PAGE, no glycophorin A was observed on the gel by PAS staining, whereas glycophorin B band was observed. The S and the s antigens of the propositus erythrocytes were appeared to be normal. These results suggested that N activity of the propositus erythrocytes may be derived from glycophorin B components on the erythrocyte membranes. The amounts of bound sialic acid of the erythrocyte membranes were significantly lower in the En(a-) erythrocytes than the ordinary OMN erythrocytes. Neither the OMN nor the En(a-) erythrocytes showed the agglutinability to Arachis hypogaea lectin. The number of lectin receptor sites on the En(a-) erythrocyte membranes was significantly lower than on the OMN erythrocyte membranes for Limulus polyphemus, Triticum vurgaris and Bauhinia purpurea lectins. These results provide further support for the contention that En(a-) cells lack the glycophorin A as major erythrocytes sialoglycoprotein on the membranes.
Asian People↗
[Complex chromosome aberrations between no. 17 and no. 21 in acute myelo-megakaryocytic leukemia: a case report].
A 10 month-old boy presented with fever. He was diagnosed as having acute myelo-megakaryocytic leukemia by electron microscopic cytochemical examination. In spite of aggressive chemotherapy, complete remission could not be achieved and he died seventeen months after the diagnosis was made. G-band karyotypes of the bone marrow cells revealed 45, XY, -17, -21, + dir tan dup (17;21) (17pter----cen----17q25::17q21----17q25;21q11 ----21qter). Furthermore, the same chromosomal aberrations were detected in the cells which were tetraploid and octaploid. Although, neoplastic changes in the progenitor cells immediately before differentiating to CFU-Meg and CFU-GM, are suggested there is a possibility of clonal evolution.
Chromosome Aberrations↗
[A case of mediastinal cavernous hemangioma].
A case of mediastinal cavernous hemangioma was reported. An asymptomatic 6-year-old girl was discovered to have a mass in the left anterior superior mediastinum on a routine chest x-ray film. Computed tomograms demonstrated a mediastinal mass with calcification. Under a median sternotomy, a 10 x 9 x 5 cm mass was resected after dissecting the connections to the pericardium. As the mass surrounded the left phrenic nerve, the nerve was resected with the tumor. The histopathology was cavernous hemangioma. The calcification was not found in the vessels as the phleboliths but was showed in the interstitial tissues.
Calcinosis↗
[A case report of anomalous left brachiocephalic vein].
An anomalous case of a left brachiocephalic vein passing behind the ascending aorta was observed in a 49-year Japanese man. This is known as anomalous left brachiocephalic vein. The anomalous left brachiocephalic vein descended along the left mediastinum in a position identical to that of a persistent left superior vena cava, so the diagnosis of this venous abnormally require carefully considered. Many cases of anomalous left brachiocephalic vein have been reported based on autopsy findings, but this venous anomaly was recently demonstrated by ultrasonography, CT, and MRI.
Brachiocephalic Veins↗