[Case of relapsing polychondritis].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
S Eto
Publications and source records attributed to S Eto.
[Chronic thyroiditis and myxedema].
Explore the source record for details and available documents.
Adult↗
Clinical significance of anti-TSH antibody in sera from patients with Graves' disease and other thyroid disorders.
In a survey of patients having anti-TSH antibody (TSH Ab), data from 167 subjects were collected from 8 Japanese Institutions. They were divided into a high TSH Ab group consisting of 63 cases; since the means of assay was via a subnormal thyrotropin binding inhibitor immunoglobulin (TBII) assay, this group had TBII values less than -20%. An additional low TSH Ab group was made up of 104 cases. Out of a total of 11,211 patients, the incidence of TSH Ab for the high and low groups were 0.57% and 13.4%, respectively. More than 95% of these TSH Ab carriers had Graves' disease or some other autoimmune thyroid disorder, and anti-thyroglobulin and anti-thyroid microsomal antibodies were detected similarly in both groups. It was significant that TSH receptor antibodies could also be detected in both groups, namely, thyroid stimulating antibody and long acting thyroid stimulator (LATS) in 4 of 9 patients in the high TSH Ab group and TBII in 55 of 104 in the low TSH Ab group, respectively. The high TSH Ab levels tended to persist, but 26% of cases showed disappearance or appearance of the antibody during the observation period. In one Graves' patient, a moderate TBII activity (64.2%) was followed by markedly elevated TSH Ab (TBII: -83.4%) within 2 months. The TSH Ab in the low TSH Ab group disappeared in most cases. Also, fluctuations in TSH Ab did not always parallel those seen for TBII and reciprocal fluctuation pattern (transient or otherwise) were observed in 33%. In conclusion, anti-TSH antibody is produced frequently in patients with either Graves' disease or some other autoimmune thyroid disorder.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Enzyme linked immunosorbent assay (ELISA) for human IgG (Gm) allotype determination.
An inhibition enzyme-linked immunosorbent assay (inhibition-ELISA) was developed for the quantitative determination of human IgG (Gm) allotypes using rabbit anti-Gm antisera, alkaline-phosphatase-conjugated goat anti-rabbit IgG and, as the calibrant, purified human myeloma proteins possessing the relevant Gm allotype. The assay is reproducible and can detect as little as 10 ng/ml of G1m(a), G2m(n) or G3m(st), and 100 ng/ml of G1m(f) or G3m(g). Using this assay, the "gene dosage effect" and "allelic balance" in healthy Japanese were studied.
Antibodies, Anti-Idiotypic↗
Recent advance in the treatment of diabetic nephropathy: anticoagulant therapy.
Explore the source record for details and available documents.
Diabetic Nephropathies↗
Clinical significance of urinary enzymes in diabetic nephropathy.
Urinary enzyme activities (N-acetyl-beta-D-glucosaminidase [NAG], alkaline phosphatase [ALP], leucine aminopeptidase [LAP], gamma-glutamyl transpeptidase [gamma-GTP]) were investigated to determine their clinical significance in diabetic nephropathy. There were correlations among ALP, LAP, and gamma-GTP, though no correlation existed between NAG and the other three enzymes. Activities of NAG isozymes (both A and B) were higher than in normal controls. It has been reported that NAG isozyme A might be associated with glomerular diseases, and isozyme B might be associated with proximal tubular damage. The results of our study suggest that NAG reflects lysosomal dysfunction of both glomerular and proximal tubular epithelial cells, which may be caused by poor glycemic control, and that ALP, LAP, and gamma-GTP reflect brush border damage of proximal tubules, which may be caused by diabetic nephropathy.
Acetylglucosaminidase↗
The characteristics of renal hemodynamics in diabetic spontaneously hypertensive rats in comparison with diabetic Wistar-Kyoto rats.
Diabetic Sprague-Dawley (SD) rats are known to exhibit renal hyperfiltration and hyperperfusion accompanied by renal hypertrophy. We examined whether such characteristics of renal hemodynamics in diabetic SD rats are also observed in diabetic spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. SHR and WKY rats were divided into four groups: D-S, diabetic SHR; N-S, nondiabetic SHR; D-W, diabetic WKY rats; and N-W, nondiabetic WKY rats. Streptozotocin (STZ), 90 mg, was intraperitoneally injected to induce diabetes. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by a clearance method with paraaminohypurate and insulin, respectively, 7-12 days after diabetes induction. In D-S and D-W, there was no increase in the kidney weight and RBF, in spite of significant increases in GFR and fasting blood sugar levels. These results indicate that, in both WKY and SHR, diabetes does not always produce renal hypertrophy and does not result in an increase in RBF.
Animals↗
Acute effect of calcium blocker on renal hemodynamics in diabetic spontaneously hypertensive rat.
This study was done to examine the acute effect of a calcium channel blocker on renal hemodynamics in the diabetic spontaneously hypertensive rat (SHR). Streptozotocin was used to induce diabetes, and barnidipine (B) was used as a calcium blocker. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by a clearance method with paraaminohypurate (PAH) and inulin, respectively. Rats were divided into two groups: nondiabetic SHR, N-SHR; diabetic SHR, DM-SHR. B increased RBF in N-SHR (7.44 +/- 1.99 versus 8.50 +/- 1.97 mL/min/g.kw) while there was no change in DM-SHR. B reduced renovascular resistance (RVR) in DM-SHR and N-SHR. B increased GFR in N-SHR (1.15 +/- 0.24 versus 1.34 +/- 0.25 mL/min/g.kw), in spite of no changes in DM-SHR. B did not modify filtration fraction (FF) in both groups. These results indicate (1) in SHR, B exerts beneficial effects on hypertensive renal damage by reducing mean arterial pressure (MAP), RVR, RBF, and GFR; (2) in diabetic SHR, B is less effective in restoring renal hyperfiltration in spite of reducing RVR.
Analysis of Variance↗
Alterations in hepatic delta-aminolevulinic acid synthetase and heme oxygenase activities after chronic ethanol consumption in rats.
In the present study, the effect of chronic ethanol consumption in rats on the hepatic heme metabolism was investigated. Male Wistar rats were fed a nutritionally adequate liquid diet containing ethanol as 36% of the total calories for 5 weeks. After an overnight fast, the livers were excised and centrifuged to obtain mitochondrial and microsomal fractions. Chronic ethanol feeding of rats resulted in about 19% hepatomegaly as represented by the increased liver/body weight ratio. There was no difference in the mitochondrial protein content between the ethanol-treated and control rats, but the microsomal protein content was significantly increased in the ethanol-treated rats. Hepatic microsomal content of cytochrome P-450 (P-450) was markedly enhanced by chronic ethanol ingestion. Microsomal contents of cytochrome b5 (b5) and total heme were also increased to a lesser extent. After chronic ethanol abuse, the hepatic activity of delta-aminolevulinic acid (ALA) synthetase, which is a rate-limiting enzyme for heme production, was significantly increased and that of the heme oxygenase was slightly increased. These data indicate that ALA synthetase activity is induced by the negative feedback mechanism in order to compensate the depletion of heme caused by the utilization of heme for P-450. It is also speculated that, in response to excessive production of heme as described above, heme oxygenase activity is secondarily induced to regulate the amount of heme.
5-Aminolevulinate Synthetase↗
Effect of acute thromboxane A2 inhibition on the renal hemodynamics in a spontaneously non-insulin-dependent diabetic rat, Otsuka Long-Evans Tokushima Fatty rat.
Thromboxane (TX) A2 plays important roles on renal injuries in streptozotocin (STZ)-induced diabetic rats, whereas its role on the renal injuries in non-insulin-dependent diabetic (NIDDM) rats remains unknown. We evaluated the effects of an intravenous infusion of TXA2 synthetase inhibitor (OKY-046, 6 mg/kg/h) on the clearances on inulin and para-aminohippurate (Cin, C(PAH)) in a spontaneously NIDDM rats, Otsuka Long-Evans Tokushima Fatty (OLETF) rats (n = 8), and Long-Evans Tokushima Otsuka (LETO) rats (n = 7), served as control rats, at the age of 40-44 weeks. OLETF rats showed obesity, moderate hyperglycemia, and hyperinsulinemia. Urinary excretion of TXB2 was slightly higher and the ratio of TXB2 to 6-keto prostaglandin F1alpha (6-kPG) was significantly higher in OLETF rats (TXB2/6-kPG: 0.22 +/- 0.04 versus 0.12 +/- 0.02, P < 0.05). Both Cin and C(PAH) were significantly higher in OLETF rats than in LETO rats (Cin: 1.1 +/- 0.1 versus 0.7 +/- 0.1 mL/min/100 g BW, C(PAH): 3.1 +/- 0.2 versus 2.3 +/- 0.3 mL/min/100gBW, P < 0.01). OKY-046 did not restore Cin and C(PAH) in OLETF rats although it significantly decreased urinary excretion of TXB2, and thus ameliorated TXB2/6-kPG in OLETF rats. These data suggested that TXA2 was not involved in the renal hyperfiltration in OLETF rats at the age of 40-44 weeks, and that TXA2 might contribute to renal injuries in OLETF rats through mechanisms other than hemodynamic injury.
6-Ketoprostaglandin F1 alpha↗
Reduced plasma LH concentration in postmenopausal depressed women.
Mean plasma LH concentration in postmenopausal women suffering unipolar depressive illness was 33% less than that of normal postmenopausal women (P less than 0.05). Since LH secretion after menopause is probably noradrenergically regulated, the finding provides support for the hypothesis of a functional noradrenaline deficit in depression.
Aged↗
Modulation of cytokine function by heparan sulfate proteoglycans: sophisticated models for the regulation of cellular responses to cytokines.
Cytokines are diffusible, soluble factors with pleiotropic actions. The ability of some cytokines to blind to and be immobilized by heparan sulfate proteoglycan (HS-PG) on either the surface of cells or within the extracellular matrix accentuates their action by 1) promoting the accumulation of cytokines at high concentrations in the appropriate location to encounter their target cells; 2) activating cytokines by inducing conformational changes in the bound cytokine; 3) promoting conformation-dependent association or polymerization of cytokines and their cell-surface receptors and facilitating the assembly of the appropriate molecular complex to initiate signal transduction; and 4) protecting cytokines from both chemical and physiological degradation. Furthermore, many interactions between HS-PG and cytokines are highly specific. Thus, variations in the HS-PG, core protein, or carbohydrate sequences that are seen at different sites or that occur with inflammation will determine which cytokines bind to a particular HS-PG, providing multiple options for cytokine binding and regulation. HS-PG therefore plays a pivotal role in regulating the function of the large number of heparin-binding cytokines. The involvement of HS-PG in promoting paracrine, autocrine, juxtacrine, and matricrine functions provides a powerful and sophisticated model for regulating cytokine-mediated cellular interactions. These functions of HS-PG have direct relevance for the control of cell growth as well as for the pathogenesis of leukocyte trafficking and inflammation, cell infiltration, and tumor metastasis. Therapies aimed at modulating HS-PG/cytokine binding may provide powerful tools for inhibiting unwanted cytokine effects in several disease processes.
Cytokines↗