Biomedical subjects

Y Mitani

Publications and source records attributed to Y Mitani.

At least 37 records · Page 2Linked to original sources

PubMed1999

Relationship between severity of middle ear mucosal lesion and middle ear pneumatic space volume in patients with otitis media with effusion.

If we assume that the state of suppression of pneumatic cells is the result of suppression of pneumatic cell growth by inflammatory stimulation in the middle ear pneumatic space, it is possible to improve the state of suppression by performing sufficient treatment during the growth period of the pneumatic cells. We indwelt a tympanic membrane ventilation tube (hereinafter referred to as tube) for treatment of otitis media with effusion (OME) in child patients aged 3-13 years and investigated the following points: i) relationship between the severity of inflammation of the lamina propria of middle ear mucosal specimens (hereinafter referred to as lamina propria) collected at the time of tube indwelling and the degree of growth of the pneumatic space; and ii) changes in the pneumatic space associated with treatment by tube indwelling, which was studied by comparing the above-described mucosal severity with the pneumatic space area of 2 years after tube indwelling, and with increase in the pneumatic space volume measured periodically after tube indwelling. The results indicated that mastoid cell growth suppression is higher in patients with a higher degree of inflammatory changes in the lamina propria. In association with treatment by tube indwelling, effusion accumulated in the pneumatic space and mucosal swelling disappeared early after the treatment, or 2 months of tube indwelling. After that, in patients with severe mucosal lesion, a long time, 1.5-2 years, was found to be required for repneumatization accompanying regrowth of the temporal bone. We confirmed that the severity of inflammation of the lamina propria is deeply involved in the growth and repneumatization of the pneumatic cells.

Adolescent↗

PubMed1999

Development of primary hypothyroidism with the appearance of blocking-type antibody to thyrotropin receptor in Graves' disease in late pregnancy.

Spontaneous remission of Graves' disease with a decrease of thyroid stimulating antibody (TSAb) activity is commonly observed in pregnancy. In this article, however, a Graves' patient who developed primary hypothyroidism with an appearance of thyroid stimulation-blocking antibody (TSBAb) activity in late pregnancy is reported. A 25-year-old woman presented with clinical and biochemical hyperthyroidism with an elevation of 99mTcO4- thyroid uptake (4.7%; normal range, 0.7%-3.0%) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulin (TBII; 30.4%). She was euthyroid with normal TBII (8.0%) and TSAb (126%) before pregnancy, when the patient was taking a 5-mg daily dose of methimazole (MMI). MMI was stopped by the patient when she became pregnant. Subsequently, the patient progressed into primary hypothyroidism with a marked elevation of TBII activity (78.4%) in the third trimester of the pregnancy (at that time, TSAb activity was not detected). TSBAb measured 2 weeks later was detected at the activity of 85.0%. Replacement therapy was initiated with levothyroxine (LT4) (0.05-0.1 mg/day), which was discontinued on the 55th day postpartum because of the onset of mild thyrotoxicosis followed by short-term euthyroid state despite high TSBAb activity. Subsequently, because the patient developed primary hypothyroidism 5 months after delivery, replacement therapy with LT4 (0.1-0.125 mg/day) was readministered. Thus, it is suggested that the development of hypothyroidism with the appearance of TSBAb in Graves' patients can occur even in late pregnancy.

Adult↗

PubMed1999

An automated method for the analysis of T-cell receptor repertoires. Rapid RT-PCR fragment length analysis of the T-cell receptor beta chain complementarity-determining region 3.

The examination of T-cell receptor (TCR) repertoires has an important role in the study of lymphoproliferative disorders and autoimmune diseases. Analysis of the complementarity-determining region 3 (CDR3) of the TCR beta chain is used to assess the clonality of T-cell populations. We developed a rapid fluorescence-based method for CDR3 length analysis of expressed TCR gene families. TCR beta chain complementary DNA is amplified by a nested polymerase chain reaction with V beta family-specific oligonucleotide primers and a fluorochrome-labeled C beta primer. The polymerase chain reaction products were analyzed on a compact automated DNA sequencing system (OpenGene system, Visible Genetics, Toronto, Ontario). To demonstrate the usefulness of our technique, we examined the CDR3 length distribution of peripheral blood T cells from a healthy subject, intestinal T cells from a patient with ulcerative colitis, and the T-cell leukemia cell line Jurkat. The analysis revealed polyclonal, oligoclonal, and monoclonal CDR3 distributions, respectively, for the 3 T-cell populations. Our new method shows virtually identical CDR3 length patterns compared with the traditional radioisotope-based method. The new technique offers the convenience of rapid throughput, nonradioactive labeling, and quality data analysis.

Automation↗

PubMed1999

Mast cell chymase in pulmonary hypertension.

Mast cells are known to be involved in various types of tissue remodelling but their role in pulmonary hypertension is still poorly understood. Two subtypes of mast cells have recently been identified by demonstrating one protease, chymase. This enzyme might be implicated in vascular remodelling. The changes in mast cells in lung tissue from three patients with primary or secondary pulmonary hypertension were therefore investigated. Compared with tissue from four control subjects the number of mast cells in the three patients was markedly increased, which suggests that chymase containing mast cells are involved in tissue remodelling accompanied by fibrotic changes in primary and secondary pulmonary hypertension.

Adult↗

PubMed1999

Exercise training does not alter acetylcholine-induced responses in isolated pulmonary artery from rat.

In chronic exercise-trained animals, acetylcholine (ACh)-stimulated endothelial nitric oxide (NO) release is enhanced in the systemic circulation. The purpose of the present study was to determine whether chronic exercise training also enhances NO-mediated relaxation in rat pulmonary artery. Sprague-Dawley rats were randomly divided into groups of exercise-trained and sedentary control rats. The exercise-trained rats ran on a motor-driven treadmill at 30 m x min(-1) up a 15 degree incline 10-60 min x day(-1), 5 days per week for 10 weeks, and had less body weight, lower serum total cholesterol and triglyceride levels than sedentary rats. Contraction induced by potassium chloride and prostaglandin (PG)F2alpha were similar between isolated conduit pulmonary arterial rings from sedentary and exercise-trained rats. There were no differences between PGF2alpha-precontracted rings from sedentary and exercise trained rats in both ACh and sodium nitroprusside-induced relaxations. The NO synthase inhibitor, nitro-L-arginine, suppressed ACh-induced relaxation in both sedentary and exercise-trained rats. These results suggested chronic exercise training did not alter the acetylcholine-induced endothelial NO production and release and the sensitivity of vascular smooth muscle cell to NO in isolated conduit pulmonary artery of rat.

Acetylcholine↗

PubMed1999

Evolutionary alterations of the minimal promoter for notochord-specific Brachyury expression in ascidian embryos.

The Brachyury genes of two divergent ascidians, As-T of Halocynthia roretzi and Ci-Bra of Ciona intestinalis, are expressed exclusively in notochord precursor cells. A previous study showed that the notochord-specific expression of Ci-Bra is controlled by a minimal promoter that is composed of three distinct regions: a region responsible for repression of expression in non-notochord mesoderm cells, a region for activation of expression in notochord cells, and a region for activation of expression in non-notochord mesoderm cells, distal to proximal to the transcription initiation site, respectively. We examined various deletion constructs of the As-T/lacZ fusion gene and demonstrate that a module between -289 and -250 bp of the 5'-flanking region is responsible for notochord-specific expression of the reporter gene. Gel-shift assays suggested the binding of nuclear protein(s) to this module. The 5'-flanking region of As-T contains a potential T-binding motif (-ACCTAGGT-) around -160 bp. Deletion of this motif from the p(-289)As-T/lacZ diminished the reporter gene expression. In addition, coinjection of p(-289)As-T/lacZ and synthetic As-T mRNA resulted in ectopic expression of lacZ in non-notochord cells, suggesting that the T-binding motif is responsible for autoactivation of the gene. These findings revealed striking differences between the minimal promoters of As-T and Ci-Bra so far revealed, with respect to their notochord-specific expression. Furthermore, reciprocal injections of reporter gene constructs, namely As-T/lacZ into Ciona eggs and Ci-Bra/lacZ into Halocynthia eggs, suggest alterations in the cis-regulatory elements and trans-activation factors that have occurred during evolution of the two ascidian species.

Animals↗

PubMed1999

[Eustachian tube function of adhesive tympanum--pre and post operative evaluation].

We examined the eustachian tube function of 48 patients with adhesive tympanum who had undergone operations. Preoperative tubal openings were observed and determined in 57% of these cases by the dynamic movement of the tympanic membrane, 35% by the impedance method, and 74% by the sonotubometry and was found to be lower than in healthy subject. Furthermore the tubal opening duration in sonotubometry was significantly shortened in patients with adhesive tympanum as compared to healthy subjects. However, in a few cases of adhesive tympanum, tubal opening was prolonged remarkably, and indicated a mixed tendency of stenotic and patulous types. Postoperative tubal opening was not seen in 90.9% of the cases as determined by the inflation-deflation test. Mucociliary function was poor in 81.3% of the cases. No remarkable differences were seen between cases of total adhesion and those of posterosuperior quadrant adhesion by any method. The condition of the tympanic membrane and the tympanic cavity after operation, and the eustachian tube function were not correlated in some cases and indicated possible involvement of other factors.

Adolescent↗

PubMed1999

[Three-phase gadolinium infusion in moving-table three-dimensional MR angiography].

Moving-table three-dimensional (3D) MR angiography provides images of long segments of arteries. However, deep veins are sometimes superimposed on the arteries below the knee, and peripheral arteries sometimes fail to be visualized. We have developed an imaging method with three-phase gadolinium infusion according to the mean blood flow velocity of the leg. Nineteen patients with various blood flow velocities were studied. Eighteen of the patients had no venous superimposition. All 19 patients showed good configuration of peripheral arteries with 16-18 ml of gadolinium. This method is useful for better visualization of peripheral arteries without venous superimposition.

Adult↗

PubMed1998

Mechanism of synergism between antimicrobial peptides magainin 2 and PGLa.

The antimicrobial peptides magainin 2 and PGLa, discovered in the skin of the African clawed frog, Xenopus laevis, exhibit marked synergism [Westerhoff, H. V., Zasloff, M., Rosner, J. L., Hendler, R. W., de Waal, A., Vaz Gomes, A., Jongsma, A. P. M., Riethorst, A., and Juretic, D., Eur. J. Biochem. 228, 257-264 (1995)], although the mechanism is not yet clear. They are believed to kill bacteria by permeabilizing membranes. In this study, we examined the interactions of these peptides in lipid bilayers. PGLa, like magainin 2, preferentially interacts with acidic lipids, forming an amphipathic helix. The peptide induces the release of a water-soluble dye, calcein, entrapped within liposomes. The coexistence of magainin 2 enhances membrane permeabilization, which is maximal at a 1:1 molar ratio. Fluorescence experiments using L18W-PGLa revealed that both peptides form a stoichiometric 1:1 complex in the membrane phase with an association free energy of -15 kJ/mol. Single amino acid mutations in magainin 2 significantly altered the synergistic activity, suggesting that precise molecular recognition is involved in complex formation. The complex as well as each component peptide form peptide-lipid supramolecular complex pores, which mediate the mutually coupled transbilayer transport of dye, lipid, and the peptide per se. The rate of pore formation rate is in the order complex >/= PGLa > magainin 2, whereas the pore lifetime is in the order magainin 2 > complex > PGLa. Therefore, the synergism is a consequence of the formation of a potent heterosupramolecular complex, which is characterized by fast pore formation and moderate pore stability.

Amino Acid Sequence↗

PubMed1998

Pyk2 is a downstream mediator of the IL-2 receptor-coupled Jak signaling pathway.

Many cytokines transmit signals to the cell interior through activation of receptor-associated, Janus family protein tyrosine kinases (Jak PTKs). The interleukin-2 receptor (IL-2R) is associated with the Jak1 and Jak3 PTKs, and ligand-induced activation of these PTKs is essential for lymphocyte proliferation. Here, the nonreceptor PTK, Pyk2, was found to be activated following IL-2 stimulation in a Jak-dependent manner. Furthermore, physical association was detected between endogenous Pyk2 and Jak3, and a dominant interfering mutant of Pyk2 inhibited IL-2-induced cell proliferation without affecting Stat5 activation. Collectively, these results suggest that Pyk2 is a newly identified component of the Jak-mediated IL-2 signaling pathway.

Binding Sites↗

PubMed1998

Relationship between middle ear pressure, mucosal lesion, and mastoid pneumatization.

OBJECTIVES: The inflammatory changes of pneumatic space mucosa are thought to affect the development of pneumatic space and the function of transmucosal gas exchange. So, it is assumed that the mucosal change is deeply involved in the onset and healing process of otitis media with effusion (OME). The objective of this study is to investigate whether the growth of the mastoid cells and the middle ear transmucosal gas exchange function in patients with OME are affected by the histopathologic changes in middle ear mucosa, and whether these two factors are changed by the treatment of OME. MATERIALS AND METHODS: From 65 children with OME, middle ear mucosal specimens were collected during indwelling of a tympanic tube, and their histopathologic changes were compared with cell growth area measured on radiographic films and with the change in the middle ear total pressure (METP). RESULTS: Suppression of the cell growth area was stronger and the METP stayed lower in cases with a higher degree of mucosal lesion. Significant expansion of pneumatic area was observed after 2 years of tube indwelling, and the peak METP showed a significant increase after 1.5 years. This increase in the METP was caused by diffusion/absorption of CO2 and O2 and indicated recovery of the transmucosal gas exchange function. CONCLUSIONS: The growth of the mastoid cells and the middle ear transmucosal gas exchange function are closely affected by the subepithelial histopathologic changes in middle ear mucosa, and these two factors recover by the treatment of OME.

Adolescent↗

PubMed1998

[Middle ear mucosa pathophysiology and healing processes in children with otitis media with effusion (OME)].

Most otitis media with effusion (OME) in children heals spontaneously, but it is sometimes persistent and intractable. The major factors determining these different courses of OME are unknown. Identifying such factors would be clinically helpful. Factors affecting on the outcome of OME were studied experimentally and clinically. In animal experiment OME was induced in rabbit by occluding the Eustachian tube. Clinical study was conducted by investigating a histology of the middle ear mucosa, sampled from 64 children with OME (87 ears) who underwent middle ear tube ventilation. Furthermore, these cases studied how the degree of mastoid pneumatization before and after treatment, changes in the volume of the middle ear air cavity and the course after removal of the middle ear ventilation tube affected lesions in the middle ear mucosa. In animals, histology of the middle ear mucosa showed that in the early stages, the subepithelial layer of the middle ear mucosa was characterized by edematous hypertrophy and enlarged blood vessels. In later stages, it became fibrous as a result of chronic inflammation. These results suggest that lesions of the subepithelial layer are unlikely to recover. In clinical cases, histological changes in mucosal samples were rated on a two-point scale: changes in the epithelium and changes in the subepithelial layer. Re-pneumatization, a sign of healing of middle ear mucosal inflammation, was seen 12 months to 18 months after surgery. Among patients in whom the tube was left inserted for more than 18 months, only 11% had unfavorable outcomes and the recurrence rate was low. All patients who had recurrence of disease despite more than 18 months of tube insertion had prolonged inflammation in the middle ear mucosa. There results indicate that the air cavity returns to approximately normal degree of pneumatization more than 18 months after surgery, and that the extent of lesions in the middle ear mucosa, especially the subepithelial layer, is closely related to the healing of OME.

Adolescent↗

PubMed1997

Hyperinsulinemia but no diabetes in transgenic mice homozygously expressing the tyrosine kinase-deficient human insulin receptor.

We generated transgenic mice homozygous for the tyrosine kinase-deficient human insulin receptor (hIRK1030M(+/+)) under control of the insulin receptor promoter. Similar growth patterns and results of glucose tolerance tests were observed among normal, heterozygous, and homozygous mice. Insulin tolerance test indicated no significant difference in the hypoglycemic response to insulin among the three genotypes. However, the serum insulin levels of the homozygous mice before and after glucose loading (201.42 +/- 58.15 pg/ml to 578.57 +/- 49.03 pg/ml) were significantly higher than in the control mice (100.92 +/- 19.55 pg/ml to 356.36 +/- 55.08 pg/ml; p < 0.01 and p < 0.01, respectively) and heterozygous mice (74.46 +/- 18.55 pg/ml to 352.33 +/- 52.43 pg/ml; p < 0.005 and p < 0.01, respectively). Immunohistological evidence of pancreatic islets showed no significant difference among the three genotypes. Taken together, these results suggest that the tyrosine kinase-deficient insulin receptor causes hyperinsulinemia but not diabetes in these homozygous transgenic mice.

Animals↗

PubMed1997

Impaired endothelial function in epicardial coronary arteries after Kawasaki disease.

BACKGROUND: Intimal lesions observed in the coronary arteries (CAs) of patients who have suffered episodes of Kawasaki disease (KD) raise concern about the premature development of arteriosclerosis. Accordingly, we investigated endothelial function in the epicardial and resistance CAs after KD during long-term observation. METHODS AND RESULTS: We assessed the responses of left epicardial and resistance CAs to serial intracoronary infusions of acetylcholine (final concentrations, 0.1 and 1 micromol/L) and nitroglycerin in subjects by using quantitative angiography and a Doppler flow wire system. Three age-matched groups were evaluated: 8 control subjects (group 1), 10 KD patients with normal left CA from the onset (group 2), and 8 KD patients with a persistent or regressed aneurysm in the left anterior descending CA (LAD) (group 3). Acetylcholine (1 micromol/L) changed the LAD area to 114.0+/-2.6%, 72.7+/-3.9% (P<.05 versus group 1), and 88.9+/-4.3% (P<.05 versus groups 1 and 2) of baseline in groups 1, 2, and 3, respectively, with a similar degree of increased coronary blood flow in each group. Nitroglycerin increased the LAD area to 143.5+/-7.7%, 132.3+/-1.9%, and 120.8+/-5.6% (P<.05 versus group 1), respectively. CONCLUSIONS: Results demonstrate a persistent endothelial dysfunction in the epicardial but not resistance CAs in patients after KD and enhanced stiffness of persistent or regressed aneurysms. The concern over early arteriosclerosis warrants the surveillance of KD patients from childhood to adulthood.

Acetylcholine↗

PubMed1997

Prolonged administration of L-arginine ameliorates chronic pulmonary hypertension and pulmonary vascular remodeling in rats.

BACKGROUND: Endothelium-dependent nitric oxide-mediated vasodilation is impaired in rats with pulmonary hypertension (PH) induced by chronic hypoxia or by monocrotaline injection. We therefore investigated whether the prolonged administration of the nitric oxide precursor L-arginine would alleviate PH in both rat models. METHODS AND RESULTS: Fifty-nine rats were exposed to hypobaric hypoxia (380 mm Hg, 10 days) or room air and injected intraperitoneally with L-arginine (500 mg/kg), D-arginine (500 mg/kg), or saline once daily from day -3 to day 10. An additional 38 rats injected subcutaneously with monocrotaline (60 mg/kg) or saline were treated similarly with L-arginine or saline from day -3 to day 17. At the end of the experiment, awake mean pulmonary arterial pressure was determined. The heart was dissected to weigh the right ventricle, and the lungs were obtained for vascular morphometric analysis. Hypoxic rats developed PH (30.8+/-0.7 versus 19.2+/-0.4 mm Hg in controls; P<.05) and right ventricular hypertrophy. Their pulmonary arterial wall thickness and the proportion of muscular arteries in the peripheral arteries increased. L-Arginine but not D-arginine reduced PH (24.8+/-0.7 mm Hg; P<.05), right ventricular hypertrophy, and pulmonary vascular disease. Monocrotaline rats developed PH (34.9+/-2.1 versus 18.8+/-1.2 mm Hg in controls; P<.05), right ventricular hypertrophy, and pulmonary vascular disease. Again, L-arginine reduced PH (24.3+/-1.7 mm Hg; P<.05), right ventricular hypertrophy, and pulmonary vascular disease. CONCLUSIONS: We conclude that L-arginine ameliorated the changes associated with PH in rats, perhaps by modifying the endogenous nitric oxide production.

Animals↗

PubMed1997

Different electrophysiological character of I-, ClO4-, and SCN- in the transport by Na+/I- symporter.

The electrophysiological characteristics of the Na+/I- symporter were examined using the Chinese hamster ovary (CHO) cell line, which was transfected with the rat Na+/I- symporter gene and stably expressed the Na+/I- symporter. In this cell line, iodide uptake was dependent on Na+, and kinetic studies revealed that the K(m) for iodide was 35 microM, similar to that of FRTL-5 cells. The maximal velocity at the cell protein level was 6- to 10-fold higher than in FRTL-5 cells. ClO-4 and SCN- dose-dependently inhibited iodide uptake in a competitive manner. Electrophysiological characteristics were examined using the whole-cell patch-clamp technique. The holding current at-40 mV rapidly shifted inwardly when the cells were perfused with 1 mEq I- or SCN-. The inward current induced by 1 mEq I- did not increase when bathing solution was replaced with a Tyrode solution with 10 mEq I-, indicating that 1 mEq I- was a saturating amount. The inward current induced by 1 mEq I- increased 1.5-fold by changing the bathing solution to a Tyrode solution containing 1 mEq I- and 1 mEq SCN-. The inward current induced by 0.5 mEq SCN- decreased when the bathing solution was changed to a Tyrode solution containing 0.5 mEq SCN- and 10 mEq I-. These findings indicated that the I- ion and the SCN- ion were carried by the NA+/ I- symporter with at least two Na+ ions. The current induced by the transport of SCN- was larger than that induced by the transport of I-, possibly because the number of Na+ ions that was carried with one SCN- ion was larger than the number of Na+ ions carried with one I- ion. Surprisingly, the perfusion of ClO-4 did not induce an inward current, indicating that ClO-4 bound to the Na+/I- symporter, but was not carried by it, or that one ClO-4 ion was carried with one Na+ ion.

Animals↗

PubMed1997

A novel mutation causing complete deficiency of thyroxine binding globulin.

OBJECTIVE: Thyroxine binding globulin (TBG) is a serum protein that transports thyroxine. Three naturally occurring mutations have been reported to produce complete deficiency of TBG (TBG-CD). The first to be reported was TBG-CD5 in caucasian families of French-Canadian origin and consists of substitutions in exons 2 and 3. TBG-CD of English ethnic origin (TBG-CD6) is characterized by a thymine deletion in codon 165 (exon 1). In Japanese families with TBG-CD (TBG-CDJ), a variant has been characterized with a deletion of the first base of the codon for amino acid 352 (exon 4) in the common type TBG. In this communication we report a new type of TBG-CD in a family of Japanese ethnic origin that is characterized by a single nucleotide substitution in place of two nucleotides in exon 1. This is an uncommon mutation which we have been unable to find in other genes. DESIGN: Exons of the TBG gene amplified by the polymerase chain reaction (PCR) were subcloned and sequenced. To examine for the presence of the same mutation in potentially affected individuals, we performed PCR using primer-directed mutagenesis or allele-specific amplification. PATIENTS: The index case was of Japanese ethnic origin, and was diagnosed as having TBG deficiency on the basis of undetectable serum TBG. The patient consented to this evaluation and the protocol was in accordance with IRB standards. MEASUREMENTS: Serum thyroid hormones, thyrotrophin binding inhibitory immunoglobulin and TBG concentrations were measured by conventional radio-immunoassay. Genomic DNA was extracted from white blood cells. RESULTS: In the index case exons 2, 3 and 4 were normal, but nucleotides 144 (cytosine) and 145 (thymine) in exon 1 were substituted with a single base (adenine) which induced a frame shift in the reading frame, resulting in an early stop codon at codon 51. The patient and his daughters were confirmed as having this mutation using primer-directed mutagenesis or allele-specific amplification. CONCLUSIONS: We have described a novel mutation in the TBG gene in a Japanese family. This results in a frame shift and premature stop codon, and was associated with undetectable serum TBG in the index case.

Exons↗

PubMed1997

Pertechnetate thyroid uptake is not always suppressed in patients with subacute thyroiditis.

The authors studied the clinical courses and immunologic aspects in 15 patients (age range, 32-69 years old; 14 women) with clinical features that were similar to subacute thyroiditis (SAT). In 2 patients (group A) whose thyrotropin-binding inhibitory immunoglobulins (TBII) and thyroid stimulating antibody (TSAb) showed strongly positive activity at the initial visit, Tc-99m pertechnetate thyroid uptake (Tc-99m uptake) was elevated (5.6% and 3.8%, respectively, normal; 0.7-3.0%). In 6 (group B) of 13 other patients, Tc-99m uptake was not completely suppressed (2 normal, 4 near normal) and imaging showed uptake in one lobe. In 7 (group C), however, there was no evidence of uptake in either lobe. Inflammatory process was localized in one lobe in all group B patients, and was in both lobes in all group C patients but one. Serum TSH levels were detectable in at least 4 patients (2 group B, 2 group C) low in all. There were no patients in both groups B and C in whom TBII and/or TSAb were detected at the initial visit. In SAT, marked suppression of Tc-99m uptake may be ascribed mainly to inflammatory follicular cell damage, but it is not always suppressed, owing to an association similar to Graves' disease and other unknown mechanism(s).

Adult↗