Transport properties of high-Tc superconductors: Fermi-liquid local-density electronic-structure predictions.
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Biomedical subjects
Publications and source records attributed to N Hamada.
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In order to discover whether or not thyroid function in patients with Hashimoto's disease will move toward hypothyroidism with age, we investigated the thyroid function and antithyroid antibody titers at the initial examination and 5 years later in 181 patients with goitrous Hashimoto's thyroiditis. Pregnant patients and those within 1 year of the postpartum period were excluded. The thyroid function was assessed before medication or at least one month after stopping it. At the initial examination, 52% (94 cases) of the cases were euthyroid, 24% (44 cases) were subclinically hypothyroid and 24% (43 cases) were hypothyroid. It was not observed whether the incidence of hypothyroidism tended to be greater in older patients or in patients with longer duration of illness. Five years later, 68% of euthyroid patients at the initial examination remained in euthyroid state, 18% had become subclinically hypothyroid, and 9% were hypothyroid. The thyroid function was not evaluated in 5% of the patients because they were under treatment with 1-thyroxine. In the patients with subclinical hypothyroidism at the initial examination, 30% had become euthyroid, 23% remained subclinically hypothyroid, 32% had become hypothyroid and 16% were not evaluated. Thirty percent of the patients with hypothyroidism at the initial examination had become euthyroid, 7% were subclinically hypothyroid, 28% remained hypothyroid and 35% were not evaluated. The higher the titer of TGHA, the higher the percentage of hypothyroidism at the first examination. A similar but much stronger tendency was observed in the patients with a higher titer of MCHA. In the patients with a higher titer of TGHA, the number of hypothyroid patients approximately doubled after 5 years, although such a tendency was not observed in the patients with a higher titer of MCHA. In patients with persistent hypothyroidism, the age was significantly higher, the serum concentration of T3 lower and the titer of TGHA at the initial examination and MCHA 5 years later higher than in the patients with transient hypothyroidism. The titer of MCHA was significantly decreased 5 years later in patients with transient hypothyroidism. From these results, it is indicated that in patients with goitrous hypothyroidism, the incidence of hypothyroidism was higher in the cases with high titers of antithyroid antibody than in those with low titers, and that in the patients with transient hypothyroidism, the age was lower, the serum level of T3 higher and the titer of TGHA lower than in the cases with permanent hypothyroidism.(ABSTRACT TRUNCATED AT 400 WORDS)
A simple and selective method for the determination of sulphamethazine (SMT) and its metabolite, N4-acetylsulphamethazine (N4-AcSMT), in meat by high-performance liquid chromatography (HPLC) with photodiode-array detection was developed. The drugs were extracted from meat with 0.2% metaphosphoric acid-methanol (6:4), followed by a Bond-Elut C18 clean-up procedure. The HPLC separation was carried out on a Supersphere RP-18e column (125 X 4.0 mm I.D.) using 0.05 M sodium dihydrogenphosphate (pH 4.5)-acetonitrile (8:2) as the mobile phase at a flow-rate of 0.5 ml/min, and monitored with a photodiode-array detector. The recoveries of SMT and N4-AcSMT from meat fortified at 0.5 micrograms/g were 90.1-93.3 and 93.0-94.4%, respectively, with coefficients of variation of 1.9-3.2 and 1.5-2.7%. The limits of detection were 0.02 micrograms/g for each drug. SMT was found in ten samples of imported meat (12.5%) at levels ranging from 0.05 to 1.05 micrograms/g.
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Enteroviruses were isolated monthly for one year from feces in the intestine of 47 cattle. Judging from the isolation panel, it was suggested that endemic infection occurs. Genetic changes of isolated enteroviruses were traced using RNase T1 oligonucleotide fingerprint analysis and nonparametric distance scaling. Using some characteristics transitions of fingerprint patterns we could also trace some strains. These analyses suggested that in some strains drastic genetic changes may occur, which coincide with additional infections transmitted from other cows. Furthermore, it was indicated that the genetic changes of viruses isolated from cow R13 were not very drastic, but genetic changes were drastic for viruses isolated from cow R19. Overall, we could never observe the same fingerprint pattern using RNase T1. This study suggests that genetic changes tend to accumulate as time elapses, and at the same time, infection decreases.
Chronic energy-intake restriction inhibits mouse mammary tumor virus (MMTV)-induced mammary tumors in C3H/Ou mice by greater than 90%. We have shown that associated with suppression of mammary tumorigenesis there is a reduction or inhibition of circulating prolactin, MMTV particles expressed, and MMTV mRNA transcription in mammary glands (and in most organs tested). To understand the concerted action of prolactin, energy-consumption level, and MMTV on inducing mammary tumors, experiments were designed to control prolactin and energy levels in order to evaluate their effects on MMTV mRNA expression. Mice on restricted diets were grafted with adenohypophyses, and mice fed ad libitum were treated with the dopaminomimetic agent octahydrobenzo [g]quinoline. Adenohypophyseal grafting significantly increased prolactin in dietary (energy)-restricted mice, and this effect was associated with an increase in MMTV mRNA expression within the mammary gland; a linear correlation between prolactin levels and MMTV mRNA expression in the mammary gland was found. Conversely, elimination of the nocturnal peak of circulating prolactin by i.p. injection of dopaminomimetic octahydrobenzo [g]quinoline to mice fed ad libitum delayed (by 8 weeks) and reduced (even as long as 25 weeks) mammary gland MMTV mRNA expression. These findings associate prolactin influences with MMTV mRNA production in mice and help explain the link between chronic energy-intake restriction and reduced MMTV gene expression.
Chronic energy intake restriction (CEIR) reduces mouse mammary tumor virus (MMTV)-induced mammary tumors in C3H/Ou mice. Fewer than 10% of C3H/Ou mice developed mammary tumors during 88 wk of study when subjected to CEIR regardless of calorie source (fat vs. carbohydrate). By contrast, 100% of mice fed ad libitum diets relatively high in fat or carbohydrate or a commercial diet developed tumors by 35-40 wk. MMTV proviral DNA transcription was shown to be activated in spleen, liver, lung, kidney, small intestine, and mammary gland of mice consuming these diets ad libitum. By contrast, these messages were suppressed by CEIR in all tissues analyzed except spleen. MMTV proviral messages in liver and mammary gland increased with age in full-fed mice and were suppressed by CEIR. These findings suggest that the nutritional regulation of MMTV proviral DNA expression is tissue-specific. In CEIR mice the suppressed MMTV proviral DNA transcripts in mammary gland and liver increased with time in association with the delayed onset of mammary tumors. Mammary tumorigenesis in C3H mice is associated with integration of MMTV proviral DNA, which appears to activate a putative mammary tumor protooncogene, int-1. CEIR apparently decreases the frequency of viral reintegration adjacent to the int-1 gene and thus inhibits expression of int-1 and probably an initiation step in mammary tumorigenesis. Expression of other putative protooncogenes, int-2 and ras, in liver tissue was also reduced by CEIR. These findings indicate that both initiation and promotion of mammary tumorigenesis are influenced by CEIR in C3H/Ou mice.
Recently, thyroid microsomal antigen was identified as thyroid peroxidase, and thyroid microsomal antibody was found to inhibit thyroid peroxidase activity in vitro. We investigated the possibility that anti-microsomal antibody inhibits the iodination of tyrosine, in vivo. Immunoglobulin G with or without anti-microsomal antibody from hypothyroid patients with goitrous Hashimoto's thyroiditis inhibited thyroid hormone synthesis in cultured slices of normal human thyroid tissue. IgGs with anti-microsomal antibody inhibited 125I thyroidal uptake and thyroid hormone synthesis stimulated by TSH more than normal IgG did. However, the same results were obtained with IgGs without anti-microsomal antibody. This effect did not involve anti-microsomal antibody, anti-thyroglobulin antibody, TSH-binding inhibitor immunoglobulin, thyroid stimulation-blocking immunoglobulin, or the cAMP level of the thyroid tissue. The ratio of organic I to inorganic I with stimulation by TSH in slices incubated with IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis or normal IgG was not significantly different, but was significantly higher in slices incubated with methylmercaptoimidazole. Therefore, IgG from hypothyroid patients with goitrous Hashimoto's thyroiditis mainly suppressed 125I thyroidal uptake, rather than inhibiting thyroid peroxidase activity. In addition, this IgG was present in the serum of 11 of the 12 hypothyroid patients with Hashimoto's thyroiditis studied. This IgG may be involved in the mechanism that causes hypothyroidism in some patients with goitrous Hashimoto's disease.
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Reverse triiodothyronine (rT3) had been believed biologically inactive, but recently we demonstrated nuclear binding sites for rT3 in human placenta. In this study we examined rT3 binding sites in rat brain. Male Wistar normal rats aged 2, 4 and 9 weeks were killed and the brain was removed for rT3 binding assay. In another series, male Wistar rats weighing about 40g were divided into two groups: group 1 (rickets group), kept on our original rachitogenic diet and group 2, kept on standard diet. After 28 days on either diet they were killed and the brain was removed for assay. Cerebral nuclear protein was extracted with 0.4M KCl buffer. In normal 2 week-old rats specific binding sites for rT3 were detected in all parts of the brain, but at 7 weeks of age the density of the binding sites was decreased and at 9 weeks it is almost 0. Scatchard analysis performed in rachitic rats showed a curvilinear pattern, suggesting two sets of receptors existing in brain tissue; in cerebral cortex one with a association constant (Ka) of 1.07 X 10(8)M-1 and a limited capacity (Bmax) of 0.75 X 10(-15) moles/mg tissue and the other with Ka = 4.93 X 10(6), Bmax = 12.1 X 10(-15), and in thalamus including hypothalamus, one with Ka = 1.00 X 10(8), Bmax = 1.00 X 10(-15) and the other with Ka = 4.57 X 10(6) and Bmax = 18.6 X 10(-15).
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Isolates of type 3 poliovirus from vaccine-recipients were characterized in terms of virulence, sensitivity of growth to high temperatures, and differences in genome structure from the Sabin type 3 vaccine strain. These included point mutations in the region of the genome coding for the structural proteins and in the 5' noncoding region, and the presence of type 1 or type 2 poliovirus genomic sequences resulting from intertypic recombination. Isolates from healthy vaccinees resembled those from vaccine-associated cases of poliomyelitis in all of these properties. Suppression of the temperature-sensitive phenotype was strictly correlated with reversion to virulence in nonrecombinant type 3 strains. Recombinant isolates were more attenuated than expected, even when they had lost all mutations known to attenuate the type 3 vaccine strain.
The antibody to TSH (TSH-Ab) found in some patients with Graves' disease may be either an antiidiotype (anti-id-Ab) to the TSH receptor antibody (TRAb) or the antigen (idiotype) for which the anti-id-Ab is in fact TRAb. Four groups have found antibodies to bovine TSH (bTSH-Ab) in Graves' disease patients in a TSH binding-inhibiting immunoglobulin (TBII) RRA that uses [125I]bTSH. In this assay serum samples containing bTSH-Ab give highly negative TBII values. The purpose of this study was to look for any clinical significance of potential idiotypic-antiidiotypic network regulation related to bTSH-Ab. Twenty-one (0.49%) of 4285 Graves' disease patients had TBII values less than the mean -4 SD of normal subjects. In all 21, bTSH-Ab was found by incubation of [125I]bTSH with the patient's serum, and significant inhibition of binding of bTSH-Ab to bTSH by human TSH was found in only 3 of these serum samples. We investigated next whether the binding site of the anti-TSH-Ab mimicked the TSH receptor-binding site. Binding of [125I]bTSH to bTSH-Ab-positive serum was not inhibited by bTSH-Ab-negative, thyroid-stimulating immunoglobulin-positive [(+)], and/or TBII(+) immunoglobulin G. In one patient with human TSH-Ab, TSH-Ab appeared and disappeared, and when TSH-Ab was negative, TBII was positive. Inhibition of [125I]bTSH binding to TSH-Ab by the same patient's serum when that patient was serum thyroid-stimulating immunoglobulin(+), TBII(+), and TSH-Ab-negative was sought but not found. Changes in serum TSH-Ab activity and disease activity were not correlated in this patient. In six untreated patients with Graves' hyperthyroidism with bTSH-Ab, the serum T3 and T4 concentrations and the time required to become euthyroid during antithyroid drug treatment were not significantly different from those in 52 such patients without bTSH-Ab. These data suggest that bTSH-Ab is not an anti-id-Ab to TRAb and that TSH-Ab does not directly modulate the activity of Graves' disease.
The thyroid microsomal antibody (M-Ab) has been found to be an antibody against thyroid peroxidase (TPO), and such antibodies have been reported not only to bind TPO but also to directly inhibit TPO activity. In this study we investigated the relationship between TPO activity-inhibiting immunoglobulin (TPII) and thyroid function in 55 untreated patients with hyperthyroidism due to Graves' disease and 35 untreated patients with Hashimoto's disease. TPO partially purified from the microsomal fraction of Graves' thyroid tissue by Sephacryl S-300 gel filtration was incubated with immunoglobulin (Ig) fractions of serum prepared by precipitation with 15% polyethylene glycol. At the end of incubation, TPO activity was measured by a guaiacol assay. The TPII level was expressed as the TPII index, defined as the inhibition of TPO activity by patient Ig divided by inhibition produced by a known positive Ig. We also measured serum free T4, free T3, and TSH concentrations and anti-M-Ab titers, the latter by a microenzyme-linked immunosorbent assay. When a positive TPII index was defined as more than the mean + 2 SD of the TPII index (0.38) for 15 normal subjects, 13 patients with Graves' disease and 14 patients with Hashimoto's disease had positive TPII index values. There was a positive correlation between the TPII index values and the M-Ab titers in patients with either Graves' disease (r = 0.38; P less than 0.01) or Hashimoto's disease (r = 0.52; P less than 0.01). The mean TPII index in patients with Hashimoto's disease was significantly higher than that in patients with Graves' disease [0.38 +/- 0.42 (+/- SD) vs. 0.19 +/- 0.41; P less than 0.05]. The slope of the regression line between the TPII index values and the M-Ab titers for patients with Hashimoto's disease was steeper than that for patients with Graves' disease. The mean serum free T4 concentration was significantly lower in those patients with Hashimoto's disease who had positive TPII index values than in those with negative TPII index values (14.0 +/- 5.0 vs. 9.6 +/- 3.7 pmol/L; P less than 0.01). There was no significant difference in thyroid function between the patients with Graves' disease with positive and negative TPII index values. TPII appears to inhibit thyroid function in some patients, but no simple relationship between TPII and thyroid function in autoimmune thyroid disease was demonstrated. Understanding the factors that control access of anti-TPO antibody to its antigen may help to elucidate the significance of circulating anti-TPO antibody.
To investigate the role of parathyroid function in transient hypocalcemia after subtotal thyroidectomy for Graves' disease, the serum parathyroid hormone (PTH) concentration and nephrogenous (N) cAMP were measured in 16 patients before and after surgery. Serum PTH was measured with two commercially available kits (PTH-M, PTH-C), PTH-M is a recently developed highly sensitive assay using an antibody recognizing the mid-portion of human PTH and a synthetic 125I-tyr45-human PTH (43-68) as a radioligand. One of the 16 patients had severe clinical tetany and had a markedly lower PTH-M concentration and NcAMP after thyroidectomy. However, no significant change in serum PTH-M, PTH-C and NcAMP were observed in the other patients, although their serum calcium (Ca) concentrations decreased significantly. The Data were analyzed by dividing the patients according to the change in serum Ca or PTH. Serum PTH-M and PTH-C significantly decreased in 4 patients whose serum Ca clearly decreased after surgery. Serum Ca on the first postoperative day was significantly lower in patients whose serum PTH decreased after thyroidectomy than in patients whose serum PTH did not. Furthermore, the serum Ca concentration was significantly correlated with PTH-M, and with NcAMP on the third postoperative day. These data proved that hypofunction of the parathyroid gland is important in transient hypocalcemia after subtotal thyroidectomy for Graves' disease. The pathogenetic mechanism of transient hypocalcemia was discussed in comparison with the data from a patient who had overt parathyroid injury.
We found an anomalous branch of the aortic arch during the students' dissection practice at Fukuoka Dental College in 1988. The results are as follows; This case was found in a 92-year-old female cadaver (cause of death: cardiac dissufficiency), whose brachiocephalic trunk arose from the aortic arch forming a striking trunk with the left common carotid artery. The diameter of this trunk was 17.2 mm at its origin and the longitudinal length was 11.0 mm. This case corresponded to Typus B of Adachi's classification, while to Type C of De Garis's.
No accurate method to detect thyroid microsomal (MC) antibody (Ab) in serum has been generalized. In this study, the titer of MC Ab obtained by the method of MC autoantibody particle agglutination (MCPA) was analyzed by enzyme linked immunosorbent assay (ELISA). MC and thyroglobulin (Tg) were prepared from Graves' thyroid. ELISA was done by coating the plate with MC, adding Tg to buffer and using peroxidase-conjugated anti-h IgG. 1) The titer of MCPA correlated with the MC Ab ELISA index in serum without Tg Ab, but it did not in serum with Tg Ab. MC Ab was negative by ELISA while it was positive by MCPA in some of the sera with Tg Ab. 2) When ELISA was done using buffer without Tg, the amount of IgG bound to MC was greater in serum with TGPA: + and MCPA: - than in serum with MCPA: + and TGPA: -. 3) The zone phenomenon observed in MCPA did not always indicate an excess of MC Ab. 4) MC Ab was positive by ELISA in some of the negative MCPA sera obtained from patients with Hashimoto's disease in which diagnosis was confirmed by biopsy. In conclusion, the result obtained in MCPA now in use is strongly influenced by Tg Ab. Furthermore, since binding of Ab to MC is judged by agglutination of particles in MCPA, ELISA is superior in sensitivity and accuracy in detecting MC Ab.