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Biomedical subjects

H Seo

Publications and source records attributed to H Seo.

At least 127 records · Page 7Linked to original sources
PubMed1996

Differential induction of fos and jun family genes by thyrotropin in rat thyroid FRTL-5 cells.

Effect of thyrotropin (TSH) on the expression of the members of fos and jun family genes in a rat thyroid cell line (FRTL-5) was examined by the reverse transcription-polymerase chain reaction (RT-PCR) method. FRTL-5 cells were maintained in a TSH-deprived medium for 5 days. After 1 mU/mL TSH addition, the cells were harvested at intervals. Total RNA extracted from the cells was subjected to RT-PCR. TSH induced a rapid and transient expression of c-fos, fosB, and fra-1 with different kinetics. Increase in c-fos mRNA was most rapid with a peak level at 30 min after TSH addition. The fosB mRNA reached a peak level at 60 min poststimulation with a rapid decline at 90 min. The fra-1 mRNA increased at 60 min followed by a gradual decrease until 120 min. The change in fra-2 mRNA level was similar to that of fra-1. TSH induced similar changes in the levels of c-jun and junB mRNAs. They significantly increased within 30 min followed by a sustained high level until 90 min. The differential induction of fos and jun family genes suggests an important role of their gene products on the regulation of thyroid cell function by TSH.

Animals↗
PubMed1996

Chest pain during daily life in patients with hypertrophic cardiomyopathy: an ambulatory electrocardiographic study.

Patients with hypertrophic cardiomyopathy frequently complain of chest pain during daily activities. ST-segment depression is described in association with sudden death and pacing, but its prevalence during ambulatory electrocardiographic monitoring is unknown. The aim of this study was to determine the relation of ambulatory ST-segment depression to clinical characteristics, risk factors for sudden death and thallium-201 perfusion in patients with hypertrophic cardiomyopathy. Continuous 48 h ambulatory electrocardiographic monitoring was performed in 113 patients (age 38 +/- 14 years) with hypertrophic cardiomyopathy. Ninety-four (83%) recordings were suitable for ST-segment analysis. A total of 109 episodes of ST-segment depression (> or = 1 mm from baseline) were recorded in 25 (27%) patients (mean 4 +/- 5). In patients < or = 30 years of age (but not > 30) there was an association between ST-segment depression and a history of exertional chest pain (seven of 12 vs one of 20; P = 0.001), and dyspnoea NYHA class II/III (seven of 15 vs one of 17; P = 0.008). There was no association between ST-segment depression and risk markers for sudden death, i.e. family history of sudden death, syncope and non-sustained ventricular tachycardia, in any group. Reversible thallium-201 defects occurred in 27 (29%) of the 94 patients with analysed recordings but were not associated with symptoms, risk factors for sudden death or ambulatory ST-segment depression. In young patients with hypertrophic cardiomyopathy, ischaemia-like ST-segment depression is common and is associated with a history of typical angina and dyspnoea. Reversible thallium-201 perfusion defects are associated with neither symptomatic status nor ambulatory ST-segment depression.

Activities of Daily Living↗
PubMed1996

Oxyphil cell function in secondary parathyroid hyperplasia.

Oxyphil cell function in secondary parathyroid hyperplasia due to chronic renal failure was evaluated using in situ hybridization and heterotransplantation of parathyroid tissue. In situ hybridization and histologic analysis were performed on continuous frozen sections using 22 parathyroid tissues. A restricted area composed exclusively of oxyphil cells was observed in 10 specimens, and an area of only chief cells was found in 12 specimens. Silver grains demonstrating the existence of parathyroid hormone (PTH) mRNA were 18.8 +/- 7.8 (mean +/- SD) in oxyphil cells while those in chief cells were 17.2 +/- 7.5. PTH mRNA was abundant in both the oxyphil and chief cells. Further analysis of oxyphil cell function was assessed by the heterotransplantation of parathyroid nodules, consisting exclusively of oxyphil or chief cells, into nude mice. The function of these implants was assessed by measuring the concentration of human intact PTH which did not cross-react with mouse PTH. Serum PTH concentrations were correlated with the volume of implanted tissue. Elevations of PTH concentrations were similar in the mice transplanted with oxyphil or chief cells, indicating that both cell types had similar PTH secretory activity. The basic histologic characteristics of both cell types were not altered following transplantation. These results demonstrate that oxyphil cells in secondary parathyroid hyperplasia synthesize and secrete PTH, and that this secretion contributes to the pathophysiology of hyperparathyroidism.

Alkaline Phosphatase↗
PubMed1996

Amino acid substitutions of thyroid hormone receptor-beta at codon 435 with resistance to thyroid hormone selectively alter homodimer formation.

Thyroid hormone action is mediated through its nuclear receptors (TRs), which bind to target DNA sequences [thyroid hormone response element (TRE)] as a homodimer or a heterodimer with 9-cis-retinoic acid receptors. Mutations of TR beta identified in patients with resistance to thyroid hormone (RTH) cluster primarily at two areas separated by the putative dimerization region. Two TR beta mutations were newly found in patients with RTH at codon 435 histidine (H435L and H435Q) close to the dimerization region. Recent crystallographic study suggested that H435 is critical for direct contact with T3. To study how the side-chain charge of amino acids at this position affects receptor characteristics, T3-binding activity, receptor dimerization, transcriptional activity, and dominant negative action were analyzed in two RTH mutants and two additional artificial mutants (H435R and H435E). The T3 binding affinities of all four mutants were below detection. In electrophoretic mobility shift assay using TRE-DR4 or the inverted palindrome (Lap), heterodimer formation of mutant receptors with 9-cis-retinoic acid receptor was similar to that of wild type receptors. However, homodimer formation varied among mutant receptors, especially using TRE-DR4, with a rank order of wild type = H435R > H435Q > H435L > > H435E. In the presence of a basic amino acid at codon 435, homodimer formation was preserved, whereas substitution to neutral or acidic amino acids resulted in decreased homodimer formation. In transient transfection assays using reporter genes under the control of 2xPal-thymidine kinase (TK), DR4-TK, Lap-TK, or TSH alpha promoter, these four mutants were inactive in T3-dependent transcriptional activation. Dominant negative inhibition was similar for all four mutants. These results indicate that 1) newly found TR beta mutations at codon 435 are responsible for RTH; and 2) codon 435 in TR beta is located at a position that can predominantly alter homodimer formation on certain TREs, such as DR4.

Amino Acid Sequence↗
PubMed1996

Dominant inheritance of resistance to thyroid hormone not linked to defects in the thyroid hormone receptor alpha or beta genes may be due to a defective cofactor.

Resistance to thyroid hormone (RTH) is an inherited syndrome of reduced tissue responsiveness to thyroid hormone. To date, all individuals expressing the RTH phenotype have been found to harbor mutations in the thyroid hormone receptor beta (TR beta) gene that impair T3-mediated function. We describe a unique family in which the dominantly inherited RTH is not associated with abnormalities in the TR beta or TR alpha genes, as determined by gene sequencing and linkage analysis. However, affected family members manifest a severe form of RTH, with reduced responses of thyrotrophs and peripheral tissues requiring 8- to 10-fold the normal replacement doses of L-T4 and L-T3. No other endocrine abnormalities were detected. The defect developed de novo in the proposita and was transmitted to her two children of unrelated fathers. As cultured fibroblasts from the proposita responded poorly to T3 despite a normal concentration of TR, other abnormalities in the mediation of T3 action were sought. Nucleotide sequences of the TSH beta promoter, containing thyroid hormone response elements, and TR-interacting protein 1 were normal. Nuclear extracts (NE) of cultured skin fibroblasts from affected individuals of this family were tested for their interaction with normal TR beta and thyroid hormone response elements by the electrophoretic mobility shift assay. NE from the proposita showed a strong additional band compared to NEs from normal individuals and patients with RTH caused by TR beta mutations or deletion. Far Western analysis of NE from the affected daughter hybridized with labeled TR beta demonstrated an additional band that was not seen in NEs from a normal control or patients with TR beta gene defects. It is concluded that the etiology of RTH is not confined to abnormalities in the TR beta gene. An abnormal cofactor with a specific function in the regulation of thyroid hormone action is probably involved in the expression of the RTH phenotype in this family.

Child, Preschool↗
PubMed1996

Gene screening of thyroxine-binding globulin (TBG) deficiencies in the Japanese: only two mutations account for TBG deficiencies in the Japanese.

T4-binding globulin (TBG) is the principal transport protein for thyroid hormone in the circulation. Twelve mutations in the human TBG gene have been reported, and the inheritance of those variant TBGs was shown to be X-chromosome linked. We previously reported a nucleotide deletion at the codon 352 (TBG-CDJ) and a nucleotide substitution at the codon 362 (TBG-PDJ) of the TBG gene in a Japanese male manifesting TBG complete deficiency and partial TBG deficiency, respectively. In this communication we investigate the prevalence of both mutations among 50 unrelated Japanese subjects manifesting complete or partial TBG deficiency from various areas of the Japanese Archipelago. Mutant alleles were identified by amplification of their genomic DNAs by PCR with allele-specific primers. In addition, the presence of a polymorphic mutation in codon 283 (TBG-Poly) in these variants was investigated. All male subjects manifesting complete TBG deficiency (n = 30) and all female subjects manifesting partial TBG deficiency (n = 4) were demonstrated to be hemizygotes and heterozygotes for the mutation of TBG-CDJ, respectively. All male subjects manifesting partial TBG deficiency (n = 16) were shown to have the mutation of TBG-PDJ as hemizygotes. TBG-Poly was consistently absent from these variants. We conclude that only TBG-CDJ and TBG-PDJ may account for complete and partial TBG deficiencies in the Japanese.

Alleles↗
PubMed1996

Redox regulation of thyroid-transcription factors, Pax-8 and TTF-1, is involved in their increased DNA-binding activities by thyrotropin in rat thyroid FRTL-5 cells.

Thyroid-enriched transcription factors, Pax-8 and TTF-1, are involved in the thyroid-specific expression of thyroglobulin (TG) gene. Here we demonstrate redox regulation of both factors in vitro and in vivo. When analyzed by electrophoretic mobility shift assay (EMSA), oxidation with diamide abolished the DNA binding of Pax-8. Subsequent reduction with dithiothreitol (DTT) restored the binding. Thioredoxin (TRX), a cellular reducing catalyst, restored the binding more efficiently than DTT. When TTF-1 was oxidized with diamide, its binding was decreased and the TTF-1-DNA complex migrated faster on EMSA. DTT reversed these effects. These observations indicate that reduction is required for full DNA binding of Pax-8 and TTF-1 in vitro. We then examined whether TSH modulates their binding through redox regulation. Whole cell extracts were prepared from FRTL-5 cells at intervals after TSH treatment without reducing agents and subjected to EMSA. Pax-8 and TTF-1 binding activities were gradually increased during the initial 6 h after TSH. This increase was due to reduction of the factors, since treatment of the extracts with DTT masked the increase by enhancing their binding activities. These results suggest that TSH up-regulates the binding of Pax-8 and TTF-1, at least in part, by reducing the preexisting, oxidized forms in FRTL-5 cells. Northern analysis showed that the increase in TRX mRNA level by TSH in FRTL-5 cells was associated with the increase in the binding activities. Cotransfection of luciferase-reporter plasmid driven by TG promoter with Pax-8- and TRX-expressing plasmids into a heterologous cells revealed that TRX up-regulated the Pax8-mediated TG promoter activity. Taken together, the present study suggests that the redox regulation of Pax-8 and TTF-1 by TSH, probably through TRX, modulates the TG gene expression.

Animals↗
PubMed1996

Histopathology of enzootic ataxia in Sika deer (Cervus nippon Temminck).

Thirteen Sika deer (Cervus nippon Temminck) showing ataxia on a stock farm in the north eastern district of China were examined histopathologically. The principal pathological changes were spongy vacuolation and myelin deficiency in the white matter of the spinal cord and brain stem, fibrosis and rupture of the elastic lamina of the spinal arterioles, and mesothelial hyperplasia in the spinal arachnoid. Other findings included defective formation of the elastic laminae of the aorta, and the blood vessels in the kidney and lung, hemosiderosis in the spleen and liver, and lymphocyte depletion in the systemic lymph nodes. Copper concentrations were low in the serum and liver. In the white matter of the spinal cord and brain stem, demyelination appeared to coexist with dysmyelination and secondary myelin breakdown. It was inferred that decreased activity of copper containing enzyme induced various lesions. The possible role of copper deficiency in the pathogenesis of the ataxic conditions is discussed.

Animals↗
PubMed1996

Synthesis and release of glycosylated prolactin in transfected cells with human prolactin complementary deoxyribonucleic acid.

To analyze how the synthesis and release of glycosylated PRL (G-PRL) is regulated, we transfected human PRL complementary deoxyribonucleic acid (cDNA) into three different cell lines consisting of GH3 cells that originated in rat pituitary tissue, Chinese hamster ovary cells, and COS-1 cells generated from monkey renal tissue. 35S-labeled PRLs produced by the cells were immunoprecipitated with anti-human PRL antiserum, and the ratios of G-PRL to total PRL were compared. PRLs of 23 kDa and 25 kDa were detected in the cell lysate and medium. The 25-kDa PRL was confirmed to be a glycosylated form by endoglycosidase treatments. The ratios of G-PRL/total PRL were 0.17-0.33, which were similar in lysates and media and among different cell lines. Pulse-chase experiments revealed that the autonomaous secretion rates of G-PRL and non-glycosylated PRL were almost identical. These results indicate that synthesis and secretion kinetics of human PRL may not be affected by its glycosylation in the cells transfected with PRL cDNA.

Animals↗
PubMed1996

Mediation of the hormone- and serum-dependent regulation of thyroglobulin gene expression by thyroid-transcription factors in rat thyroid FRTL-5 cells.

The molecular mechanism for hormone- and serum-dependent regulation of thyroglobulin (TG) gene expression was studied. A construct of rat TG promoter (-178 to -3) linked to a luciferase gene was transfected into TSH-, insulin- and serum-deprived FRTL-5 cells. Addition of TSH, insulin or serum augmented the luciferase activity. The endogenous TG mRNA level was also increased, indicating that the promoter used confers responsiveness of TG gene to these additives. The possible involvement of thyroid-transcription factors, TTF-1, TTF-2 and Pax-8, in the induction of TG gene transcription was studied using an electrophoretic mobility shift assay. Since the protein/DNA ratio in FRTL-5 cell extracts was significantly increased by these additives, binding activities of these factors per unit of DNA were examined. It was demonstrated that TSH, insulin or serum increased not only TTF-2 binding activity but also the binding activities of TTF-1 and Pax-8. However, the magnitude of the increase in TTF-1 and Pax-8 mRNA levels per unit of DNA was less than that of the binding activity. Taken together, our results suggest that TSH, insulin and serum increase the binding activities of TTF-1 and Pax-8 to the TG promoter presumably through the posttranslational modification of the factors, thereby enhancing TG gene transcription.

Animals↗
PubMed1996

[Two cases of Candida endocarditis associated with abdominal disease].

Two cases of Candida endocarditis are reported. The first case was of a 63-year-old man who had a positive blood culture for Candida albicans during treatment for liver abscess and early gastric cancer. He was transferred to our department, and aortic and tricuspid regurgitation due to Candida endocarditis was diagnosed. The patient was successfully treated with aortic valve replacement, tricuspid valve plasty and anti-fungal agents. The second case was of a 65-year-old man who complained of fever. Despite a diagnosis of common bile duct cancer and resection of the tumor, the fever persisted. He was transferred to our department and was diagnosed having aortic regurgitation due to Candida endocarditis, complicated by heart failure. Although intense medical therapy including antifungal agents, diuretics, catecholamines and digoxin was initiated, the patient died from multiple embolisms 9 days later. In the treatment of Candida endocarditis, early diagnosis and early decision-making for either surgical or medical therapy is indispensable. Although the prevalence of Candida endocarditis is low, the differentiation of this disease should be taken into account in febrile elderly patients with long-standing therapy with antibiotics.

Aged↗
PubMed1996

Effects of bisphosphonate on bone metabolism in tail-suspended rats.

Our previous studies demonstrated that tail suspension causes early, transient increases in osteoclastic activity, followed by a decrease in osteoblastic activity in the hind limbs of rats. To assess whether this early increase in bone resorption is important in the development of disuse atrophy, the effect of YH529, a third generation bisphosphonate, was studied on hind limb atrophy in rats subjected to tail suspension. YH529 (YH group) or PBS (control group) were administered subcutaneously in 5-week-old male Wistar rats suspended for 7 days. In the control group, wet weight, calcium and phosphorus contents decreased significantly in the femur but they did not change in the humerus. In the YH group, however, these parameters did not change significantly in the femur, but both calcium and phosphorus increased significantly in the humerus. These results indicate that the inhibition of bone resorption by YH529 prevents the development of disuse atrophy induced by tail suspension. It is thus suggested that early increases in bone resorption are important for the development of disuse bone atrophy.

Animals↗
PubMed1996

Changes in serum concentrations of calcium and its regulating hormones during tail suspension in rats.

To study the effects of mechanical unloading on systemic calcium homeostasis, we determined the changes in serum concentration of calcium, 1,25-dihydroxyvitamin D3 and parathyroid hormone (PTH) during tail-suspension experiments in rats. The serum concentration of ionized calcium significantly increased during the 14 days of the suspension, reflecting increased bone resorption in the hind limbs. This hypercalcemic condition should cause suppression in PTH secretion. Indeed, serum PTH levels decreased on Day 3 of the suspension. This decrease was associated with lower serum levels of 1,25-dihydroxyvitamin [correction of dihyroxyvitamin] D3 probably due to a decrease in the activity of 1 alpha-hydroxylase in the kidneys resulting from a decrease in PTH secretion. Since it is known that 1,25-dihydroxyvitamin D3 stimulates osteoblastic function, it is suggested that endocrine responses evoked by tail suspension aggravate disuse atrophy of the hind limbs.

Amino Acids↗
PubMed1996

[Radiologic-pathologic correlation between tumor edge and surrounding inherent structures in peripheral lung cancer].

PURPOSE: To evaluate the radiologic-pathologic relationship between the tumor edge of peripheral lung cancers and surrounding normal structures. MATERIALS AND METHODS: Tissue samples from 16 lung cancers with diameters less than 2 cm were examined: 7 adenocarcinomas, 5 squamous cell carcinomas, 2 small cell carcinomas, 1 large cell carcinoma, and 1 that had metastasized to the lung. Inflation-fixed lung specimens containing tumor tissue were sliced to a thickness of 2 mm: The tumor edge of each section was traced under a stereomicroscope and its relationship to marginal structure, including bronchi, pulmonary arteries, and pulmonary veins containing interlobular septa, was analyzed. The tumor edge and marginal structures were classified into four types: Type 1, clear margin formed by marginal structures; Type 2, tumor involving the marginal structures; Types 3 and 4, marginal structures penetrating the tumor with and without a notch, respectively. RESULTS: Type 1 was found in 23 of 47 pulmonary arteries (49%), 23 of 49 bronchi (47%), and 12 of 31 pulmonary veins or interlobular septa (39%). Type 2 was found in 11% (14/127), Type 3 in 15% (19/127) and Type 4 in 28% (36/127) of marginal structures. Type 1 was common in all histological types of carcinomas studied. CONCLUSION: In small peripheral lung cancers, the tumor edge sometimes has a clear margin formed by surrounding structures such as interlobular septa. This can make it difficult to differentiate benign from malignant lesions.

Adenocarcinoma↗
PubMed1996

[Comparison between high-resolution computed tomography and 99mTc-technegas SPECT pulmonary emphysema].

Scintigraphy with 99mTc-technegas was recently introduced for clinical imaging of lung ventilation. This method has been found to be useful in emergencies, to be more suitable for single photon emission computed tomography (SPECT) than other agents used in ventilation scintigraphy, and could reveal abnormalities in ventilation more easily than high resolusion computed tomography (HRCT) in pulmonary emphysema. We compared 99mTc-technegas SPECT with HRCT in six regions: the right upper, middle, and lower lobes, the left upper lobe, the lingula, and the left lower lobe, in 15 patients with pulmonary emphysema. Patients with centrilobular emphysema tended to show stronger changes in upper lobes than in lower lobes on both 99mTc-technegas SPECT and HRCT. Some regions showed no change on HRCT but various changes on 99mTc-SPECT. Patients with panlobular emphysema showed severe changes on 99mTc-SPECT in lower lung fields in which well-demarcated areas of low attenuation were not seen on HRCT. We conclude that 99mTc-SPECT is useful for detecting early changes and panlobular changes in pulmonary emphysema.

Adult↗
PubMed1996

Antioxidants inhibit tumor necrosis factor-alpha mediated stimulation of interleukin-8, monocyte chemoattractant protein-1, and collagenase expression in cultured human synovial cells.

OBJECTIVE: To study whether the induction of mRNA for interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and collagenase by tumor necrosis factor-alpha (TNF-alpha) is suppressed by antioxidants in human synovial cells. TNF-alpha has been shown to exert some of its effects by stimulating production of reactive oxygen intermediates in some cell lines other than synovial cells. METHODS: Amounts of mRNA for IL-8, MCP-1, and collagenase were determined by Northern blot analysis. Electrophoretic mobility shift assays were performed for the detection of a transcription factor, nuclear factor-kappa B(NF-kappa B). The concentration of IL-8 in the medium was determined by ELISA. RESULTS: TNF-alpha increased the expression of IL-8, MCP-1, and collagenase mRNA in human synovial cells. NF-KB known to induce IL-8 gene transcription was also increased in nuclear extracts from the synovial cells treated with TNF-alpha. Prior addition of antioxidant, N-acetyl-L-cysteine (NAC) or 2-oxothiazolidine-4-carboxylate (OTC), suppressed TNF-alpha stimulated expressions of IL-8, MCP-1, and collagenase mRNA in a dose dependent manner. Treatment with NAC also suppressed TNF-alpha induced increase in NF-kappa B. The changes of IL-8 in the medium reflected the mRNA levels. Hydrogen peroxide (H2O2) induced the expression of mRNA for the cytokines but not collagenase mRNA, and NAC suppressed the effect of H2O2. CONCLUSION: Our data suggest that TNF-alpha induces expression of proinflammatory cytokines such as IL-8 and MCP-1 through generation of reactive oxygen intermediates and subsequent activation of NF-kappa B in human synovial cells, and the antioxidants may inhibit, at least in part, the activation of NF-kappa B by TNF-alpha. These results indicate that antioxidants such as NAC may be useful in treating rheumatoid arthritis.

Acetylcysteine↗