Assessment of the diagnostic value of head-up tilt testing in the evaluation of syncope in hypertrophic cardiomyopathy.
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Adult↗
Biomedical subjects
H Seo
Publications and source records attributed to H Seo.
Anti-(glioma surface antigen) monoclonal antibody G-22 recognizes overexpressed CD44 in glioma cells.
We raised an anti-glioma monoclonal antibody, named G-22, that specifically recognizes a human glioma-associated surface antigen. Proven to be useful for target imaging of malignant gliomas after radioisotope labeling and cerebrospinal fluid diagnosis by enzyme-linked immunospecific assay, G-22 was found to immunoprecipitate an 85-kDa glycoprotein of the human glioma U-251MG cell. We purified this antigen by G-22-coupled cyanogenbromide-activated Sepharose affinity chromatography, and sequence analysis demonstrated that the 54 amino acid residues were identical to positions 55-108 of human CD44. The results show that the smallest spliced form (85 kDa) of CD44 is strongly expressed in glioma cells.
Amino Acid Sequence↗
Stimulation of interleukin-4 of cell proliferation and mRNA expression of alkaline phosphatase and collagen type I in human osteoblast-like cells of trabecular bone.
Interleukin-4 (IL-4) potently inhibits bone resorption by preventing the differentiation of osteoclast precursors to osteoclasts. To elucidate the role of IL-4 in bone formation, we studied the effects of human IL-4 on human osteoblast-like cells obtained from trabecular bone, which showed increased osteocalcin production in response to 1,25-(OH)2D3 in more than 10 passages. IL-4 stimulated the proliferation of osteoblast-like cells in a concentration-dependent manner, showing the minimal and maximal stimulatory effects at 10 pg/ml and 100-1000 pg/ml, respectively. IL-4 also stimulated the expression of alkaline phosphatase mRNA (1.7-fold) and the enzyme activity to the same extent at 10-100 pg/ml. Furthermore, IL-4 stimulated collagen type I mRNA expression in human osteoblast-like cells. The cytokine did not affect osteocalcin production in a short culture period (3 days). These in vitro findings suggest that IL-4, a bone-resorption-inhibitory cytokine produced by activated T cells in bone marrow, may exert an anabolic effect on osteoblast-like cells in trabecular bone through a paracrine mechanism.
Adult↗
Plasma interleukin 8 levels are increased by hemodialysis.
The effects of hemodialysis on plasma interleukin 8 (IL-8) levels and the expression of IL-8 mRNA in peripheral blood mononuclear cells (PBMC) were studied in uremic patients undergoing maintenance hemodialysis (HD) using regenerated cellulose dialyzers. The plasma IL-8 levels in the patients after HD sessions were significantly higher than before HD. Comparison of the IL-8 mRNA levels obtained from PBMC before and after HD indicated that the expression of IL-8 mRNA was increased by HD. The enhancement of production of IL-8 in PBMC during HD may be responsible for inflammatory complications and impaired host defense in HD patients.
Adult↗
Involvement of beta 2-microglobulin modified with advanced glycation end products in the pathogenesis of hemodialysis-associated amyloidosis. Induction of human monocyte chemotaxis and macrophage secretion of tumor necrosis factor-alpha and interleukin-1.
beta 2-Microglobulin (beta 2M) is a major constituent of amyloid fibrils in hemodialysis-associated amyloidosis (HAA), a complication of long-term hemodialysis. However, the pathological role of beta 2M in HAA remains to be determined. Recently, we demonstrated that beta 2M in the amyloid deposits of HAA is modified with advanced glycation end products (AGEs) of the Maillard reaction. Since AGEs have been implicated in tissue damage associated with diabetic complications and aging, we investigated the possible involvement of AGE-modified beta 2M (AGE-beta 2M) in the pathogenesis of HAA. AGE- and normal-beta 2M were purified from urine of long-term hemodialysis patients. AGE-beta 2M enhanced directed migration (chemotaxis) and random cell migration (chemokinesis) of human monocytes in a dose-dependent manner. However, normal-beta 2M did not enhance any migratory activity. AGE-beta 2M, but not normal-beta 2M, increased the secretion of TNF-alpha and IL-1 beta from macrophages. Similar effects were also induced by in vitro prepared AGE-beta 2M (normal-beta 2M incubated with glucose in vitro for 30 d). When TNF-alpha or IL-1 beta was added to cultured human synovial cells in an amount equivalent to that secreted from macrophages in the presence of AGE-beta 2M, a significant increase in the synthesis of collagenase and morphological changes in cell shape were observed. These findings suggested that AGE-beta 2M, a major component in amyloid deposits, participates in the pathogenesis of HAA as foci where monocyte/macrophage accumulate and initiate an inflammatory response that leads to bone/joint destruction.
Adult↗
Glucocorticoids potentiate the action of atrial natriuretic polypeptide in adrenalectomized rats.
Adrenal insufficiency in human and rat is associated with an impairment of the diuretic response to water load, and only glucorticoids (GCs) restore this deficit. Our observation that GCs potentiate atrial natriuretic polypeptide (ANP)-stimulated cGMP production in cultured renal cells prompted us to examine the possibility that GCs may restore the diuretic response through the potentiation of ANP action. Initially, changes in urine volume and ANP levels were studied in adrenalectomized (Adx) and sham-operated intact rats after an oral water load of 5 ml/100 g BW. Urine volume after water load was 4.5 +/- 0.5 ml/30 min in the intact rats, whereas it was 0.8 +/- 0.2 ml/30 min in the Adx rats. In the intact rats, a significant increase in plasma ANP level was observed 30 min after the water load, whereas no increase was observed in Adx rats. This defective ANP response may be involved in the impairment of the diuretic response in Adx rats. Indeed, pretreatment of Adx rats with dexamethasone (Dex, 20 micrograms/100 g BW) increased plasma ANP levels even before water load and improved diuretic response. Subsequently, effect of iv administration of human or rat ANP at a pharmacological dose (2.5 micrograms/100 g BW) on urine volume, osmolarity, and urinary excretion of cGMP, and sodium was studied in Adx rats that received an oral water load 30 min before ANP. Dex treatment was achieved by per os administration 3 h before the ANP injection. In Adx rats, the urine volume after ANP administration was 1.2 +/- 0.1 ml/30 min, and pretreatment with Dex markedly increased the urine volume to 6.3 +/- 0.4 ml/30 min. Dex also increased ANP-induced osmolar and sodium excretion by 2.6- and 2.9-fold, respectively. Although urinary excretion of cGMP was increased in Adx rats by ANP administration, a further significant increase was observed by the pretreatment with Dex. Injection of (Bu)2cGMP to Adx rats pretreated with Dex resulted in a significant increase in urine volume and osmolar and sodium excretion. However, no significant increase in urine volume was observed in Adx rats not pretreated with Dex. The present study suggests that GCs restore the diuretic response to acute water load not only by increasing the secretion of ANP but also by potentiating ANP-stimulated cGMP production. Furthermore, GCs may augment ANP action at one or more steps other than cGMP formation because administration of (Bu)2cGMP to Adx rats did not correct the diuretic response to water load.
Adrenalectomy↗
A truncated thyroxine-binding globulin due to a frameshift mutation is retained within the rough endoplasmic reticulum: a possible mechanism of complete thyroxine-binding globulin deficiency in Japanese.
We have previously reported six unrelated Japanese families having the same mutation in the TBG gene and manifesting complete TBG deficiency (TBG-CDJ). The deficiency consists of a single nucleotide deletion resulting in the production of C-terminal truncation due to a frameshift and premature termination. However, the reason for the failure to detect TBG in the serum of subjects harboring this mutation remains unknown. In this communication we investigated the mechanism of the TBG deficiency associated with TBG-CDJ. The complementary DNAs of TBG-CDJ and normal TBG (TBG-N) were expressed in COS-1 cells. Pulse-chase experiments revealed a complete absence of secretion of TBG-CDJ, whereas TBG-N was already present in the medium at time 0 and was almost entirely secreted by 3 h. In cell lysates, TBG-CDJ had a smaller molecular mass [52 kilodalton (kDa)] than TBG-N (54 kDa) and gradually decreased during the chase. Thus, failure of TBG-CDJ secretion accounts for the complete TBG deficiency. The molecular mass of TBG-CDJ (42 kDa) was also smaller than that of TBG-N (44 kDa) when synthesized in the presence of tunicamycin. These findings are consistent with the premature termination of the TBG-CDJ molecule deduced from the nucleotide sequence analysis. Intracellular TBG-N was resistant to endoglycosidase H but not TBG-CDJ, suggesting the retention of TBG-CDJ within the rough endoplasmic reticulum. Indeed, subcellular fractionation revealed that most of TBG-CDJ was located in the rough endoplasmic reticulum compartment, and TBG-N was distributed in the Golgi fractions. Our results suggested that the lack of intracellular transport of the truncated TBG molecule is the cause for the absence of immunoreactive TBG in the serum of subjects harboring the TBG-CDJ variant.
Animals↗
Impaired intracellular transport contributes to partial thyroxine-binding globulin deficiency in a Japanese family.
We have previously reported a Japanese family manifesting partial TBG deficiency (TBG-PDJ). This variant was characterized by a decreased level of serum TBG concentration, heat lability, and normal isoelectric focussing pattern, but the affinity to iodothyronine is unknown. The TBG-PDJ gene possesses a single nucleotide substitution replacing the normal Pro363(CCT) with Leu(CTT); however, the precise mechanism that results in the reduction of the TBG concentration in the serum of the subjects harboring this mutation remains unknown. This was investigated in the current communication by expressing the complementary DNAs of TBG-PDJ and the common type TBG (TBG-C) in COS-1 cells. Pulse-chase experiments revealed impaired secretion of TBG-PDJ. TBG-C secretion into the medium was evident during 60 min of the pulse period and was almost completed by 12 h. On the other hand, TBG-PDJ was secreted slowly and continued to accumulate between 12-24 h of the chase period. The molecular mass of TBG-PDJ in the cell lysate was identical to that of TBG-C when estimated by gel electrophoresis (54 kilodaltons). The content of TBG-PDJ in the cell lysate decreased less rapidly than that of TBG-C, indicating that impaired TBG-PDJ secretion accounts for the partial TBG deficiency. Oligosaccharide units of intracellular TBG-C were resistant to endoglycosidase-H, but half of those of TBG-PDJ were sensitive to the enzyme digestion, suggesting partial retention of TBG-PDJ within the rough endoplasmic reticulum. Northern blot analysis revealed abundant messenger ribonucleic acid for the glucose-regulated protein-78, the level of which was 3.54-fold greater in the cells transfected with TBG-PDJ than in nontransfected COS-1 cells, whereas that in TBG-C-transfected cells was same as that in the nontransfected cells. Increased expression of glucose-regulated protein-78 together with the sensitivity to endoglycosidase-H suggests impairment of intracellular processing of TBG-PDJ. Our results indicate that the impaired intracellular transport of the TBG-PDJ molecule is the main cause of the reduced concentration of immunoreactive TBG in the serum of subjects harboring this TBG variant.
Base Sequence↗
Diagnostic value of transient dilatation of the left ventricle in negative dipyridamole-thallium imaging.
To evaluate the diagnostic value of a transient dilatation of the left ventricle during dipyridamole-thallium imaging (DTI) for detecting significant coronary artery disease (CAD) in patients with negative DTI results, 81 consecutive patients were studied. Twenty one patients (26%) had CAD and 60 patients had normal coronary anatomy (NCA). The initial/delayed ratio of the left ventricular dimension, which was measured as the distance between the 2 peaks of a count profile curve on a 45 degrees left anterior oblique planar image, was defined as the dilatation ratio (DR) of the left ventricle. Patients with CAD had a higher incidence of chest pain after dipyridamole infusion (35 vs 13%; p < 0.05), and ST depression during exercise testing (50 vs 25%; p < 0.05) than those with NCA. DR was significantly greater in CAD patients than in NCA patients (1.08 +/- 0.10 vs 0.97 +/- 0.03; p < 0.0001). DR was considered abnormal (> 1.03) when it was greater than the mean +2 standard deviations of the DR in NCA patients. Seventy-six percent of CAD patients had an abnormal DR. A stepwise discriminant analysis revealed that an abnormal DR alone had the same ability to predict CAD (sensitivity 76%, specificity 98%, chi-square 80.9, p < 0.0001) as the best combination of abnormal DR, chest pain during exercise testing, age and gender (sensitivity 76%, specificity 98%, chi-square 98.5, p < 0.0001). When abnormal DR was excluded from this analysis, the best combination of the variables showed a reduced ability to predict CAD (sensitivity 81%, specificity 77%, Wilks' Lambda 0.71, chi-square 26.7, p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Octreotide treatment results in the inhibition of GH gene expression in the adenoma of the patients with acromegaly.
Seven patients with growth hormone (GH)-secreting pituitary adenoma were treated preoperatively with octreotide (Sandostatin or SMS 201-995; a somatostatin analogue), and were compared with 18 non-treated patients in their clinical courses and adenoma analyses. Octreotide treatment improved the endocrinological data in all 7 cases. The octreotide-treated adenomas were soft and easily removed by suction and curettage. The postoperative normalization of endocrinological data was encountered more often in the octreotide-treated cases than in the non-treated, although the statistical significance was not observed by the limited number of cases. The adenoma tissues were examined with conventional histology and immunohistochemistry, and the amount of GH messenger ribonucleic acid (mRNA) was quantitatively assessed. The studies demonstrated: 1) No fibrosis nor necrosis was observed in the adenomas from the octreotide-treated patients. 2) Immunohistochemistry for human GH revealed no remarkable differences between the octreotide-treated and the non-treated adenomas. 3) The amounts of GH mRNA in the adenoma from the octreotide-treated patients were 4.2 +/- 1.8 (mean +/- SEM; expressed in an arbitrary unit) and were significantly less than those from the non-treated (33.6 +/- 9.1). These data suggest that octreotide inhibits not only GH release from the adenoma but also its biosynthesis.
Acromegaly↗
Increase in Pit-1 mRNA is not required for the estrogen-induced expression of prolactin gene and lactotroph proliferation.
Estrogen has been shown to stimulate lactotroph proliferation and expression of the prolactin (PRL) gene. Recently it has been established that Pit-1, a pituitary-specific transcription factor, is required for lactotroph proliferation. Furthermore, in vitro studies showed that an increase in the PRL promoter activity caused by estrogen was dependent of the amount of cotransfected Pit-1-expressing plasmid. These findings led us to examine whether the induction of Pit-1 mRNA is required for the estrogen-increased PRL gene expression in the rat anterior pituitary in vivo. Short term estrogen treatment was achieved by means of a single intramuscular injection of estradiol dipropionate. DNA synthesis, the levels of PRL and Pit-1 messenger RNAs in the anterior pituitary were determined. Estradiol dipropionate resulted in a significant increase in DNA synthesis 24 h after administration and in PRL mRNA after 48 h. In contrast, the Pit-1 mRNA level was not altered. Since Pit-1 is expressed not only in lactotroph but also in somatotroph and thyrotroph, and the lactotroph cell population has been reported to be less than 10% in the pituitary, the change in the Pit-1 mRNA level in lactotrophs was not seen following only short term estrogen treatment. An increase in the lactotroph cell population was therefore achieved by chronic estrogen treatment (subcutaneous implantation of a silastic tube containing 17 beta-estradiol powder for 30 days). This treatment resulted in the marked proliferation of lactotrophs and a 3-fold increase in PRL mRNA. However, no alteration in Pit-1 mRNA was observed. These results suggest that the increase in Pit-1 mRNA is not required for the estrogen-induced lactotroph proliferation or PRL gene expression.
Animals↗
Adrenocortical response to tail-suspension in young and old rats.
We recently showed that increased glucocorticoid secretion aggravates disuse atrophy when induced by skeletal unloading. Disuse atrophy in the elderly is becoming a serious problem in many developed countries. In this study we attempted to examine how aging affects the glucocorticoid response to skeletal unloading. Three groups of rats (aged 5 weeks, 12 months and 18 months) were subjected to 7 days of hind limb unloading by tail-suspension. Urinary excretion of corticosterone over a 24-hr period were monitored every other day. Corticosterone excretion in the control group of 5-week-old rats was initially 87.4 +/- 12.8 ng/day and did not change throughout the experiment. Tail-suspension experiments yielded a significant increase (more than 3 fold) in excretion on days 1 and 3 of the suspension before returning to control levels. In the 12-month-old rats, a marked increase in the basal corticosterone level was observed in the control rats throughout the experiment, while the increase by tail-suspension was attenuated with a transient, significant increase on day 5. In 18-month-old rats, a further increase in the basal level was observed in the control group, although excretions tended to increase steadily from day 1 to day 3 and remained high until day 7. Urinary excretion of corticosterone among the 18-month-old suspension group was similar to those observed in the control group. These results indicate that the younger (5-week-old) rats adapted the stress load caused either by tail-suspension or manipulation alone faster than the older rats did (12 or 18 months old). The observation that basal corticosterone excretion increases with age suggests, alterations in the hypothalamic-pituitary-adrenal axis among the aged rats which might aggravates disuse atrophy induced by skeletal unloading.
Adaptation, Physiological↗
Changes in serum 1,25-dihydroxyvitamin D3 and mRNAs for osteocalcin and alkaline phosphatase in femur unloaded by tail suspension in rats.
To elucidate the mechanism involved in the development of disuse atrophy of bone by skeletal unloading, changes in osteocalcin and alkaline phosphatase mRNAs, markers for bone formation, were studied in the hind limb bones of tail-suspended rats. Tail suspension for 8 and 14 days resulted in a significant decrease in osteocalcin mRNA in the femur when compared with age-matched non-suspended controls. Serum 1,25-dihydroxyvitamin D3 decreased to 60% of the control level after 8 days of skeletal unloading but regained almost normal levels over the next 7 days. Since it is known that vitamin D3 up regulates and glucocorticoid down regulates transcription of the osteocalcin gene, the endocrine response evoked by tail suspension may have aggravated the disuse atrophy caused by skeletal unloading in this study.
Alkaline Phosphatase↗
[A comparative study on fine structure of the glomerular changes of kidney in pure toxemia of pregnancy and superimposed toxemia of pregnancy].
It is known that changes occur in the renal glomerulus in toxemia of pregnancy, but what are extremely rate are the reports on a comparative study of the difference between the pure toxemia of pregnancy (called the pure type) and the superimposed toxemia of pregnancy (called the superimposed type). I have therefore clarified the difference between the morbidities by making observations of the two types mainly by transmission electron microscopy (TEM). The subjects were 19 cases of the pure type and 6 cases of the superimposed type, and light microscopic (LM) and TEM observations were made both after informed consent by performing a needle biopsy in the right kidney at cesarean section. By TEM observation, comparisons were made by giving 0-3 points for the findings in the endothelial cells epithelial cells, mesangium and basement membrane. By LM, the changes in the renal glomeruli in the pure type were classified roughly into the extracapillary type, endocapillary type and capillary type, but what was seen in many cases was a mixture of these changes. Regarding the morbidities in the superimposed type cases, my attention was attracted to adhesion with Bowman's capsule and a sclerotic image. In TEM observations, greater changes in the mesangium and basement membrane were seen in the superimposed type cases than in the pure type cases, compared with the changes in endothelial cells and epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effects of interleukins on EGF-stimulated growth promotion in human thyroid cells: differential modifications by IL-2 and IL-6 in Graves' and normal thyroid cells.
To investigate the role of interleukins on the growth of human thyroid cells, the effect of IL-2, IL-4 and IL-6 was studied on EGF-induced [3H]-thymidine uptake, cell cycle by flow cytometry, and mRNA levels of cellular proto-oncogene c-fos in thyroid monolayer cells from eighteen patients with Graves' disease and sixteen with non-thyroidal disease. EGF stimulated the DNA synthesis and the expression of c-fos mRNA both in Graves' thyroid cells and in normal thyroid cells. A dose-dependent inhibition of Graves' thyroid cell growth was observed with increasing concentration of IL-2 regardless of coculture with EGF. IL-2 did not influence [3H]-thymidine uptake nor the percentage of S+G2/M phase in cell cycle in normal thyroid cells. Such effects were not modified by the elimination or addition of lymphocytes. IL-2 did not affect the EGF-induced expression of c-fos mRNA in both Graves' and normal thyroid cells. IL-6 (10(-2)-10 ng/ml) stimulated the [3H]-thymidine uptake up to 218-303 % of control level, and the percentage of cells in S+G2/M phase was increased in IL-6-treated normal thyroid cells as compared to EGF-treated cells. IL-6 did not augment these parameters in Graves' thyroid cells. When EGF was included with IL-6, the level in c-fos mRNA was further augmented in normal thyroid cells. Such an additive effect was not seen in Graves' thyroid cells. Incubation of Graves' or normal thyroid cells with IL-4 did not affect the [3H]-thymidine uptake nor the percentage of S+G2/M. These data suggest that, compared with normal cells, the growth factors (such as cytokines), may act in an opposite way in Graves' thyroid cells. The different behavior between Graves' and normal thyroid cells in response to IL-2 and IL-6 might contribute to the pathogenesis of goiter formation.
Cell Cycle↗
[anorexia nervosa; an association with certain types of soft tissue emphysema].
A 17-year-old female with anorexia nervosa developed pneumomediastinum, subcutaneous emphysema, retroperitoneal emphysema, interstitial pulmonary emphysema and epidural emphysema (epidural emphysema; air between the dura mater and the vertebral arch). She had no history of bronchial asthma. The mechanism was presumed to be weakness of the alveolar wall due to malnutrition, leading to rupture of alveoli, followed by air entering the interstitium and dissecting along perivascular sheaths (interstitial pulmonary emphysema) into the mediastinum. A further increase in mediastinal pressure may bring about opening of the fascial planes along great vessels and allow air to penetrate into subcutaneous tissues and the spinal canal. These types of emphysema have been reported in bronchial asthma cases and in those on positive pressure breathing. To our knowledge, there are no previous reports of anorexia nervosa associated with these phenomena.
Adolescent↗
Migraine equivalent and hemorrhagic infarction.
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Aged↗
[Estimation of malignancy using SPECT with 201Tl chloride in astrocytic tumors].
This study was designated to estimate the usefulness of SPECT with 201Tl chloride (Tl-SPECT) for the determination of the malignancy in astrocytic tumors. The subjects consisted of 39 astrocytic tumors in supra-tentorial regions. Tl-SPECT undertaken ten minutes to obtain an early image and four hours to obtain a delayed image, after intravenous injection of 74MBq 201Tl chloride (Tl). Tl index (L/N) was defined as the RI count ratio in the tumor lesion (L) to that in the normal parenchyma (N). Histological classification was determined by the WHO grading, and the results showed one case at Grade I, 11 cases at Grade II, 23 cases at Grade III and 4 cases at Grade IV. The proliferating activity was determined by the labeling index using the monoclonal antibody of proliferating cell nuclear antigen (PCNA). In both of the early and delayed images, Tl index was significantly higher (p < 0.01) in high grade astrocytomas compared with low grade tumors. There was a close correlation between the Tl index and the proliferating activity. The relationship between the Tl index and prognosis indicated that the high Tl index was corresponded to the poor prognosis. These results showed that the Tl index is useful to determine the malignancy of astrocytic tumors.
Adolescent↗