243 results on '"Seiichiro Tarui"'
Search Results
2. Type VII Glycogenosis (Muscle and Erythrocyte Phosphofructokinase Deficiency)
- Author
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Yuji Ikura, Masamichi Kuwajima, Seiichiro Tarui, and Norio Kono
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Phosphofructokinase deficiency ,medicine.medical_specialty ,Endocrinology ,Biochemistry ,business.industry ,Internal medicine ,medicine ,business ,medicine.disease - Published
- 2015
3. Serum Level of �-N-Acetylglucosaminidase and �2-Microglobulin in Diabetic Nephropathy
- Author
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Hisako Fushimi, Kyohei Nonaka, and Seiichiro Tarui
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Diabetic nephropathy ,Diabetic microangiopathy ,medicine.medical_specialty ,Endocrinology ,business.industry ,Beta-2 microglobulin ,Internal medicine ,N acetylglucosaminidase ,Medicine ,business ,medicine.disease - Published
- 2015
4. Clinical efficacy of fluvastatin for hyperlipidemia in Japanese patients
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Motoo Tsushima, Sho Yoshida, Kiyoshi Kurokawa, Toru Kita, Yoshiya Hata, Hiroshi Mabuchi, Goro Kajiyama, Yuji Matsuzawa, Nobuhiro Yamada, Tamio Teramoto, Noriaki Nakaya, Akira Yamamoto, Yuichiro Goto, Tadao Ishioka, Seiichiro Tarui, Kikuo Arakawa, Fumimaro Takaku, Hiroshige Itakura, Haruo Nakamura, Fumio Kuzuya, and Yasushi Saito
- Subjects
medicine.medical_specialty ,Indoles ,Dose ,Hypercholesterolemia ,Familial hypercholesterolemia ,Gastroenterology ,Fatty Acids, Monounsaturated ,Hyperlipoproteinemia Type II ,Placebos ,Apolipoproteins E ,Japan ,Internal medicine ,Hyperlipidemia ,medicine ,Humans ,In patient ,Longitudinal Studies ,Dosing ,Clinical efficacy ,Fluvastatin ,Adverse effect ,Apolipoproteins A ,Triglycerides ,Apolipoproteins B ,business.industry ,Anticholesteremic Agents ,Cholesterol, HDL ,Cholesterol, LDL ,Middle Aged ,medicine.disease ,Cholesterol ,Endocrinology ,Cardiology ,Hydroxymethylglutaryl CoA Reductases ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,Safety ,Cardiology and Cardiovascular Medicine ,business ,medicine.drug - Abstract
The objective of the study was to evaluate theefficacy and safety of fluvastatin in patients with hypercholesterolemia, including heterozygous familial hypercholesterolemia, in a 1-year study (a 12-week open assessment, followed by 40 weeks of active treatment). Of the 337 patients enrolled in the study, the effects of fluvastatin were analyzed in 296 patients at baseline and at 12 weeks. Of these, 265 were receiving 20 mg/day fluvastatin at week 12 and in 20 patients the dose had been increased to 30 mg/day; 11 patients violated the dosing protocol. A total of 229 patients continued into the 40-week, long-term phase, and 212 patients were analyzed at baseline and after 24 and 52 weeks. At the end of treatment, 153 evaluable patients were still taking 20 mg/day fluvastatin, 1 was taking 10 mg/day, and 48 patients were taking 30 mg/day, and 10 were taking 40 mg/day. In the 20 mg/day fluvastatin group, low density lipoprotein cholesterol (LDL-C) levels decreased by 24.1 % at week 12 and by 29.3% at week 52. In those patients requiring the higher doses, the corresponding reductions in LDL-C were 20.2% (week 12) and 26.7% (week 52). Total cholesterol was also reduced at week 12 by 17.0% (20 mg/day) and 15.7% (20–30 mg/ day), and at week 52 by 20.4% (≤20 mg/day) and 19.2% (≥30 mg/day). Throughout the study, fluvastatin was generally well tolerated and no serious clinical adverse events were observed. In conclusion, long-term treatment of hypercholesterolemia with fluvastatin at dosages of 20–40 mg daily can be considered both safe and effective.
- Published
- 1995
5. Myogenic hyperuricemia: What can we learn from metabolic myopathies?
- Author
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Seiichiro Tarui and Ikuo Mineo
- Subjects
Adult ,Male ,Purine ,medicine.medical_specialty ,Physiology ,Biology ,AMP Deaminase ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Adenosine Triphosphate ,Muscular Diseases ,Physiology (medical) ,Internal medicine ,medicine ,Humans ,Glycogen storage disease ,Glycolysis ,Hyperuricemia ,Myopathy ,Exercise ,Glycogen ,AMP deaminase ,Glycogen Storage Disease ,medicine.disease ,Uric Acid ,Adenosine Diphosphate ,Endocrinology ,Genes ,chemistry ,Biochemistry ,Uric acid ,Neurology (clinical) ,medicine.symptom ,Energy Metabolism - Abstract
The association of muscle glycogenosis with hyperuricemia led to the identification of a unique purine disorder. Myogenic hyperuricemia is ascribed to excessive degradation of muscle purine nucleotides, secondary to impaired ATP generation. Although this pathophysiological condition has been observed not only in glycolytic defects but also in mitochondrial diseases affecting lipid and carbohydrate oxidation, it is most common and prominent in muscle phosphofructokinase deficiency, in which neither glycogen nor glucose can be used as metabolic fuels. The first key reaction of muscle purine degradation is catalysis by AMP deaminase. Numerous studies have indicated that AMP deaminase may play an important role in energy metabolism in contracting muscle. Arguments against this hypothesis have emerged through analyses on muscle AMP deaminase deficiency. According to a recent study, the mutant allele is extremely frequent among Caucasians and African-Americans, suggesting that many individuals with this enzyme defect may be clinically asymptomatic. Further study is required to explain the significance of muscle purine degradation in energy metabolism.
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- 1995
6. A new variant case of muscle phosphofructokinase deficiency, coexisting with gastric ulcer, gouty arthritis, and increased hemolysis
- Author
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Misako Kaido, Ikuo Mineo, Seiichiro Tarui, Tomoya Hamaguchi, Takao Shimizu, Harutoshi Fujimura, Chisa Nakagawa, and Hiromu Nakajima
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Adult ,Male ,medicine.medical_specialty ,Physiology ,Phosphofructokinase-1 ,Arthritis ,Physical exercise ,Hemolysis ,Cellular and Molecular Neuroscience ,Muscular Diseases ,Physiology (medical) ,Internal medicine ,medicine ,Humans ,Glycolysis ,Stomach Ulcer ,Hyperuricemia ,Myopathy ,Exercise ,Glycogen Storage Disease Type VII ,Arthritis, Gouty ,business.industry ,Myoglobinuria ,medicine.disease ,Gout ,Endocrinology ,Mutation ,Neurology (clinical) ,medicine.symptom ,business ,Phosphofructokinase - Abstract
Muscle phosphofructokinase (PFK) deficiency includes both clinically and genetically heterogeneous conditions. A 22-year-old man with muscle PFK deficiency due to previously unrecognized mutation was admitted because of gastric ulcer. He had noticed mild fatigability on vigorous exercise, but had never experienced painful cramps and myoglobinuria. His history included five time relapses of gastric ulcer and gouty arthritis at ages 19 and 21 years. His laboratory data showing impaired muscle glycolysis, increased hemolysis, and myogenic hyperuricemia had aspects in common with those reported for the classic form of this disease, except that lactate concentrations in his blood increased considerably after exercise. The mutant PFK enzyme of this patient, who was demonstrated to have a missense mutation, could exert some catalytic activity that permitted glycolytic flux in vivo, thus leading to the absence of typical myopathic symptoms. The association of relapsing gastric ulcer with muscle PFK deficiency was detected for the first time. There is a possibility that oxygen radical-induced tissue damage resulting from increased hypoxanthine on exertion plays a role in the pathogenesis of ulceration, since the patient is more tolerant to exercise than reported cases with the classic form of muscle PFK deficiency © 1995 John Wilev & Sons. Inc.
- Published
- 1995
7. Impaired ketogenesis in patients with adult-type citrullinemia
- Author
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Yuichi Maeda, Kazuto Fukuda, Masamichi Kuwajima, Takumi Igura, Seiichiro Tarui, Sumio Kawata, Yoshiaki Inui, Yuji Matsuzawa, and Norio Kono
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Adult ,Male ,medicine.medical_specialty ,Ketone Bodies ,Urine ,Fatty Acids, Nonesterified ,chemistry.chemical_compound ,Internal medicine ,Ketogenesis ,medicine ,Citrulline ,Humans ,Triglycerides ,chemistry.chemical_classification ,Hepatology ,Triglyceride ,business.industry ,Citrullinemia ,Osmolar Concentration ,Fatty liver ,Gastroenterology ,Fatty acid ,Fasting ,Lipid Metabolism ,medicine.disease ,Circadian Rhythm ,Endocrinology ,Liver ,chemistry ,Ketone bodies ,Female ,business - Abstract
Background/Aims: To clarify the mechanism causing fatty liver in adult-type citrullinemia, the effect of fasting on blood levels of free fatty acids, triglycerides, and ketone bodies was investigated in two cases. Methods: Blood and urine samples were collected from two patients and healthy volunteers 12, 15, 17, 21.5, and 24 hours after their last meal. Results: During 24-hour fasting free fatty acid concentrations increased in both cases to the concentrations found in the healthy volunteers. The levels of blood ketone bodies (β-hydoxybutyrate and acetoacetate) were markedly suppressed throughout the fasting test without any increase in urinary excretion of ketone bodies or organic acids in both cases when plasma citrulline concentrations were more than 10-fold higher than in controls. Serum triglyceride concentrations in case 1 paradoxically increased from 185 mg/dL to 294 mg/dL during 24-hour fasting when the citrulline concentration was extremely high. When hemodialysis was performed and plasma citrulline consequently decreased to near the normal level in case 1, levels of both serum triglycerides and blood ketone bodies responded normally to 24-hour fasting. Conclusions: These data suggest that ketogenesis was impaired in adult-type citrullinemia.
- Published
- 1994
8. Contribution of visceral fat accumulation to the development of coronary artery disease in non-obese men
- Author
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A. H. M. Waliul Islam, Yuji Matsuzawa, Tadashi Nakamura, Y Keno, Yoshiyuki Nagai, Shigenori Fujioka, Seiichiro Tarui, S Yoshida, Katsuto Tokunaga, Iichiro Shimomura, T Kobatake, Kazuaki Kotani, and Makoto Nishida
- Subjects
Blood Glucose ,Male ,medicine.medical_specialty ,genetic structures ,medicine.medical_treatment ,Coronary Disease ,Gastroenterology ,Body Mass Index ,Coronary artery disease ,Insulin resistance ,Risk Factors ,Internal medicine ,Hyperlipidemia ,medicine ,Humans ,Risk factor ,Glucose tolerance test ,medicine.diagnostic_test ,business.industry ,Insulin ,Glucose Tolerance Test ,Middle Aged ,medicine.disease ,Lipids ,Obesity ,Viscera ,Endocrinology ,Adipose Tissue ,Cardiology and Cardiovascular Medicine ,business ,Body mass index - Abstract
Associations between intra-abdominal visceral fat accumulations and coronary risk factors were studied in a sample of 29 non-obese men aged 57 ± 10 years with coronary artery disease (CAD). Their body mass indexes (BMI) were 23.8 ± 1.5 (range 18.7–26.3). The visceral fat area (VFA) and the subcutaneous fat area (SFA) were measured at the level of the umbilicus by computed tomography. In patients with CAD, the average VFA was significantly increased compared with that in 54 control subjects without CAD, matched for sex, age, and BMI (117.2 ± 53.1 vs. 93.8 ± 38.6 cm2, P < 0.05). However, their average SFA was not statistically different (111.2 ± 33.3 vs. 106.3 ± 35.7 cm2, N.S.). Eleven CAD patients (38%) and nine control subjects (17%) had greater than 2S. D. higher than the mean VFA obtained from 22 healthy subjects extracted from the control subjects. Accordingly, the proportion of the subjects with high VFA was significantly higher in the CAD group. This group also had significantly higher levels of plasma glucose and insulin areas than controls determined by oral glucose tolerance tests. This may be due to insulin resistance. The proportion of the subjects with multiple risk factors including hyperlipidemia, hyperglycemia, and hypertension was significantly higher in the CAD patients with high VFA compared with the control subjects with normal VFA (CAD with high VFA 82% and control with normal VFA 33%). These findings suggest that visceral fat accumulations may play an important role in the occurrence of CAD regardless of obesity. Accordingly, we propose the term ‘visceral fat syndrome’, which encompasses visceral fat accumulation, glucose intolerance, hyperlipidemia, and hypertension. Patients with this syndrome have increased susceptibility to coronary sclerosis from these risk factors based on visceral fat accumulation.
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- 1994
9. Nephrosialidosis: ultrastructural and lectin histochemical study
- Author
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Masako Taniike, S. Okada, Koji Inui, Harutoshi Fujimura, Hiroo Yoshikawa, Takehiko Yanagihara, Seiichiro Tarui, Shiro Yorifuji, and Keiko Toyooka
- Subjects
Male ,Peanut agglutinin ,medicine.medical_specialty ,Cerebellum ,Pathology ,Central nervous system ,Neuraminidase ,Kidney ,Pathology and Forensic Medicine ,Cellular and Molecular Neuroscience ,Mucolipidoses ,Lectins ,Internal medicine ,Peripheral Nervous System ,Basal ganglia ,medicine ,Humans ,Neurons ,biology ,Histocytochemistry ,Brain ,Infant ,medicine.disease ,Wheat germ agglutinin ,Microscopy, Electron ,medicine.anatomical_structure ,Endocrinology ,nervous system ,Cerebral cortex ,Peripheral nervous system ,biology.protein ,Neurology (clinical) ,Lysosomes ,Galactosialidosis - Abstract
The neuropathological findings in a Japanese male with nephrosialidosis are reported. Clinically, coarse face, psychomotor retardation, macular cherry-red spot and proteinuria were noted at 1 year and 7 months. He was diagnosed to have nephrosialidosis on the basis of a deficiency of alpha-neuraminidase activity in both lymphocytes and cultured skin fibroblasts, and of severe glomerular and tubular involvement on renal biopsy. He died of multiple organ failure at 8 years and 6 months. There were numerous vacuoles and storage materials in visceral organs, particularly in the glomerular and tubular epithelial cells of the kidney and Kupffer cells as well as hepatocytes in the liver. Neuropathological examination revealed severe neuronal storage in the selected part of the central nervous system: lower motor neurons of the brain stem and spinal anterior horn cells, as well as neurons in the basal nucleus of Meynert. In the peripheral nervous system, sympathetic ganglia were severely affected. There was little or no neuronal storage in the basal ganglia, cerebral cortex or cerebellum, and demyelination was not found. Electron microscopic examination showed fine wavy multilamellar structures in the spinal anterior horn cells or Zebra body-like structures in the neurons of the Meynert's basal nucleus. Lectin histochemistry was positive for wheat germ agglutinin, Ricinus communis agglutinin-1 and peanut agglutinin within distended neurons. We conclude that the neuropathological feature in nephrosialidosis is not specific except for the selectiveness of the anatomical sites of involvement. It shares some aspects found in other types of sialidosis or galactosialidosis.
- Published
- 1993
10. Clinical evaluation of biosynthetic glucagon treatment for recovery from hypoglycemia developed in diabetic patients
- Author
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Mitsuyoshi Namba, Toshiaki Hanafusa, Norio Kono, Seiichiro Tarui, N. Horiuchi, K. Hasegawa, H. Fushimi, Y. Yamada, Y. Minami, G. Okuno, F. Kawakami, A. Ohki, S. Sumi, S. Noda, H. Toyoshima, K. Kuroda, and Y. Fukumoto
- Subjects
Chemotherapy ,medicine.medical_specialty ,business.industry ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Insulin ,General Medicine ,Hypoglycemia ,medicine.disease ,Glucagon ,law.invention ,Endocrinology ,law ,Diabetes mellitus ,Internal medicine ,Internal Medicine ,medicine ,Recombinant DNA ,Complication ,business ,Adverse effect - Abstract
Biosynthetic glucagon (GL-G) produced by recombinant DNA technology with transformed yeast strains is already available for clinical use. We studied the effects of 1 mg GL-G injection on plasma glucose level and hypoglycemic symptoms in 38 diabetic patients treated with insulin or oral hypoglycemic agents during spontaneous hypoglycemic episodes. In both intramuscularly and intravenously administered GL-G groups, plasma glucose significantly increased from 58.1 +/- 11.4 to 113.2 +/- 6.9 mg/dl (i.m., n = 17, P < 0.01) and from 76.4 +/- 4.4 to 125.7 +/- 5.9 mg/dl (i.v., n = 15, P < 0.01), respectively 20 min after the administration and the symptoms due to hypoglycemia subsided promptly after the injection of GL-G in 27 cases. The hyperglycemic effect of intramuscularly injected GL-G was more potent and long-standing than when intravenously injected, particularly in insulin-dependent diabetic (IDDM) patients. Neither significant changes of antibody levels against yeast proteins nor serious adverse effects were observed after GL-G administration. Biosynthetic glucagon is safe and useful for the treatment of hypoglycemia developing in diabetic patients.
- Published
- 1993
11. Glycogenosis Type V (McArdle’s Disease) with Hyperuricemia
- Author
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Y Yamamoto, M Tsutsumi, Yuya Yamada, Kenji Jinnai, N. Kono, S Ohno, F Kanda, Takuo Fujita, Masanori Kawachi, and Seiichiro Tarui
- Subjects
Purine ,medicine.medical_specialty ,business.industry ,nutritional and metabolic diseases ,Physical exercise ,Xanthine ,medicine.disease ,chemistry.chemical_compound ,Endocrinology ,Neurology ,chemistry ,Internal medicine ,medicine ,Uric acid ,Aerobic exercise ,Neurology (clinical) ,Hyperuricemia ,Inosine ,business ,Hypoxanthine ,medicine.drug - Abstract
A 28-year-old male with glycogenosis type V associated with continuous hyperuricemia during mild daily activities is reported. An aerobic exercise test using a bicycle ergometer revealed that purine metabolites, i.e., ammonia, inosine, hypoxanthine and xanthine, were transiently increased by the exercise and that a subsequent increment in uric acid continued until the following day. The accelerated purine degradation by the muscle exercise was thus shown to be able to cause the overt hyperuricemia in a patient with glycogenosis type V. Therapeutic use of fructose for glycogenosis was disappointing due to fructose-induced hyperuricemia. A search for myogenic hyperuricemia is essential for therapeutic trials.
- Published
- 1993
12. Visceral fat type obesity
- Author
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Seiichiro Tarui
- Subjects
medicine.medical_specialty ,Endocrinology ,business.industry ,Internal medicine ,medicine ,General Medicine ,medicine.disease ,business ,Obesity ,Visceral fat - Published
- 1993
13. Polydisperse low-density lipoproteins in hyperalphalipoproteinemic chronic alcohol drinkers in association with marked reduction of cholesteryl ester transfer protein activity
- Author
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Masaharu Kubo, Shuichi Nozaki, Ken-ichi Hirano, Tohru Funahashi, Yuji Matsuzawa, Naohiko Sakai, Hisatoyo Hiraoka, Seiichiro Tarui, and Shizuya Yamashita
- Subjects
Adult ,Male ,Hyperlipoproteinemias ,medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,Alcohol ,chemistry.chemical_compound ,Endocrinology ,Internal medicine ,Mole ,Cholesterylester transfer protein ,medicine ,Humans ,Aged ,Glycoproteins ,Ethanol ,biology ,Cholesterol ,Cholesterol, HDL ,Metabolism ,Middle Aged ,Cholesterol Ester Transfer Proteins ,Lipoproteins, LDL ,Alcoholism ,Apolipoproteins ,chemistry ,Toxicity ,biology.protein ,Electrophoresis, Polyacrylamide Gel ,lipids (amino acids, peptides, and proteins) ,Carrier Proteins ,Lipoproteins, HDL ,Lipoprotein - Abstract
Long-term heavy alcohol intake is well known to increase serum high-density lipoprotein (HDL) cholesterol concentrations. Epidemiologic studies have shown that the protective effect of alcohol intake against coronary heart disease (CHD) is observed in moderate alcohol drinkers, but not in heavy ones. To clarify whether heavy alcohol intake may cause abnormalities in lipoprotein metabolism, we analyzed the plasma lipoproteins in eight male chronic heavy alcohol drinkers with marked hyperalphalipoproteinemia. Although their serum HDL cholesterol levels were remarkably high, ranging from 2.67 to 3.58 mmol/L, three patients had CHD and corneal arcus was present in seven patients. Cholesteryl ester transfer protein (CETP) activity was reduced in all subjects (7.3% +/- 4.2%/10 microL/18 h in alcohol drinkers v 20.5% +/- 2.4%/10 microL/18 h in control; mean +/- SD, P < .001). The CETP mass levels were also markedly reduced in these subjects. The analysis of low-density lipoprotein (LDL) on nondenaturing polyacrylamide gradient gel electrophoresis revealed that four subjects with severely low CETP activity (< 25% of control) had polydisperse LDLs, similar to those observed in genetic CETP deficiency. The other four subjects with approximately half the normal CETP activity had homogeneous but smaller-sized LDLs, as compared with control subjects. Particle size of HDL was larger than that of normal control HDL in all subjects. After cessation of alcohol intake, plasma HDL cholesterol levels were decreased and LDLs became more homogeneous and normal in size, in parallel with elevation of CETP activity.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1992
14. Retrovirus gag protein p30 in the islets of non-obese diabetic mice: relevance for pathogenesis of diabetes mellitus
- Author
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Seiichiro Tarui, Akira Hakura, Jun-ichiro Miyagawa, K. Yamamoto, M. Yutsudo, N. Kono, Toshiaki Hanafusa, Koji Tomita, Chisa Nakagawa, and Hiromu Nakajima
- Subjects
medicine.medical_specialty ,viruses ,Endocrinology, Diabetes and Metabolism ,Blotting, Western ,Gene Products, gag ,Biology ,Endoplasmic Reticulum ,medicine.disease_cause ,Autoimmunity ,Islets of Langerhans ,Mice ,Western blot ,Mice, Inbred NOD ,Diabetes mellitus ,Internal medicine ,Internal Medicine ,medicine ,Animals ,Cyclophosphamide ,medicine.diagnostic_test ,Pancreatic islets ,Group-specific antigen ,medicine.disease ,Diabetes Mellitus, Type 1 ,Retroviridae ,Endocrinology ,medicine.anatomical_structure ,biology.protein ,Beta cell ,Antibody ,Insulitis - Abstract
We investigated the presence of retroviral protein in the pancreatic islets of non-obese diabetic mice to prove that the virus-like particle observed specifically in the pancreatic Beta cell of these mice was retrovirus. Western blot analysis probed with anti-retrovirus antibody demonstrated the existence of retroviral gag (group specific antigen) protein p30 in the islets of female non-obese diabetic mice. Islets of non-obese diabetic mice which were treated with cyclophosphamide, known to accelerate the development of insulitis and diabetes mellitus, have shown both a significantly increased number of retrovirus-like particles (type C) and enhanced expression of gag protein p30, compared to those of mice not treated with cyclophosphamide. These results confirmed the presence of type C retrovirus in non-obese diabetic mouse Beta cells and suggest a role for retrovirus in the development of insulitis and diabetes in these mice.
- Published
- 1992
15. Transthyretin (prealbumin) in the pancreas and sera of newly diagnosed type I (insulin-dependent) diabetic patients
- Author
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Masami Inada, Toshiaki Hanafusa, N. Kono, Jun-ichiro Miyagawa, Seiichiro Tarui, Sumio Kawata, Shinji Tamura, and Naoto Itoh
- Subjects
Adult ,Male ,endocrine system ,medicine.medical_specialty ,Biopsy ,T-Lymphocytes ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Clinical Biochemistry ,Fluorescent Antibody Technique ,Biochemistry ,Glucagon ,Immunoenzyme Techniques ,Islets of Langerhans ,Endocrinology ,Internal medicine ,Diabetes mellitus ,Blood plasma ,medicine ,Humans ,Prealbumin ,Pancreas ,Autoantibodies ,Delta cell ,biology ,business.industry ,Insulin ,Histocompatibility Antigens Class I ,Biochemistry (medical) ,Histocompatibility Antigens Class II ,nutritional and metabolic diseases ,medicine.disease ,Transthyretin ,Diabetes Mellitus, Type 1 ,medicine.anatomical_structure ,biology.protein ,Immunohistochemistry ,Female ,business - Abstract
We investigated transthyretin (TTR) in the pancreases and sera of 10 newly diagnosed type I diabetic patients by immunohistochemistry and nephelometry. In the type I diabetic pancreases, glucagon-positive A-cells showed strong immunoreactivity for TTR, the intensity and distribution pattern of which corresponded to those in normal subjects. Morphometric analysis revealed that the amount of strongly TTR-positive A-cells was not significantly different from that in normal subjects. On the contrary, insulin-positive B-cells, which normally show uneven and weak TTR immunoreactivity, decreased in number, and only a few residual B-cells showed faint immunoreactivity. Neither somatostatin cells nor pancreatic polypeptide cells were positive for TTR. The serum TTR concentration showed a significant decrease in type I diabetic patients compared with that in normal subjects (P less than 0.005). These data suggest that the synthesis or storage of TTR in A-cells is not affected, but that in B-cells is impaired in type I diabetes. The decrease in serum TTR might be one of the features of metabolic disorders in type I diabetes.
- Published
- 1992
16. Function of DR-positive thyrocytes from patients with Graves' disease: quantitative analysis of thyroid peroxidase content by fluorescent photometry
- Author
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Toshiaki Hanafusa, Kanji Kuma, Hideki Asakawa, N. Kono, and Seiichiro Tarui
- Subjects
Adult ,Male ,endocrine system ,medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,Graves' disease ,Clinical Biochemistry ,Thyroid Gland ,Fluorescent Antibody Technique ,Immunofluorescence ,Iodide Peroxidase ,Biochemistry ,Autoimmune thyroiditis ,Endocrinology ,Antigen ,Thyroid peroxidase ,Internal medicine ,medicine ,Humans ,Lymphocytes ,Thyroid Epithelial Cells ,medicine.diagnostic_test ,biology ,Chemistry ,Biochemistry (medical) ,Thyroid ,HLA-DR Antigens ,medicine.disease ,Immunohistochemistry ,Graves Disease ,medicine.anatomical_structure ,biology.protein ,Female ,Hormone - Abstract
A considerable number of thyrocytes in patients with autoimmune thyroiditis ectopically express HLA-DR antigen. Furthermore, it has been reported that interferon-gamma-induced DR-positive thyrocytes in vitro secrete less thyroid hormone in response to TSH stimulation compared with DR-negative ones. However, the function of the intrinsically DR-positive thyrocytes is unknown. To evaluate their function, we stained by immunofluorescence for both DR antigen and thyroid peroxidase (TPO) in thyroid epithelial cells from patients with Graves' disease. We also measured the quantity of DR antigen and TPO using fluorescent photometry. The content of TPO was not significantly reduced in DR-positive thyrocytes compared with that in DR-negative thyrocytes. The TPO content is one measure of thyrocyte function. There was no significant difference between DR-positive and DR-negative thyrocytes. In conclusion, the function of DR-positive thyrocytes in vivo was not suppressed compared with that of DR-negative thyrocytes.
- Published
- 1992
17. Mechanisms of corticosteroid action in immune thrombocytopenic purpura (ITP): experimental studies using ITP-prone mice, (NZW x BXSB) F1
- Author
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Takeshi Yonezawa, Hironori Take, S Ikehara, Yoshiyuki Kurata, Seiichiro Tarui, Hirokazu Kashiwagi, Takayasu Furubayashi, Shigenori Honda, Yasuharu Imai, and Hajime Mizutani
- Subjects
Blood Platelets ,Male ,medicine.medical_specialty ,Erythrocytes ,Cell Survival ,medicine.drug_class ,Prednisolone ,Immunology ,Spleen ,Receptors, Fc ,Biochemistry ,Immunoglobulin G ,Mice ,Phagocytosis ,Internal medicine ,Animals ,Medicine ,Platelet ,Receptor ,Autoantibodies ,Mice, Inbred BALB C ,Purpura, Thrombocytopenic, Idiopathic ,biology ,Platelet Count ,business.industry ,Macrophages ,Cell Biology ,Hematology ,Flow Cytometry ,medicine.disease ,Thrombocytopenic purpura ,Endocrinology ,medicine.anatomical_structure ,Liver ,biology.protein ,Corticosteroid ,Female ,Antibody ,business ,medicine.drug - Abstract
To determine the mechanism by which platelet counts increase after corticosteroid therapy for human immune thrombocytopenic purpura (ITP), we studied the platelet kinetics using prednisolone (PDN)-treated ITP- prone mice, (NZW x BXSB) F1 (W/B F1). An increase in platelet counts was observed in W/B F1 mice (n = 10, mean +/- SD, 1,202 +/- 202 x 10(3)/microL) 4 weeks after treatment with PDN (2 mg/kg/d); no increase occurred in nontreated W/B F1 mice (n = 5,651 +/- 126, P less than .005). Prolonged platelet life-spans (PLSs) were observed in treated W/B F1 mice (1.29 +/- 0.40 days), but not in nontreated controls (0.60 +/- 0.24 days, P less than .01). No increase in platelet production (platelet turnover) was found in PDN-treated W/B F1 mice, but significant decreases in platelet-associated antibodies (PAAs) and platelet-bindable serum antibodies (PBAs) were noted. Studies on organ localization of radiolabeled platelets showed that hepatic uptake significantly decreased in the treated W/B F1 mice, but not in nontreated W/B F1 mice. To elucidate the effect of PDN on the reticulo- endothelial phagocytic activity in W/B F1 mice, we studied in vivo clearance of IgG-sensitized, 51Cr-labeled autologous erythrocytes. W/B F1 mice treated with PDN showed a marked impairment of their ability to clear these cells, although PDN had little effect on the number of splenic or hepatic macrophage Fc gamma receptors. These results and our previous findings of splenectomy suggest that PDN improves platelet counts not only by suppressing systemic reticulo-endothelial phagocytic function but also by reducing antibody production.
- Published
- 1992
18. Decreased Renal Clearance of Xanthine and Hypoxanthine in a Patient with Renal Hypouricemia: A New Defect in Renal Handling of Purines
- Author
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Hiromu Nakajima, Takao Shimizu, Shiro Yorifuji, Norio Kono, Seiichiro Tarui, Masamichi Kuwajima, Ikuo Mineo, Hiroaki Kiyokawa, and Masanori Kawachi
- Subjects
Male ,Purine ,medicine.medical_specialty ,Metabolic Clearance Rate ,Metabolite ,Xanthine ,chemistry.chemical_compound ,Tubulopathy ,Internal medicine ,medicine ,Humans ,Hypouricemia ,Purine metabolism ,Hypoxanthine ,Probenecid ,business.industry ,Parkinson Disease ,Middle Aged ,medicine.disease ,Pyrazinamide ,Uric Acid ,Endocrinology ,chemistry ,Hypoxanthines ,Xanthines ,Uric acid ,Kidney Diseases ,business - Abstract
Renal handling of urate, xanthine and hypoxanthine was studied in a hypouricemic patient who had increased plasma concentrations of xanthine and hypoxanthine. The patient, a 50-year-old man, had been suffering from Parkinson's disease, while neither systemic disorders nor particular renal diseases known to affect plasma purine levels were found. His serum urate level was 58 +/- 6 mumol/l (healthy controls for males, 310 +/- 48 mumol/l, mean +/- SD) and the renal uric acid clearance was 3 times higher than that of the controls, establishing a diagnosis of renal hypouricemia. Xanthine and hypoxanthine concentrations in the plasma were elevated to 1.3 +/- 0.1 mumol/l (controls, 0.5 +/- 0.3) and 5.9 +/- 3.5 mumol/l (controls, 1.6 +/- 0.4), respectively. Both renal xanthine and hypoxanthine clearance was only half the value of the controls, indicating reduced urinary excretion of xanthine, and hypoxanthine appears to be responsible for their elevation in plasma. A probenecid loading test revealed no response of urinary urate excretion but normal responses of xanthine and hypoxanthine excretion. However, urinary excretion of urate, xanthine or hypoxanthine did not respond at all to pyrazinamide administration. These findings indicate that the patient had a defective renal handling of xanthine and hypoxanthine as well as urate.
- Published
- 1992
19. Peptide YY enhances NaCl and water absorption in the rat colon in vivo
- Author
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Tatsuya Kiyohara, Takashi Nakanishi, H. Ishikawa, Yasuhisa Shinomura, Masaru Okuno, and Seiichiro Tarui
- Subjects
Male ,medicine.medical_specialty ,Colon ,Potassium ,Sodium ,Vasoactive intestinal peptide ,chemistry.chemical_element ,Sodium Chloride ,Peptide hormone ,Chloride ,Gastrointestinal Hormones ,Cellular and Molecular Neuroscience ,In vivo ,Internal medicine ,medicine ,Animals ,Peptide YY ,Molecular Biology ,Pharmacology ,Water transport ,digestive, oral, and skin physiology ,Water ,Rats, Inbred Strains ,Cell Biology ,Rats ,Endocrinology ,Intestinal Absorption ,chemistry ,Molecular Medicine ,Peptides ,hormones, hormone substitutes, and hormone antagonists ,Vasoactive Intestinal Peptide ,medicine.drug - Abstract
Peptide YY (PYY) is thought to possess paracrine and endocrine functions. The highest concentrations of this peptide are in the colonic mucosa. The effect of PYY on electrolyte and water transport in the rat colon was studied in vivo. Under urethane anesthesia, rat colonic loops were perfused at a constant rate with physiological buffer solution containing phenol red as a nonabsorbable volume marker, and net movements of water, sodium, chloride and potassium in the perfused colon were determined every 10 min. Intravenous administration of PYY produced a dose-dependent increase in the net absorption of sodium chloride and water, as well as a decrease in the net secretion of potassium. PYY inhibited the reduction in net absorption of sodium chloride and water evoked by vasoactive intestinal peptide (VIP), but did not affect the VIP-evoked increase in net potassium secretion. These findings suggest that PYY acts as an enhancer of sodium chloride and water absorption and as an antagonist to VIP-induced secretion in the colon.
- Published
- 1992
20. ENDOTHELIAL AND MICROVASCULAR ABNORMALITIES IN THE ISLET OF NON-OBESE DIABETIC (NOD) MICE: TRANSMISSION AND SCANNING ELECTRON MICROSCOPIC STUDIES
- Author
-
A. Miyazaki, Jun-ichiro Miyagawa, Toshiaki Hanafusa, Naoto Itoh, Yuji Matsuzawa, Chisa Nakagawai, Koji Yamamoto, N. Kono, and Seiichiro Tarui
- Subjects
Autoimmune disease ,medicine.medical_specialty ,geography ,Pancreatic disease ,geography.geographical_feature_category ,Endothelium ,Ratón ,Microangiopathy ,General Medicine ,Biology ,medicine.disease ,Islet ,General Biochemistry, Genetics and Molecular Biology ,Pathogenesis ,Endocrinology ,medicine.anatomical_structure ,Internal medicine ,medicine ,NOD mice - Published
- 1992
21. α1-adrenergic regulation of thyrotropin-stimulated release of 3, 5, 3’ -triiodothyronine and thyroxine from perifused mouse thyroid
- Author
-
Jun-ichiro Miyagawa, Koji Tajima, Seiichiro Tarui, Misuzu Mori-Tanaka, Toshiaki Hanafusa, Kazuhiko Mashita, Koichi Kitajima, Yasuo Oda, and Ikuko Matsui
- Subjects
Male ,Agonist ,endocrine system ,medicine.medical_specialty ,4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone ,endocrine system diseases ,medicine.drug_class ,Endocrinology, Diabetes and Metabolism ,Thyroid Gland ,Thyrotropin ,Adrenergic ,Biology ,Methoxamine ,Mice ,Endocrinology ,1-Methyl-3-isobutylxanthine ,Internal medicine ,Cyclic AMP ,medicine ,Prazosin ,Animals ,Phosphodiesterase inhibitor ,Receptor ,Triiodothyronine ,Dose-Response Relationship, Drug ,Thyroid ,Receptors, Adrenergic, alpha ,Thyroxine ,medicine.anatomical_structure ,Calcium ,hormones, hormone substitutes, and hormone antagonists ,medicine.drug - Abstract
The effect of methoxamine, a specific alpha 1-adrenergic agonist, on the release of T3, T4 and cAMP from perifused mouse thyroid was studied to clarify the role of the alpha 1-adrenergic receptor in the regulation of thyroid hormone secretion. TSH-stimulated T3 and T4 release was inhibited significantly by methoxamine. With regard to cAMP release, methoxamine inhibited TSH-stimulated cAMP release in the presence of 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone but did not inhibit TSH-stimulated cAMP release in the presence of 3-isobutyl-1-methylxanthine. Methoxamine did significantly suppress TSH-stimulated release of T3 and T4 in the presence of each phosphodiesterase inhibitor. Depletion of Ca2+ in the perifusion buffer abolished completely the inhibitory effect of methoxamine on TSH-stimulated T3 and T4 release. The present study suggests that activation of the alpha 1-adrenergic receptor inhibits TSH-stimulated T3 and T4 secretion through a Ca(2+)-dependent mechanism in the mouse thyroid gland.
- Published
- 1991
22. Quantitative Comparison of Aromatase Induction by Dexamethasone in Fibroblasts from a Patient with Familial Cortisol Resistance and a Patient with Cortisol Hyperreactive Syndrome*
- Author
-
Teruo Kitani, Seiichiro Tarui, Masahiro Gomi, Mamiko Tsugawa, Sayomi Iida, Kaname Moriwaki, Yoshihisa Nakamura, and Hiroshi Fujii
- Subjects
Male ,medicine.medical_specialty ,Hydrocortisone ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Clinical Biochemistry ,Drug Resistance ,Endocrine System Diseases ,Biochemistry ,Dexamethasone ,Aromatase ,Endocrinology ,Glucocorticoid receptor ,Internal medicine ,medicine ,Humans ,Enzyme inducer ,Cells, Cultured ,biology ,business.industry ,Biochemistry (medical) ,Syndrome ,Mifepristone ,Fibroblasts ,Kinetics ,Steroid hormone ,Enzyme Induction ,biology.protein ,business ,Glucocorticoid ,medicine.drug - Abstract
The ability of dexamethasone to induce aromatase activity was tested in fibroblasts from a patient with familial cortisol resistance, a patient with cortisol hyperreactive syndrome, and five normal subjects. Dexamethasone increased enzyme activity in all cases in a concentration-dependent manner (over a range of 1-1000 nmol/L). In fibroblasts from a patient with familial cortisol resistance, the response curve of dexamethasone-induced aromatase activity was shifted to the right compared to that of normal cells. However, the maximal induction of the enzyme at 1 mumol/L dexamethasone was unchanged in cortisol-resistant fibroblasts. On the other hand, in fibroblasts from the patient with the cortisol hyperreactive syndrome, the half-maximal effect of dexamethasone was similar to that in normal cells, but maximum induction of aromatase activity was 2 times greater than that in normal cells. The glucocorticoid antagonist RU 486 inhibited dexamethasone-induced aromatase activity in these patients' cells and in normal cells in a concentration-dependent manner, indicating that the altered effects of dexamethasone on aromatase induction observed in each cell type were mediated through glucocorticoid receptors.
- Published
- 1991
23. Low glucose-1, 6-bisphosphate and high fructose-2, 6-bisphosphate concentrations in muscles of patients with glycogenosis types VII and V
- Author
-
Takao Shimizu, Hiraoki Kiyokawa, Seiichiro Tarui, Norio Kono, Hiromu Nakajima, Masanori Kawachi, Takamichi Nishimura, Akira Ono, Masamichi Kuwajima, and Yuya Yamada
- Subjects
medicine.medical_specialty ,Allosteric regulation ,Biophysics ,Glucose-6-Phosphate ,Biology ,Biochemistry ,chemistry.chemical_compound ,Glycogen phosphorylase ,Reference Values ,Internal medicine ,Fructosediphosphates ,medicine ,Humans ,Glycolysis ,Phosphoglucokinase ,Kinase activity ,Molecular Biology ,Glycogen Storage Disease Type VII ,Glycogen ,Activator (genetics) ,Muscles ,Glucosephosphates ,Cell Biology ,Endocrinology ,chemistry ,Glycogen Storage Disease Type V ,Phosphofructokinase - Abstract
The level of glucose-1, 6-bisphosphate, a potent allosteric activator of phosphofructokinase, was markedly decreased in muscles of patients with glycogenosis type VII (muscle phosphofructokinase deficiency) and type V (muscle phosphorylase deficiency). Glucose-1-phosphate kinase activity in muscle was virtually absent in a patient with glycogenosis type VII, whereas it was normal in a patient with type V blycogenosis. Glucose-1-phosphate level was increased in type VII glycogenosis, whereas it was decreased in type V glycogenosis. Another activator of phosphofructokinase, fructose-2, 6-bisphosphate was increased in muscles of patients with both types of glycogenosis although it was much higher in type VII than in type V. This finding may be partly related to the difference of fructose-6-phosphate concentrations. The results suggest that phosphofructokinase would contribute to the major glucose-1-phosphate kinase activity in normal human muscle and would also form a kind of self-activating system.
- Published
- 1991
24. Modulation of cholesterol 7α-hydroxylase activity by nonspecific lipid transfer protein in human liver — possibly altered regulation of its cytosolic level in patients with gallstones
- Author
-
Hiroki Kakimoto, Seiichiro Tarui, Sumio Kawata, Masami Inada, Yasuharu Imai, Yoshiaki Inui, Yuichi Maeda, and Kazuto Fukuda
- Subjects
Adult ,Male ,medicine.medical_specialty ,Blotting, Western ,Immunoblotting ,Clinical Biochemistry ,Biology ,Biochemistry ,Bile Acids and Salts ,chemistry.chemical_compound ,Cytosol ,Cholelithiasis ,Internal medicine ,medicine ,Humans ,Cholecystectomy ,Cholesterol 7-alpha-Hydroxylase ,SCP2 ,Antiserum ,Human liver ,Cholesterol ,Biochemistry (medical) ,General Medicine ,Gallstones ,Middle Aged ,medicine.disease ,Endocrinology ,Liver ,chemistry ,Microsomes, Liver ,Microsome ,Female ,Carrier Proteins ,Plant lipid transfer proteins - Abstract
Nonspecific lipid transfer protein (nsLTP) partially purified from human liver stimulated human microsomal cholesterol 7 alpha-hydroxylase activity. Addition of the nsLTP preparation to the reaction mixture enhanced the activity two-fold. Treatment of the nsLTP preparation with anti-rat nsLTP antiserum, which cross-reacts with human nsLTP, reduced the 7 alpha-hydroxylase-stimulating ability. These observations suggested that nsLTP plays a role in regulating the 7 alpha-hydroxylase activity in the human liver. 7 alpha-Hydroxylase activity in eight patients with cholesterol gallstones (4.7 +/- 1.6 pmol/min per mg microsomal protein) was significantly lower than that in five controls (7.9 +/- 3.4) (P less than 0.05). The amount of nsLTP in the cytosolic fraction (105,000 X g supernatant) of human liver was determined by dot-blotting immunoquantitation with the antiserum. The cytosolic level of nsLTP in the liver of the patients (716 +/- 239 cpm/3 micrograms protein) was higher than that in the controls (438 +/- 184) although the difference between the two groups was not statistically significant. This suggested that control of the cytosolic level may be affected in patients with cholesterol gallstones.
- Published
- 1991
25. Hypogalactosylation of immunoglobulin G sugar chains and elevated serum interleukin 6 in Castleman's disease
- Author
-
Yoshio Kanayama, Seiichiro Tarui, Atsushi Nishikawa, Naoyuki Taniguchi, Hirohisa Nakao, and Tetsuo Nishiura
- Subjects
Adult ,Male ,medicine.medical_specialty ,Glycosylation ,Molecular Sequence Data ,Clinical Biochemistry ,Oligosaccharides ,Immunoglobulin E ,Biochemistry ,Immunoglobulin G ,chemistry.chemical_compound ,Internal medicine ,medicine ,Humans ,Sugar ,Interleukin 6 ,Chromatography, High Pressure Liquid ,chemistry.chemical_classification ,biology ,Interleukin-6 ,Castleman Disease ,Biochemistry (medical) ,Galactose ,General Medicine ,Middle Aged ,Oligosaccharide ,Carbohydrate ,Endocrinology ,Carbohydrate Sequence ,chemistry ,Immunology ,biology.protein ,Electrophoresis, Polyacrylamide Gel ,Antibody - Abstract
Immunoglobulin G (IgG) molecule has two N-linked complex type oligosaccharides, consisting of a mixture of at least 12 different structures. The pattern of these oligosaccharides is fairly constant in healthy individuals. In three patients with Castleman's disease, in whom serum interleukin 6 (IL-6) levels were elevated, agalactosyl species of serum IgG oligosaccharides were markedly increased as compared to those of normal healthy controls. A close relationship between increased IL-6 and altered IgG oligosaccharide structure is suggested.
- Published
- 1991
26. Neoplastic epithelial cells express α-subunit of muscle nicotinic acetylcholine receptor in thymomas from patients with myasthenia gravis
- Author
-
Tomoyuki Uemichi, Yoshitaka Fujii, Shiro Yorifuji, Seiichiro Tarui, Yasuo Hara, Satoshi Ueno, and Nobuyuki Takahashi
- Subjects
medicine.medical_specialty ,Thymoma ,Molecular Sequence Data ,Biophysics ,Receptors, Nicotinic ,Biology ,Polymerase Chain Reaction ,Biochemistry ,Epithelium ,Antigen ,Structural Biology ,hemic and lymphatic diseases ,Internal medicine ,Myasthenia Gravis ,Gene expression ,Tumor Cells, Cultured ,Genetics ,medicine ,Humans ,Acetylcholine receptor ,Amino Acid Sequence ,RNA, Messenger ,Northern blot ,Molecular Biology ,Binding Sites ,Base Sequence ,Muscles ,mRNA expression ,DNA ,Cell Biology ,Blotting, Northern ,medicine.disease ,Molecular biology ,Reverse transcriptase ,Myasthenia gravis ,Epithelial cell ,Nicotinic acetylcholine receptor ,Endocrinology ,Electrophoresis, Polyacrylamide Gel - Abstract
We studied the expression of mRNAs coding for the alpha-subunit of the muscle nicotinic acetylcholine receptor (AChR) in thymomas from patients with myasthenia gravis (MG). Northern blot analysis failed to detect the expression, but amplification of mRNAs derived from thymomas by reverse transcription and polymerase chain reaction produced the DNA fragments containing the nucleotide sequence coding for part of the alpha-subunit. We further revealed that the alpha-subunit mRNA was derived from neoplastic epithelial cells of thymoma. Our results support the hypothesis that AChR expressed in thymoma is a candidate for the primary antigen which induces autoimmune responses to muscle AChR. The close relationship between MG and thymoma may be at least in part explained by this hypothesis.
- Published
- 1991
27. Age-related changes in adrenergic alpha 1, alpha 2, and beta receptors of rat white fat cell membranes: an analysis using [3H]bunazosin as a novel ligand for the alpha 1 adrenoceptor
- Author
-
Shigenori Fujioka, Hiroyuki Yoshida, Yasuhiro Watanabe, Seiichiro Tarui, Y Keno, Yuji Matsuzawa, T Kobatake, Toshiharu Kawamoto, and Koh Tokunaga
- Subjects
Male ,Aging ,medicine.medical_specialty ,Bunazosin ,Adrenergic receptor ,Adrenergic beta-Antagonists ,Rauwolscine ,Alpha (ethology) ,QD415-436 ,Biochemistry ,Propanolamines ,chemistry.chemical_compound ,Endocrinology ,Internal medicine ,Receptors, Adrenergic, beta ,medicine ,Animals ,Obesity ,Binding site ,Receptor ,Adrenergic alpha-Antagonists ,Epididymis ,Binding Sites ,Chemistry ,Cell Membrane ,Yohimbine ,Rats, Inbred Strains ,Cell Biology ,Receptors, Adrenergic, alpha ,Ligand (biochemistry) ,Rats ,Kinetics ,Adipose Tissue ,Quinazolines ,Alpha-2 adrenergic receptor ,medicine.drug - Abstract
Age-related changes in alpha 1-, alpha 2-, and beta-catecholamine receptors on membrane of rat epididymal fat cells were investigated. Both young (6 weeks old, weight about 190 g) and aged (20 weeks old, weight about 490 g) Sprague-Dawley male rats were used. For the alpha 1-adrenoceptor binding experiment, we developed a novel analytical method using the hydrophilic alpha 1-receptor selective antagonist, [3H]bunazosin. The binding of [3H]bunazosin to its binding sites was rapid, reversible, saturable, and stereospecific. Scatchard binding analysis showed a single class of binding site. The sites were characterized as alpha 1-adrenoceptors by inhibition experiments using various agonists and antagonists. The number of maximum binding sites (Bmax) of alpha 1-receptor binding was 37.0 +/- 6.5 (young) versus 24.0 +/- 3.2 (aged) fmol/mg protein (P less than 0.01). [3H]Rauwolscine and [3H]CGP-12177 were used for alpha 2- and beta-receptor binding, respectively. In alpha 2-receptor detection using [3H]rauwolscine as a ligand, Bmax increased markedly from 19.8 +/- 4.9 to 86.2 +/- 19.5 fmol/mg protein (P less than 0.01). In contrast, Bmax for beta-receptor decreased from 69.7 +/- 9.7 to 45.4 +/- 13.9 fmol/mg protein with increasing rat age (P less than 0.05). Kd showed no change in each of the binding experiments between young and aged rats. The cell volume increased from 0.07 +/- 0.02 to 0.15 +/- 0.06 nl. It is implied that anti-lipolytic activity strengthened on the whole mainly with the marked increase of alpha 2-receptor number and decrease of beta-receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1991
28. Animal model of systemic carnitine deficiency: Analysis in C3H-H-2° strain of mouse associated with juvenile visceral steatosis
- Author
-
Jun-ichiro Hayakawa, Seiichiro Tarui, Sumio Kawata, Akira Ono, Yasushi Imamura, Takeyori Saheki, Masamichi Kuwajima, Yoshiaki Inui, Norio Kono, Tsutomu Koizumi, and Masahisa Horiuchi
- Subjects
Aging ,medicine.medical_specialty ,Biophysics ,Carbohydrate metabolism ,Hypoglycemia ,Biology ,Muscle Development ,Biochemistry ,Mice ,Reference Values ,Carnitine ,Internal medicine ,medicine ,Animals ,Molecular Biology ,chemistry.chemical_classification ,Mice, Inbred C3H ,Muscles ,Fatty liver ,Hyperammonemia ,Cell Biology ,Metabolism ,Lipid Metabolism ,medicine.disease ,Mice, Mutant Strains ,Amino acid ,Fatty Liver ,Disease Models, Animal ,Endocrinology ,Liver ,chemistry ,Steatosis ,medicine.drug - Abstract
We analyzed carnitine profiles in C3H-H-2° strain of mouse associated with fatty liver, hyperammonemia and hypoglycemia (Koizumi et al., 1988). Carnitine levels in serum, liver and muscle of mouse with fatty liver were markedly decreased in comparison with those of control mouse (littermates without fatty liver). This is a useful animal model to analyze the role of carnitine in lipid, amino acid and carbohydrate metabolism.
- Published
- 1991
29. STIMULATION OF INTESTINAL CHOLECYSTOKININ SECRETION BY FREE FATTY ACID IN RATS IS NOT ASSOCIATED WITH AN INCREASE IN THE CCK mRNA LEVEL
- Author
-
Shuji Kanayama, Kaname Moriwaki, Yasuhisa Shinomura, Seiichiro Tarui, and Masayuki Tsuji
- Subjects
chemistry.chemical_classification ,Messenger RNA ,medicine.medical_specialty ,Fatty acid ,Neuropeptide ,Stimulation ,General Medicine ,Peptide hormone ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Endocrinology ,chemistry ,Mechanism of action ,Internal medicine ,medicine ,Secretion ,medicine.symptom ,Cholecystokinin - Published
- 1991
30. STIMULATION OF DUODENAL CHOLECYSTOKININ RELEASE BY FATTY ACID OR TRYPSIN INHIBITOR IS MARKEDLY INHIBITED BY LUMINAL WASHING
- Author
-
Seiichiro Tarui, Shuji Kanayama, Yasuhisa Shinomura, and Yasuhisa Sakamura
- Subjects
chemistry.chemical_classification ,medicine.medical_specialty ,Trypsin inhibitor ,digestive, oral, and skin physiology ,Fatty acid ,Bombesin ,General Medicine ,Trypsin ,digestive system ,General Biochemistry, Genetics and Molecular Biology ,chemistry.chemical_compound ,Endocrinology ,medicine.anatomical_structure ,Gastrointestinal hormone ,chemistry ,Internal medicine ,Pancreatic juice ,medicine ,Duodenum ,hormones, hormone substitutes, and hormone antagonists ,medicine.drug ,Cholecystokinin - Abstract
To investigate the influence of intestinal fluid containing bile, pancreatic juice and intestinal secretions on the regulation of cholecystokinin (CCK) release, arterial perfusion of bombesin or intraduodenal infusion of trypsin inhibitor or fatty acid was performed in vascularly perfused rat duodenum
- Published
- 1991
31. A delayed-addition enzyme immunoassay for the relative cholesteryl ester transfer protein mass in patients with deficient plasma cholesteryl ester transfer activity
- Author
-
Judith A.K. Harmony, Yuji Matsuzawa, Seiichiro Tarui, John R. Wetterau, Naohiko Sakai, Dennis L. Sprecher, and Shizuya Yamashita
- Subjects
Adult ,Male ,Hyperlipoproteinemias ,medicine.medical_specialty ,Lipoproteins ,Clinical Biochemistry ,Sterol O-acyltransferase ,Biochemistry ,Immunoenzyme Techniques ,chemistry.chemical_compound ,Internal medicine ,Cholesterylester transfer protein ,Blood plasma ,medicine ,Humans ,Triglycerides ,Glycoproteins ,chemistry.chemical_classification ,biology ,Triglyceride ,medicine.diagnostic_test ,Biochemistry (medical) ,General Medicine ,Middle Aged ,Lipids ,Cholesterol Ester Transfer Proteins ,carbohydrates (lipids) ,Apolipoproteins ,Endocrinology ,Enzyme ,chemistry ,Polyclonal antibodies ,Immunoassay ,Cholesteryl ester ,biology.protein ,lipids (amino acids, peptides, and proteins) ,Cholesterol Esters ,Carrier Proteins - Abstract
The biochemical basis for the apparent deficiency of cholesteryl ester (CE) transfer activity was investigated in two unrelated subjects with markedly elevated high density lipoprotein-cholesterol (Atherosclerosis 1988; 70:7–12). Essentially no CE or triglyceride transfer activity was detected in the patients' plasma, utilizing four different lipid transfer assays. Using polyclonal antibodies raised against human plasma cholesteryl ester transfer protein (CETP), a delayed-addition enzyme immunoassay was developed to determine plasma CETP mass. CETP could not be detected with this assay in the plasma of the two subjects with transfer activity deficiency, indicating that the CE transfer activity deficiency in these subjects is due to the absence of plasma CETP. In addition, three hyperalphalipoproteinemic subjects with a partial deficiency of CE transfer activity had a reduced level of CETP mass. There was a good correlation between plasma CETP activity and mass levels. The principles of this immunoassay may be applicable to measure the mass levels of other proteins with catalytic activities.
- Published
- 1990
32. Interferon-γ Reduces Actin Filaments and Inhibits Thyroid-Stimulating Hormone-Induced Formation of Microvilli and Pseudopods in Mouse Monolayer Thyrocytes
- Author
-
Toshiaki Hanafusa, Koji Tajima, Seiichiro Tarui, Akihito Otsuka, Kazuya Yamagata, Kazuhiko Mashita, A. Miyazaki, Norio Kono, Hideki Asakawa, Hayato Katsura, Jun-ichiro Miyagawa, and Chisa Nakagawa
- Subjects
medicine.medical_specialty ,Thyroid Gland ,Fluorescent Antibody Technique ,Thyrotropin ,Stimulation ,Biology ,Microfilament ,Immunofluorescence ,Epithelium ,Interferon-gamma ,Mice ,Endocrinology ,Thyroid-stimulating hormone ,Internal medicine ,medicine ,Animals ,Interferon gamma ,Pseudopodia ,Cells, Cultured ,Actin ,Mice, Inbred C3H ,Microvilli ,medicine.diagnostic_test ,Actins ,Microscopy, Fluorescence ,Cell culture ,Microscopy, Electron, Scanning ,Keratins ,Female ,medicine.drug - Abstract
To study the role of interferon-gamma (IFN gamma), which is released from activated lymphocytes in the development of lymphocytic thyroiditis, we investigated the effects of IFN gamma on the morphology of mouse thyrocytes, using scanning electron microscopy. Thyrocytes were cultured in monolayers for 5-7 days and incubated with TSH (10 mU/ml) for 1 h before fixation. IFN gamma (200 U/ml) was added to the culture medium for 1 h to 5 days before TSH stimulation. Coculture of thyrocytes with IFN gamma for more than 24 h inhibited TSH-induced morphological changes in the thyrocytes; IFN gamma inhibited the increase in the number of and elongation of microvilli and the appearance of pseudopods. IFN gamma also reduced the number of actin filaments in thyrocytes, as confirmed by immunofluorescence photometry. These results suggest that IFN gamma inhibits the morphological response of thyrocytes to TSH stimulation by the reduction of actin filaments.
- Published
- 1990
33. Decreased xanthine oxidase activities and increased urinary oxypurines in heterozygotes for hereditary xanthinuria
- Author
-
Masanori Kawachi, Seiichiro Tarui, Yuya Yamada, Norio Kono, and Ikuo Mineo
- Subjects
Adult ,Male ,Purine ,Heterozygote ,Purine-Pyrimidine Metabolism, Inborn Errors ,Xanthine Oxidase ,medicine.medical_specialty ,Clinical Biochemistry ,Urine ,Biology ,Biochemistry ,chemistry.chemical_compound ,Internal medicine ,Blood plasma ,medicine ,Humans ,Xanthine oxidase ,Hypoxanthine ,Oxidase test ,Biochemistry (medical) ,General Medicine ,Xanthine ,Pedigree ,Uric Acid ,Kinetics ,Endocrinology ,chemistry ,Purines ,Creatinine ,Hypoxanthines ,Xanthines ,Uric acid ,Female - Abstract
Two brothers with hereditary xanthinuria (xanthine oxidase deficiency) and several members of their family were studied. In both subjects, plasma and urinary concentrations of uric acid were low whereas xanthine and hypoxanthine concentrations were markedly elevated. Xanthine oxidase activity was virtually absent in the patients' duodenal mucosa, a finding that established the diagnosis of hereditary xanthinuria. In their parents (obligate heterozygotes), the duodenal xanthine oxidase activity was about 50% of that in control subjects (father 9.3 and mother 12.8 mU/g tissue compared with 21.3 +/- 5.0 mU/g tissue, mean +/- SD). The residual xanthine oxidase from the parents exhibited normal kinetics with respect to hypoxanthine. The parents' urinary xanthine and hypoxanthine concentrations were significantly greater than those of control subjects, while their plasma concentrations of oxypurines were normal. Similar findings were observed in at least 6 other relatives, a finding that suggested that they were heterozygotes. This study suggests that obligate hereditary xanthinuria heterozygotes have only 50% of the xanthine oxidase activity of controls; this deficiency results in a partial metabolic blockage at this enzymatic step in heterozygotes.
- Published
- 1990
34. Demonstration of high-affinity interleukin-2 receptors on B-chronic lymphocytic leukemia cells: Functional and structural characterization
- Author
-
Tetsuo Nishiura, Yoshiaki Tomiyama, Toshiharu Tamaki, Shuichi Katagiri, Takeshi Yonezawa, Nobuhiko Tominaga, Hirosuke Yagura, T. Furitsu, and Seiichiro Tarui
- Subjects
Interleukin 2 ,medicine.medical_specialty ,Macromolecular Substances ,Chronic lymphocytic leukemia ,medicine.medical_treatment ,Fluorescent Antibody Technique ,Immunoglobulins ,Biology ,Cell surface receptor ,Internal medicine ,medicine ,Humans ,Receptor ,B-Lymphocytes ,Ligand binding assay ,Receptors, Interleukin-2 ,DNA ,Hematology ,General Medicine ,medicine.disease ,Leukemia, Lymphocytic, Chronic, B-Cell ,Recombinant Proteins ,In vitro ,Molecular Weight ,Endocrinology ,Cytokine ,Cell culture ,Interleukin-2 ,Cell Division ,medicine.drug - Abstract
Functional and structural characteristics of interleukin 2 (IL-2) receptors on B-cell chronic lymphocytic leukemia (B-CLL) cells were analyzed by a proliferation assay, IL-2 binding assay and cross-linking study. In the 3H-thymidine incorporation assay, purified B-CLL cells from four out of sixteen cases, in which the percentage of Tac antigen (Tac Ag) positive cells in peripheral blood lymphocytes ranged from 0 to 48.8%, responded to IL-2 (100 U/ml) after both 3- and 6-day incubation. No relationship was found between the responsiveness to IL-2 and the percentage of Tac Ag positive cells. In the radiolabeled IL-2 binding assay, however, B-CLL cells from all seven cases examined, including three cases with mitogenic response to IL-2 and four cases without mitogenic response, were shown to have both high- and low-affinity receptors. The number of high- and low-affinity receptors per cell ranged from 29-186 and from 420 to 1,800, respectively. Furthermore, with the affinity cross-linking method p55 (Tac Ag) and p70/75 were found even in cases without mitogenic response in their B-CLL cells. In conclusion, the B-CLL cells so far examined possessed high-affinity IL-2 receptors consisting of p55 and p70/75; nevertheless, this was not sufficient to respond to the mitogenic signal of IL-2.
- Published
- 1990
35. A Patient with Hypocortisolism and Cushing's Syndrome-Like Manifestations: Cortisol Hyperreactive Syndrome*
- Author
-
Yoshihisa Nakamura, Junichi Fukata, Teruo Kitani, Junichi Nishimura, Kaname Moriwaki, Seiichiro Tarui, Masahiro Gomi, Hiroshi Fujii, Mamiko Tsugawa, and Sayomi Iida
- Subjects
Male ,endocrine system ,Vasopressin ,medicine.medical_specialty ,Cortisol awakening response ,Hydrocortisone ,Corticotropin-Releasing Hormone ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Lypressin ,Dermatitis, Contact ,Biochemistry ,Dexamethasone ,Cushing syndrome ,Aromatase ,Endocrinology ,Adrenocorticotropic Hormone ,Internal medicine ,medicine ,Humans ,Insulin ,Cushing Syndrome ,Glucocorticoids ,Cells, Cultured ,Chromatography, High Pressure Liquid ,Skin ,Metyrapone ,business.industry ,Biochemistry (medical) ,Fibroblasts ,Middle Aged ,medicine.disease ,Enzyme Activation ,Addison's disease ,Gonadotropins, Pituitary ,business ,hormones, hormone substitutes, and hormone antagonists ,Glucocorticoid ,Thymidine ,medicine.drug - Abstract
One patient is reported who has the manifestations of Cushing's syndrome in spite of persistent hypocortisolemia. His serum levels of cortisol and free cortisol were below normal, and 24-h urinary excretion of 17-hydroxycorticosteroids and cortisol were decreased. There was a rapid and substantial increase in serum cortisol in response to synthetic ACTH-(1-24). Plasma levels of ACTH were marginally increased by successive administration of CRH and vasopressin, which were followed by substantial increases in serum cortisol. Glucocorticoid activity of the patient's serum, as measured by a RRA was low. There were no responses of urinary 17-hydroxycorticosteroids after metyrapone treatment. These laboratory examinations ruled out any known clinical conditions resulting in hypocortisolemia. The clinical condition could also be explained by cortisol hyperreactivity of the patient's cells. In vitro hyperreactivity to glucocorticoids was demonstrated in cultured skin fibroblasts whose aromatase activity was increased 1.5- to 1.8-fold above that of normal cells, and [3H]thymidine incorporation was inhibited more effectively by the addition of cortisol or dexamethasone. The mechanism by which the patient is hyperreactive to glucocorticoids remains unexplained.
- Published
- 1990
36. Simple estimation of ideal body weight from body mass index with the lowest morbidity
- Author
-
Yuji Matsuzawa, Seiichiro Tarui, Katsuto Tokunaga, Kazuaki Kotani, Takashi Kobayashi, and Y Keno
- Subjects
Adult ,Male ,Ideal (set theory) ,Body volume index ,business.industry ,Endocrinology, Diabetes and Metabolism ,Body Weight ,nutritional and metabolic diseases ,General Medicine ,Middle Aged ,Body weight ,Body Mass Index ,Endocrinology ,Internal Medicine ,Humans ,Medicine ,Female ,Obesity ,business ,Body mass index ,Mathematics ,Demography - Abstract
Body mass index (BMI) is expressed by the body weight (kg) divided by height (m) squared. Therefore, if we know ideal BMI, ideal body weight (kg) of each individual can be calculated by a formula: Ideal BMI x height (m)2. In order to estimate ideal BMI, we investigated average BMI with the lowest morbidity using 4565 Japanese men and women aged 30 to 59 years. Their BMI distributed widely with the highest frequency at 23 in men and 21 in women. The morbidity was evaluated by the number of medical problems that the subjects with each BMI have. The BMI associated with the lowest morbidity was calculated to be 22.2 kg/m2 in men and 21.9 kg/m2 in women according to the quadratic regression curves derived from the relation between BMI and morbidity. From these data, we propose that an ideal body weight in Japanese is 22 x height (m)2.
- Published
- 1990
37. TROPHIC EFFECT OF GLUCAGON-(1-21)-PEPTIDE ON THE RAT SMALL INTESTINE AND COLON
- Author
-
Tsukuru Hashimoto, Mitsuyoshi Namba, Hidehiko Itoh, Tatsuo Matsuyama, Seiichiro Tarui, Yasuhiro Tanaka, Norio Kono, Ryoya Komatsu, Nobuaki Watanabe, and Toshiko Ohara
- Subjects
chemistry.chemical_classification ,medicine.medical_specialty ,Peptide ,Radioimmunoassay ,General Medicine ,Peptide hormone ,Biology ,Glucagon ,Rat Small Intestine ,General Biochemistry, Genetics and Molecular Biology ,Small intestine ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Internal medicine ,medicine ,Pancreatic hormone ,Trophic level - Published
- 1990
38. MULTIPLE FORMS OF GLUCAGON-LIKE PEPTIDE-1 AND GLUCAGON-LIKE IMMUNOREACTIVITIES IN CANINE GASTROINTESTINAL TRACT AND THEIR RELEASE INTO CIRCULATION
- Author
-
Meisei Hirota, Mitsuyoshi Namba, Kenji Shima, Norio Kono, Tatsuo Matsuyama, Hidehiko Itoh, Nobuaki Watanabe, Ryoya Komatsu, and Seiichiro Tarui
- Subjects
medicine.medical_specialty ,Gastrointestinal tract ,Endocrinology ,Multiple forms ,Chemistry ,Internal medicine ,medicine ,General Medicine ,Glucagon-like peptide-1 ,Glucagon ,General Biochemistry, Genetics and Molecular Biology - Published
- 1990
39. NH2-terminal big gastrin immunoreactivity in human urine
- Author
-
Kazuhiro Nagao, Shuji Kanayama, Yoshifumi Higashimoto, Yasuhisa Shinomura, Seiichi Himeno, and Seiichiro Tarui
- Subjects
Adult ,medicine.medical_specialty ,Radioimmunoassay ,Urine ,Chemical Fractionation ,General Biochemistry, Genetics and Molecular Biology ,chemistry.chemical_compound ,Column chromatography ,Internal medicine ,Gastrins ,Blood plasma ,medicine ,Humans ,Protein Precursors ,General Pharmacology, Toxicology and Pharmaceutics ,Big gastrin ,Chromatography, High Pressure Liquid ,Gastrin ,Kidney ,Chromatography ,General Medicine ,Chromatography, Ion Exchange ,medicine.anatomical_structure ,Endocrinology ,chemistry ,Sephadex - Abstract
The concentrations and molecular forms of urinary and plasma gastrin from normal subjects were studied by radioimmunoassays using two region-specific antisera. Urinary concentration of NH 2 -terminal big gastrin (G-34) immunoreactivity was several hundred times as great as that of COOH-terminal gastrin immunoreactivity. Fractionation of urine extract showed a broad giant peak of NH 2 -terminal G-34 immunoreactivity (gastrin fragments “U”) eluting in a later position than G-34 (1–17) by Sephadex G-50 column chromatography. HPLC revealed that urinary NH 2 -terminal G-34 immunoreactivity was composed of four fragments including G-34 (1–8), G-34(1–9), and G-34 (1–10). Sephadex G-50 column chromatography of plasma extract revealed two or three peaks of NH 2 -terminal G-34 immunoreactivity, and a major peak eluted in the same position as urinary gastrin fragments “U”. These results and data on renal clearances suggest that most of all gastrin fragments “U” in plasma are excreted in urine without renal reabsorption, whereas almost all of plasma COOH-terminal gastrin peptides including G-34 and little gastrin (G-17) are removed and metabolized in the kidney.
- Published
- 1990
40. Glucose infusion paradoxically accelerates degradation of adenine nucleotide in working muscle of patients with glycogen storage disease type VII
- Author
-
Akira Ono, Chisa Nakagawa, Y. Matsuzawa, Ikuo Mineo, Norio Kono, M. Kuwajima, and Seiichiro Tarui
- Subjects
Adult ,Blood Glucose ,Male ,medicine.medical_specialty ,Time Factors ,Glycogen Storage Disease Type VII ,medicine.medical_treatment ,Physical Exertion ,Fatty Acids, Nonesterified ,chemistry.chemical_compound ,Adenine nucleotide ,Ammonia ,Reference Values ,Internal medicine ,medicine ,Humans ,Insulin ,Inosine ,Muscle, Skeletal ,Hypoxanthine ,chemistry.chemical_classification ,Adenine Nucleotides ,Fatty acid ,Skeletal muscle ,Carbohydrate ,medicine.anatomical_structure ,Endocrinology ,Glucose ,chemistry ,Hypoxanthines ,Exercise Test ,Female ,Neurology (clinical) ,medicine.drug - Abstract
Article abstract-We investigated the effect of glucose infusion on adenosine triphosphate degradation in skeletal muscle of patients with glycogen storage disease type VII. Three patients and six healthy subjects exercised on a bicycle ergometer twice, once with 20% glucose infusion and once with saline infusion. The glucose infusion increased plasma glucose levels to 170 to 182 mg/dl and serum insulin levels to 30 to 50 microunits/ml, while it markedly decreased plasma free fatty acid levels. The exercise-induced increases in plasma ammonia, inosine, and hypoxanthine were much larger with glucose than with saline infusion in the patients. Urinary excretion of inosine and hypoxanthine with glucose infusion was twice as high as that with saline infusion. No such differences were present between glucose and saline infusion in the healthy subjects. Glucose infusion therefore accelerates the energy crisis in working muscle of patients with glycogen storage disease type VII, probably due to a decrease in fatty acid utilization.NEUROLOGY 1995;45: 161-164
- Published
- 1995
41. The NOD mouse
- Author
-
Jun-ichiro Miyagawa, Seiichiro Tarui, Yuji Matsuzawa, Toshiaki Hanafusa, Koji Tomita, Hiromu Nakajima, and Masamichi Kuwajima
- Subjects
Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,medicine.disease_cause ,Autoimmunity ,Pathogenesis ,Islets of Langerhans ,Mice ,Endocrinology ,Retrovirus ,Mice, Inbred NOD ,Diabetes mellitus ,Internal Medicine ,medicine ,Animals ,Autoimmune disease ,biology ,business.industry ,General Medicine ,Immunotherapy ,medicine.disease ,biology.organism_classification ,Disease Models, Animal ,Diabetes Mellitus, Type 1 ,Retroviridae ,Immunology ,business ,Insulitis ,Biobreeding rat - Abstract
The NOD mouse was discovered and established as an inbred strain in Japan. It is an excellent animal model for human Type 1 (insulin-dependent) diabetes mellitus in many aspects, including genetics, immunology, virology, and prevention and therapy. The diabetes and/or insulitis is controlled by at least 10 genes and results from the T cell-mediated destruction of beta cells. Retrovirus might also play a role in the pathogenesis. Insulitis and/or diabetes of the mice is easily prevented by a number of agents or manipulations, suggesting that diabetes of the mice develops only when many diabetogenic factors assemble. Some of the intervention trials using the mice are hoped to be applied to human Type 1 diabetes.
- Published
- 1994
42. Marked reduction of pancreatic insulin content in male ventromedial hypothalamic-lesioned spontaneously non-insulin-dependent diabetic (Goto-Kakizaki) rats
- Author
-
Iichiro Shimomura, Kazuaki Kotani, Shigenori Fujioka, Seiichiro Tarui, Makoto Nishida, Yoshiaki Keno, Shingo Yoshida, Yuji Matsuzawa, Takao Matsuo, Takashi Kobatake, Hiroyuki Odaka, and Katsuto Tokunaga
- Subjects
Blood Glucose ,Male ,medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Hypothalamus, Middle ,Carbohydrate metabolism ,Biology ,Diabetes Mellitus, Experimental ,Endocrinology ,Internal medicine ,Diabetes mellitus ,Hyperinsulinism ,medicine ,Hyperinsulinemia ,Animals ,Insulin ,Rats, Wistar ,Pancreas ,Pancreatic hormone ,Sex Characteristics ,Pancreatic insulin ,Metabolism ,medicine.disease ,Rats ,medicine.anatomical_structure ,Diabetes Mellitus, Type 2 ,Female ,Hypothalamic Diseases - Abstract
The effects of ventromedial hypothalamic (VMH) lesions were examined in male and female non-obese non-insulin-dependent diabetic (Goto-Kakizaki [GK]) rats with respect to glucose metabolism and pancreatic insulin content. VMH lesions produced hyperphagia and hyperinsulinemia in both male and female GK rats. In male rats, plasma glucose levels of VMH-lesioned GK rats (22.7 ± 3.1 mmol/L) were significantly greater than the levels of sham-operated GK rats (10.6 ± 1.0 mmol/L, P < .001) at 7 weeks after the operation, although there were no differences in these levels between VMH-lesioned and sham-operated groups in Wistar rats. Plasma insulin levels in male VMH-lesioned GK rats tended to be lower at 7 weeks than at 1 week. VMH lesions caused a significant decrease in the pancreatic insulin content of male GK rats (12.0 ± 2.3 nmol/L/g pancreas) compared with male sham-operated rats (15.8 ± 1.4 nmol/L/g pancreas, P < .05) 9 weeks postoperatively. In contrast to the results in male rats, female GK rats showed no differences in plasma glucose levels between VMH-lesioned and sham-operated groups at 7 weeks. Female VMH-lesioned GK rats also showed no difference in plasma insulin levels between 1 week and 7 weeks. The pancreatic insulin level of female VMH-lesioned GK rats was unchanged from that of female sham-operated GK rats. The insulin content was significantly greater in the VMH-lesioned Wistar group than in the sham-operated Wistar group, regardless of sex. These observations suggest that the increased requirement for insulin secretion caused by VMH lesions may lead to B-cell exhaustion, producing, at least in part, marked hyperglycemia in male GK rats. Male VMH-lesioned GK rats might be a good model for obese Japanese patients with the genetic predisposition to non-insulin-dependent diabetes mellitus (NIDDM).
- Published
- 1994
43. Decrease of hepatic triglyceride lipase levels and increase of cholesteryl ester transfer protein levels in patients with primary biliary cirrhosis: relationship to abnormalities in high-density lipoprotein
- Author
-
Masaharu Kubo, Naohiko Sakai, Shuichi Nozaki, Yuji Matsuzawa, Hisatoyo Hiraoka, Seiichiro Tarui, Shizuya Yamashita, Sumio Kawata, and Ken-ichi Hirano
- Subjects
Apolipoprotein E ,Adult ,Male ,medicine.medical_specialty ,Very low-density lipoprotein ,Hypercholesterolemia ,Biology ,chemistry.chemical_compound ,High-density lipoprotein ,Apolipoproteins E ,Internal medicine ,Cholesterylester transfer protein ,medicine ,Humans ,Aged ,Glycoproteins ,Triglyceride lipase ,Lipoprotein lipase ,Hepatology ,Cholesterol ,Liver Cirrhosis, Biliary ,Cholesterol, HDL ,Lipase ,Middle Aged ,Cholesterol Ester Transfer Proteins ,Microscopy, Electron ,Endocrinology ,chemistry ,Liver ,biology.protein ,lipids (amino acids, peptides, and proteins) ,Electrophoresis, Polyacrylamide Gel ,Female ,Carrier Proteins ,Lipoproteins, HDL ,Lipoprotein - Abstract
Serum levels of high-density lipoprotein cholesterol are often increased in patients with primary biliary cirrhosis. To elucidate the mechanism of the elevation of high-density lipoprotein cholesterol levels in this disease, lipoprotein abnormalities were analyzed in 10 patients subdivided into two groups according to concentration of high-density lipoprotein cholesterol. Activities and protein masses of lipoprotein lipase, hepatic triglyceride lipase and cholesteryl ester transfer protein were also determined. Serum high-density lipoprotein cholesterol concentration exceeded 90 mg/dl in 5 of 10 patients. Lipoprotein particles in the high-density lipoprotein2 fraction (with density between 1.063 and 1.125 gm/ml) were enriched with apolipoprotein E and larger in size than those of normal controls. In patients with and without hyperalphalipoproteinemia, hepatic triglyceride lipase activity was significantly decreased (p < 0.05); this was due to the reduction of its protein mass. Lipoprotein lipase activity and protein mass were normal. It is noteworthy that increases in cholesteryl ester transfer protein activity and mass were observed. The enhancement of cholesteryl ester transfer protein activity was more remarkable in the patients with hyperalphalipoproteinemia than in those without hyperalphalipoproteinemia. Because a significant positive correlation was demonstrated between activity and protein mass (r = 0.90, p < 0.001), the increase of cholesteryl ester transfer protein activity may be attributed to the increase of its protein mass. These data suggest that the decrease of hepatic triglyceride lipase levels at least partly explains the appearance of apolipoprotein E-rich large high-density lipoprotein particles in patients with primary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1993
44. Aromatase activity in human hepatocellular carcinoma. Relationship with the degree of histologic differentiation
- Author
-
Yasuo Matsuda, Minoru Nishioka, Yuji Matsuzawa, Seiichiro Tarui, Nobuyuki Ito, Sumio Kawata, Kaname Moriwaki, Shinji Tamura, and Iwao Yabuuchi
- Subjects
Male ,Cancer Research ,medicine.medical_specialty ,Pathology ,Carcinoma, Hepatocellular ,medicine.drug_class ,Aromatase ,Internal medicine ,Liver tissue ,medicine ,Humans ,Aged ,chemistry.chemical_classification ,biology ,business.industry ,Liver Neoplasms ,Cytochrome P450 ,Middle Aged ,Androgen ,medicine.disease ,digestive system diseases ,Enzyme ,Endocrinology ,Oncology ,chemistry ,Liver ,Estrogen ,Hepatocellular carcinoma ,biology.protein ,Microsome ,Microsomes, Liver ,Female ,business - Abstract
Human hepatocellular carcinomas (HCC) were examined aromatase activity, an enzyme that converts androgen into estrogen. Such activity was detected in all 13 specimens of HCC (mean activity, 120 fmol/30 min/mg microsomal protein). The activity tended to be lower in the HCC tissue than in the surrounding liver tissue (mean activity, 230 fmol/30 min/mg microsomal protein), although it was higher in the HCC tissue from three of eight patients with Edmondson's Grade 2 disease. This relationship was not found in the five with Grade 3 disease. On the whole, aromatase activity was significantly higher in specimens from patients with Edmondson's Grade 2 tumors than in the less differentiated Grade 3 type (P < 0.05). These observations suggested that aromatase activity was present in human HCC and was related to the degree of histologic differentiation.
- Published
- 1993
45. Amyloid polyneuropathy with transthyretin Arg50 in a Japanese case from Osaka
- Author
-
Shiro Yorifuji, Tomoyuki Uemichi, Nobuyuki Takahashi, Satoshi Ueno, Harutoshi Fujimura, and Seiichiro Tarui
- Subjects
Adult ,Male ,endocrine system ,medicine.medical_specialty ,Pathology ,Amyloid ,Cardiomyopathy ,Arginine ,Internal medicine ,Medicine ,Humans ,Prealbumin ,Wasting ,Chromatography, High Pressure Liquid ,biology ,business.industry ,Amyloidosis ,nutritional and metabolic diseases ,Peripheral Nervous System Diseases ,medicine.disease ,Immunohistochemistry ,Sciatic Nerve ,Pedigree ,Transthyretin ,Endocrinology ,Neurology ,Heart failure ,Mutation ,biology.protein ,Neurology (clinical) ,medicine.symptom ,business ,Polyneuropathy - Abstract
A Japanese patient with systemic amyloidosis associated with a transthyretin (TTR) variant Arg50 is presented. This 41-year-old man became impotent and developed decreased pain sensation in his hands, and then sensory loss and muscle wasting in his lower legs, and cardiomyopathy appeared. The symptoms progressed and he died of congestive heart failure at age 46. There were amyloid deposits in all organs studied and massive amyloid deposition was seen in the peripheral nerves and cardiac muscles. Amyloid fibrils extracted from heart tissue contained TTR. A genetic mutation, causing a Ser50 → Arg substitution of the TTR molecule, was identified in another family member. Plasma TTR was shown to be a mixture of normal TTR Ser50 and mutant TTR Arg50 in the 2 subjects.
- Published
- 1992
46. Familial amyloid polyneuropathy associated with the transthyretin Cys114 gene in a Japanese kindred
- Author
-
Satoshi Ueno, Yusaku Nakamura, M. Takahashi, Shiro Yorifuji, Harutoshi Fujimura, Takehiko Yanagihara, and Seiichiro Tarui
- Subjects
Adult ,Male ,medicine.medical_specialty ,Amyloid ,Molecular Sequence Data ,Blood Pressure ,Sudden death ,Japan ,Heart Rate ,Internal medicine ,Medicine ,Humans ,Prealbumin ,Amino Acid Sequence ,Cysteine ,biology ,business.industry ,Amyloidosis ,Peripheral Nervous System Diseases ,medicine.disease ,Pedigree ,Transthyretin ,Amyloid Neuropathy ,Autonomic nervous system ,Endocrinology ,Autonomic Nervous System Diseases ,Heart failure ,Mutation ,biology.protein ,Neurology (clinical) ,Nervous System Diseases ,business ,Polyneuropathy - Abstract
A Japanese kindred with dominantly inherited amyloid polyneuropathy, commonly called familial amyloid polyneuropathy (FAP), has been identified. Amyloid protein was transthyretin (TTR) related and the patients were heterozygous for the mutant gene encoding TTR with a single amino acid substitution of cysteine for tyrosine at position 114. This family originated in Nagasaki Prefecture, Japan, and 12 of the 36 known members of six generations have been affected. The initial symptoms occurred in their thirties with the cardinal features of polyneuropathy, vitreous opacities and cardiac disease. Sensory neuropathy was severe in the lower limbs. Autonomic disturbances, especially postural hypotension, were the most debilitating to the patients. Amyloid deposits were detected widely in most organs except for the central nervous system. The duration from the onset of the disease to death was within 10 yrs. Heart failure caused by heavy amyloid deposits was the most common cause of sudden death.
- Published
- 1992
47. Familial amyloid polyneuropathy related to transthyretin Gly42 in a Japanese family
- Author
-
Tadashi Umekage, Harutoshi Fujimura, Satoshi Ueno, Shiro Yorifuji, Tomoyuki Uemichi, Yuji Matsuzawa, and Seiichiro Tarui
- Subjects
Adult ,Male ,medicine.medical_specialty ,Amyloid ,Physiology ,Biopsy ,Cardiomyopathy ,Cellular and Molecular Neuroscience ,Exon ,Sural Nerve ,Polymorphism (computer science) ,Physiology (medical) ,Internal medicine ,medicine ,Humans ,Prealbumin ,chemistry.chemical_classification ,biology ,business.industry ,Amyloidosis ,nutritional and metabolic diseases ,Peripheral Nervous System Diseases ,Exons ,Middle Aged ,medicine.disease ,Amino acid ,Pedigree ,Transthyretin ,Muscular Atrophy ,Endocrinology ,chemistry ,Autonomic Nervous System Diseases ,Mutation ,biology.protein ,Female ,Neurology (clinical) ,business ,Polyneuropathy ,Polymorphism, Restriction Fragment Length - Abstract
A Japanese family is described in which 6 persons showed familial amyloid polyneuropathy (FAP). Mean ages of onset were 38 for 4 males and 54 for 2 females. Three of the 6 became emaciated and died after 4 to 10 years. In 5, muscular weakness and autonomic dysfunction were the initial symptoms followed by sensory disturbances. Amyloidotic cardiomyopathy was present in 3 of the subjects. Amyloid deposits showed an immunohistological relation to transthyretin (TTR). Analysis of 1 patient's TTR gene revealed a single base change (A----G) that led to amino acid substitution (Glu42----Gly). This base change produced a new restriction site for endonuclease Cfr13 I in exon 2. Polymorphic analysis of the length of the Cfr13 I-restriction fragment confirmed the base change, and made it possible to detect the mutant TTR Gly42 gene in the FAP subjects. Amino acid sequencing analysis showed a variant of TTR Gly42 in 1 patient's serum.
- Published
- 1992
48. Changes in lipid composition of erythrocyte membranes with administration of S-adenosyl-L-methionine in chronic liver disease
- Author
-
Yuji Matsuzawa, Seiichiro Tarui, Masami Inada, Sumio Kawata, Yasuharu Imai, and Hiroki Kakimoto
- Subjects
Adult ,Liver Cirrhosis ,Male ,medicine.medical_specialty ,S-Adenosylmethionine ,Cirrhosis ,Membrane Fluidity ,Phospholipid ,Chronic liver disease ,chemistry.chemical_compound ,Liver disease ,Primary biliary cirrhosis ,Internal medicine ,medicine ,Membrane fluidity ,Humans ,Phospholipids ,Aged ,business.industry ,Liver Cirrhosis, Biliary ,Erythrocyte Membrane ,Gastroenterology ,Hepatology ,Middle Aged ,medicine.disease ,Membrane ,Endocrinology ,Cholesterol ,chemistry ,Biochemistry ,Chronic Disease ,Injections, Intravenous ,Phosphatidylcholines ,Female ,business - Abstract
This study was undertaken to determine whether S-adenosyl-L-methionine (SAMe) changes the lipid composition and fluidity of erythrocyte membranes in chronic liver disease. SAMe was administered intravenously at a daily dose of 600 mg for 2 weeks to 10 patients; 6 patients with cirrhosis and four with primary biliary cirrhosis. The elevated free cholesterol to phospholipid molar (C/PL) ratio of the erythrocyte membranes of the patients (0.857 +/- 0.018) significantly decreased after the administration of SAMe (1 week, 0.823 +/- 0.021; 2 weeks, 0.823 +/- 0.013). In all of the four patients whose erythrocyte membrane fluidity was measured, fluidity improved with the administration of SAMe and correlated with the C/PL ratio of the membranes. These results suggest that SAMe decreases the C/PL ratio of erythrocyte membranes and thus improves membrane fluidity in chronic liver disease.
- Published
- 1992
49. Interferon-gamma reduces the thyroid peroxidase content of cultured human thyrocytes and inhibits its increase induced by thyrotropin
- Author
-
Seiichiro Tarui, Tetsuro Kobayashi, Toshiaki Hanafusa, Shin-ichiro Takai, Norio Kono, and Hideki Asakawa
- Subjects
Adenoma ,Adult ,Male ,endocrine system ,medicine.medical_specialty ,endocrine system diseases ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Thyroid Gland ,Fluorescent Antibody Technique ,Thyrotropin ,Biochemistry ,Iodide Peroxidase ,Interferon-gamma ,Endocrinology ,Antigen ,Thyroid peroxidase ,Internal medicine ,medicine ,Humans ,Interferon gamma ,Thyroid Neoplasms ,Child ,Cells, Cultured ,Autoimmune disease ,biology ,Biochemistry (medical) ,Thyroid ,HLA-DR Antigens ,Middle Aged ,medicine.disease ,Recombinant Proteins ,Kinetics ,medicine.anatomical_structure ,biology.protein ,Thyroidectomy ,Female ,Antibody ,Peroxidase ,Hormone ,medicine.drug - Abstract
To clarify the role of interferon-gamma (IFN gamma) in autoimmune thyroid diseases, we investigated the effects of IFN gamma on the content of thyroid peroxidase (TPO) and the expression of HLA-DR antigens in cultured normal human thyrocytes. The effect of TSH on the action of IFN gamma was investigated. Immunofluorescence staining and photometric analysis showed that IFN gamma not only induced the expression of DR antigen, but also reduced the content of TPO in a concentration-dependent manner. The addition of TSH increased the content of TPO and enhanced the IFN gamma-induced expression of DR antigen. IFN gamma also inhibited the increase in TPO content induced by TSH. Thus, complex interactions appear to exist between IFN gamma and TSH or thyroid-stimulating antibodies in the modulation of hormone secretion and autoimmune phenomena in the thyroid.
- Published
- 1992
50. Effects of splenectomy on immune thrombocytopenic purpura in (NZW x BXSB) F1 mice: analyses of platelet kinetics and anti-platelet antibody production
- Author
-
Seiichiro Tarui, Shigenori Honda, Hajime Mizutani, Takayasu Furubayashi, Yoshiyuki Kurata, Takeshi Yonezawa, Hirokazu Kashiwagi, Hironori Take, and Susumu Ikehara
- Subjects
Blood Platelets ,Male ,medicine.medical_specialty ,Cell Survival ,medicine.medical_treatment ,Splenectomy ,Spleen ,Mice ,Immune system ,Internal medicine ,medicine ,Animals ,Platelet ,Autoantibodies ,Purpura, Thrombocytopenic, Idiopathic ,biology ,business.industry ,Platelet Count ,Indium Radioisotopes ,Hematology ,medicine.disease ,Thrombocytopenic purpura ,Purpura ,Kinetics ,Endocrinology ,medicine.anatomical_structure ,Immunology ,biology.protein ,Bone marrow ,medicine.symptom ,Antibody ,business - Abstract
SummaryEffects of splenectomy on platelet kinetics and production of anti-platelet antibodies were studied in male (NZW × BXSB) F1 (W/B F1) mice, which are known as the animal model of immune thrombocytopenic purpura (ITP). Studies on organ localization of radiolabeled platelets revealed that splenic uptake significantly increases in W/B F1 mice in comparison with that of normal controls. W/B Fj mice showed a significant increase in platelet counts and, in contrast with sham-operated controls, high levels of platelet counts were maintained up to 6 weeks after splenectomy. Platelet lifespans (PLSs) did not reach normal levels, although prolonged PLSs were observed. In addition, platelet-associated antibody (PAA) values showed a tendency towards transient decrease, but there was no change in platelet-bindable serum antibodies (PBAs). These findings indicate that the suppression of anti-platelet antibody production is essential to the treatment of ITP; splenectomy may not be effective in treating severely affected ITP patients because, although the spleen is one of the major sites of platelet sequestration and antibody production, reticulo-endothelial systems (RESs) (liver, bone marrow, lymphnodes, etc.) other than the spleen are also responsible for the destruction of platelets. We therefore consider the W/B F1 mouse to be a useful model of human ITP, and believe that it provides valuable information for the development of new therapeutic agents in patients with ITP, especially those who do not respond to splenectomy.
- Published
- 1992
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