Unpleasant alcohol effect in diabetes associated with 3243 bp mitochondrial tRNALeu(UUR) mutation.
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Adult↗
Biomedical subjects
M Taniyama
Publications and source records attributed to M Taniyama.
Stimulatory effect of human insulin on erythroid progenitors (CFU-E and BFU-E) in human CD34+ separated bone marrow cells and the relationship between insulin and erythropoietin.
Erythropoietin is known to be effective for the treatment of anemia in chronic renal failure, but the efficacy of erythropoietin for anemia in other diseases is not so great. Insulin exerts a growth promoting activity in various kinds of cells. In the present study, the effects of insulin on erythroid progenitors (colony forming units-erythroid, CFU-E; and burst forming units-erythroid, BFU-E) in human bone marrow were examined at various concentrations of recombinant human erythropoietin (rh-Epo) to clarify the relationship between erythropoietin and insulin. Human insulin stimulated the formation of CFU-E and BFU-E in the presence of three concentrations (0.25, 5, and 100 U/ml) of rh-Epo. Stimulatory effects of human insulin on CFU-E and BFU-E were also observed in the nonphagocytic and nonadherent bone marrow fraction (NP-NA fraction) and in the NP-NA and T cell-depleted fraction at each concentration of rh-Epo. Human insulin further stimulated the CFU-E and BFU-E growth in CD34+ separated bone marrow cells. These results indicate that the enhancing effect of human insulin on erythroid progenitors is not mediated through monocytes and macrophages or T cells, suggesting a direct action on erythroid progenitors.
Animals↗
Specific PCR amplification for N-ras mutations in neoplastic thyroid diseases.
We analyzed point mutations of N-ras protooncogene codon 61 in thyroid neoplasms by means of a mutation-specific PCR method. In this method, one of the paired primers has a base at the 3' terminal that is complementary to a mutated base of the DNA sequence to be analyzed. With this primer, only alleles which have the same mutation can be amplified. Among 24 thyroid tissues, we detected 2 point mutations out of 7 follicular carcinomas (29%). One tumor had a cytosine to adenine substitution mutation at the first base of codon 61, and the other had an adenine to guanine substitution mutation in the second base of the same codon. The same mutations were not detected in 7 follicular adenomas or 1 papillary carcinoma. These results were confirmed by both dot blot hybridization and direct sequencing method. Mutation of N-ras codon 61 may be significant in malignant transformation of follicular thyroid tumors. Because of its easy availability, the mutation-specific PCR method is a useful screening test for N-ras mutations.
Adenocarcinoma, Follicular↗
Circulating activated T lymphocyte subsets in patients with silent thyroiditis.
In order to investigate the immunological aspects of silent thyroiditis, T lymphocyte subsets were analyzed by two-color flow cytometry in 10 patients with silent thyroiditis in the thyrotoxic phase, 12 patients with silent thyroiditis in the recovery phase, and 11 healthy volunteers as a control. The percentages of CD3+, CD4+, and CD8+ cells were similar in all three groups. In contrast, activated matured T (HLA-DR+CD3+), activated helper/inducer T (HLA-DR+CD4+) and activated suppressor/cytotoxic T (HLA-DR+CD8+) cells were more numerous in both the thyrotoxic and the recovery phases of patients with silent thyroiditis when compared with healthy controls. In a serial study of 6 patients with silent thyroiditis, the percentage of activated helper/inducer T (HLA-DR+CD4+) cells was higher in the thyrotoxic phase than in the recovery phase. These data indicate that the activation of T cells, especially of helper/inducer T cells, might be important for the induction of silent thyroiditis.
Adolescent↗
[Specific amplification by PCR for N-ras mutation in thyroid follicular cartinoma].
Mutation-specific PCR amplification, a special version of allele-specific amplification, is a method for detection of known mutation. In this method, one of the paired primers has a base at the 3' terminal that is complementary to a mutated base. With this primer, only alleles which have the same mutation can be amplified. We analyzed point mutations of N-ras protooncogene codon 61 in thyroid neoplasms using this mutation-specific PCR amplification method. This method is easy to perform, and many samples can be treated at one time. We detected 2 point mutations of N-ras codon 61 out of 7 follicular carcinomas. One was a cytosine to adenine substitution mutation at the first base, and the other was an adenine to guanine substitution mutation in the second base. These mutations were not detected in 7 follicular adenoma and 1 papillary carcinoma. The results were confirmed by both dot blot hybridization and direct sequencing. Mutation-specific amplification is a powerful method for detection of known mutations of protooncogenes or tumor suppressor genes in investigation of the cancer biology.
Adenocarcinoma, Follicular↗
Urinary cortisol metabolites in the assessment of peripheral thyroid hormone action: application for diagnosis of resistance to thyroid hormone.
Urinary cortisol metabolites are altered both quantitatively and qualitatively in thyroid dysfunction. This study was conducted to elucidate the usefulness of urinary cortisol metabolites in the assessment of peripheral thyroid hormone action, particularly in the patients with inappropriate thyrotropin secretion. Twenty-four hour urinary 17-hydroxycorticosteroid (17-OHCS) level and gas chromatographical steroid profile were studied in 25 hyperthyroid, 18 hypothyroid, and 24 euthyroid control subjects. Five patients with generalized thyroid hormone resistance and two patients with thyrotropin secreting pituitary tumor were also studied. The ratio of urinary tetrahydrocortisone to tetrahydrocortisol (THE/THF) was significantly elevated in hyperthyroidism (4.58 +/- 1.49) and depressed in hypothyroidism (1.31 +/- 0.55) compared to control (1.93 +/- 0.35). There were good correlations between THE/THF and serum thyroid hormone levels, especially in hypothyroidism. THE/THF can be a good biochemical indicator for deficiency of peripheral thyroid hormone action. Two patients with thyrotropin-secreting tumor showed high THE/THF, which reflected thyroid hormone excess. In contrast, THE/THF in the patients with generalized thyroid hormone resistance was low as compared to high serum thyroid hormone levels. Similar findings were demonstrated with 17-OHCS but discrimination of thyroid hormone resistance was insufficient. Thus, the ratio of the urinary concentrations of cortisol metabolites, THE/THF, appears to be a good marker for peripheral thyroid hormone resistance.
17-Hydroxycorticosteroids↗
Graves' thyrotoxicosis and Moyamoya disease.
Cerebrovascular accidents due to Moyamoya disease, a disorder characterized by arterial stenosis at the base of the brain accompanied by typical net-like collateral vessels, occurred in two young Japanese women with Graves' disease when they were in thyrotoxicosis. In one patient, a second attack of cerebral infarction occurred with the recurrence of thyrotoxicosis. Association of Moyamoya disease and Graves' thyrotoxicosis is rare and the pathegenetic relationship is discussed.
Adult↗
Simultaneous development of insulin dependent diabetes mellitus and alopecia areata universalis.
Alopecia areata universalis developed gradually over nine months in a 25-year-old woman. When her scalp hairs were totally lost and other body hair began to fall out, the symptoms of insulin dependent diabetes mellitus, an organ-specific autoimmune disease, developed rapidly and progressed to diabetic coma. Alopecia did not regress after the metabolic state improved following insulin therapy. Biopsy of the scalp skin revealed significant reduction of the total number of hair bulbs and prominent lymphocyte infiltration into the remaining hair follicles. Insulin dependent diabetes mellitus and alopecia areata universalis are both thought to be related to the autoimmune mechanism and sometimes coexist. However, simultaneous development of these two disorders is extremely rare.
Adult↗
[The significance of serum fructosamine measurement in patients with thyroid diseases].
Serum fructosamine was measured in patients with Graves' disease and primary hypothyroidism. Fructosamine levels and fructosamine per albumin ratio were significantly lower in patients with Graves' disease than in normal subjects, while they were significantly higher in patients with primary hypothyroidism. Fructosamine levels were normalized by treatment in the euthyroid state in patients with Graves' disease. Along with the normalization of thyroid stimulating hormone levels, fructosamine levels returned to the normal range in patients with primary hypothyroidism with treatment. There were significant correlations between fructosamine levels and free triiodothyronine levels, free thyroxine levels, thyroid stimulating hormone levels, hemoglobin A1C levels, albumin levels, and creatine phosphokinase levels. We concluded that it was useful to measure serum fructosamine as an indicator of peripheral metabolic function in patients with thyroid diseases.
Creatine Kinase↗
[Phosphorylation of 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase and enzyme activities].
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Animals↗
Effects of streptozotocin-induced diabetes on glucose utilization that was stimulated by various agents in rat thymocytes.
Post receptor insulin resistance has been demonstrated in insulin sensitive tissues from streptozotocin induced diabetic animals. Insulin deficiency itself or metabolic derangements of diabetes seem to contribute to this insulin resistant state. However, the mechanism is presently unknown. Using largely insulin insensitive rat thymocytes, we have studied glucose oxidation stimulated by agents that mimic insulin action but that work independently of the insulin receptor. Glucose oxidations stimulated by these agents were markedly diminished in the thymocytes from streptozotocin induced diabetic rats. These findings as well as our finding that the thymocytes from diabetic rats possess a normal complement of insulin receptor provide further evidence that post insulin receptor impairment of glucose metabolism occurs in streptozotocin diabetes. Thus although thymocytes are not sensitive to insulin, they are useful for the investigation of the impaired glucose metabolism.
Animals↗
Isozymes of fructose 6-phosphate,2-kinase:fructose-2,6-bisphosphatase in rat and bovine heart, liver, and skeletal muscle.
The distribution of Fructose 6-P,2-kinase:Fructose 2,6-bisphosphatase in rat and bovine heart, liver, and skeletal muscle tissues was examined. With DEAE-cellulose chromatography, two peaks (I and II) of Fru 6-P,2-kinase activity were detected in all tissue extracts. Peak I was the predominant form both in rat and bovine heart tissue, while peak II was the major form in liver and skeletal muscle. Antibodies to heart enzyme reacted specifically with peak I, and antibodies to liver enzyme reacted with peak II from both liver and skeletal muscle. All the isozymes were bifunctional. All the tissues examined contained other isozymes in minor amounts.
Animals↗
Elevated serum creatine kinase level in diabetic patients with nephrotic syndrome: a role of fluid retention.
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Adult↗
Transient elevation of serum growth hormone level during pituitary apoplexy in acromegaly.
We report a case of acromegaly followed by pituitary apoplexy in which hormonal changes during the course of an acute episode were investigated. Serum growth hormone level increased markedly during the acute phase, and, subsequently, decreased rapidly. Finally, serum growth hormone level remained low and did not respond to stimulation. In contrast, the serum cortisol level remarkably decreased during the most serious stage and returned to the previous level after pituitary apoplexy. The low level of cortisol during the acute phase is compatible with the patient's manifestation of adrenal insufficiency, and hydrocortisone sodium succinate administration improved the critical state of the patient dramatically.
Acromegaly↗
Cell-mediated cytotoxic islet cell surface antibodies to human pancreatic beta cells.
Sera containing islet cell surface antibodies show a complement-dependent cytotoxic reaction against islet cells, but it has not yet been clarified whether islet cell surface antibodies exhibit cell-mediated cytotoxicity to these cells. By 51Cr release assay we investigated whether islet cell surface antibodies showed a cytotoxic reaction to human pancreatic B cells (JHPI-1 clone) in the presence of normal human lymphocytes. The sera from 14 islet cell surface antibody-positive, 16 islet cell surface antibody-negative Type 1 (insulin-dependent) diabetic patients and 18 islet cell surface antibody-negative healthy subjects were studied. Four sera containing islet cell surface antibodies showed specific cytotoxicity above the mean +3SD value of healthy subjects, and the mean specific cytotoxicity of islet cell surface antibody-positive sera differed significantly from that of both islet cell surface antibody-negative groups. These results suggest that this cell-mediated cytotoxic mechanism may play an important role in the pathogenesis of Type 1 diabetes.
Adolescent↗
Immunological aspect of non-obese diabetic mice: immune islet cell-killing mechanism and cell-mediated immunity.
The non-obese diabetic mouse is thought to be one of the best available animal models for human Type 1 (insulin-dependent) diabetes. By 51Cr release assay we investigated cell-mediated cytotoxicity to the islet cell of Balb/C mice, natural killer activity, and antibody-dependent cell-mediated cytotoxicity activity of spleen lymphocytes from pre-diabetic non-obese diabetic mice. The cell-mediated cytotoxicity to islet cells of non-obese diabetic mice was significantly higher than that of control ICR mice. In contrast, natural killer and antibody-dependent cell-mediated cytotoxicity activities of the spleen cells from the non-obese diabetic mice were significantly lower than those of ICR mice spleen cells. These results suggest that lymphocytes from non-obese diabetic mice were sensitized to the antigen of islet cells and that the non-specific cellular immunity of non-obese mice was reduced. They suggest also that this immune islet cell-killing mechanism may play an important role in the pathogenesis of diabetes in non-obese diabetic mice.
Animals↗
Mode of enhancement in ribonucleic acid synthesis directed by chromium (III)-bound deoxyribonucleic acid.
By forming a complex with calf thymus DNA, Cr(III), i.e., CrCl3 and Cr(NO3)3, significantly enhanced its template activity for in vitro RNA synthesis as assayed by 3H incorporation from [5-3H]uridine triphosphate (UTP). The extent of the augmentation in RNA synthesis was proportional to the binding ratio of Cr(III) to the template DNA. K2CrO4, on the other hand, neither bound to DNA nor enhanced its template activity. Experiments using rifampicin and heparin suggested that incorrect and nonviable initiation sites for RNA synthesis became functional in Cr(III)-bound DNA. The incorporation of [gamma-32P]adenosine triphosphate (ATP) into RNA synthesized on Cr(III)-bound DNA was 8 to 9 times greater than that on control DNA. This value was much higher than that of the 3H incorporation form [5-3H]UTP, i.e., the incorporation of 32P on Cr(III) bound DNA was 8 to 9 times greater that of 3H and less than twice that on control DNA. These results suggest that Cr(III) possibly induces the abnormal synthesis of RNA of a very low molecular weight, for most if not all the molecules, by binding to the template DNA.
Animals↗
Alterations in ribonucleic acid synthesis by chromium (III).
The effect of Cr(III) on in vitro RNA synthesis directed by DNA and chromatin isolated from mouse liver was investigated in comparison with other inorganic metals. At 1 mM, CrCl3 significantly stimulated RNA synthesis when incubated with DNA or chromatin prior to the addition of Escherichia coli RNA polymerase, while other metals inhibited it. This stimulation by Cr(III) was caused even at 1 muM CrCl3 on either DNA- or chromatin- directed RNA synthesis. The Cr(III)-complexes of DNA and chromatin also showed significantly enhanced template activities. On the other hand, when RNA polymerase was preincubated with Cr(III), a remarkable inhibition was observed in RNA synthesis directed by both DNA and chromatin. In isolated mouse liver nuclei with endogenous RNA polymerases, Cr(III) stimulated Mg2+-activated RNA synthesis but not Mn2r-(NH4)2SO4-activated synthesis. These results suggest that Cr(III) may alter or regulate gene expressions in mammals.
Animals↗