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Biomedical subjects

N Amino

Publications and source records attributed to N Amino.

At least 163 records · Page 9Linked to original sources

A case of postpartum hypopituitarism associated with empty sella: possible relation to postpartum autoimmune hypophysitis.

A fifty-year-old woman was admitted to our hospital because of generalized edema, progressive symptoms of fatigue and weakness of ten years' duration. After an uneventful third delivery, 24 years before admission, she could not lactate and developed oligomenorrhea and then amenorrhea. Laboratory evaluation revealed panhypopituitarism and pituitary cell antibodies were positive. Both CT scans and MR images showed empty sella. This case is postpartum hypopituitarism without a preceding history of excessive bleeding and may be autoimmune hypophysitis.

Autoimmune Diseases↗

[T4 autoantibody].

Explore the source record for details and available documents.

Autoantibodies↗

[Effect of theophylline on the thyroid function in healthy subjects: comparison between the short- and long-term medication].

Effect of theophylline on the thyroid function was studied in 9 healthy subjects. Theophylline (200mg) was taken two times (AM8:00, PM10:00) and blood was collected two times (AM9:00, PM4:00) a day for five days. Five of these 9 subjects took same dose two times (AM8:00, PM10:00) a day and blood was collected once (AM9:00) a week for four weeks. In short-term medication, serum free thyroxine (FT4) increased significantly (1.19 +/- 0.19 ng/dl, before medication) in 4th day AM (1.29 +/- 0.14 ng/dl, p < 0.05), in 4th day PM (1.30 +/- 0.12 ng/dl, p < 0.05) and in 5th day AM (1.30 +/- 0.16 ng/dl, p < 0.05). Serum free triiodothyronine (FT3) increased significantly (3.9 +/- 0.36 pg/ml, before medication) in 4th day AM (4.3 +/- 0.66 pg/ml, p < 0.05) and in 5th day AM (4.3 +/- 0.61 pg/ml, p < 0.05). Serum thyroid stimulating activity (TSA), which was measured as an increase in cAMP in FRTL-5 cells, increased significantly (116.5 +/- 49.5%, before medication) in 1st day PM (152.3 +/- 60.0%, p < 0.05), in 2nd day PM (192.6 +/- 86.7%, p < 0.05), in 3rd day PM (208.5 +/- 94.1%, p < 0.05) and in 4th day AM (183.5 +/- 80.1%, p < 0.05). In contrast, serum FT4, FT3, TSH, and TSA did not increase significantly in long-term medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[A clue for discovery and recent progress in gene abnormalities].

With the striking progress in analytic technology for detecting gene abnormalities, genetic analysis, such as polymerase chain reaction (PCR), has become a routine procedure in laboratory medicine. Consequently, the role of laboratory medicine in detecting genetic disease is increasing. However, in the process of genetic analysis maintaining consistency with clinical expression is necessary. In this symposium, the discussion includes the following items: (1) Genetic analysis of Maple Syrup Urine Disease (MSUD), (2) Analytic study of abnormal antithrombin III (TOYAMA), (3) Diagnostic procedures for anemia attributed to RBC membrane protein abnormality, (4) Genetic analysis of LDH-M subunit deficiency, (5) Development of a new prospect for hereditary hyperlipidemia, (6) Genetic analysis of hormone resistance syndromes: T3 receptor abnormality, and (7) Etiologic genetic analysis of pituitary cretinism. In general, DNA analysis in these cases can demonstrate wide variations in gene structural abnormalities. In MSUD, for instance, enzyme abnormalities, which occur in enzyme complex of various kinds include E1 alpha, beta, or E2. Currently, the cell fusion method, and PCR-SSCP method, miss-match PCR-DGGE method and so on are commonly used analytic methods. To sum up the issues discussed at this symposium, the most important function of genetic analysis is to clarify the relationship between the many clinical phenotypic expressions and the essential abnormality in the structure of the gene and/or function of the controlling proteins.

Chromosome Aberrations↗

[Molecular pathology of congenital pituitary hypothyroidism--discovery of new clinical entities].

Congenital pituitary hypothyroidism (pituitary cretinism) results in severe mental and growth retardation when it is not treated soon after birth. Since the introduction of neonatal mass screening of thyrotropin (TSH), most congenital hypothyroidism has been detected except for pituitary and hypothalamic hypothyroidism. In 1971, we reported the first familial case of congenital isolated TSH deficiency and thereafter began intensively investigating the molecular pathology of congenital pituitary hypothyroidism. After determining the entire structure of the human TSH beta gene, we identified the molecular pathology in this patient. Recently, we reported a familial case of congenital combined pituitary hormone deficiency (PIT1 abnormality). To examine the PIT1 gene, which encodes pituitary specific transcription factor, Pit-1/GHF-1, we determined its genomic structure. Sequence comparisons using PCR amplified PIT1 gene sequences revealed only one nonsense mutation in the patient, and established that this alteration caused the combined deficiencies of TSH, GH and PRL. We also discuss other recent progress in molecular pathology of congenital pituitary hypothyroidism.

Congenital Hypothyroidism↗

[A quantitative measurement of polymorphonuclear leukocyte oxidative metabolism using plasma depleted blood by flow cytometry].

We investigated a method measuring the superoxide production in peripheral polymorphonuclear leukocytes (PMN) in whole blood by flow cytometer using DCFH-DA as marker dye. The DCFH-DA which is colorless in its form and is freely permeable into blood cells is converted into DCF, a fluorescent substance, by oxidative reaction of superoxide in PMN. Thus, the superoxide production in PMN is measurable by counting number of fluorescence positive cells and their intensity by flow cytometer. However, when the DCFH-DA is added to the whole blood, a considerable amount of it is trapped not only in PMN but also in red blood cell, thus giving rise an inconsistent incorporation of the DCFH-DA in PMN due to differences in number of red blood cell among samples. Furthermore, there are several anti-oxidative factors in blood plasma. In order to avoid possible effects of plasma oxidative factors and red blood cell-numbers in whole blood on the measurement of PMN-superoxide production, we prepared plasma depleted blood by washing and the number of red blood cells was adjusted to 5 x 10(6) microliters before addition of DCFH-DA. This improved reproducibility and gave within assay coefficient of variance (CV) of 3.62% for a sample with normal value and 7.09% for a low value sample. The value obtained by this method correlated well with those of NBT reduction test (r = -0.887). It is concluded that this method is simple, reliable and useful for the clinical determination of superoxide production instead of NBT test.

Cells, Cultured↗

Nucleotide sequence of the complementary DNA for human Pit-1/GHF-1.

Human cDNA clones encoding Pit-1/GHF-1, a pituitary-specific DNA binding factor, were obtained by PCR following reverse transcription of human pituitary RNA. It is approx. 1.3 kb in size with 0.1 kb 5' non-coding region, 0.9 kb protein-coding region and 0.3 kb 3' non-coding region. The predicted human Pit-1/GHF-1 peptide structure has 291 amino acids and is highly conserved among mouse, rat and bovine. In addition, the 5' non-coding region is highly conserved with rat pit-1/GHF-1 sequence to the transcription start site.

Amino Acid Sequence↗

Chinese medicine, Coix seeds increase peripheral cytotoxic T and NK cells.

Coix seeds, a Chinese medicine have been used in Japan and reported to be effective in patients with verruca vulgaris and verrucae planae juveniles. We investigated the in vivo effects on lymphocyte subsets in seven healthy volunteers who took six tablets of Coix seeds three times a day (a typical dose) for four weeks. Leukocyte counts and the percentage of total lymphocytes did not change but the percentages of CD3+CD56+ cells and CD16+CD57- cells increased significantly. These results indicate that Coix seeds increase peripheral cytotoxic lymphocytes and may be effective to viral infection through the enhancement of cytotoxic activity.

Adult↗

Cretinism with combined hormone deficiency caused by a mutation in the PIT1 gene.

Cretinism is marked by irreversible mental and growth retardation. We describe here an entirely new case of cretinism showing combined pituitary hormone deficiencies of thyrotropin, growth hormone and prolactin that appears to be caused by homozygosity for a nonsense mutation in the gene for the pituitary specific transcription activator, Pit-1/GHF-1 (designated PIT1 in humans for pituitary specific factor 1). This is the first report in humans of a defect in a transcription activator causing deficiency of multiple target genes.

Amino Acid Sequence↗

Decreases in alpha beta T cell receptor negative T cells and CD8 cells, and an increase in CD4+ CD8+ cells in active Hashimoto's disease and subacute thyroiditis.

We examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from alpha beta T cell receptor (TCR) negative T (WT31-CD3+) cells and CD8 (CD4-CD8+) cells decreased and those of CD4+CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+CD8-) cells, non-T, non-B (CD5-CD19-) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, alpha beta+ TCR T (WT31+CD3+) cells, CD8 cells, and non-T, non-B cells. A serial study of some of the patients showed opposite changes in alpha beta TCR- T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. alpha beta TCR- T cells were mostly gamma delta TCR+ T (IIF2+ CD3+) cells in these patients. These data suggest that alpha beta TCR-T (gamma delta TCR+ T), CD8, and CD4+ CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells are important in thyroid stimulation in Graves' disease.

Adult↗