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H Namba

Publications and source records attributed to H Namba.

At least 19 recordsLinked to original sources
PubMed1992

Molecular cloning and sequencing of an alternatively spliced form of the human thyrotropin receptor transcript.

In the present study, we report the molecular cloning and sequencing of an alternatively spliced form of the human thyrotropin receptor (hTSHR) mRNA transcript, which has previously been detected on Northern blot analysis of human thyroid cells. The smaller hTSHR cDNA, designated hTSHR cDNA-I, is approximately 1 kb in size and encodes a protein of 253 amino acids. Comparison of the nucleotide sequence of hTSHR cDNA-I with available hTSHR genomic sequence data reveals that the cDNA-I contains exons 1-8 and unidentified DNA tract, presumably an intron. Thus, the hTSHR cDNA-I encodes for the N-terminal half of the extracellular domain of the hTSHR (approximately 60%). The truncated TSHR-I may be secreted and function as a TSH binding protein.

Alternative Splicing↗
PubMed1992

Growth hormone deficiency and empty sella syndrome in a boy with dup(X) (q13.3----q21.2).

A 2 8/12-year-old boy with severe growth failure and mental retardation was found to have a maternally derived tandem duplication of the long arm of X chromosome, dup(X) (q13.3----q21.2). Karyotypic interpretation was further confirmed in this patient by a double gene dose for red blood cell phosphoglycerate kinase. DNA replication study showed that the duplicated X chromosome was always late replicating in peripheral blood lymphocytes as well as in skin fibroblasts from the mother. Endocrine studies in the patient demonstrated growth hormone deficiency. Magnetic resonance imaging of the head then disclosed the empty sella syndrome. This appears to be the first report of a dup(Xq) patient associated with a growth hormone deficiency and the empty sella syndrome. We emphasize that duplication of the proximal Xq in males represents another microduplication syndrome (Thode-Leonard syndrome).

Child, Preschool↗
PubMed1992

Unique karyotypes in two patients with Prader-Willi syndrome.

A physical disruption of the Prader-Willi syndrome (PWS) chromosome region is thought to cause PWS. We describe 2 girls with PWS phenotype, who had unique chromosome 15 abnormalities. The first patient showed mosaicism: 45,XX,t(15;15)(qter----p11.1::q11.200----qter)/46,XX,t(15;15)(qter----p1 1.1::q 11.200----qter), +mar. The band 15q11.2 apparently remained intact in the t(15;15) chromosome, and the mar chromosome was considered as r(15) (p11.1q11.1). The second patient had a karyotype of 47,XX,del(15)(q11.200----q11.207), +idic (15)(pter----q11.1::q11.1----pter). The complex breakage and reunion involving the 15q11.2 regions of the father's homologous chromosomes 15 at meiosis appeared to have resulted in the idic(15) and the del(15) chromosomes. These cytogenetic findings suggest that the PWS chromosome region may be localized on the very proximal portion of band 15q11.2.

Child↗
PubMed1992

Multiple endocrine neoplasia type 2 with malignant pheochromocytoma--long term follow-up of a case by 131I-meta-iodobenzylguanidine scintigraphy.

The case of a 33-year-old Japanese man, who has Multiple Endocrine Neoplasia Type 2 (MEN IIa) (Sipple's syndrome) with malignant pheochromocytoma, is reported. He had survived for twelve years since the initial diagnosis of malignant pheochromocytoma. Within this period, he had undergone 131I-meta-iodobenzylguanidine scintigraphy twice, in 1983 and 1990. This is the first case in Japan of a longterm surviving patient with malignant pheochromocytoma followed up by 131I-MIBG scintigraphy. Although he had no exacerbation of clinical symptoms or urinary catecholamine levels, second scintigraphy clearly showed an increase in the tumor size, new metastasis of the malignant pheochromocytoma and exacerbation of the medullary thyroid carcinoma. Compared with any other roentgenological device and hormonal data, 131I-MIBG scintigraphy was seen to be a good tool for evaluating the localization and the progression of tumors. 131I-MIBG scintigraphy is a useful procedure not only for initial diagnosis but also for judging progression in a case of advanced malignant pheochromocytoma.

3-Iodobenzylguanidine↗
PubMed1992

Impairment of the TSH signal transduction system in human thyroid carcinoma cells.

In order to further evaluate the role of TSH in the proliferation and the differentiation of human thyroid carcinoma cells, we have analyzed the function of the TSH receptor in the established thyroid carcinoma cell lines NPA and WRO. The TSH signal transduction system in the carcinoma cells was also compared with that in normal thyroid cells. Although unresponsiveness to bovine and human TSH was demonstrated by measurement of cAMP production and [3H]thymidine incorporation after treatment of TSH, cAMP production was induced after stimulation of these cells by forskolin, cholera toxin, and isoproterenol. Specific binding to 125I-TSH was demonstrated in both NPA and WRO cells in addition to the existence of a TSH receptor mRNA and thyroglobulin mRNA species, although thyroid-specific gene expression in these cells was not regulated by TSH. These findings suggest that the unresponsiveness to TSH in these cells may be due to an abnormality of TSH receptor-G protein coupling rather than to a decreased level of TSH-receptor expression or a Gs protein abnormality.

Base Sequence↗
PubMed1992

Interleukin-1 inhibits human thyroid carcinoma cell growth.

In order to further clarify the growth regulating effect of cytokines on thyroid cell proliferation, the effect of interleukin-1 (IL-1) was tested on growth of human papillary and follicular thyroid carcinoma cells (NPA and WRO). Although fetal bovine serum stimulated DNA synthesis, TSH did not affect cell growth and the level of thyroglobulin messenger RNA (mRNA) in NPA. Eight-bromo-cAMP and forskolin, however, significantly suppressed DNA synthesis, suggesting the impairment of TSH receptor signal transduction in NPA cells despite of the presence of [125I]TSH binding. Both IL-1 alpha and beta inhibited [3H] thymidine uptake into NPA cell DNA in a dose- and time-dependent manner at concentrations ranging from 5 x 10(2) to 10(5) U/L; 10(5) U/L of IL-1 suppressed DNA synthesis by more than 40% of control. The suppressive activity of IL-1 beta was more potent than that of IL-1 alpha in spite of the same lymphocytes activating factor (LAF) activity. Steady state levels of c-myc mRNA transcripts were also inhibited by both IL-1 alpha and beta, respectively. On the other hand, IL-1 alpha and beta did not affect the WRO cell growth. Although forskolin stimulated cAMP production in NPA cells, IL-1 did not induce cAMP generation. Indomethacin (1.0 approximately 10 mg/L) did not alter the suppressive activity of IL-1. Neither IL-1 alpha and beta caused a cytotoxic effect on the NPA cells. Although changes in c-myc mRNA content may just be an epiphenomenon of the decrease in proliferative activity in response to IL-1, and not a direct target of action of the peptide, these results demonstrate the inhibitory effect of IL-1 on cell growth of NPA. IL-1 may have an aspect of antitumorigenic action in some human thyroid carcinoma differentiation and replication.

Adenocarcinoma↗
PubMed1992

Acute adrenal insufficiency due to symptomatic Rathke's cleft cyst.

A 65-year-old Japanese man who suffered from secondary hypopituitarism due to Rathke's cleft cyst is reported. Although computed tomography failed to detect any pituitary abnormality, magnetic resonance imaging demonstrated the presence of a cystic intrasellar mass, initially suggesting craniopharyngioma or abscess. Operative findings revealed Rathke's cleft cysts within the pituitary fossa which resulted in secondary hypopituitarism. Among cases of secondary hypopituitarism with abnormal findings in the pituitary, symptomatic Rathke's cleft cysts should be included in the differential diagnosis of adrenal insufficiency.

Adrenal Insufficiency↗
PubMed1992

[A case of medically treated type A acute aortic dissection: trial of antifibrinolytic therapy while monitoring the thrombotic and fibrinolytic parameters].

A 56-year-old male was admitted with severe chest and abdominal pain. Enhanced CT revealed type-A acute aortic dissection. Enhancement of false lumen was complete in the aortic arch, but it was incomplete in the ascending and descending aorta. This finding suggested a thrombosing tendency of the false lumen. Marked elevation of Thrombin-Antithrombin III complex (TAT) and Plasmin-alpha 2 Plasmin inhibitor complex (PIC) indicated the activation of both coagulation and fibrinolysis in the false lumen. Aprotinin and Tranexamic acid were used in order to suppress the fibrinolysis. Both TAT and PIC were completely normalized at the 20th hospital day. Enhanced CT on the 40th hospital day showed that the false lumen had disappeared, and the adventitia had thickened. Care should be taken to notice activated coagulation and fibrinolysis in the false lumen. This report appears to be the first statement about the effectiveness of antifibrinolytic therapy to facilitate thrombosing and healing of the false lumen in the treatment of acute aortic dissection.

Acute Disease↗
PubMed1992

[A successful surgical case of thoracoabdominal aortic aneurysm ruptured into the right pleural cavity].

A 55-year-old man was transferred to our cardiovascular center because of right hemothorax and hemorrhagic shock. Emergency CT scan revealed a thoracoabdominal aortic aneurysm (Crawford's type I-A) ruptured into the right thorax. The aneurysm was exposed by Stoney's spiral opening approach. A 24 mm Cooley Dacron graft was implanted in end-to-end fashion between the descending thoracic aorta and the abdominal aorta just above the celiac artery. The use of aortic artery cannula, femoral artery cannula and flexible polyvinyl tube provided safe and simple means as a temporary bypass during this graft replacement. Postoperative course was uneventful.

Aorta, Abdominal↗
PubMed1991

Specification of small distal 6q deletions in two patients by gene dosage and in situ hybridization study of plasminogen and alpha-L-fucosidase 2.

Gene-dosage and in situ hybridization study of plasminogen (PLG) and alpha-L-fucosidase 2 (FUCA2) was performed on two patients with a small deletion of the distal long arm of chromosome 6, to define the structural abnormality more precisely. The results led to the cytogenetic diagnosis of an interstitial 6q deletion, del(6)(q25.1q25.3), in one patient and of a terminal 6q deletion resulting from a paternal t(1;6)(q44;q2605) translocation in the other patient. The latter patient had congenital noncommunicating hydrocephalus due to obstruction at the level of the foramen of Monro or the third ventricle which has not previously been described in terminal 6q deletions. Review of the literature suggests the emergence of a clinical syndrome associated with terminal 6q deletions.

Abnormalities, Multiple↗
PubMed1991

Lesion of the nucleus basalis magnocellularis does not affect cerebral cortical blood flow in rats.

The effects of a unilateral ibotenic acid lesion of the nucleus basalis magnocellularis (NBM) on blood flow of the cerebral cortex and striatum were studied at 2, 4, 8 and 16 weeks after the lesion in conscious rats. In the cerebral cortex, no side-to-side difference in blood flow was observed, though cholinergic enzyme activity was markedly reduced on the side of the lesion. The results suggest that NBM lesion produces disturbance of cholinergic neurons in the cerebral cortex without significant alteration of blood flow.

Acetylcholinesterase↗
PubMed1991

Lack of evidence for the presence of human immunodeficiency virus type 1-related sequences in patients with Graves' disease.

The pathogenesis of human autoimmune diseases, including Graves' disease, remains to be elucidated. Recently, Ciampolillo et al. proposed that human immunodeficiency virus type 1 (HIV-1)-related retroviruses were involved in Graves' disease. Using Southern blot analysis, they found specific integration of exogenous sequences homologous to HIV-1 gag region in genome DNA of thyrocytes and peripheral blood lymphocytes (PBL) of patients with Graves' disease. In order to test their hypothesis, we examined the presence or the absence of HIV-1 gag-related sequences in Japanese Graves' patients using the polymerase chain reaction (PCR) in addition to Southern blotting. Sets of primer pairs used in PCR were designed to cover the whole span of the HIV-1 gag region. Hybridization was performed in both relaxed and stringent conditions. Our results showed that neither Southern blot hybridization nor PCR gave positive signals in any of the samples examined from Graves' patients. This suggests that HIV-1 or its closely associated viruses are unlikely to be involved in the pathogenesis of Graves' disease in Japan.

Adolescent↗
PubMed1991

Assignment of human porphobilinogen deaminase to 11q24.1----q24.2 by in situ hybridization and gene dosage studies.

In situ hybridization and gene dosage-effect studies were conducted to determine the detailed chromosomal location of the gene encoding human porphobilinogen deaminase (PBGD). Red cell PBGD activity was normal in one patient with monosomy for 11q24.2----qter but was increased 1.5 times in another patient with trisomy for 11q22.2----qter. The cDNA probe for PBGD was found to be specifically hybridized to band 11q24. These results suggest that the gene for PBGD is localized within the region 11q24.1----q24.2.

Abnormalities, Multiple↗
PubMed1991

Solitary polyclonal autonomous thyroid nodule: a rare cause of childhood hyperthyroidism.

Solitary autonomous thyroid tumors are an unusual cause of hyperthyroidism, particularly in childhood. We describe the youngest individual so far reported with this condition, a 22 month child with a large hyperfunctioning thyroid nodule who became overtly hyperthyroid after iodinated contrast administration. The histology of the nodule was compatible with follicular cell hyperplasia. These tumors are often called toxic adenomas, although there is no solid evidence that they are true neoplasms. We examined the clonal composition of the child's thyroid tumor by X-chromosome inactivation analysis, taking advantage of a polymorphism in the X-chromosome gene phosphoglycerate kinase. The tumor consisted of an even mixture of cells containing activated paternal and maternal PGK alleles, indicating that the tumor was polyclonal. Furthermore, the nodule had no structural rearrangements or activating point mutations of ras oncogenes, which are found in up to 50% of solitary monoclonal follicular adenomas. Solitary hot nodules may at least in some cases be secondary to hyperplasia, and not to clonal expansion of an abnormal, mutated cell. This may also explain the relatively low frequency of malignant transformation observed in hyperfunctioning thyroid tumors.

Adenoma↗
PubMed1991

[Physiologically active compounds in the extracts from tochukaso and cultured mycelia of Cordyceps and Isaria].

Tochukaso is a Chinese traditional medicine composed of a fruit body of Cordyceps sinensis and its parasitic host larva. Tochukaso (C. sinensis) and the cultured mycelia of five species of Cordyceps and four species of Isaria were each extracted with hot water and examined for the inotropic effect on guinea-pig right atrium in vitro system. The extracts from C. militaris and I. felina showed a negative inotropic effect to approximately the same extent as that from Tochukaso. These three extracts also showed inhibitory action on twitch response of guinea-pig ileum and aggregation of human blood platelet. It is suggested that these activities are ascribed to the combination of adenosine, 5'-adenosine monophosphate and several other nucleic acid-related compounds, all of which have been shown to be present in the extracts.

Animals↗
PubMed1991

Lack of PTC gene (ret proto-oncogene rearrangement) in human thyroid tumors.

PTC gene, which is derived from the rearranged form of the ret proto-oncogene, was originally discovered in human thyroid papillary carcinomas. This gene has been thought to act as a tumorigenetic factor in thyroid carcinoma, although the action of PTC oncogene products is still unknown. To study the frequency of the PTC gene present in human thyroid carcinomas, we investigated four cell lines derived from thyroid carcinoma and 22 thyroid tumor tissue specimens. The reverse transcriptase-polymerase chain reaction (RT-PCR) method was performed to detect putative PTC mRNA. The presence of the PTC gene in genomic DNA was analyzed by Southern blot hybridization. PTC mRNA was detected by the RT-PCR method in only one papillary carcinoma cell line (TPC-1 cell). Southern gel analysis confirmed the rearrangement of the ret proto-oncogene in this cell line. In the other three cell lines and 22 tumor tissue specimens, however, neither the PTC gene or mRNA was detected. These results demonstrate that the prevalence of the PTC gene in thyroid tumor is low and may not be essential for human thyroid tumorigenesis. That our present results conflict with previous reports may be due to general differences in genetic background among races.

Base Sequence↗
PubMed1991

[Blood flow measurement of brain tumor by 123I-IMP using 3-heads rotating gamma camera SPECT].

Using 3-heads rotating gamma camera SPECT system, regional blood flow was measured from the super-early image obtained 4 to 6 minutes after the intravenous injection of 123I-IMP on 11 patients with various brain tumors. Two cases of olfactory groove meningioma and malignant astrocytoma showed significantly high 123I-IMP uptake by the lesion visualized by MRI compared to the uptake by normal brain cortex on super-early image but 123I-IMP uptake by the tumor decreased on early image. In both cases, blood flow of the tumor measured from super-early image showed values much higher than those of normal brain cortex. It was thought that usual correction method based on early image did not correctly represent the blood flow of the lesion but that the present method based on super-early image could show the increase of blood flow of the tumor.

Adult↗