Successful birth in a hemodialysis patient with SLE.
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Adult↗
Biomedical subjects
H Namba
Publications and source records attributed to H Namba.
Overexpression of the intact thyrotropin receptor in a human thyroid carcinoma cell line.
Although thyrotropin is known to regulate thyroid cell differentiation and proliferation, human thyroid carcinoma cells are relatively insensitive or resistant to TSH stimulation. The expression levels of TSH receptor are significantly lower in carcinoma tissues than in normal tissues. Furthermore, in vitro human thyroid cell growth is not regulated by TSH itself. We, therefore, isolated neomycin-resistant stable human thyroid carcinoma cell (WRO cell) transfectants overexpressing intact human TSH receptor to evaluate the functional role of TSH receptor on carcinoma cells. Southern blot analysis confirmed incorporation and amplification of human TSH receptor complementary DNA sequences into genomic DNA. Northern gel analysis and reverse transcriptase-polymerase chain reaction analysis revealed the presence of specific TSH receptor messenger RNA (4.0 kilobases), and the specific binding and the affinity of [125I]TSH on stably transfected WRO cells were demonstrated compared to wild type. Nevertheless, impaired cAMP production to transfectants by TSH was observed. cAMP production was confirmed after stimulation of both wild type and transfectants by forskolin, cholera toxin, and isoproterenol. In contrast, TSH could affect the cytoplasmic calcium mobilization immediately after the addition of TSH to WRO transfectants. These results suggest that the impairment of TSH action on human thyroid carcinoma cells is not due to a major structural abnormality of the TSH receptor, reduction in the receptor number, or receptor affinity, but much more likely due to a TSH receptor-guanyl nucleotide-binding protein coupling defect.
8-Bromo Cyclic Adenosine Monophosphate↗
Evidence of thyroid volume increase in normal subjects receiving excess iodide.
A prospective study was conducted on 10 normal male volunteers to investigate the effect of the administration of excess iodide on thyroid volume. After 1 week of dietary iodide restriction, all subjects were given daily oral doses (27 mg daily total iodine dose) of licorice lecithin-bound iodine tablets for 4 weeks. Thyroid function studies, total serum iodine concentration, and urinary iodine excretion were monitored. Thyroid volume was measured by high resolution echoscanner before treatment, on the day of the last treatment, and 1 month after the treatment. There was a significant rise in serum TSH levels, with a small decline in serum free T4 concentration during iodide administration; the values remained within the normal range except for two subjects. Serum thyroglobulin levels were increased in parallel with serum TSH levels, which became higher than normal after 1 week of treatment. The volume of the thyroid gland became significantly enlarged after 28 days of iodide intake. When iodide was discontinued, thyroid volume and function returned to baseline levels within 1 month for all subjects. This is the first documentated objective evidence that the compensatory rise in serum TSH in response to iodide administration elicits reversible thyroid hypertrophy in normal subjects.
Adult↗
Interferon-gamma inhibition of human thyrotropin receptor gene expression.
To evaluate the role of interferon-gamma (IFN gamma) on human thyroid-specific gene expression, the effect of IFN gamma on TSH- and cAMP-induced TSH receptor gene expression was studied using cultured thyroid cells obtained from normal thyroid glands and those from patients with Graves' disease. Incubation of Graves' thyroid cells with 1.0 U/L bovine TSH or 1.0 mM 8-bromo-cAMP resulted in a 2-fold increase in TSH receptor mRNA expression, which was markedly inhibited in the presence of IFN gamma in a dose- and time-dependent manner. This inhibitory effect was completely neutralized by monoclonal antibody against IFN gamma. IFN alpha and -beta had no influence on TSH- and cAMP-stimulated TSH receptor mRNA expression. Paranodular normal thyroid cells showed the same results as those obtained using Graves' thyroid cells. Scatchard analysis of the [125I]TSH binding study showed that IFN gamma inhibited the number of TSH receptors up-regulated by TSH on the cell surface at the low affinity binding site (4.1 vs. 8.2 x 10(5)/cell). These results indicate that IFN gamma suppresses TSH- and cAMP stimulated human TSH receptor gene expression, resulting in a decrease in the number of TSH receptors. In conclusion, IFN gamma interacts via an intermediate pathway of TSH signal transduction and attenuates TSH receptor synthesis in normal and Graves' thyroid cells.
8-Bromo Cyclic Adenosine Monophosphate↗
[Intra-arterial ACNU, CDDP chemotherapy for brain metastases from lung cancer: comparison of cases with and without intra-arterial mannitol infusion].
To assess whether therapeutic efficacy is related to intra-arterial (IA) mannitol infusion prior to ACNU and cisplatin (CDDP) for brain metastases from lung cancer, clinical results of patients with and without IA mannitol infusion were compared. Thirty-nine patients were randomly assigned to either a mannitol infusion group (group A) or a non-mannitol infusion group (group B). There were 22 patients in group A and 17 in group B. During radiotherapy, ACNU and CDDP, at a dose of 100 mg/body, were given through the common carotid artery at a rate of 20 mg/min. In group A, 50 ml of 20% mannitol was injected intra-arterially at a rate of 50 ml/min immediately prior to the injection of chemotherapeutic agents. Major complications, such as seizure and neurotoxicity, were not observed. Complete response (disappearance of enhanced tumor mass) was obtained in 72% of group A and in 67% of group B. The median time to tumor progression was 40 weeks for group A and 22 weeks for group B. The median survival time (MST) was 45 weeks for group A and 30 weeks for group B. The survival time was significantly longer in group A as compared to group B (p < 0.05). When the patients who died of failure of vital organ systems other than brain complications were excluded in calculating the survival time, the MST was 69 weeks for 11 patients of group A and 34 weeks for 7 patients of group B. These data suggest that an effort to increase drug delivery to the brain tumor may indeed lengthen the survival time of patients with brain metastases from lung cancer.
Adult↗
[A surgical case report of severe valvular aortic stenosis with atrial septal defect in a 78-year-old female].
We have experienced open heart surgery of severe valvular aortic stenosis associated with atrial septal defect in a 78-year-old female patient. This is the oldest case in Japanese literature. Because balloon valvuloplasty can not produce improvement in hemodynamic and clinical status, open heart surgery was performed as the final decision. The operative procedure consisted of aortic valve replacement with a 19 mm St. Jude Medical valve and direct closure of atrial septal defect. Postoperative course was excellent. The patient is doing well at the two years and three months of follow-up period.
Aged↗
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↗
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↗
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↗
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↗
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↗
Pituitary adenoma and cerebral infarction demonstrated by Tc-99m HMPAO using a high-resolution SPECT system.
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Adenoma, Acidophil↗
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↗
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↗
[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↗
[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↗
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↗
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↗