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Biomedical subjects

J Takeda

Publications and source records attributed to J Takeda.

At least 199 records · Page 11Linked to original sources
PubMed1996

Superficial spreading-type mucosa-associated lymphoid tissue (MALT) lymphoma in the stomach--a case report.

We presented a case of a 71-year-old woman who presented irregular mucosal folds with tiny depressions and multiple erosions with ulceration in the stomach, on endoscopy and roentgenography. Histological findings from biopsy specimens showed dense and mildly atypical lymphoid-like cells invading the submucosa. Immunohistochemical examinations revealed monoclonal reactivity of Heavy-chain. She was then diagnosed to have low grade malignant lymphoma in the stomach and underwent total gastrectomy. The resected cancer demonstrated the pathological features including small lymphocytic plasmacytoid cells and lymphoepithelial lesions characteristic of a mucosa-associated lymphoid tissue (MALT) lymphoma. The lymphoma cells expressed B cell markers with a phenotype of IgG and lambda type. It is difficult to make a firm diagnosis of a MALT lymphoma from only small biopsy specimens. Accordingly it is necessary to complete the observed clinical process, endoscopic and roentgenographic findings with immunohistochemical characteristics to determine diagnosis. The MALT lymphoma should be treated as a low-grade malignancy and diagnosis sufficiently early can lead to a favorable prognosis.

Aged↗
PubMed1996

[The effect of droperidol and sevoflurane on serotonin-induced bronchoconstriction in dog].

Serotonin is a potent bronchoconstrictor, but the site of bronchoconstriction has not been determined. The present study was performed in dogs to clarify the site of bronchoconstriction induced by serotonin as well as to clarify the bronchodilating effect of droperidol and sevoflurance on the serotonin-induced bronchoconstriction by means of deflation flow-volume curve (DFVC) method, passive expiratory flow volume curve (PEFVC) method and respiratory system impedance measurement by forced oscillation method. Infusion of serotonin (60 micrograms.kg-1.min-1) induced a significant decrease in maximal expiratory flow at 10% of maximal expiratory volume (DEF10) by DFVC method and a significant increase in respiratory system impedance (Z). After droperidol (0.1 mg.kg-1) injection, DEF10 and Z returned to the control level and they remained unchanged even after the termination of serotonin infusion. Respiratory system compliance and resistance by PEFVC were unchanged by both serotonin and droperidol infusion or sevoflurane. Inhalation of 5% sevoflurane during serotonin infusion caused no significant change in DEF10. These findings indicate that serotonin-induced bronchoconstriction involves the small airway as well as the large airway. It is suggested that droperidol reversed serotonin-induced small airway constriction probably due to the antagonism of serotonin receptor in the airway. Bronchodilating effect of sevoflurane is probably limited in the small airway constricted by serotonin.

Anesthetics, Inhalation↗
PubMed1996

[Immunohistochemical analysis of c-erB-2 and nm23 expression in early gastric carcinoma].

The expression of c-erB-2 and nm23 genes product were investigated immunohistochemically in 108 resected cases of early gastric cancer. The expression rate of c-erB-2 was significantly higher in the cases of submucosal cancer or in the cases with lymph node metastasis. The expression rate of c-erB-2 was higher in the metastatic tumor than in the primary tumor. There was no significant correlation between the expression of nm23 and depth of invasion. The expression rate of nm23 was lower in the cases with lymph node metastasis than in the cases without lymph node metastasis. The expression could not be found in the metastatic tumor. These results suggest that there would be correlation between the expression of c-erB-2 and depth of invasion and lymph node metastasis, and the nm23 may suppress metastatic potential in early gastric cancer.

Humans↗
PubMed1995

Structure and chromosomal localization of the GPI-anchor synthesis gene PIGF and its pseudogene psi PIGF.

Posttranslational modification by the GPI glycolipid anchor is essential for the surface expression of many membrane proteins. Defect of GPI biosynthesis due to somatic mutation in the hematopoietic stem cell is the basis for an acquired genetic disease, paroxysmal nocturnal hemoglobinuria (PNH). Previously, an X-linked gene PIGA (phosphatidylinositol glycan class A), which participates in the first step of the biosynthesis, was shown to be mutated in abnormal cells from all 60 patients with PNH. The cDNA of another GPI synthesis gene PIGF was previously cloned, but it is not involved in pathogenesis of PNH. In the present study, we have analyzed PIGF genomic clones. The PIGF gene contained six exons spanning about 40 kb and was located to the short arm of chromosome 2 at 2p16-p21. The frequency of mutations on both alleles of PIGF should be much lower than that of mutation in the X-linked PIGA, accounting for a lack of involvement of PIGF in PNH. We also identified the processed pseudogene of PIGF (psi PIGF) and mapped it to 5q35.

Base Sequence↗
PubMed1995

Somatic mutations of PIG-A in Thai patients with paroxysmal nocturnal hemoglobinuria.

Paroxysmal nocturnal hemoglobinuria (PNH) is a hematopoietic stem cell disorder characterized by clonal blood cells that are deficient in the surface expression of glycosylphosphatidylinositol (GPI)-anchored proteins. In the affected cells, the X-chromosomal gene PIG-A, which participates in biosynthesis of the GPI anchor, is somatically mutated. Analyses of Japanese, British, and American patients with PNH have shown somatic mutations of PIG-A in all of them, indicating that PIG-A is responsible for PNH in most, if not all, patients in those countries. Twenty-nine of the reported somatic mutations are small, mostly involving 1 or 2 bases, except for one with a 4-kb deletion. Here we describe an analysis of PIG-A in neutrophils from 14 patients from Thailand where PNH is thought to be more common. We found small somatic PIG-A mutations in all patients. These consisted of six single base deletions, one each of 2-, 3-, 5- and 10-base deletions, two single base insertions and two base substitutions. Thus, the small somatic mutation in the PIG-A gene is also responsible for PNH in Thailand. However, base substitutions were rarer (2 of 14) than in Japan (8 of 16), and deletions of multiple bases were more common, suggesting various causes of mutation.

Base Sequence↗
PubMed1995

Human fructose-1,6-bisphosphatase gene (FBP1): exon-intron organization, localization to chromosome bands 9q22.2-q22.3, and mutation screening in subjects with fructose-1,6-bisphosphatase deficiency.

Fructose-1,6-bisphosphatase (EC 3.1.3.11) is a key regulatory enzyme of gluconeogenesis that catalyzes the hydrolysis of fructose-1,6-bisphosphate to generate fructose-6-phosphate and inorganic phosphate. Deficiency of fructose-1,6-bisphosphatase is associated with fasting hypoglycemia and metabolic acidosis because of impaired gluconeogenesis. We have cloned and characterized the human liver fructose-1,6-bisphosphatase gene (FBP1). FBP1, localized to chromosome bands 9q22.2-q22.3 by fluorescence in situ hybridization, consists of seven exons that span > 31 kb, and the six introns are in the same position as in the rat gene. FBP1 was screened for mutations in two subjects with fructose-1,6-bisphosphatase deficiency. Four nucleotide substitutions were identified, two of which were silent mutations in the codons for Ala-216 (GCT-->GCC) and Gly-319 (GGG-->GGA). The other substitutions were in intron 3, a C-->T substitution 7 nucleotides downstream from the splice donor site, and in the promoter region, an A-->T substitution 188 nucleotides upstream from the start of transcription. These nucleotide substitutions were also found in normal unaffected subjects and thus are not the cause of fructose-1,6-bisphosphatase deficiency in the two subjects studied. The molecular basis of hepatic fructose-1,6-bisphosphatase deficiency in these subjects remains undetermined but could result from unidentified mutations in the promoter that decrease expression or from mutations in another gene that indirectly lead to decreased fructose-1,6-bisphosphatase activity.

Amino Acid Sequence↗
PubMed1995

Somatic mutations of the PIG-A gene found in Japanese patients with paroxysmal nocturnal hemoglobinuria.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematologic disorder caused by deficient biosynthesis of the glycosylphosphatidylinositol (GPI) anchor. PIG-A, an X-linked gene that participates in the first step of GPI-anchor synthesis, is responsible for PNH. Abnormalities of the PIG-A gene have been demonstrated in all patients with PNH that have been studied to date. In this study, we analyzed 14 Japanese patients with PNH and identified 15 somatic mutations of PIG-A. The mutations included eight single-base changes and seven frame shift mutations. The single-base changes were two nonsense, three missense, and three splice site mutations. The frame shift mutations were four single-base deletions, two single-base insertions, and a replacement of two bases with one. They were all different, except for the same missense mutation being found in two patients. Moreover, these mutations were distributed in various regions of the gene. These results indicated that the mutations occurred at random sites and that there is no mutation hot spot in the PIG-A gene. All the mutations resulted in complete loss of function. Interestingly, the granulocytes in these patients contained variable proportions of mutant cells, suggesting that clonal expansion is not determined solely by mutations but is influenced by another factor(s).

Antigens, CD↗
PubMed1995

Bioactivity of recombinant feline interleukin-2 on human and feline leukocytes.

Interleukin (IL)-2 is a 16,000 Da protein product of T lymphocytes which is the principle cytokine responsible for clonal expansion of T lymphocytes as a response to antigen exposure. Deficiency of functional IL-2 plays a pivotal role in the pathogenesis of human immunodeficiency syndrome and may be important in the pathogenesis of feline immunodeficiency syndrome as well. Additionally, IL-2 may enhance secretion of interleukin-5 from the TH2 subset of CD4+ T cells, promote peripheral and systemic eosinophilia, and contribute to the eosinophilia which characterizes the inflamed airways of human beings and cats with asthma. We recently reported the sequence of feline IL-2 and the synthesis of recombinant feline IL-2. The purpose of the present study was to evaluate the bioactivity of recombinant feline IL-2 on human and feline leukocytes. We established dose-response relationships between recombinant feline IL-2 and radiolabeled proliferating human and feline leukocytes using thymidine incorporation as a marker of bioactivity. We found that recombinant human IL-2 promotes proliferation of both human and feline leukocytes. However, recombinant feline IL-2 promotes proliferation of feline cells, but not human cells.

Animals↗
PubMed1995

GPI-anchor biosynthesis.

Many eukaryotic proteins bind to membranes using a glycosylphosphatidylinositol (GPI) anchor. GPI anchors are essential in yeasts and probably also in protozoa. Although mammalian cells can survive without GPI anchors, their deficiency in haemopoietic cells cause a haemolytic disease, paroxysmal nocturnal haemoglobinuria (PNH). Here, we discuss recent progress in our understanding of GPI-anchor biosynthesis that could lead to a better understanding of PNH and chemotherapeutic agents to treat protozoal and fungal infections.

Animals↗
PubMed1995

Plasma N-methylhistamine concentration as an indicator of histamine release by intravenous d-tubocurarine in humans: preliminary study in five patients by radioimmunoassay kits.

Histamine disappears rapidly from plasma because of its short half-life. Because a metabolite of histamine, N-methylhistamine, is stable and has a longer half-life, determination of its plasma concentration can be useful in retrospective determination of histamine release. In this study, we measured plasma histamine and N-methylhistamine concentrations after d-tubocurarine (dTc) administration to evaluate the use of plasma N-methylhistamine measurement for confirming histamine release. After the induction of anesthesia, five patients received dTc, 0.8 mg/kg intravenously. A radioimmunoassay kit was used to determine plasma histamine and N-methylhistamine before and 1, 3, 5, and 10 min after administration of dTc. Histamine released by the injection of dTc reached a maximum level at 1 min, but decreased rapidly, whereas N-methylhistamine increased at 1 min and remained increased for at least 10 min. Good correlations were found between histamine concentration at 1 min and N-methylhistamine concentrations at 1, 3, 5, and 10 min, especially r = 0.999 (n = 5) at 10 min. N-Methylhistamine measurement with this kit can ascertain histamine release retrospectively in a semiquantitative manner.

Anesthesia↗
PubMed1995

Evolution of beta-cell dysfunction in the male Zucker diabetic fatty rat.

The molecular basis for the beta-cell dysfunction that characterizes non-insulin-dependent diabetes mellitus (NIDDM) is unknown. The Zucker diabetic fatty (ZDF) male rat is a rodent model of NIDDM with a predictable progression from the prediabetic to the diabetic state. We are using this model to study beta-cell function during the development of diabetes with the goal of identifying genes that play a key role in regulating insulin secretion and, thus, may be potential targets for therapeutic intervention aimed at preserving or improving beta-cell function. As a first step, we have characterized morphology, insulin secretion, and pattern of gene expression in islets from prediabetic and diabetic ZDF rats. The development of diabetes was associated with changes in islet morphology, and the islets of diabetic animals were markedly hypertrophic with multiple irregular projections into the surrounding exocrine pancreas. In addition, there were multiple defects in the normal pattern of insulin secretion. The islets of prediabetic ZDF rats secreted significantly more insulin at each glucose concentration tested and showed a leftward shift in the dose-response curve relating glucose concentration and insulin secretion. Islets of prediabetic animals also demonstrated defects in the normal oscillatory pattern of insulin secretion, indicating the presence of impairment of the normal feedback control between glucose and insulin secretion. The islets from diabetic animals showed further impairment in the ability to respond to a glucose stimulus. Changes in gene expression were also evident in islets from prediabetic and diabetic ZDF rats compared with age-matched control animals. In prediabetic animals, there was no change in insulin mRNA levels. However, there was a significant 30-70% reduction in the levels of a large number of other islet mRNAs including glucokinase, mitochondrial glycerol-3-phosphate dehydrogenase, voltage-dependent Ca2+ and K+ channels, Ca(2+)-ATPase, and transcription factor Islet-1 mRNAs. In addition, there was a 40-50% increase in the levels of glucose-6-phosphatase and 12-lipoxygenase mRNAs. There were further changes in gene expression in the islets from diabetic ZDF rats, including a decrease in insulin mRNA levels that was associated with reduced islet insulin levels. Our results indicate that multiple defects in beta-cell function can be detected in islets of prediabetic animals well before the development of hyperglycemia and suggest that changes in the normal pattern of gene expression contribute to the development of beta-cell dysfunction.

Animals↗