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Biomedical subjects

J Takeda

Publications and source records attributed to J Takeda.

At least 217 records · Page 12Linked to original sources
PubMed1995

Early mucosal gastric cancer with lymph node metastasis.

From 1976 to 1992, a total of 358 cases of mucosal early gastric cancer (m-cancer) were treated by resection in the First Department of Surgery, Kurume University Hospital. Eight (2.2%) of these 358 cases of m-cancer were associated with lymph node metastasis. In these 358 cases, the mean diameter of the tumor was 2.75 cm, and the mean age was 59.6 years. In the 8 cases of m-cancer with positive lymph node metastasis (n(+)), the mean diameter was 5.2 cm and the mean age was 51.6 years. Seven (87.5%) out of the 8 cases of m-cancer with n(+) were IIc macroscopic cancer type and were associated with ulcer and/or ulcer scar.

Adenocarcinoma↗
PubMed1995

Resected early gastric cancer--clinicopathological studies on 610 cases.

A total of 610 cases of early gastric cancer were studied, retrospectively. Of these, 541 (88.7%) cases were single and 62 (10.1%) cases were multiple cancers. Lymph node metastasis occurred in 11.2% of the elevated, in 8.2% of the depressed and in 15.1% of the mixed type. There was no lymph node metastasis when a mucosal or submucosal cancer was less than 10 mm in diameter. By contrast, in the cases in which the preoperative diagnosis was suspected advanced cancer, the incidence of lymph node metastasis was high, at 33%. Therefore, when the preoperative diagnosis is advanced cancer, standard radical gastrectomy and/or extended radical gastrectomy should be selected even though they are found to be early gastric cancer. The age-corrected 5-year survival rate was 98.5% in the cases with no lymph node metastasis and 93.0% in the cases with lymph node metastasis (p > 0.05). The 5-year survival rate was 100% in mucosal cancer and 95.5% in submucosal cancer (p > 0.05).

Adult↗
PubMed1995

[A case of unresectable advanced gastric cancer responding remarkably to combined chemotherapy with 5-fluorouracil and low-dose cisplatin].

A 62-year-old male patient complaining epigastralgia was diagnosed as having Borrmann type 2 gastric concer (por). The primary lesion was unresectable, so the patient was treated by combined chemotherapy with 5-fluorouracil and low-dose cisplatin for 4 weeks, which resulted in the disappearance of primary tumor and a remarkable reduction of metastatic lymph nodes. The patient has a good quality of life without any sign of recurrence now.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

[Air pollution by sevoflurane in operating room and serum and urine inorganic fluoride of anesthetists].

Since lower blood-gas partition coefficient of sevoflurane provides rapid induction and emergence from anesthesia, sevoflurane has been used widely for inhalational anesthesia. However, because higher minimum alveolar concentration of sevoflurane requires a large dosage of anesthetic than other volatile anesthetics, air pollution with sevoflurane in the operating room might be of great concern. Anesthetists may keep inhaling the low concentration of anesthetics every day, even though scavenging system is equipped in the operating room. The purpose of this study is to evaluate the effects on anesthetists of the low concentration of anesthetics by measuring the inorganic fluoride concentration in the urine and serum of anesthetists and operating room nurses. Healthy 29 anesthesiologists and two operating room nurses were studied. Informed consent was obtained. Inorganic fluoride ions in the serum and urine were measured. Simultaneously sevoflurane concentration in operating room was measured in three operating rooms, at two places in the corridor and in the recovery room. Sevoflurane concentrations in three operating rooms were 1.22 ppm, 2.13 ppm and 6.05 ppm respectively. Concentration in the recovery room was 0.544 ppm. Serum and urine concentrations of inorganic fluoride were 1.1 +/- 0.1 mumol.l-1 and 36.2 +/- 17.1 mumol.l-1, respectively (mean +/- SD). Serum concentration of inorganic fluoride was within normal ranges. Although it is possible that fluoride concentration in urine is influenced by urine volume and a half of fluoride deposits in bone, no abnormal values in urine were found in this study. These results suggest that long term exposure to low concentration of sevoflurane and isoflurane causes no significant increase in their metabolites in operating room staffs.

Adult↗
PubMed1995

[Augmentation by succinylcholine of the neuromuscular blocking effect of vecuronium in children].

To evaluate the influence of succinylcholine (Scc) on the neuromuscular blocking effect of subsequently administered vecuronium in children, 30 patients aged 2-14 years scheduled for elective surgery were studied after obtaining the informed consent from the parents. Anesthesia was induced with inhalation of sevoflurane, nitrous oxide and oxygen. T1 of the adductor pollicis muscle to ulnar nerve stimulation elicited by train of four stimulation at 2 Hz was monitored continuously by an acceleration transducer. The patients were divided into two groups; group V (16 patients) received vecuronium (0.03 mg.kg-1) and group SV (14 patients) received vecuronium (0.03 mg.kg-1) after 100% recovery of twitch from neuromuscular blockade induced with Scc (1.0 mg.kg-1). Short onset of action and potentiation of maximal block were demonstrated in group SV. After vecuronium administration, a complete suppression of T1 was observed in 8 patients of group SV and only 1 patient of group V. The present study demonstrates that the neuromuscular blockade of vecuronium can be potentiated with the prior administration of Scc in pediatric patients.

Adolescent↗
PubMed1995

[Effects of nitrous oxide on electroencephalographic activity during sevoflurane anesthesia: a zero-crossing analysis].

We have investigated the influence of nitrous oxide (N2O) on central nervous system (CNS) during sevoflurane anesthesia by using zero-crossing method of EEG in 31 patients. The study was divided into three parts: Study 1 (n = 18), Study 2 (n = 6) and Study 3 (n = 7). (Study 1) After induction of anesthesia, sevoflurane 1.0 % in oxygen (O2), and sevoflurane 1.0 % with 67 % N2O in O2 were given to the patients sequentially in a random fashion, and EEG was recorded. (Study 2) Sevoflurane 1.7 % in O2, and sevoflurane 0.7 % with 67 % N2O in O2, which were considered to be the same anesthetic depth (= sevoflurane 1 MAC), were inhaled, and EEG was recorded in the same manner as in the study 1. (Study 3) We compared the effects of N2O on EEG during intravenous administration of fentanyl and midazolam with 67 % N2O, and without N2O, and EEG was recorded in the same manner. In all studies, percentage of each frequency range (delta, theta, alpha, beta) and average frequency were calculated by zero-crossing method. During sevoflurane anesthesia, the EEG activity was decelerated with N2O, depending on minimum alveolar concentration (MAC). But there were no significant changes in EEG activity of the patient with and those without N2O during intravenous anesthesia. We concluded that the influences of N2O on CNS can be evaluated by quantitative analysis of EEG.

Adult↗
PubMed1995

PIG-A gene abnormalities in Thai patients with paroxysmal nocturnal hemoglobinuria.

Deficient biosynthesis of the glycosyl phosphatidyl inositol (GPI)-anchor in blood cells is implicated in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH). Abnormal clonal cells appear in various hematopoietic cell lineages, suggesting that PNH arises as a result of somatic mutation occurred at the multipotential hematopoietic stem cell stage. We previously cloned a gene which is responsible for PNH. The gene termed PIG-A (for Phosphatidyl Inositol Glycan-class A) participates in the early step of GPI-anchor biosynthesis. Studies with cell lines and granulocytes from patients with PNH revealed that in all cases so far characterized, PIG-A is the target for the somatic mutation. In the present study, we analyzed PIG-A abnormality in granulocytes from 14 Thai-patients with PNH. PIG-A RNA was reversed transcribed and the coding region was amplified by polymerase chain reaction and cloned into plasmids. The cDNA thus obtained and genomic DNA were analyzed by mutation detection enhancement gel electrophoresis and sequencing. The assessment of function of PIG-A cDNA was based on the ability to correct the phenotype of a PIG-A deficient cell line after transfection. The result showed that all patients had PIG-A abnormality. Three patients had size abnormality of PIG-A transcripts caused by mutations at the splicing sites in the genomic DNA level. Eleven patients had PIG-A transcripts of normal sizes but had mutations in the coding region which included small deletions and insertions. Taken together with the result from Japanese and British patients, the PIG-A somatic mutations in patients with PNH are small mutations widely distributed throughout coding region and the splicing sites.

DNA Transposable Elements↗
PubMed1994

Localization of the gene encoding a neutral amino acid transporter-like protein to human chromosome band 19q13.3 and characterization of a simple sequence repeat DNA polymorphism.

The gene encoding a human neutral amino acid transporter-like protein (SLC1A5) was mapped to chromosome band 19q13.3 by fluorescence in situ hybridization to metaphase chromosomes. A simple sequence repeat DNA polymorphism of the form (GT)n was identified in the 3'-untranslated region of SLC1A5 mRNA. Studies in the CEPH families showed significant evidence of linkage between this DNA polymorphism and markers localized to the distal long arm of chromosome 19.

Amino Acid Transport Systems↗
PubMed1994

Agonists and antagonists bind to different domains of the cloned kappa opioid receptor.

Opium and its derivatives are potent analgesics that can also induce severe side effects, including respiratory depression and addiction. Opioids exert their diverse physiological effects through specific membrane-bound receptors. Three major types of opioid receptors have been described, termed delta, kappa, and mu. The recent molecular cloning of these receptor types opens up the possibility to identify the ligand-binding domains of these receptors. To identify the ligand-binding domains of the kappa and delta receptors, we have expressed in COS-7 cells the cloned mouse delta and kappa receptors and chimeric delta/kappa and kappa/delta receptors in which the NH2 termini have been exchanged. The opioid antagonist naloxone binds potently to wild-type kappa receptor but not to wild-type delta receptor. The kappa/delta chimera bound [3H]naloxone with high affinity. In contrast, the kappa-specific agonist [3H]U-69,593 did not bind to the kappa/delta chimera. These findings indicate that selective agonists and antagonists interact with different recognition sites in the kappa receptor and localize the antagonist-binding domain to the NH2 terminus. Consistent with the results of radioligand-binding studies, the kappa/delta chimera did not mediate kappa-agonist inhibition of cAMP formation. In contrast, the delta/kappa chimera did mediate kappa-agonist inhibition of cAMP formation, but this effect was not blocked by naloxone. Furthermore, a truncated kappa receptor lacking its NH2 terminus was able to mediate agonist inhibition of cAMP accumulation in a naloxone-insensitive manner. This result further indicates that the NH2 terminus of the kappa receptor contains the selective antagonist-binding domain. The ability to dissociate agonist- and antagonist-binding sites will facilitate the development of more specific kappa agonists, which could have analgesic properties devoid of side effects.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1994

Regulation of expression of the human fructose transporter (GLUT5) by cyclic AMP.

The effect of cyclic AMP on the expression of the fructose transporter, GLUT5, was studied in Caco-2 cells, a human colon cancer cell line that differentiates spontaneously in culture into cells with the properties of small intestine enterocytes. Treatment of differentiated Caco-2 cells with 50 microM forskolin, which stimulates adenylate cyclase and raises intracellular cyclic AMP levels, increased fructose uptake 2-fold and raised GLUT5 protein and mRNA levels 5- and 7-fold respectively. The increased GLUT5 mRNA levels in forskolin-treated cells are a result of stabilization of GLUT5 mRNA in these cells and increased transcription. The effect of cyclic AMP on GLUT5 transcription was assessed by measuring the activity of human GLUT5 promoter-reporter gene constructs in forskolin-treated differentiated Caco-2 cells. The results showed that forskolin stimulated the activity of the GLUT5-reporter gene constructs and this stimulatory effect was mediated by cis-acting regulatory sequences.

Animals↗
PubMed1994

Characterization of genomic PIG-A gene: a gene for glycosylphosphatidylinositol-anchor biosynthesis and paroxysmal nocturnal hemoglobinuria.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia characterized by the presence of abnormal subpopulations of blood cells that are deficient in surface expression of glycosylphosphatidylinositol (GPI)-anchored proteins. Recent studies showed that the gene termed PIG-A, which participates in the first step of GPI-anchor biosynthesis, is mutated in the abnormal blood cells from patients with PNH. In this study the genomic PIG-A gene was cloned and characterized to obtain nucleotide sequence information for analyzing somatic mutations of PIG-A in patients with PNH. The PIG-A gene is at least 17 kb long and has six exons. The exon-intron boundaries and 583 bp of the 5' flanking region were sequenced. The 5' flanking region has no TATA-like sequence, but includes four CAAT boxes, two AP-2 sequences, and a CRE sequence, some of which are present in regions necessary for the promoter activity. We report pairs of oligonucleotide primers for polymerase chain reaction that should be useful to amplify and analyze various regions of the PIG-A gene in patients with PNH.

Base Sequence↗
PubMed1994

Abnormalities of PIG-A transcripts in granulocytes from patients with paroxysmal nocturnal hemoglobinuria.

BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder in which there is a deficiency in the synthesis by hematopoietic cells of the glycosyl-phosphatidylinositol molecules that anchor proteins to the cell membrane. Recently, we demonstrated that a gene termed PIG-A (for phosphatidylinositol glycan class A), a component of glycosyl-phosphatidylinositol biosynthesis, was responsible for PNH in two patients. The present study was undertaken to elucidate whether PIG-A is the gene responsible for all cases of PNH and to characterize further the somatically acquired abnormalities of this gene. METHODS: We studied granulocytes from 15 patients with PNH. The cell content of CD55 and CD59 was assessed by fluorescence-activated flow cytometry. PIG-A transcripts were reverse-transcribed, amplified by the polymerase chain reaction, and cloned into plasmids. The structure of the cloned complementary DNA was analyzed by nucleotide sequencing, and its function was assessed on the basis of its ability to restore to normal the abnormal phenotype of a PIG-A-deficient cell line after transfection. RESULTS: Three patients had size abnormalities of PIG-A transcripts with different patterns, and in one patient a very low level of the PIG-A transcript was found. Eleven patients had transcripts of normal size, but the transfection assay revealed that in each patient some of them were nonfunctional. The percentage of nonfunctional PIG-A transcripts was correlated with the percentage of affected granulocytes (P < 0.001). Sequence analysis demonstrated somatic mutations in two of the patients. CONCLUSIONS: PIG-A is the gene responsible for PNH in all patients studied to date.

Base Sequence↗
PubMed1994

Paroxysmal nocturnal haemoglobinuria (PNH) is caused by somatic mutations in the PIG-A gene.

Paroxysmal nocturnal haemoglobinuria (PNH), an acquired clonal blood disorder, is caused by the absence of glycosyl phosphatidylinositol (GPI)-anchored surface proteins due to a defect in a specific step of GPI-anchor synthesis. The cDNA of the X-linked gene, PIG-A, which encodes a protein required for this step has recently been isolated. We have carried out a molecular and functional analysis of the PIG-A gene in four cell lines deficient in GPI-linked proteins, obtained by Epstein-Barr virus (EBV) transformation of affected B-lymphocytes from PNH patients. In all four cell lines transfection with PIG-A cDNA restored normal expression of GPI-linked proteins. In three of the four cell lines the primary lesion is a frameshift mutation. In two of these there is a reduction in the amount of full-length mRNA. The fourth cell line contains a missense mutation in PIG-A. In each case the mutation was present in the affected granulocytes from peripheral blood of the patients, but not in normal sister cell lines from the same patient. These data prove that PNH is caused in most patients by a single mutation in the PIG-A gene. The nature of the mutation can vary and most likely occurs on the active X-chromosome in an early haematopoietic stem cell.

Amino Acid Sequence↗
PubMed1994

Molecular cloning of murine pig-a, a gene for GPI-anchor biosynthesis, and demonstration of interspecies conservation of its structure, function, and genetic locus.

Many membrane proteins are anchored to the cell membrane by glycosylphosphatidylinositol (GPI). The core structure and biosynthesis of the GPI anchor are well conserved in eukaryote cells. We previously cloned a human PIGA gene that participates in GPI anchor biosynthesis. We have now cloned complementary and genomic DNA of Pig-a, the murine homologue of PIGA, and compared its function and gene structure with those of PIGA. The deduced amino acid sequence of mouse PIG-A is 88% identical with that of human PIG-A. Transfection of Pig-a cDNA complemented the defects of both a PIG-A-deficient murine cell line and a PIG-A-deficient human cell line, demonstrating that functions of mouse and human PIG-A are conserved. Like human PIGA, the chromosomal Pig-a gene has six exons and spans approximately 16 kb. Moreover, Pig-a was mapped to X-F3/4, which is syntenic to human Xp22.1, where PIGA is located. Thus, murine Pig-a provides a good animal model to study paroxysmal nocturnal hemoglobinuria, a disease caused by a somatic mutation of PIGA. Database analysis demonstrated that a yeast gene, SPT14, is homologous to Pig-a and PIGA and that these genes are members of a glycosyltransferase gene family.

Amino Acid Sequence↗
PubMed1994

GPI-anchor synthesis.

The glycosyl phosphatidylinositol (GPI) anchor of membrane proteins is widely distributed in eukaryotes and parasitic protozoa. The structure and biosynthetic pathway of its core have been elucidated and appear to be conserved in various species. Some of the genes involved in mammalian GPI-anchor biosynthesis have recently been isolated using GPI-anchor-deficient mutant cell lines and expression cloning methods. One of these genes proved to be responsible for a GPI-anchor deficiency known as paroxysmal nocturnal hemoglobinuria. Since the core of the GPI anchor is variously modified in different species and since there may be other differences between its biosynthetic pathway in parasites and their hosts, this pathway could be a target for chemotherapy. In this review, Taroh Kinoshita and Junji Takeda focus on the GPI-anchor biosynthetic pathway and the genes involved in it.

Journal Article↗
PubMed1994

Effects of sevoflurane, isoflurane, enflurane, and halothane on left ventricular diastolic performance in dogs.

The effects of volatile anesthetics on active (ventricular relaxation) and passive (chamber stiffness) indices of diastolic function and on left ventricular filling rates in dogs were studied to determine how these agents affect left ventricular diastolic performance. Thirty-five mongrel dogs were randomly assigned to receive sevoflurane, isoflurane, enflurane, or halothane. Left ventricular pressure waveforms, phonocardiograms, and echocardiograms were recorded after administering the anesthetics at concentrations of 0% (control), 1%, 2%, and 3%. Ventricular relaxation was defined as the time constant of the decline in left ventricular pressure. Chamber stiffness was derived from the ventricular pressure-volume relationship during passive filling. Rapid filling rate, slow filling rate, and atrial filling rate were obtained from echocardiograms and phonocardiograms. No change in the time constant or in chamber stiffness was observed at any concentration of sevoflurane or isoflurane. However, the highest studied concentration of enflurane and halothane produced a significant increase in the time constant and in chamber stiffness. Rapid filling rate as well as atrial filling rate decreased significantly with the volatile anesthetics, especially with enflurane and halothane. Sevoflurane and isoflurane did not alter ventricular relaxation or chamber stiffness, but did affect diastolic function as manifested by their alteration of filling rates. In contrast, enflurane and halothane each prolonged ventricular relaxation and increased chamber stiffness. With the administration of the volatile anesthetics, the rapid filling rate decreased with the deterioration of diastolic function; in addition, atrial filling rates decreased and did not compensate for the reduction in early ventricular filling.

Anesthetics, Inhalation↗