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Biomedical subjects

T Oda

Publications and source records attributed to T Oda.

At least 289 records · Page 16Linked to original sources
PubMed1995

Relationship between cytotoxic and microtubule disruptive activities of (+)-, (-)- and (+/-)-indenestrol A and B monomethyl ethers in Chinese hamster V79 cells in culture.

We report the effects of indenestrol A, a metabolite of diethylstilbestrol, and its analogue, indenestrol B, on the relative plating efficiency and cellular microtubular architecture of Chinese hamster V79 cells. In this study, the effects of the monomethyl ethers of indenestrols A and B on these biological activities and their affinity for estrogen receptors in cytosol from mouse uteri were investigated. The results indicate that among eight optically active and four racemic methyl ethers, the 4'-methyl ether of [(-)-3S]indenestrol B exhibits both the strongest cytotoxicity in, and greatest disruption of, the cellular microtubular architecture of Chinese hamster V79 cells in culture. For the 6- and 4'-monomethyl ethers of optically active indenestrols A and B, some correlation was found between cytotoxicity and the effect on the distribution of cellular microtubular networks in Chinese hamster V79 cells. Estrogen receptor competitive binding studies revealed that stereochemistry and the position (6 or 4') of the methyl ether group contributed greatly to their binding affinity. However, no correlation was observed between the affinity for estrogen receptors and the cytotoxicity of the monomethyl ester tested. This suggests that the important causes of cytotoxicity in this series of compounds involve the inhibitory activity on cellular microtubule networks and not the affinity for estrogen receptors.

Aneuploidy↗
PubMed1995

Propranolol inhibits the spontaneous closure of the ductus arteriosus in newborn rats.

Newborn rats delivered by cesarean section were given subcutaneously propranolol (PRO), a beta-adrenergic blocker, (1) immediately or (2) 180 min after delivery. The diameter of the ductus arteriosus (DA) of the newborn pups was calibrated at 30, 60 and 90 min after the PRO-administration. The results were as follows: (1) the DA calibers of the pups given 0.2, 1.0., 5.0 mg/kg PRO immediately after cesarean delivery remained significantly larger than those of controls in a dose-dependent manner for 30 min after treatment. In the 5 mg/kg group, the enlargement of the DA was prolonged for 90 min after treatment. (2) In untreated pups, the DA completely closed by 180 min after cesarean delivery. The DA was not affected by the administration of 5 mg/kg PRO at 3 hr after delivery. It was concluded that, PRO inhibits the spontaneous constriction of the DA, suggesting an important role of beta-adrenergic stimulation on the spontaneous closure of the DA in newborn rats.

Adrenergic beta-Antagonists↗
PubMed1995

[Abnormal expression of E-cadherin in human pancreatic carcinoma cell lines].

Nineteen human pancreatic cancer cell lines were analyzed for possible abnormal mRNA and/or protein expression of the E-cadherin. Five lines showed no or markedly reduced expression of the E-cadherin, and protein was absent. In 9 lines, mRNA was positive but protein distribution was abnormal, i.e. diffusely positive in cytoplasm instead of membrane, or mixed distribution to membrane and cytoplasm. These 14 cell lines with abnormal E-cadherin expression grow in isolated fashion or loose sheet formation, indicating the loss of cell-cell adhesion system. These findings that the strong relation between E-cadherin abnormalities and loss of physical cell-cell interaction may explain the extensively poor prognosis of the patients with pancreatic carcinoma.

Cadherins↗
PubMed1995

[Non-invasive monitoring of cerebral oxygenation by NIR spectrophotometry (clinical trial)].

A Shimazu OM-100A near infrared spectrophotometer was used to monitor the cerebral oxygenated hemoglobin (Oxy-Hb), deoxygenated hemoglobin (Deoxy-Hb) and total hemoglobin (Total-Hb) in 3 patients with a) massive hemorrhage, b) ruptured aneurysm in the abdominal aorta, or c) hypercapnia. The hematocrit value of the patient with massive hemorrhage decreased rapidly to 18 %; the Total-Hb and Oxy-Hb also decreased significantly. Red blood cell transfusion raised the Oxy-Hb level, indicating an improvement in cerebral oxygenation. In the patient with a ruptured aneurysm, changes in blood flow brought about by clamping or declamping of the abdominal aorta were immediately reflected by corresponding changes in Total-Hb and Oxy-Hb. Oxy-Hb increased significantly and correlated well with the PETCO2 value in the patient with hypercapnia. Thus, NIR spectrophotometry is a useful non-invasive tool which can monitor metabolic and hemodynamic changes in the brain in various pathological conditions.

Adult↗
PubMed1995

[Clinical analysis of the surgical therapy of DeBakey type I acute aortic dissection].

We investigated relation of operative mortality with factors such as during from onset to operation, cardiac tamponade, age (more than 70 years old), aortic regurgitation, and shock. Fourteen patients underwent emergent surgery for DeBakey type I acute aortic dissection. These patients were the basis for this reports. Operative mortality was 43% (6/14). Although not statistically significant, there was a trend toward preoperative cardiac tamponade, namely the patients with preoperative tamponade had a poor prognosis. Causes of death were as follows, two patients related to the residual false lumen, two patients to surgical procedure, one patients to ischemic heart and one to mis-swallowing after operation. Among two patients who related to the residual false lumen, one died of rupture of the descending aorta that the clamping was performed during operation and the other occlusion of superior mesenteric artery 43 days after operation. Causes of deaths in patients in relation with surgical procedure were brain death and postoperative bleeding in 1 each. We concluded that the residual false lumen is a risk factor in the peri-operative stage.

Adult↗
PubMed1995

The SH2 domain of ABL is not required for factor-independent growth induced by BCR-ABL in a murine myeloid cell line.

Chronic myelogenous leukemia (CML) is characterized by the presence of a specific chromosomal translocation between the long arms of chromosomes 9 and 22 that results in the fusion of BCR encoded sequences upstream of exon 2 of c-ABL. This fusion gene produces a 210-kDa chimeric BCR-ABL protein that has elevated tyrosine kinase activity. Several substrates of this activated tyrosine kinase have been reported. However, their necessity for the transforming functions of BCR-ABL has not been determined. A specific deletion of the SH2 domain of ABL was created to determine whether this mutation would alter the ability of BCR-ABL to induce factor-independent growth of a murine myeloid cell line and to determine whether the SH2 domain mediates the interaction of BCR-ABL with any of its substates. Our results indicate that the SH2 domain of BCR-ABL is not required for the induction of growth factor independence and is not required for the association of BCR-ABL with rasGAP or SHC. However, myeloid cells expressing this mutant lack the tyrosine phosphorylation of a 62-kDa rasGAP associated protein.

Animals↗
PubMed1995

Analysis of the neurofibromatosis 2 gene in human breast and hepatocellular carcinomas.

The neurofibromatosis 2 gene (NF2) mapped to chromosome 22q is a recently isolated tumor suppressor gene that participates in the tumorigenesis of cells of embryonic neural crest origin. The structural similarities between the NF2 product, merlin-schwannomin, and the band 4.1 family raise the possibility that merlin may participate in a wide range of cell activities, in which the cytoskeleton latticework has important roles to play. In order to examine the significance of NF2 in general carcinogenesis, comprehensive analyses of 68 cases of breast carcinoma, which shows frequent loss of heterozygosity at chromosome 22, and 48 hepatocellular carcinomas of different histological grade were performed. No mutation was detected by the polymerase chain reaction-single-strand conformation polymorphism method for six exons of NF2 in any of the cases examined, suggesting that NF2 may be less important in the tumorigenesis of breast and liver cancers than in that of cancers originating from the neural crest.

Base Sequence↗
PubMed1995

[An autopsy case of corticobasal degeneration clinically misdiagnosed as Pick's disease].

We report a 69-year-old woman who was clinically diagnosed as having a frontal lobe-type of Pick's disease. The initial symptoms were personality changes and problematic behaviors. The patient showed intellectual decline, "stehende Redensarten" and abnormal attitude in interpersonal situations such as inattentiveness and indifference in the course of the disease. Brain CT revealed a marked atrophy of the frontal lobes. In the terminal stage the patient had severe dementia, mutism, parkinsonism and cervical dystonia. Neuropathologically, there was a marked atrophy of the frontal lobes. The superior frontal gyrus was most severely atrophic. Histological study revealed mild to moderate loss of neurons, hyperplasia of protoplasmic astrocytes and many balooned neurons in the deep layers of the atrophied cerebral cortex. Severe neuronal loss was even seen only in a part of the superior frontal gyrus. The cerebral white manner showed marked diffuse fibrillary gliosis. There was neuronal loss with gliosis in the thalamus, lentiform nucleus, subthalamic nucleus, substantia nigra and inferior olivary nucleus. Marked gliosis was seen in the midbrain and pontine tegmentum. Sections from several levels of the spinal cord also showed marked gliosis of the gray matter. Antibodies against human tau stained massive argyrophilic thread-like structures and oligodendroglial microtubular masses in the affected lesions. Neurofibrillary tangles were localized in the hippocampus and parahippocampal region. Neither Pick's body nor senile plaque were observed. Corticobasal degeneration (CBD) is a neurodegenerative disease initially presenting with unilateral motor disturbances. Typical initial symptoms are rigidity, akinesia and apraxia of an affected arm. The clinical phenotype might depend upon the affected areas of the cerebral cortex. Our patient initially exhibited personality changes and was clinically diagnosed as having Pick's disease. Although our case had unusual distribution pattern of the cerebral atrophy, it was pathologically diagnosed as CBD. The review of the literature suggests the presence of clinical varieties in CBD.

Aged↗
PubMed1995

[Anesthetic management of a patient with congenital cystic adenomatoid malformation].

Congenital cystic adenomatoid malformation (CCAM) is a rare disease that is diagnosed by severe respiratory dysfunction from birth. A 5-day-old-boy with CCAM underwent removal of a large cyst which was present at lower lobe of right lung. Anesthesia was induced slowly and maintained with oxygen and sevoflurane. Severe airway obstruction occurred transiently by the secretion from the lung cyst. Thereafter, the surgery was completed safely and his postoperative course was uneventful. Perioperative anesthetic management of the patient with CCAM is also discussed.

Airway Obstruction↗
PubMed1995

Characterization of human proteins that bind the repeated sequences in the squirrel monkey retrovirus enhancer.

We have recently identified two different human DNA-binding proteins, SMBP1 (35 kDa) and SMBP2 (17 kDa), that specifically interact with the direct repeats of the enhancer sequence in the squirrel monkey retrovirus long terminal repeat. Herein, we report several biochemical properties of the human DNA-binding proteins. SMBP1 and 2 recognized an overlapped sequence of the 5' region of the repeat which contains a palindrome of CCAATGG. Both proteins required divalent cations such as Mg2+ and Ca2+ for their specific DNA binding at the optimum concentration of 1 mM. SMBP2 is a thermostable protein that binds tightly to the DNA sequence even by treatment at 80 degrees C for 15 min. The SMBP2-DNA complex was also stable in the presence of 300 mM NaCl. The resistance of SMBP2 to heat and salt treatment is a prominent character distinguishable from SMBP1 and other known transcriptional factors. SMBP1 and 2 can be easily separated by heparin-agarose chromatography. These DNA-binding proteins were found to be present in nuclear extracts from several human cell lines including T cell, B cell, and epithelial cell.

Animals↗
PubMed1994

A truncated beta-catenin disrupts the interaction between E-cadherin and alpha-catenin: a cause of loss of intercellular adhesiveness in human cancer cell lines.

Cadherin cell adhesion molecules play an essential role in creating tight intercellular association and are considered to work as an invasion suppressor system of cancer cells. They form a molecular complex with catenins, a group of cytoplasmic proteins including alpha- and beta-catenins. While alpha-catenin has been demonstrated to be crucial for cadherin function, the role of beta-catenin is not yet fully understood. In this study, we analyzed the cadherin-catenin system in two human cell lines, HSC-39 and its putative subline HSC-40A, derived from a signet ring cell carcinoma of stomach. These cells grow as loose aggregates or single cells, suggesting that their cadherin system is not functional. In these cell lines, an identical 321-base pair in-frame mRNA deletion of beta-catenin was identified; this led to a 107-amino-acid deletion in the NH2-terminal region of the protein. Southern blot analysis disclosed a homozygous deletion in part of the beta-catenin gene. On the other hand, these cells expressed E-cadherin, alpha-catenin, and plakoglobin of normal size. Immunoprecipitation analyses showed that E-cadherin was coprecipitated with the mutated beta-catenin but not with alpha-catenin, and antibodies against beta-catenin did not copurify alpha-catenin. However, the recombinant fusion protein containing wild-type beta-catenin precipitated alpha-catenin from these cells. These results suggest that the dysfunction of E-cadherin in these cell lines is due primarily to its failure to interact with alpha-catenin, and that this defect results from the mutation in beta-catenin. Thus, it is most likely that the association between E-cadherin and alpha-catenin is mediated by beta-catenin, and that this process is blocked by NH2-terminal deletion in beta-catenin. These findings indicate that genetic abnormality of beta-catenin is one of the mechanisms responsible for loosening of cell-cell contact, and may be involved in enhancement of tumor invasion in human cancers.

Animals↗
PubMed1994

Purification and characterization of brain clusterin.

Clusterin, a 70-80 kDa sulfated glycoprotein found in numerous tissues, is also known as complement lysis inhibitor (CLI), apolipoprotein J, SP-40,40, TRPM-2, and SGP-2. In Alzheimer disease (AD), clusterin mRNA is increased, whereas clusterin protein is found in deposits of beta-amyloid (A beta). These studies characterized clusterin protein from human brain. In extracts from cortex and hippocampus, clusterin was about 40% higher in AD than in controls. Purified clusterin from human brain was slightly smaller than serum clusterin. Brain and serum clusterin were indistinguishable in the inhibition of complement-mediated hemolysis. Both serum and brain clusterin were indistinguishable in inhibiting the aggregation of A beta and promoting oxidative stress in rat pheochromocytoma PC12 cells (MTT assay). The inhibition of A beta aggregation and enhancement of A beta toxicity by clusterin suggest new mechanisms in AD.

Alzheimer Disease↗
PubMed1994

Crkl is the major tyrosine-phosphorylated protein in neutrophils from patients with chronic myelogenous leukemia.

The Philadelphia chromosome (Ph1), detected in virtually all cases of chronic myelogenous leukemia (CML), is formed by a reciprocal translocation between chromosome 9 and 22 that fuses Bcr-encoded sequences upstream of exon 2 of c-Abl. This oncogene produces a fusion protein, p210bcr-abl, in which the Abl tyrosine kinase activity is elevated. Using anti-phosphotyrosine immunoblotting, we have compared the pattern of phosphotyrosine-containing proteins from freshly prepared neutrophils of patients in the stable phase of CML to normal controls. The only consistent difference was the presence of a 39-kDa tyrosine-phosphorylated protein in 18 out of 18 neutrophil samples from CML patients that was not seen in normal controls. This same protein, as assessed by two-dimensional anti-phosphotyrosine immunoblotting, was also present in cell lines expressing p210bcr-abl, including K562 cells. Using K562 cells as a source of protein, the 39-kDa protein was purified and identified by microsequencing as Crkl, an SH2/SH3 adaptor protein related to the crk oncogene of the avian sarcoma virus, CT10. A direct interaction between Crkl and Abl has also been shown using a yeast two-hybrid screen.

Adaptor Proteins, Signal Transducing↗
PubMed1994

Different mutations of the p53 gene in nodule-in-nodule hepatocellular carcinoma as a evidence for multistage progression.

The p53 gene was analysed for mutation in three macro- and micro-scopically different areas of a nodule-in-nodule hepatocellular carcinoma (HCC). Two inner nodules revealed distinct mutations while the surrounding early HCC lesion was negative for mutation. This case clearly demonstrated that the p53 mutation was associated with the progression of HCC from an early to a more advanced stage, and that the primary HCC lesion was composed of genetically heterogeneous subclones. These findings provide direct proof of the involvement of genetic abnormalities in one step of multistage tumor progression.

Carcinoma, Hepatocellular↗
PubMed1994

Urate oxidase is imported into peroxisomes recognizing the C-terminal SKL motif of proteins.

Rat liver urate oxidase synthesized from cDNA through coupled transcription and translation was incubated at 26 degrees C for 60 min with purified peroxisomes from rat liver. Urate oxidase was efficiently imported into the peroxisomes, as determined by resistance to externally added proteinase K. The amount of imported urate oxidase increased with time and the import was temperature dependent. A synthetic peptide composed of the C-terminal 10 amino acid residues of acyl-CoA oxidase (the C-terminal tripeptide is Ser-Lys-Leu) inhibited the import of urate oxidase, whereas other peptides, in which the C-terminal Ser-Lys-Leu (SKL) sequence was deleted or mutated, were not effective. Two mutant urate oxidase proteins in which the C-terminal Ser-Arg-Leu (SRL) sequence was deleted or mutated to Ser-Glu-Leu (SEL) were not imported into peroxisomes. With substitution of a lysine residue for arginine in the SRL tripeptide at the C-terminus the import activity was retained. These results show that urate oxidase is important into peroxisomes via a common pathway with acyl-CoA oxidase, and that the C-terminal SRL sequence functions as a peroxisomal-targeting signal.

Amino Acid Sequence↗