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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 487 records · Page 27Linked to original sources

Presence of different types of procollagen messenger RNAs in human hepatoma cell lines.

Human hepatoma cell lines were shown for the first time to contain various types of procollagen mRNAs. The amounts and types of procollagen mRNAs differed depending on the cell lines. Pro alpha 1 (III) and pro alpha 1 (IV) collagen mRNAs were present in PLC/PRF/5, a hepatocellular carcinoma cell line, whereas pro alpha 1 (I), pro alpha 2 (I), pro alpha 1 (IV) and pro alpha 2 (V) collagen genes contrast, HepG2 cells derived from hepatoblastoma contained little, if any, mRNAs for these types of procollagens we had examined.

Actins↗

Conservation of E6 and E7 regions of human papillomavirus types 16 and 18 present in cervical cancers.

The E6 and E7 regions of human papillomavirus (HPV) type 16 were present in the DNA samples from cervical cancer cell lines, SKG-IIIa and SKG-IIIb, and those from cervical cancer tissues of three different patients. T601 cells, an NIH3T3 transformant obtained by transfection of DNA from a surgical specimen of a cervical cancer, also contained the E6 and E7 regions. The E6 region of HPV type 16 was expressed as mRNA in SKG-IIIa, SKG-IIIb and T601 cells. The E6 and E7 regions of HPV type 18 were present in the DNA samples from cervical cancer cell lines, SKG-I and SKG-II, and those from cervical cancer tissues of two different patients. SKG-I and SKG-II cells expressed the E6 region of HPV type 18 as mRNAs. These results strongly suggest that the E6 and E7 regions or the sequence surrounding these regions are important for maintaining malignant phenotype of cervical cancer cells.

Cell Line↗

Genomic clone of hst with transforming activity from a patient with acute leukemia.

We have previously reported the identification of a novel transforming gene, hst, in DNA samples taken from human stomach cancers and a noncancerous portion of stomach. Five clones, containing the genomic hst gene, were isolated from a human cosmid library constructed from leukocyte DNA from a patient with acute leukemia. All clones possessed transforming activity when transfected to NIH3T3 cells. From one clone, an 8.7 kb BamHI fragment was subcloned into pBR322, and this subclone was active in transforming NIH3T3 cells. This is the first isolation of transformation-competent genomic hst clones directly from a human genomic library, that is, without prior passage through NIH3T3 cells.

Acute Disease↗

Effects of milbemycin D on adult Angiostrongylus cantonensis in rats.

Effects of milbemycin D against adult Angiostrongylus cantonensis in rats were examined. The first-stage larval counts in rat faeces (larvae per gram of faeces per female worm recovered, LPG/female) were most conspicuously reduced in the group treated with nine consecutive weekly doses of 5.0 mg/kg. The effect was more marked in the group treated with five or ten successive daily doses of 5.0 mg/kg than the group treated with a single dose of 25.0 or 5.0 mg/kg. Host lung-body weight ratio and number of recovered worms were reduced significantly only in the group treated with five or ten successive daily doses of 5.0 mg/kg. These results suggest that the action of milbemycin D on the reproductive system of the worms might be differentiated from its killing action. The in vitro motility of females recovered from rats medicated with nine consecutive weekly doses of 5.0 mg/kg was inhibited, and almost all females and males were semitransparent and colourless. Results obtained from sectioned worms showed little content in their digestive tracts and uteri. In addition, there were few eggs and first-stage larvae in the lung tissues of treated rats. These suggest that milbemycin D affects the reproductive functions of the worms through an indirect mode of action including paralysis and inhibition in food intake and energy and/or synthetic metabolism.

Angiostrongylus↗

Genomic sequence of hst, a transforming gene encoding a protein homologous to fibroblast growth factors and the int-2-encoded protein.

hst is a transforming gene first identified from transformed NIH 3T3 cells that were transfected with DNA of a human stomach cancer. A genomic fragment of hst obtained directly from a human genomic library also has transforming activity. This fragment has a coding sequence identical to that of the hst cDNA prepared from an NIH 3T3 transformant induced by DNA from a stomach cancer. The deduced amino acid sequence of the hst protein is 43%, 38%, and 40% homologous, respectively, to human basic fibroblast growth factor, human acidic fibroblast growth factor, and mouse int-2 protein in selected regions. This suggests that hst encodes a protein related to fibroblast growth factors, which are wide-spectrum mitogens, and to the int-2 protein, a potential oncogene product implicated in murine mammary carcinogenesis.

Amino Acid Sequence↗

Loss of heterozygosity on chromosomes 3, 13, and 17 in small-cell carcinoma and on chromosome 3 in adenocarcinoma of the lung.

By a molecular genetic approach using polymorphic DNA markers that detect allelic deletion of specific chromosomal regions, we analyzed for possible loss of chromosomal heterozygosity in five different histological types of lung cancers obtained from 47 patients. In small-cell carcinomas, the incidence of allelic deletions at three different chromosomal loci was extremely high; loss of heterozygosity was detected on chromosomes 3p in 7 of 7 patients (100%), 13q in 10 of 11 patients (91%), and 17p in 5 of 5 patients (100%). The deletions at these loci in small-cell carcinomas were observed even in the tumors without any clinical evidence of metastasis. Furthermore, loss of heterozygosity on chromosomes 3p and 13q occurred prior to NMYC amplification and chromosome 11p deletion. Loss of heterozygosity on chromosome 3p was also detected with high frequency in adenocarcinomas [5 of 6 patients (83%)]. Heterozygosity of chromosomes 13q and 17p was lost in 10 of 31 patients (32%) and in 3 of 12 patients (25%), respectively, of lung cancers other than small-cell carcinomas. These results indicate that recessive genetic changes involving sequences on chromosomes 3p, 13q, and 17p may play important roles in the genesis of small-cell carcinoma, and those on chromosome 3p may play an important role in the genesis of adenocarcinoma.

Adenocarcinoma↗

cDNA sequence of human transforming gene hst and identification of the coding sequence required for transforming activity.

The hst gene was originally identified as a transforming gene in DNAs from human stomach cancers and from a noncancerous portion of stomach mucosa by DNA-mediated transfection assay using NIH3T3 cells. cDNA clones of hst were isolated from the cDNA library constructed from poly(A)+ RNA of a secondary transformant induced by the DNA from a stomach cancer. The sequence analysis of the hst cDNA revealed the presence of two open reading frames. When this cDNA was inserted into an expression vector containing the simian virus 40 promoter, it efficiently induced the transformation of NIH3T3 cells upon transfection. It was found that one of the reading frames, which coded for 206 amino acids, was responsible for the transforming activity.

Amino Acid Sequence↗

An improved cryopreservation procedure for human fetal pancreas tissues.

Improved viability and function of insulin-producing beta (B) cells of frozen-stored human fetal pancreatic tissue was obtained by a two-step method utilizing high concentrations of dimethyl sulfoxide (DMSO). Human fetal pancreata (14-23-week gestation) obtained from pathologic abortions were teased and cultured overnight. Prior to freezing the tissues were immersed in 0.9% saline containing 0.5 M DMSO for 30 min (room temperature) and then placed in 2.1 M DMSO on ice for 5 min. The tissues were frozen by the method previously developed in our laboratory and stored at -196 degrees C. The frozen-stored tissues were subsequently thawed at 24 degrees C and cultured overnight before viability testing. Viability and function of the B cells were assessed by several specific assay methods; glucose plus theophylline-induced insulin release during static incubation and perifusion, 3H-leucine incorporation into insulin, and insulin content of the tissue grown in athymic mice for 7 days. The response to glucose plus theophylline stimulation, measured on the frozen-thawed tissue one day after thawing, was 80% of the level measured in control tissue maintained in organ culture. Frozen-thawed tissues maintained in organ culture for 1 week responded comparably in the in vitro assay systems. The insulin content of frozen-thawed pancreatic tissue removed from athymic mice 1 week after transplantation was approximately 60% of the amount measured in the control grafts. These results demonstrate the utility of our procedure in the maintenance of the viability and function of frozen-stored human B cells both in culture and after transplantation.

Animals↗

Thyrotropin-releasing hormone reduces myo-inositol content in rat cerebellum pretreated with lithium.

The effect of thyrotropin-releasing hormone (TRH) and lithium on myo-inositol metabolism has been assessed in rat cerebral cortex, cerebellar cortex, and sciatic nerves. Sprague-Dawley male rats were injected subcutaneously with 10 mEq/kg of LiCl and intraperitoneally with 10 mg/kg of TRH-tartrate, alone or in combination. Either lithium or TRH alone had little effect on the myo-inositol concentration in cerebellar cortex, whereas the combination of lithium and TRH significantly lowered the level. The myo-inositol level of cerebellar cortex reached its nadir (70% of values in untreated control rats) 30 min after addition of TRH and then returned to the control level at 90 min. In cerebral cortex, both lithium alone and lithium plus TRH significantly reduced the myo-inositol level. No effect was seen on the myo-inositol concentration in sciatic nerves with these regimens. These results suggested that the pharmacological dose of TRH activated phosphatidylinositol turnover in rat cerebellar cortex and subsequently reduced the myo-inositol level in the presence of lithium.

Animals↗

Antitumor activity of quinocarmycin against carcinoma of the lung in human tumor clonogenic assay.

Quinocarmycin monocitrate is a novel antitumor antibiotic isolated from Streptomyces melanovinaceus. We have utilized a human tumor clonogenic assay to test the antitumor activity of this drug against carcinoma of the lung and to compare its activity with those of mitomycin C or cisplatin, which are components of the clinically effective regimens in therapy for this disease. The overall in vitro response rate (defined as less than 50% survival of tumor colony forming units) for quinocarmycin at 0.1 and 1.0 microgram/ml continuous exposure was 42% and 72%, respectively, which was superior to that of other drugs. Quinocarmycin and other antitumor drugs do not have identical spectra of antitumor activities in vitro, suggesting that this compound with good in vitro activity should be further developed for clinical trials.

Adenocarcinoma↗

Detection of gastrin-releasing peptide mRNA in small cell lung carcinomas and medullary thyroid carcinomas using synthetic oligodeoxyribonucleotide probes.

Human gastrin-releasing peptide (GRP) mRNA was detected in the tumor tissues of medullary thyroid carcinomas and small cell lung carcinomas using synthetic oligodeoxyribonucleotides as hybridization probes. The amount of GRP mRNA was estimated by radiodensitometric hybridization assay. A good correlation was found between the amount of GRP mRNA and the concentration of immunoreactive GRP in the tumor tissues.

Carcinoma↗

Identification of transforming genes as hst in DNA samples from two human hepatocellular carcinomas.

In a DNA-mediated transfection assay using NIH3T3 cells, the DNAs from two out of twelve human hepatocellular carcinomas gave transformants. The transforming gene was identified as hst, which was originally found in DNAs from stomach cancers and a noncancerous portion of stomach mucosa, the putative product being a growth factor. Transcripts were not detected in the original HCC 1 and HCC2 upon Northern blot analysis. The possible mechanisms involved in the hst gene activation are discussed.

Carcinoma, Hepatocellular↗

Activation of N-ras gene in a rat hepatocellular carcinoma induced by dibutylnitrosamine and butylated hydroxytoluene.

DNA samples from eighteen rat hepatocellular carcinomas, including those induced by oral administration of dibutylnitrosamine (DBN) with butylated hydroxytoluene (BHT), or DBN with butylated hydroxyanisole (BHA), have been tested for the presence of transforming activity by transfection assay with NIH3T3 cells. Of the eighteen samples, only one from a tumor induced by DBN and BHT gave transformants. the activated oncogene was identified as rat N-ras by Southern blot analysis.

Animals↗

Y chromosome abnormality in human stomach and lung cancer.

Sex chromosome abnormalities in human stomach and lung cancers from 33 male patients were examined by Southern blot hybridization with pDP34 DNA probe, which recognizes X and Y chromosome-linked restriction fragment length polymorphisms (RFLPs). Contrary to the recent cytogenetic observations showing high incidence of loss of the Y chromosome in solid tumors, loss of the Y chromosome was observed in only 3 of 21 stomach cancers and 2 of 12 lung cancers. Gain of the Y chromosome was found in one of 12 lung cancers, but not in any of the stomach cancers. No X chromosome abnormality was found in any of these 33 stomach cancers and lung cancers.

Humans↗