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Biomedical subjects

Y Kano

Publications and source records attributed to Y Kano.

At least 163 records · Page 9Linked to original sources
PubMed1992

Construction and characterization of an Escherichia coli mutant deficient in the metY gene encoding tRNA(f2Met): either tRNA(f1Met) or tRNA(f2Met) is required for cell growth.

The Escherichia coli metY gene, encoding tRNA(f2Met), was split by the kanamycin-resistance-encoding gene. The resulting mutant exhibited the same growth rate as the wild type, indicating that tRNA(f2Met) is not indispensable as is the case with the metZ gene encoding tRNA(f1Met) [Kenri et al., Gene 103 (191) 31-36]. beta-Galactosidase was produced efficiently from the start codon AUG of the intact lacZ gene or a trpA'::lac'Z fusion gene, in the metY mutant. The lac repressor from the lacI gene and the chimeric protein from a hupB'::lac'Z fusion gene, whose start codons are GUG, were also synthesized efficiently in the insertion mutant. These results provide evidence that tRNA(f2Met) is not essential for growth of E. coli and that the start codons, AUG and GUG, are both recognized by tRNA(f1Met), a major N-formyl methionine-specific tRNA, in the tRNA(f2Met)-depleted cells. We were unable to construct mutants deficient in both tRNA(f1Met) and tRNA(f2Met) by P1 phage-mediated transduction with the metY and metZ mutations. Moreover, the ampicillin-resistance marker of the pUC9 plasmid carrying metZ+ was not cured at 42 degrees C in host cells with the polAts and metY-metZ double mutations. These results indicate that either tRNA(f1Met) or tRNA(f2Met) is required for the growth of E. coli.

Blotting, Southern↗
PubMed1992

Effects of CPT-11 in combination with other anti-cancer agents in culture.

CPT-11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy camptothecin, is a newly developed water-soluble camptothecin derivative now undergoing phase-II evaluation. In an attempt to establish whether the combination of CPT-11 with other standard anti-cancer agents would be of any benefit, we studied the effects of CPT-11 in combination with 11 other anti-cancer agents on a human T-cell leukemia cell line, MOLT-3, in culture. We used both CPT-11 and SN-38 (active substance of CPT-11 in vivo), for our study. Cells were incubated for 3 days in the presence of 2 drugs (CPT-11 or SN-38 and another drug) and cytotoxic effects were determined by MTT assay. The effects of drug combinations on ID50 were analyzed by an improved isobologram method. Supra-additive and marginal supra-additive effects (synergism) were observed for CPT-11 in combination with cisplatin, cytosine arabinoside and mitomycin C. Additive effects were observed for its combination with amsacrine, bleomycin, doxorubicin, etoposide, 5-fluorouracil, mitoxantrone and vincristine. Alternate sub-additive and protective effects (antagonism) were observed for CPT-11 in combination with methotrexate. Similar tendencies were observed for SN-38 in combination with other agents. These results suggest that CPT-11 in simultaneous administration with a majority of anti-cancer agents has an advantage for cytokilling. Of these agents, cisplatin, cytosine arabinoside and mitomycin C are most suitable for simultaneous administration with CPT-11.

Antineoplastic Agents, Phytogenic↗
PubMed1992

Malignant transformation of human fibroblasts previously immortalized with 60Co gamma rays.

Normal human fibroblasts obtained from a whole embryo were malignantly transformed with only 60Co gamma rays, but after extensive passage. The fibroblasts were exposed intermittently to 60Co gamma rays, 13 times, 2,800 rads in total, from the primary culture to the 40th passage level. At the 50th passage level the cells became morphologically changed, showing chromosomal abnormalities, and serial passages showed them to be immortalized. They were not tumorigenic on transplantation into nude mice, but became malignant after extensive passage; i.e., at the 547th passage level and 2,800 days after initiation of the culture. Our results indicate that several different genotypic changes are necessary for malignant transformation of human cells over long periods. No mutation at codons 12 and 61 of H-, K- and N-ras was detected in the malignant cells. Thus, this system may be useful to detect other cellular genes that may contribute to the malignant phenotypes of human fibroblasts.

Base Sequence↗
PubMed1992

Can test statistics in covariance structure analysis be trusted?

Covariance structure analysis uses chi 2 goodness-of-fit test statistics whose adequacy is not known. Scientific conclusions based on models may be distorted when researchers violate sample size, variate independence, and distributional assumptions. The behavior of 6 test statistics is evaluated with a Monte Carlo confirmatory factor analysis study. The tests performed dramatically differently under 7 distributional conditions at 6 sample sizes. Two normal-theory tests worked well under some conditions but completely broke down under other conditions. A test that permits homogeneous nonzero kurtoses performed variably. A test that permits heterogeneous marginal kurtoses performed better. A distribution-free test performed spectacularly badly in all conditions at all but the largest sample sizes. The Satorra-Bentler scaled test statistic performed best overall.

Female↗
PubMed1992

The effects of ICRF-154 in combination with other anticancer agents in vitro.

We studied the effects of ICRF-154 in combination with 11 anticancer agents on four human leukaemia cell lines. Cells were incubated for 3 days in the presence of two drugs (ICRF-154 and one other), and cell growth inhibition was determined by MTT assay. Effects of drug combinations at the ID50 level were analysed using the isobologram method (Steel). In the lymphoblastic leukaemia cell lines, MOLT-3, HSB, and B-ALL, supra-additive effects were observed for ICRF-154 in combination with amsacrine, bleomycin, doxorubicin, and etoposide. Additive effects were observed for its combinations with cisplatin, CPT-11, cytosine arabinoside, 5-fluorouracil, mitomycin C, and vincristine. Sub-additive to protective effects were observed in combination with methotrexate. In an erythroleukaemia cell line, K-562, no drug showed supra-additive effects with ICRF-154, while sub-additive to protective effects were observed for ICRF-154 in combination with cisplatin and methotrexate. The other drugs showed additive effects with ICRF-154. These results indicate that the combined effects of ICRF-154 with other agents vary, depending on the cell line. Against lymphoid malignancies, ICRF-154 would be advantageous when administered simultaneously with many anticancer agents. Of such agents, amsacrine, bleomycin, doxorubicin, and etoposide are the most suitable, while methotrexate is least suitable for such combined treatment.

Antineoplastic Agents↗
PubMed1992

Pharmacokinetics of [6]-gingerol after intravenous administration in rats with acute renal or hepatic failure.

The pharmacokinetics of [6]-gingerol were investigated in rats with acute renal failure induced by bilateral nephrectomy, or those with acute hepatic failure induced by a single oral administration of carbon tetrachloride (CCl4), to clarify the contribution of the kidney and liver to the elimination process of [6]-gingerol. After bolus intravenous administration, a plasma concentration-time curve of [6]-gingerol was illustrated by a two-compartment open model. There was no significant difference in either the plasma concentration-time curve or any pharmacokinetic parameters between the control and nephrectomized rats. It is suggested, therefore, that renal excretion does not contribute at all to the disappearance of [6]-gingerol from plasma in rats. In contrast, hepatic intoxication with CCl4 elevated the plasma concentration of [6]-gingerol at the terminal phase. Its elimination half-life increased significantly, from 8.5 to 11.0 min, in CCl4-intoxicated rats. The extent of [6]-gingerol bound to serum protein was more than 90% and was affected very slightly by the CCl4-intoxication. These aspects indicate that [6]-gingerol is eliminated partly by the liver.

Acute Disease↗
PubMed1992

Comparison of the distribution of carbonic anhydrase isozymes (CA-I, CA-II, CA-III) in the rat gastrointestinal tract.

The present paper described the immunohistochemical distributions of carbonic anhydrase (CA) isozymes. CA-I, CA-II and CA-III, in the epithelium lining the rat gastrointestinal tract, with rabbit antibodies to equine CA-I, CA-II and CA-III. Prior to the immunohistochemical examinations, the crossreactivities of these antibodies to the rat-antigens were confirmed in this study. In the stomach, surface epithelial cells and parietal cells of the glandular region showed an immunoreactivity only to CA-II. In the large intestine, each immunoreactivity to CA isozyme (CA-I, CA-II and CA-III) was localized in the upper portion of intestinal glands, and decreased toward the distal digestive tract, but absent in the small intestine. The present histological findings suggested that the CA isozymes might play a role in the ion-transportation during the water absorption in the rat large intestine.

Animals↗
PubMed1992

Lectin histochemical study of the prostate gland of the rhesus monkey (Macaca mulatta).

Glycoconjugates in the secretory epithelial cells of the rhesus monkey (Macaca mulatta) prostate gland were investigated using lectin histochemistry. The monkey prostate possesses cranial and caudal lobes. Histochemical staining with a battery of 8 lectins demonstrated differences in lectin binding patterns of the secretory epithelial cells between the 2 lobes. BS-1 bound exclusively to the cranial lobe, and PNA bound exclusively to the caudal lobe. DBA bound exclusively to a number of the secretory epithelial cells of the caudal lobe. In addition, both lobes showed binding with Con-A, RCA-1, WGA and S-WGA, but were negative for binding with SBA. Specific lectin binding patterns suggest a differing carbohydrate composition for each region, and a biological difference between the cranial and caudal lobes of the rhesus monkey prostate.

Animals↗
PubMed1992

[The identification and determination of marker substances in xiaoyao wan by three dimensional HPLC].

A Chinese traditional patent medicine Xiaoyao Wan was analysed by three dimensional HPLC. The result shows that the Chinese traditional medicines involved in Xiaoyao Wan were identified excellently and the content of marker substances can be determined accurately. According to the results of determination, the content of saikosaponin b1, b2, glycyrrhizin, paeoniflorin and atractylenolide III in Xiaoyao Wan was 0.43, 0.53, 5.22, 3.95 and 0.16 (mg/g), respectively; The RSD was 1.2, 0.8, 0.4, 0.3 and 1.0 (%) respectively.

Benzoates↗
PubMed1992

Heterogeneity of monoclonal immunoglobulins with antistreptolysin-O activity detected in the cases of essential monoclonal gammopathy and multiple myeloma.

Two different types of monoclonal human immunoglobulins (M-components) with antistreptolysin-O (ASO) activity were investigated. The M-component FM with essential monoclonal gammopathy revealed to have an ASO activity, demonstrated not only by streptolysin-O neutralizing assay according to Ranz-Randall's method, but also by passive agglutination assays and precipitation on agar. The ASO activity was shown to reside in the Feb. These findings suggest that the M-component FM have a true antibody activity. On the other hand, ASO activity of M-component TT with multiple myeloma was detected only by streptolysin-O neutralizing assay, but the passive agglutinating assays and precipitation on agar showed no positive results. It has not been fully confirmed if the M-component TT behaves as a true antibody activity. Heterogeneity of the M-components with ASO activity was discussed.

Aged↗
PubMed1992

Effects of mitoxantrone in combination with other anticancer agents on a human leukemia cell line.

To investigate the effects of mitoxantrone in combination with other anticancer agents, a human T-cell leukemia cell line, MOLT-3, was incubated for 3 days in the presence of two drugs (mitoxantrone and the combined drug) and cell growth inhibition was determined by assay with 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazonium bromide. The effects of drug combinations at doses giving 80% inhibition (ID80) were analyzed by an improved isobologram method. A supra-additive (synergistic) effect was observed for mitoxantrone in combination with amsacrine, cisplatin, or cytosine arabinoside. An additive effect was observed for its combination with bleomycin, doxorubicin, etoposide, 5-fluorouracil, mitomycin C, 6-mercaptopurine, or vincristine. A sub-additive (antagonistic) effect was observed for its combination with methotrexate. These data suggest that mitoxantrone, administered simultaneously with any one of a majority of anticancer agents we studied, is advantageous for cytokilling. Of the anticancer agents tested, amsacrine, cisplatin, and cytosine arabinoside are the most suitable for combination with mitoxantrone, and these combinations are worthy of clinical investigation. Methotrexate in our system is inappropriate for simultaneous administration with mitoxantrone. These data should provide useful information for the establishment of clinical protocols involving mitoxantrone.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Participation of the histone-like protein HU and of IHF in minichromosomal maintenance in Escherichia coli.

The closely related Escherichia coli genes, hupA, hupB, himA and himD (hip), encode the bacterial histone-like protein subunits, HU-2, HU-1, IHF chi and IHF beta, respectively. We report here that E. coli minichromosomes [plasmids (2.7-12.2 kb) with oriC] carrying the intact mioC region were unable to transform mutants deficient in both HU and integration host factor (IHF), whereas they could transform mutants deficient in either HU or IHF as efficiently as the wild-type strain. Minichromosomes carrying a deletion of the proximal part of mioC or a DnaA box just upstream from mioC could not transform cells deficient in IHF, but could transform cells deficient in HU. These results suggested that HU and IHF participate in minichromosomal replication from oriC in E. coli.

Bacterial Proteins↗
PubMed1991

Construction and characterization of an Escherichia coli mutant with a deletion of the metZ gene encoding tRNA (f1Met).

The Escherichia coli metZ gene encoding tRNA (f1Met) was replaced by the chloramphenicol-resistance-encoding gene. The resulting mutant exhibited slightly lower growth rates as compared to the wild type at 37 degrees C or 42 degrees C, but grew apparently slower than the latter at 30 degrees C, indicating a slight cold sensitivity of growth. beta-Galactosidase was produced efficiently from the start codon AUG of the intact lacZ gene or trpA'::lac' Z fusion gene, in the metZ deletion mutant. The lac repressor from the lacI gene and the chimeric protein from a hupB' ::lac'Z fusion gene, whose start codons are GUG, were also synthesised in the deletion mutant. These results provide evidence that tRNA (f1Met) is not essential for growth of E. coli and that the start codons, AUG and GUG, are both recognized by tRNA (f1Met), a minor N-formyl methionine-specific tRNA, in the tRNA (f1Met)-depleted cells.

Blotting, Southern↗
PubMed1991

Effects of amsacrine in combination with other anticancer agents in human acute lymphoblastic leukemia cells in culture.

Effects of amsacrine in combination with other anticancer agents at ID80 were evaluated by cell growth assay using a human T-cell leukemia cell line (MOLT-3). The data were analyzed with the aid of an improved isobologram, using the concept of an envelope of additivity. A supra-additive effect was observed for amsacrine in combination with cytosine arabinoside and mitoxantrone. An additive effect was observed in its combinations with bleomycin, CPT-11, cisplatin, daunorubicin, doxorubicin, etoposide, 5-fluorouracil, homoharringtonine, mitomycin C, or vincristine. 6-Mercaptopurine had an additive effect with amsacrine at ID80 but a sub-additive to protective effect at ID90. A sub-additive to protective effect was shown for amsacrine in combination with methotrexate. These data suggest that cytosine arabinoside and mitoxantrone are the best of the anticancer agents we studied for use in combination with amsacrine. Bleomycin, cisplatin, CPT-11, doxorubicin, cytosine arabinoside, homoharringtonine, mitomycin C, and vincristine also yielded favorable results when administrated simultaneously with amsacrine. Simultaneous administration of amsacrine with 6-mercaptopurine and methotrexate is not appropriate. If amsacrine is combined with 6-mercaptopurine and methotrexate, other suitable schedules should be explored. These results may provide a rationale for the design of clinical protocols combining amsacrine with other anticancer agents.

Amsacrine↗
PubMed1991

Schedule-dependent synergism and antagonism between methotrexate and 6-mercaptopurine in a human acute lymphoblastic cell line.

We studied the combined cytotoxic effects of methotrexate and 6-mercaptopurine (6-MP) on a human acute lymphoblastic cell line (MOLT-3) in vitro according to various schedules. The combined effects were analysed with improved isobologram using the concept of additivity. Simultaneous and continuous exposure (72 h) to these two agents had subadditive to protective effects (antagonism). Partial simultaneous exposure to methotrexate (5 h) and 6-MP (72 h) showed additive to protective effects. Sequential exposure to methotrexate (5 h) followed by 6-MP (72 h) had an additive effect at 0 h and a supra-additive effect (synergism) at 3 h and 19 h intervals. Therefore, it would seem to be better to avoid the simultaneous administration of methotrexate and 6-MP when these two drugs are used in combination. Sequential administration of methotrexate first, followed by 6-MP at short intervals, is recommended.

Cell Division↗