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Biomedical subjects

H Imanishi

Publications and source records attributed to H Imanishi.

At least 37 records · Page 2Linked to original sources
PubMed1992

Cisplatin-induced emesis in Suncus murinus.

Emetic responses to cisplatin and participation of vagal innervation in emesis were studied in suncus. Intraperitoneal and intravenous administration of cisplatin caused dose-dependent emesis. ED50 values, latencies and frequencies were not significantly different between the two administrations. Cis-diaqodiammineplatinum (DAP), an active metabolite of cisplatin, also induced emesis, but with significantly shorter latency. Vagotomy completely abolished both types of vomiting. These results suggest that cisplatin is metabolized to DAP that subsequently causes emesis through stimulation of the vagus afferent.

Animals↗
PubMed1992

A variant serum cholinesterase and a confirmed point mutation at Gly-365 to Arg found in a patient with liver cirrhosis.

A 64-year-old man was admitted to our hospital because of possible liver cirrhosis. His serum cholinesterase was anomalously low with a delta pH of 0.1 (normal range; 0.8-1.1). His enzyme was more heat-labile than the normal controls. Km value of his enzyme for benzoylcholine was 1.1 x 10(-5) mol/l, while that for normal controls was 2.3 x 10(-6) mol/l. In addition, isozymic alteration of his enzyme was observed. Sequencing of the white blood cell DNA of the patient showed a point mutation at nucleotide 1093 (GGA to CGA), which changes codon 365 from glycine to arginine.

Amino Acid Sequence↗
PubMed1992

[The current role of devascularization and transection procedures in portal hypertension].

It is not clear which theory should be used in patients with bleeding esophageal varices that are not controlled by emergency endoscopic sclerotherapy. Definitive hemostasis is the key to successful therapy of variceal bleeding. Recurrence of haemorrhage in patients with portal hypertension is the most feared life threatening complication. Based on our management of 658 patients with esophageal varices and the availability of treatment options at our institution, the strategy of management of uncontrollable variceal haemorrhage by endoscopic sclerotherapy has evolved. Bleeding was controlled in 64 liver cirrhosis (100%) by devascularization and transection procedures and 50 patients (78%) survived to leave the hospital including 43 of 64 patients (67%) with Child grade C liver cirrhosis. Cumulative rebleeding rate at 10 years following emergency surgery was 3% (2/64). It is associated with a lower morbidity and mortality as well as a lower incidence of subsequent encephalopathy. We suggest that emergency transection and devascularization is an effective salvage treatment for the endoscopic sclerotherapy failed group.

Esophageal and Gastric Varices↗
PubMed1991

A xanthinuric family--the proposita having immunologically reactive xanthine oxidase but no xanthine oxidase activity.

The antibody was raised against purified human liver xanthine oxidase in a rabbit. In a xanthinuric patient, the double immunodiffusion method demonstrated the existence of an immunologically reactive duodenal mucosa xanthine oxidase which did not possess xanthine oxidase activity. These results indicated that xanthine oxidase protein is abnormal in structure and/or amino acid sequence.

Female↗
PubMed1991

Tea tannin components modify the induction of sister-chromatid exchanges and chromosome aberrations in mutagen-treated cultured mammalian cells and mice.

The modifying effects of tannin components extracted from green tea and black tea on mutagen-induced SCEs and chromosome aberrations were studied. These tannin components did not affect spontaneous SCEs and chromosome aberrations in cultured Chinese hamster cells. The frequency of SCEs and chromosome aberrations induced by mitomycin C (MMC) or UV was enhanced by the posttreatment with tea tannin components. When cells were post-treated with tea tannin components in the presence of metabolic enzymes of rat liver (S9 mix), the modifying effects on the induction of SCEs and chromosome aberrations by mutagens were complicated. MMC- and UV-induced SCEs and chromosome aberrations were suppressed by the posttreatment with tea tannin components at low concentrations (less than or equal to 6.7 micrograms/ml) with S9 mix. At a high concentration of tea tannin components (20 micrograms/ml) with S9 mix, a co-mutagenic effect was observed. The modifying effects of tea tannin components were shown to occur in the G1 phase of the cell cycle. In cells from a patient with xeroderma pigmentosum (XP) and a normal human embryo, MMC-induced SCEs were suppressed by the posttreatment with tea tannin components in the presence of S9 mix, and enhanced in the absence of S9 mix. On the other hand, tea tannin components modified SCE frequencies in UV-irradiated normal human cells but not in UV-irradiated XP cells. Our results suggested that tea tannin components themselves inhibited DNA-excision repair and resulted in a co-mutagenic effect, while in the presence of S9 mix metabolites of tea tannin components promoted DNA-excision repair activity and resulted in an antimutagenic effect. MMC-induced chromosome aberrations in mouse bone marrow cells were suppressed by the pretreatment with green tea and black tea tannin mixture.

Animals↗
PubMed1991

A hybrid form of alkaline phosphatase produced in FL-amnion cells.

FL-amnion cells have mainly two alkaline phosphatase (AP) isozymes, of which the faster migrating one (FL-APF) on 5% polyacrylamide gel electrophoresis has proved to be identical to the Kasahara isozyme, a tumor-associated AP of intestinal type. But the other slower migrating one (FL-APs) remains to be characterized. Immunological and enzymic examination of purified FL-APs revealed that it is a hybrid form of AP consisting of one subunit with a molecular weight of 66,200 coming from the same subunit as that of FL-APF and another one with a molecular weight of 58,000 from placental AP subunit with modified glycosylation.

Alkaline Phosphatase↗
PubMed1990

Reciprocal t(14;19)(q32.3;q13.1) in a patient with B-cell lymphoma.

A patient with B-cell lymphoma with a chromosome rearrangement of t(14;19)(q32.3;q13.1) is reported. This patient had leukemic features and an aggressive clinical course. The histopathologic diagnosis was malignant lymphoma, small noncleaved cell. Chromosome analysis of the cells from a cervical lymph node and peripheral blood showed a reciprocal translocation between chromosome 14 with a break at band q32.3 and chromosome 19 with a break at band q13.1, to which the bcl-3 gene has been mapped. Monoclonal rearrangement of the JH gene was detected by Southern blot analysis. However, we could not detect rearrangement of the bcl-3 gene. This case also had a t(2;8)(q13;q24.1), but the c-myc gene remained in its germline. This is the first case with the reciprocal t(14;19) and 8q24 chromosomal breakpoint in a B-cell lymphoid malignancy.

Chromosomes, Human, Pair 14↗
PubMed1990

Expression of a hybrid form of alkaline phosphatase isoenzyme in a newly established cell line (HuG-1) from a gastric cancer patient.

An unusual alkaline phosphatase (AP), named HuG-AP, was found in a newly established cell line (HuG-1) derived from a patient with stomach cancer. The enzyme was purified about 300-fold by affinity chromatography. On polyacrylamide gradient (4-30%) gel electrophoresis, the one band with the enzyme activity was observed. The enzymic properties of HuG-AP did not conform to those of liver, intestinal, placental, and germ cell AP isoenzymes which were recognized as homodimeric structure. Thermostability of the HuG-AP showed an intermediate value between intestinal and placental APs. Immunologically, the HuG-AP reacted with both anti-intestinal and anti-placental AP monoclonal antibodies. Dot blot analysis showed that both intestinal and placental AP mRNAs were expressed in HuG-1 cells concurrently. Therefore, we concluded that this novel AP had a hybrid form, namely heterodimeric structure, consisting of one subunit each of intestinal and placental APs. However, all of the properties of this hybrid AP did not conform to the intermediate enzymic properties between intestinal and placental APs which would be shown when they both coexist. Because an AP identical to HuG-AP had already been found in the metastatic lesion of the liver of the same patient, the expression of this novel AP seemed to occur in the patient's original cancer cells but did not result from spontaneous transformation of cultured cells.

Adenocarcinoma↗
PubMed1990

Structures of the asparagine-linked oligosaccharides of an alkaline phosphatase, kasahara isozyme, purified from FL amnion cells.

Asparagine-linked oligosaccharides were quantitatively released by hydrazinolysis from an alkaline phosphatase, Kasahara isozyme, which was purified from FL amnion cells. Almost all of the oligosaccharides (98%) were acidic components, all of which can be converted to neutral oligosaccharides upon sialidase digestion. Structural analysis of the oligosaccharides by sequential exoglycosidase digestion in combination with methylation analysis revealed that the alkaline phosphatase of FL cells contains sialylated mono-, bi-, tri-, and tetraantennary complex type sugar chains with the Gal beta 1----4GlcNAc beta 1---- outer chains. Some of the tetraantennary sugar chains contain a single Gal beta 1----4GlcNAc beta 1----3Gal beta 1----4GlcNAc beta 1---- outer chain on their Man alpha 1----6 arm. Both fucosylated and nonfucosylated trimannosyl cores were found in the sugar chains. However, it is of interest that the core portion of monoantennary oligosaccharide was not fucosylated and that of the tetraantennary oligosaccharide with a tetrasaccharide outer chain was completely fucosylated.

Alkaline Phosphatase↗
PubMed1990

Purification and some properties of the fast migrating alkaline phosphatase in FL-amnion cells (the Kasahara isoenzyme) and its cDNA cloning.

One of two main FL-amnion cell alkaline phosphatase (AP), the fast migrating one (FL-APF) has been reported to be identical to Kasahara isoenzyme (K.I.), which occurs preferentially in sera of patients with primary hepatoma. We purified FL-APF of which the apparent molecular weight was 135,000 by gel filtration, and that of the subunit was 62,000 on SDS/PAGE, indicating homodimeric structure of FL-AL-APF. FL-APF was found to react with monoclonal antibody against adult intestinal AP, but not with monoclonal antibody to placental AP. We isolated FL-APF cDNA clone from FL-amnion cells, of which cDNA was 2525 base pairs in length. Nucleotide sequence of the coding region and the 3' untranslated region was identical to the sequence of human adult intestinal AP cDNA. But the untranslated region of the 5' end of the isolated clone was slightly longer than that of intestinal AP. Hence, FL-APF (K.I.) may occur by altered glycosylation of intestinal AP.

Alkaline Phosphatase↗
PubMed1990

Discrimination of liver cirrhosis from chronic hepatitis by analysis of serum cholinesterase isozymes using affinity electrophoresis with concanavalin A or wheat germ agglutinin.

Isozymic alteration of serum cholinesterase (ChE) was investigated in patients with chronic liver diseases using affinity electrophoresis with concanavalin A (Con A) or wheat germ agglutinin (WGA). On Con A-containing agarose gel electrophoresis, three bands with enzyme activity (named bands I to III, from the anodic side to the cathodic) were observed in sera of normal controls. Disappearance of band II was observed in 50% (15/30) of cirrhotic patients, but only one of 20 patients with chronic hepatitis lacked band II of the serum ChE isozymes. Meanwhile, WGA-containing agarose gel electrophoresis revealed that normal controls had four ChE isozymes (named bands I to IV from the anodic side to the cathodic). These four isozymes were also observed in patients with chronic hepatitis. However approximately 67% (20/30) of cirrhotic patients lacked band II of ChE isozymes. When these two affinity electrophoreses were used in combination, 22 (73%) of 30 cirrhotic patients had isozymic alteration of their serum ChE on either Con A-containing or WGA-containing agarose gel electrophoresis, or both. Thus, affinity electrophoreses with Con A and WGA seemed to be useful methods in differentiating liver cirrhosis from chronic hepatitis.

Cholinesterases↗
PubMed1990

Suppressing effect of antimutagenic flavorings on chromosome aberrations induced by UV-light or X-rays in cultured Chinese hamster cells.

Chromosome aberrations induced by UV-light or X-rays were suppressed by the post-treatment with antimutagenic flavorings, such as anisaldehyde, cinnamaldehyde, coumarin, and vanillin. UV- or X-ray-irradiated surviving cells increased in the presence of each flavoring. X-ray-induced breakage-type and exchange-type chromosome aberrations were suppressed by the vanillin treatment in the G1 phase of the cell cycle and a greater decrease in the number of X-ray-induced chromosome aberrations during G1 holding was observed in the presence of vanillin. Furthermore, a greater decrease in the number of X-ray-induced DNA single-strand breaks was observed in the presence of vanillin. Treatment with vanillin in the G2 phase suppressed UV- and X-ray-induced breakage-type but not exchange-type chromosome aberrations. The suppression of breakage-type aberrations was assumed to be due to a modification of the capability of the post-replicational repair of DNA double-strand breaks. These G1- and G2-dependent anticlastogenic effects were not observed in the presence of 2',3'-dideoxythymidine, an inhibitor of DNA polymerase beta. Based on these results, the anticlastogenic effect of vanillin was considered to be due to the promotion of the DNA rejoining process in which DNA polymerase beta acts.

Animals↗
PubMed1990

Suppression of 6-TG-resistant mutations in V79 cells and recessive spot formations in mice by vanillin.

The antimutagenic effects of vanillin, anisaldehyde, cinnamaldehyde and coumarin were investigated in cultured Chinese hamster V79 cells in vitro. The frequencies of 6-TG-resistant mutations induced by UV or X-rays were decreased by treatment with each compound during the expression time. These decreases were not due to cytotoxic effects on cellular growth or killing effects on damaged cells. The antimutagenic effect of vanillin was also investigated in vivo in the mouse spot test using male PW and female C57BL/10 mice. Female mice were injected intraperitoneally with ethylnitrosourea (ENU) on the 10th day of pregnancy and received 3 successive oral administrations of vanillin. Administration of vanillin decreased the ENU-induced frequency of recessive carrier pups. These results indicate that vanillin acts as an antimutagen in mammalian cells both in vitro and in vivo.

Acrolein↗
PubMed1990

In vivo anticlastogenic and antimutagenic effects of tannic acid in mice.

The anticlastogenic effect of tannic acid was studied in vivo in the mouse micronucleus test. The frequencies of micronuclei induced by mitomycin C, ethyl nitrosourea (ENU) or 4-nitroquinoline 1-oxide in mouse bone marrow cells were decreased by the oral administration of tannic acid 6 h before the mutagen injection. The observed suppressing effect was not a reflection of a delay in the formation of micronuclei by the cytotoxic effect of tannic acid. The antimutagenic effect of tannic acid was also investigated in vivo in the mouse spot test using male PW and female C57BL/10 mice. Tannic acid was given orally to pregnant females 6 h before the intraperitoneal injection of ENU on the 10th day of pregnancy. The frequency of pups with recessive color spots induced by ENU was decreased by the administration of tannic acid. The observed decrease was not due to toxic effects on the embryo. These results indicate that tannic acid acts as an anticlastogen and antimutagen in vivo.

4-Nitroquinoline-1-oxide↗
PubMed1990

Suppressing effects of vanillin, cinnamaldehyde, and anisaldehyde on chromosome aberrations induced by X-rays in mice.

X-ray-induced chromosome aberrations were suppressed when vanillin, cinnamaldehyde, or p-anisaldehyde was given orally to mice after X-ray irradiation. Chromosome aberrations were monitored by the occurrence of polychromatic erythrocytes with micronuclei in bone marrow cells. The frequency of micronuclei was depressed about 55-60% without toxicity of the test compounds to the bone marrow.

Acrolein↗
PubMed1989

Enhancing effects of cinoxate and methyl sinapate on the frequencies of sister-chromatid exchanges and chromosome aberrations in cultured mammalian cells.

Sister-chromatid exchanges (SCEs) induced by mitomycin C (MMC), 4-nitroquinoline-1-oxide (4NQO) or UV-light in cultured Chinese hamster ovary cells (CHO K-1 cells) were enhanced by cinoxate (2-ethoxyethyl p-methoxycinnamate) or methyl sinapate (methyl 3,5-dimethoxy 4-hydroxycinnamate). Both substances are cinnamate derivatives and cinoxate is commonly used as a cosmetic UV absorber. Methyl sinapate also increased the frequency of cells with chromosome aberrations in the CHO K-1 cells treated with MMC, 4NQO or UV. These increasing effects of methyl sinapate were critical in the G1 phase of the cell cycle and the decline of the frequencies of UV-induced SCEs and chromosome aberrations during liquid holding was not seen in the presence of methyl sinapate. Both compounds were, however, ineffective in cells treated with X-rays. In cells from a normal human embryo and from a xeroderma pigmentosum (XP) patient, MMC-induced SCEs were also increased by the post-treatment with methyl sinapate. The SCE frequencies in UV-irradiated normal human cells were elevated by methyl sinapate, but no SCE-enhancing effects were observed in UV-irradiated XP cells. Our results suggest that the test substances inhibit DNA excision repair and that the increase in the amount of unrepaired DNA damage might cause the enhancement of induced SCEs and chromosome aberrations.

4-Nitroquinoline-1-oxide↗
PubMed1989

Suppressing effect of tannic acid on the frequencies of mutagen-induced sister-chromatid exchanges in mammalian cells.

The effects of tannic acid (m-galloyl gallic acid) and 7 of its analogues on the frequencies of sister-chromatid exchanges (SCEs) were investigated in cultured Chinese hamster cells. SCEs induced by UV-light or mitomycin C (MMC) were suppressed by post-treatment with tannic acid and 5 of its analogues. These effects were independent of the extension of the cell cycle. The compounds which showed an SCE-suppressing effect have a common structure of 3 neighboring hydroxy or methoxy groups substituted on the phenyl group in benzoic acid or ester. These decreasing effects of tannic acid were observed in the G1 phase but not in the S or G2 phase of the cell cycle and a greater decline of the frequencies of UV-induced SCEs during liquid holding was seen in the presence of tannic acid. However, cells irradiated with X-rays were not influenced by tannic acid. In cells from a xeroderma pigmentosum (XP) patient, a Fanconi's anemia (FA) patient, and a normal human embryo, MMC-induced SCEs were also decreased by post-treatment with tannic acid. Tannic acid reduced the SCE frequencies in UV-irradiated FA and normal human cells but not in UV-irradiated XP cells. Our results suggest that tannic acid modifies DNA-excision repair and that the decrease in the amount of unrepaired DNA damage might cause the reduction of induced SCEs.

Animals↗