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Biomedical subjects

K Furuya

Publications and source records attributed to K Furuya.

At least 325 records · Page 18Linked to original sources
PubMed1985

Abdominal repair of vaginal prolapse and the postoperative outcome as judged by a scoring system and X-ray colpography.

Three abdominal procedures were combined to suspend the prolapsed vagina in patients with post-hysterectomy vault prolapse and a narrow vagina and uterine prolapse with pelvic diseases (such as fibroids) necessitating laparotomy. We used Moschcowitz's method (obliteration of the cul-de-sac by purse-string sutures) Burch's method (fixation of the anterior vaginal wall to Cooper's ligament) and Williams and Richardson's method (suspension of the vaginal stump using fascial strips from the external oblique aponeurosis. The postoperative outcome of 8 operations was judged by a scoring system and by X-ray colpography with superimposition of films obtained at rest and during straining (subtraction technic). The scoring system indicated that the anterior vaginal wall and the vaginal vault were well supported by this combination procedures. However, the prolapse of the lower posterior vaginal wall needed an additional vaginal repair. The X-ray colpogram showed that the axis of the repaired vagina was slightly more vertical than normal. But displacement of the vagina on straining was within the normal range. Neither dyspareunia nor stress urinary incontinence were seen as complications of our procedures.

Adult↗
PubMed1985

Absence of a promoting or sequential syncarcinogenic effect in rat liver by the carcinogenic hypolipidemic drug nafenopin given after N-2-fluorenylacetamide.

The hypolipidemic agent nafenopin, (NF), has been reported to be carcinogenic to rat liver. To determine whether nafenopin exerts a promoting or syncarcinogenic effect in rat liver, its effect on liver carcinogenesis induced by N-2-fluorenylacetamide (FAA) was studied. In two separate experiments, male F344 rats were fed 0.02% FAA for either 10 or 8 weeks to induce preneoplastic liver lesions. Following a recovery period of 1 week, rats were given 0.01 or 0.02% NF in the diet for 23 weeks in one experiment and 0.05 or 0.1% for 24 weeks in the other. The final incidence of neoplasms, and their numbers, size distribution, and degrees of differentiation were not significantly different in groups given NF after FAA compared to those maintained on a basal diet after FAA. In the group treated with the highest dose level of NF following FAA, however, there was a decrease in the number of grossly visible small neoplasms. In contrast, the liver neoplasm promoter phenobarbital increased the multiplicity, although not the incidence, of liver neoplasms when given after FAA. Thus, four different dose levels of NF showed no promoting or syncarcinogenic effect on FAA-induced hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1985

Evidence for L-glutamate as the neurotransmitter of the squid giant synapse.

The effect of a spider toxin (JSTX), a specific blocker of glutamate receptors, was studied in the squid stellate ganglion. JSTX irreversibly blocked the excitatory postsynaptic potential in a dose-dependent manner. The toxin neither affected the spike in the postsynaptic nor the presynaptic fibers. Spontaneous miniature potentials recorded from thin stellate nerves were suppressed by the toxin. Iontophoretically applied L-glutamate depolarized the postsynaptic membrane of the giant axon and this potential was also blocked by JSTX. Kainic acid also depolarized the postsynaptic membrane but this was partially blocked by JSTX, indicating that JSTX differentiated kainate receptor from glutamate one. The results strongly suggest that L-glutamate is the neurotransmitter in the giant synapse of squid.

Animals↗
PubMed1985

Effects of the hepatocarcinogen nafenopin, a peroxisome proliferator, on the activities of rat liver glutathione-requiring enzymes and catalase in comparison to the action of phenobarbital.

The biochemical effects in the livers of male rats of prolonged administration of the experimental hepatocarcinogen nafenopin, a hypolipidemic agent and peroxisome proliferator, were compared to those of another experimental liver carcinogen, phenobarbital, which acts as a neoplasm promoter. Feeding of nafenopin, 0.03 mmol/kg basal diet for up to 24 weeks increased the numbers of hepatic peroxisomes, increased catalase activity, markedly decreased cytosolic glutathione transferase activities toward two substrates, decreased cytosolic glutathione peroxidase activities toward H2O2 and two organic peroxides, and suppressed the age-related increase in gamma-glutamyl transpeptidase activity. In contrast the livers of rats fed an equimolar concentration of phenobarbital displayed increases in cytosolic glutathione transferase activities and enhancement of gamma-glutamyl transpeptidase activity but no changes in glutathione peroxidase activities. There was also an enhancement of catalase activity without apparent increase in peroxisome number. Enzyme kinetic analyses revealed that the cytosolic glutathione transferase activities toward two halogenonitrobenzene substrates were inhibited in the rats fed nafenopin and displayed elevated Km and decreased Vmax. Kinetic studies of glutathione transferase activities in which nafenopin was mixed with normal rat liver cytosols in the assay system revealed competitive type inhibition toward 1-chloro-2,4-dinitrobenzene and a noncompetitive type of inhibition toward 3,4-dichloronitrobenzene. Likewise activities of glutathione peroxidases toward H2O2 and cumene hydroperoxide were suppressed by in vitro addition. Thus the effects of nafenopin and phenobarbital on liver biochemistry were very different. The inhibition of hepatic biotransformation and scavenger systems by nafenopin is suggested to be relevant to its hepatocarcinogenicity.

Animals↗
PubMed1985

[Multidisciplinary treatment of bone and soft tissue sarcomas].

The result of the group study on adjuvant chemotherapy with HD-MTX, ADR and CPM for 25 cases of osteosarcomas is as follows: Overall survival at three and a half years is 58.4% and the disease-free survival is 40%. In our clinics, 66 cases of osteosarcomas were treated by the radical surgery from 1955. Overall survival of these cases at five years was 49%. Overall survival between 1955 and 1974 was 43% and that from 1975, the year when ADR was introduced, to date was 55%. The data of the group study of soft tissue sarcoma sponsored by Ministry of Health and Welfare show that in 318 cases of soft tissue sarcomas of extremities, the recurrence rate during the period between 1962 and 1976 is 52%, metastasis rate 69%, and overall survival at 5 years 42%. From 1972 to 1983, in 414 cases treated by the orthopaedic clinics of the same group the recurrence rate become as low as 23% metastasis rate 45% and overall survival at 5 years 56%. In our clinics, 89 patients with soft tissue sarcomas were treated by the curative wide resection and the recurrence rate is 12%, metastasis rate 25%, and overall survival at 5 years 78%. In this series, in 80% of cases limb salvage is succeeded.

Adult↗
PubMed1984

Liver cell dysplasia and hepatitis B surface antigen in liver cirrhosis and hepatocellular carcinoma.

Liver tissues of 223 autopsy cases of cirrhosis and hepatocellular carcinoma were examined for liver cell dysplasia in relation to hepatitis B surface antigen (HBsAg) detected with orcein stain. Liver cell dysplasia was found in 94 cases (42.2%): 37 were from cases of cirrhosis only, and 53 were from cases of cirrhosis with hepatocellular carcinoma. There was a significant difference in the overall incidence of HBsAg in cases with and without dysplasia (70.2%:32.6%). A similar difference was found in all groups, i.e., those with cirrhosis, cirrhosis with hepatocellular carcinoma, and hepatocellular carcinoma only, in which none of 11 cases of HBsAg negative had dysplasia. A good correlation was seen between the semiquantitative grade of dysplasia and the incidence of HBsAg. These findings suggest a close relationship of HBsAg with liver cell dysplasia.

Autopsy↗
PubMed1984

Neoplastic conversion in rat liver by the antihistamine methapyrilene demonstrated by a sequential syncarcinogenic effect with N-2-fluorenylacetamide.

A study was performed to determine whether the enhancing effect of the antihistamine methapyrilene (MP) in rat liver carcinogenesis represents promotion or syncarcinogenesis . The effect on hepatocarcinogenicity induced by N-2-fluorenylacetamide (FAA) of sequential administration of MP given either before or after FAA was studied in comparison with diethylnitrosamine (DEN) also given either before or after FAA. MP in either sequence with FAA enhanced liver carcinogenicity as did DEN. Moreover, MP by itself induced liver altered foci, albeit at a high dose for a prolonged interval. A single liver neoplasm occurred with exposure to MP alone. These findings suggest that MP produces neoplastic conversion of liver cells which can be summated with the genotoxic effect of FAA to produce syncarcinogenesis .

2-Acetylaminofluorene↗
PubMed1984

Adsorption of influenza viruses to nitrocellulose membrane filters by filtration and their quantitative densitometric determination.

Influenza viruses concentrated and adsorbed onto nitrocellulose membrane filters by filtration are detected rapidly and sensitively by sequential incubation with the primary antibody and the secondary antibody conjugated with peroxidase. The bound enzyme is detected by incubation with a substrate which is converted to an insoluble colored product. A dual-wavelength TLC scanner is used for densitometric quantitation. The membrane filtration-blotting enzyme immunoassay provides a method for quantitative analysis and rapid typing of influenza isolates. The method may be also applicable for quantitative detection of influenza viruses in throat swab specimens from patients, as well as in tissue culture fluids.

Collodion↗
PubMed1984

Effects of the hepatocarcinogenic peroxisome-proliferating hypolipidemic agents clofibrate and nafenopin on the rat liver cell membrane enzymes gamma-glutamyltranspeptidase and alkaline phosphatase and on the early stages of liver carcinogenesis.

The effects of the hepatocarcinogenic peroxisome proliferating hypolipidemic agents clofibrate (CF) and nafenopin (NF) on rat liver carcinogenesis initiated by N-2-fluorenylacetamide (FAA) were studied and compared with that of the neoplasm promoter phenobarbital (PB). Male F344 rats were fed 0.02% FAA for 8 weeks to induce hepatocellular altered foci, and were then given no chemical or equimolar amounts (0.03 mmol/kg diet) of the chemicals for 24 weeks in the diet. In groups of animals killed sequentially, 0.07% PB had a marked enhancing effect on FAA-induced foci, while 0.073% CF produced only slight enhancement and 0.093% NF produced none. At the end of the experiment, only PB increased the incidence and multiplicity of liver neoplasms. NF suppressed histochemical gamma-glutamyltranspeptidase activity in the abnormal hepatocytes of foci as well as in periportal hepatocytes. In homogenates of livers from rats fed NF, gamma-glutamyl-transpeptidase activity was reduced, and this occurred to a lesser degree with CF, whereas PB enhanced activity. NF also induced alkaline phosphatase activity in hepatocytes throughout the lobule, but not in altered hepatocytes, thereby making foci demonstrable in sections reacted for alkaline phosphatase. These findings thus reveal significant cell membrane effects of NF and CF and suggest that their involvement in hepatocarcinogenesis is more complex than a promoting action.

2-Acetylaminofluorene↗
PubMed1984

Distinction between liver neoplasm promoting and syncarcinogenic effects demonstrated by exposure to phenobarbital or diethylnitrosamine either before or after N-2-fluorenylacetamide.

The effect on the liver carcinogenicity in rats of sequential administration of either phenobarbital (PB) or diethylnitrosamine (DEN) given either before or after N-2-fluorenylacetamide (FAA) was studied. DEN given in the drinking water either before or after dietary FAA enhanced liver carcinogenicity over that produced by FAA alone. In contrast, dietary PB produced enhancement only when given after FAA. Thus, the effects of DEN summate with those of FAA, whereas PB produces a promoting, but not syncarcinogenic, effect. The usefulness of reverse sequence protocols for distinguishing between initiation-promotion and syncarcinogenesis by sequentially administered chemicals is demonstrated.

2-Acetylaminofluorene↗
PubMed1984

Inhibition of chemically induced mammary carcinogenesis in rats by short-term exposure to butylated hydroxytoluene (BHT): interrelationships among BHT concentration, carcinogen dose, and diet.

Dietary butylated hydroxytoluene (BHT) fed 14 days before and 14 days after carcinogen administration resulted in a dose-dependent inhibition of 7, 12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumor incidence in outbred Sprague-Dawley rats. In addition, the inhibitory effects of BHT were strongly influenced by the dose of initiating carcinogen and the type of diet in which BHT was administered. In animals fed the NIH-07 diet and receiving a low dose of DMBA (5 mg/rat), the inhibitory effect of BHT was manifested at all four BHT concentrations (6,000 leads to 300 ppm). Maximal inhibition was approximately 50% in animals given 5 mg DMBA and receiving 6,000 ppm BHT. However, in the group administered a high dose of DMBA (15 mg/rat), the inhibitory effect of BHT was expressed only at 6,000 ppm, the highest concentration given. Lower concentrations (300 and 1,000 ppm) of BHT had no detectable effect on tumor incidence. In animals fed the defined, semipurified AIN-76A diet during the 4-week treatment period and initiated with 5 mg DMBA, BHT at 6,000 ppm inhibited tumor development. However, at 15 mg DMBA animals fed the AIN-76A diet differed markedly from those fed the NIH-07 diet. In the former group, BHT at 6,000 ppm was unable to elicit any inhibitory response; in the latter group, BHT inhibited tumor development by 40%. Dietary BHT also inhibited DMBA-induced adrenocortical hyperplastic nodules in a dose-dependent fashion. These results indicate that short-term exposure to dietary BHT can inhibit experimental mammary tumor development at environmentally relevant concentrations.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Abnormalities in liver iron accumulation during N-2-fluorenylacetamide hepatocarcinogenesis that are dependent or independent of continued carcinogen action.

The characteristics of liver iron accumulation were studied during N-2-fluorenylacetamide (FAA)-induced hepatocarcinogenesis in rats. After injection of iron-dextran in control rats, hepatocytes accumulated stainable iron evenly throughout hepatic lobules. During the feeding of FAA, iron accumulation was reduced in the midzonal and centrilobular regions. After FAA removal, hepatocytes in these regions again accumulated high amounts of iron. Hepatocellular altered foci induced by FAA displayed rather uniform (> 94%) iron-exclusion during FAA feeding. After FAA removal, however, iron-exclusion was lost in a fraction of the foci, while others (40-64%) remained resistant to iron accumulation. A large majority of liver neoplasms (> 93%) displayed resistance to cellular iron accumulation both during FAA feeding and after removal of FAA. Thus, iron-exclusion by liver neoplasms is carcinogen-independent and irreversible, in contrast with that of normal hepatocytes which is completely carcinogen-dependent and reversible. Altered foci appear to represent two populations: one is characterized by reversible iron-exclusion whereas the other, like neoplasms, possesses permanent iron-exclusion.

2-Acetylaminofluorene↗
PubMed1984

[A clinical and genetic study on the congenital dislocation of the hip].

Among 13,779 infants examined from 1974 to 1980 at Takashimadaira and Toride health centers, there were 45 patients with congenital hip dislocation, an incidence of 3.3 per 1,000 live births, that is, 0.08% and 0.53% respectively in male and female. The male to female ratio was 1: 7.4. Its incidence seems to be decreasing year by year with statistic significance, compared with the data previously reported. A family study was conducted based upon 117 patients with this disease diagnosed at the Tokyo Medical and Dental University from 1971 to 1980. Applying the recurrence rate of siblings and the incidence in the general population to the model proposed by Falconer, the heritability of liability to congenital hip dislocation in Japan is estimated to be 80 +/- 20% in males and 135 +/- 10% in females, which is beyond limitation of the heritability and much higher than Woolf's estimation (82% in male and 58% in female). This might be due to the insufficient size of the test population, but the genetic factors are presumed to play a more important role on the etiology of this abnormality.

Adult↗