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Biomedical subjects

N Ariyoshi

Publications and source records attributed to N Ariyoshi.

50 records · Page 3Linked to original sources
PubMed1993

Different characteristics of neuroblastomas in cases found by mass screening and non-screening: evaluation of mass screening for neuroblastoma in Kitakyushu City.

Neuroblastoma accounts for 24 of 109 patients who have been managed by the pediatric tumor outpatient clinic of our university hospital. Among the malignant solid tumors, neuroblastomas are the most numerous. We investigated neuroblastomas found by mass screening oncologically and epidemiologically. Up until March 31, 1991, seven cases were detected from 64,885 infants who received mass screening by the Kitakyushu City System which we had introduced in 1985. This system is based on an individual health survey program for infants in the city. Six of seven cases found by the screening were treated in our department. None of them, including stage III and stage IV cases, showed any conventional risk factors such as high serum levels of neuron specific enolase, ferritin, amplification of N-myc gene, nor cytogenetic abnormalities. Histopathological studies revealed that ganglioneuroblastoma was observed in 9 of 13 cases over one year of age, whereas it was observed only in two screened cases out of 11 cases under one year of age. According to the classification of Shimada et al., there was one stroma-rich tumor, which is rare in infants and usually a matured type, in the screened cases. Interestingly, another one of the six screened cases regressed spontaneously without any treatment. These cases suggested that some neuroblastomas in the process of maturation or spontaneous regression could be detected by mass screening. On the other hand, 9 of 13 non-screened cases over one-year-old died. Although mass screening at six months of age decreased the mortality rate by neuroblastoma in infancy, the prognosis of neuroblastoma in patients over one-year-old remained still poor. Mass screening should be carried out in a health survey program at one year and six months of age in order to improve the outcome.

Child↗
PubMed1993

Identification of in vitro metabolites of 2,4,6,2',4',6'-hexachlorobiphenyl from phenobarbital-treated dog liver microsomes.

We studied in vitro metabolites of 2,4,6,2',4',6'-hexachlorobiphenyl (HCB, IUPAC PCB No. 155) produced by liver microsomes of a phenobarbital (PB)-treated beagle dog. The major metabolites were 3-hydroxy-2,4,6,2',4',6'-HCB (M-1), 4-hydroxy-2,6,2',4',6'-pentachlorobiphenyl (PenCB, M-2) and 3,4-dihydroxy-2,6,2',4',6'-PenCB (M-3). Furthermore, 4-hydroxy-2,3,6,2',4',6'-HCB (M-4), which could be formed via the 3,4-epoxidation and the subsequent NIH-shift of the chlorine from the 4 to the 3 position, was also detected. We found that M-3 is a common secondary metabolite of the two major monohydroxy metabolites, M-1 and M-2. These results indicate that the dog seems to metabolize and eliminate this congener not only by a mechanism involving direct insertion of a hydroxyl group but also via an arene oxide intermediate.

Animals↗
PubMed1993

[Inducing ability of co-planar PCBs toward bilirubin UDP-glucuronyltransferase of liver microsomes: the remarkable difference between guinea pigs and rats].

The induction of liver microsomal UDP-glucuronyltransferase (UGT) activity toward bilirubin by pretreatment with 3, 4, 3', 4'-tetrachlorobiphenyl (TCB), 3, 4, 5, 3', 4'-pentachlorobiphenyl (PenCB) and 3-methylcholanthrene (MC) was studied in guinea pigs and rats. In addition, microsomal benzo(a)pyrene 3-hydroxylase and cytosolic DT-diaphorase activities were also measured for the comparison. All of the PenCB, TCB and MC significantly induced the bilirubin UGT activity of guinea pig liver microsomes. The highest induction (6-fold over the control) was seen in the PenCB-treated animal, and MC (3.2-fold) and TCB (2.4-fold) were less effective. On the other hand, the induction of benzo(a)pyrene 3-hydroxylase and DT-diaphorase activities of guinea pigs was not so remarkable as that of bilirubin UGT activity. In the guinea pig, the inducibility of bilirubin UGT activity seemed to be correlated with the toxicity induced with PenCB, TCB and MC. In contrast to the guinea pig, UGT activity toward bilirubin in the rat was significantly decreased by the treatment with the inducers described above. These results suggest that bilirubin UGT activity in the guinea pig can be an index for the toxicity of polychlorinated biphenyls as like as benzo(a)pyrene 3-hydroxylase and DT-diaphorase activities in the rat.

Animals↗
PubMed1993

[Metabolism in vivo of 2, 4, 6, 2', 4', 6'-hexachlorobiphenyl in dog and partial characterization of cytochrome P-450 isozyme responsible for biotransformation of the congener].

We reported previously that the dog is a unique species which can metabolize 2, 4, 5, 2', 4', 5'-hexachlorobiphenyl (HCB) by unusual mechanism via 2,3-arene oxide intermediate formation. 2, 4, 5, 2', 4', 5'-HCB is known as one of the PCB congeners showing the highest concentration in the blood of Yusho patients at present. Therefore, further investigation on the mechanism of biotransformation of PCB in the dog is very useful to obtain informations about metabolic fates of persistent congeners in the bodies of Yusho patients. In the present study, we examined in vivo metabolic pathways of 2, 4, 6, 2', 4', 6'-HCB in a dog, and also a role of cytochrome P-450 isozymes in its metabolism. In these experiments, three major metabolites were found in feces of the dog. These were identified to be 3-hydroxy-2, 4, 6, 2', 4', 6'-HCB (M-1), 4-hydroxy-2, 6, 2', 4', 6'-pentachlorobiphenyl (M-2) and 3, 4-dihydroxy-2, 6, 2', 4', 6'-PenCB (M-3), which were previously identified as the major metabolites in vitro. 4-Hydroxy-2, 3, 6, 2', 4', 6'-HCB has also been isolated as a metabolite in vitro, but not detected in this in vivo study. In conclusion, the present in vivo study supported the previous in vitro results that the dog metabolizes this congener at least two mechanisms including direct hydroxylation and arene oxide formation. It was also indicated that cytochrome P-450 isozymes responsible for metabolism of this congener may be in part different from those catalyzing the 2, 4, 5, 2', 4', 5'-HCB metabolism.

Animals↗
PubMed1993

[Vitamin K].

In this paper, highly sensitive methods for measuring of vitamin K in serum, feces and milk are described. Vitamin K1 and the menaquinone family from the serum, feces and milk were separated by high performance liquid chromatography. The separated K1 and menaquinone families were detected by a fluorescence spectrophotometer after their reduction with sodium borohydride or platinum catalyst column. In these methods, minimum detectable quantities of K1, menaquinone-4 and menaquinone-7 were 10, 10 and 50 pg, respectively. More than 95% of supplemented vitamin K1, menaquinone-4 and menaquinone-7 were recovered in the serum and feces. Furthermore, the method of Hirauchi et al. for measurement of vitamin K1 2,3-epoxide in human plasma is introduced.

Chromatography, High Pressure Liquid↗
PubMed1992

Metabolism of 2,4,5,2',4',5'-hexachlorobiphenyl with liver microsomes of phenobarbital-treated dog; the possible formation of PCB 2,3-arene oxide intermediate.

1. Metabolism of 2,4,5,2',4',5'-hexachlorobiphenyl (HCB) was investigated in vitro using liver microsomes of one male beagle dog after phenobarbital treatment. 2. Three major metabolites were isolated and identified as 3-hydroxy-2,4,5,2',4',5'-HCB, 2-hydroxy-4,5,2',4',5'-pentachlorobiphenyl (PenCB), and 2-hydroxy-3,4,5,2',4',5'-HCB, by comparison of g.l.c.-mass spectrometry and 1H-n.m.r. data with those of authentic samples. 3. 2-Hydroxy-3,4,5,2',4',5'-HCB was found as a metabolite of 2,4,5,2',4',5'-HCB for the first time using dog liver microsomes. Present result indicate that this metabolite and the dechlorinated PenCB are derived from a metabolic intermediate, namely, 2,3-epoxy-2,4,5,2',4',5'-HCB. 2,3-Epoxide formation is a new metabolic pathway of PCB.

Animals↗
PubMed1991

[Plasma levels of antithrombin III, thrombin-antithrombin III complex, alpha 2 plasmin inhibitor and plasmin alpha 2 plasmin inhibitor complex in normal and sick newborn infants].

Both bleeding and thrombosis are commonly seen in newborn infants because of their imbalance of coagulation and fibrinolysis system. In order to clarify some aspects of the hemostatic characteristics during neonatal period, we measured the levels of antithrombin-III (AT-III), thrombin AT-III complex (TAT), alpha 2-plasmin inhibitor (alpha 2PI) and plasmin alpha 2PI complex (PIC) in 137 normal and sick newborn infants. The results were as follows 1) AT-III levels in normal neonates were significantly low as compared with them in normal adults, and further lower levels were found in sick neonates. 2) TAT levels in sick neonates were significantly higher than those in either normal neonates and adults. In sick neonates, the incidence of abnormally high TAT values increased with DIC score points. 3) No significant difference of alpha 2PI level was seen between normal term neonates and adults. However, alpha 2PI levels in sick neonates were significantly low as compared with them in normal term neonates and adults. 4) PIC levels in either normal and sick infants were significantly higher than those in adults, but there was no significant difference in PIC levels between normal and sick newborn infants.

Antifibrinolytic Agents↗
PubMed1990

Purification and characterization of two forms of 2,3,4,7,8-pentachlorodibenzofuran-inducible cytochrome P-450 in hamster liver.

Two forms of cytochrome P-450 (P-450) from liver microsomes of hamsters treated with 2,3,4,7,8-pentachlorodibenzofuran (PenCDF), which possesses the potent acute toxicity and 3-methylcholanthrene (MC)-type inducing ability of liver microsomal monooxygenases in animals, were purified and characterized. These P-450 forms, designated as hamster P-450H and hamster P-450L, had the molecular masses of 52 and 50 kDa, respectively, and showed the absorption maximum of CO-reduced difference spectra at 446 nm. The absolute spectra of their oxidized forms indicated that hamster P-450H was in high-spin state and hamster P-450L was in low-spin state. A part of PenCDF injected into hamster was tightly bound to purified hamster P-450H at a ratio of 0.107 nmol PenCDF/nmol P-450. In a reconstituted system, both hamster P-450H and hamster P-450L showed relatively low catalytic activities for 3-hydroxylation of benzo[a]pyrene and O-deethylations of both 7-ethoxyresorufin and 7-ethoxycoumarin, while they both catalyzed 7 alpha- and 2 alpha-hydroxylations of testosterone effectively to a similar extent. Addition of cytochrome b5-to a reconstituted system accelerated the formation of 7 alpha-hydroxytestosterone 5.3-fold with hamster P-450L and 2.2-fold with hamster P-450H. In addition, hamster P-450H catalyzed estradiol 2-hydroxylation at a high rate but hamster P-450L did not.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMedDate not supplied

Metabolism of 2,3',4',5-tetrachlorobiphenyl by cytochrome P450 from rats, guinea pigs and hamsters.

The metabolism of 2,3',4',5-tetrachlorobiphenyl (TCB) was compared using liver microsomes and six isoforms of cytochrome P450 purified from rats, guinea pigs and hamsters. In microsomal study, the following species differences were observed: 1) Untreated guinea pigs and hamsters but not rats can metabolize this TCB to 3-hydroxy- or 4-hydroxy-2,3',4',5-TCB, 2) Guinea pig microsomes showed only 3-hydroxylating activity, whereas hamster microsomes showed higher activity of 4-hydroxylation than that of 3-hydroxylation. In common with three species, the 3-hydroxylation was accelerated by phenobarbital. The 4-hydroxylation in rats and hamsters was increased by pretreatment with 3-methylcholanthrene and 3,3',4,4',5-pentachlorobiphenyl. The hydroxylation activities of liver microsomes from the three species could be explained by an involvement of different isoforms of cytochrome P450. In addition, it is apparent that hamster CYP1A2 as well as hamster CYP2A8 is involved in the 4-hydroxylation of 2,3',4',5-TCB although it has no activity for 2,2',5,5'-TCB.

Animals↗
PubMedDate not supplied

Overview of clinical studies of childhood acute lymphoblastic leukemia for more than ten years by the Japanese Children's Cancer and Leukemia Study Group.

Since 1981, the Children's Cancer and Leukemia Study Group (CCLSG) has developed a series of protocols for treatment of acute lymphoblastic leukemia (ALL) in childhood. In the first randomized controlled study of the 811 protocol (1981-1983) a comparison of conventional daily 6-mercaptopurine and methotrexate with a pulsed regimen of the two drugs was performed. The superiority of the pulsed regimen was shown. In the next 841 protocol (1984-1987) a comparison of two drugs and three drugs during induction therapy was conducted. The three-drug regimen resulted in a significantly higher event-free survival (EFS) rate. In the 874 protocol (1987-1990) two regimens with or without cranial irradiation were randomly compared, and there was no significant difference between the two regimens for the standard-risk group. To further improve the EFS rate a risk group-directed protocol 911 was conducted starting in January 1991. Life-table analysis of serial CCLSG protocols revealed that the outcome of overall ALL has gradually improved with an increase of the EFS rate; 41.4% +/- 3.6% at 14 years for the 811 protocol, 51.3% +/- 3.5% at 11 years for the 841 protocol, 56.7% +/- 3.1% at 8 years for the 874 protocol, and 78.2% +/- 3.1% at 4 years for the more recent 911 protocol.

Antineoplastic Combined Chemotherapy Protocols↗