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Biomedical subjects

C Ishida

Publications and source records attributed to C Ishida.

45 records · Page 3Linked to original sources
PubMed1989

Further studies on metabolism in vivo of 3,4,3',4'-tetrachlorobiphenyl in rats: identification of minor metabolites in rat faeces.

1. Metabolism in vivo of 3,4,3',4'-tetrachlorobiphenyl (TCB) was investigated in male Wistar rats. 2. Five new minor metabolites in addition to two previously identified major metabolites (5-hydroxy-3,4,3',4'-TCB and 4-hydroxy-3,5,3',4'-TCB) were isolated as methylated derivatives from faeces of rats treated with 3,4,3',4'-TCB, by silica gel column chromatography and subsequent preparative t.l.c. 3. Among these methylated metabolites, three were identified as dimethoxy-TCB, and one as monomethoxy-trichlorobiphenyl (TriCB), by g.l.c.-mass spectrometry. By comparison with synthetic standards they were fully identified as 2,5-dimethoxy-3,4,3',4'-TCB, 4,4'-dimethoxy-3,5,3',5'-TCB, 5,6-dimethoxy-3,4,3',4'-TCB, and 4-methoxy-3,3',4'-TriCB, respectively. The structures of these metabolites in rat faeces should therefore be 2,5-dihydroxy-3,4,3',4'-TCB, 4,4'-dihydroxy-3,5,3',5'-TCB, 5,6-dihydroxy-3,4,3',4'-TCB, and 4-hydroxy-3,3',4'-TriCB. 4. One further metabolite was isolated, which was shown to be an oxepin, existing in a state of equilibration with the 4',5'-oxide of the major metabolite, 4-hydroxy-3,5,3',4'-TCB, by mass and 1H-n.m.r. spectra. On standing for several months, this metabolite isomerized to a new compound with a different g.l.c. retention time, which on methylation yielded a product identical with synthetic 4,4'-dimethoxy-3,5,3',5'-TCB by g.l.c.-mass spectrometry. From these results this metabolite was assumed to be an oxepin, equilibrated with 4-hydroxy-4',5'-epoxy-3,5,3',4'-TCB.

Animals↗
PubMed1989

[Comparison of walking exercises in air and in water in children with cerebral palsy].

To compare the effect of walking exercise in water with that in air in cerebral palsied children, we measured in ten subjects oxygen uptake (VO2) during walking for 3-minutes. In 7 children with spastic type of cerebral palsy, VO2 values were significantly lower in exercises in water than in air (p less than 0.05). No significant differences were found in athetotic children. In 5 children with crouched posture VO2 showed a tendency to be lower in exercises in water than in air (0.05 less than p less than 0.1). In contrast, significant differences were not found in 5 children without crouched posture. Children with spasticity or crouched posture may be able to walk in water more than in air.

Adolescent↗
PubMed1988

[Clinical and fundamental studies on intravenous drip infusion of gentamicin in the pediatric field. Pediatric study group of gentamicin].

A multiclinic study of gentamicin (GM) given by intravenous drip infusion was carried out by the Gentamicin Pediatric Study Group. The results are summarized as follows: 1. Upon intravenous drip infusion of GM at a dose range of 2.0-2.5 mg/kg over a period of 0.5-1 hour, therapeutically effective serum concentrations of 4-12 micrograms/ml were obtained. These values are similar to reported values in previous studies using GM intramuscular injection. 2. High urinary concentrations were observed up to 6 hours after administration, and the urinary recovery rate was approximately 60%. 3. Of a total of 142 cases collected, 117 cases were evaluated. Efficacy rates by diseases were: 100% in pneumonia (30/30), 98.3% in urinary tract infections (59/60), and 92.3% in other infections (skin and soft tissue) (12/13), with an overall efficacy rate of 94.9% (including 77 "excellent" cases). 4. Bacteriological examinations showed high eradication rates with the use of GM; i.e., 80% with Staphylococcus aureus (8/10), 60% with Pseudomonas aeruginosa (3/5), 100% with Haemophilus influenzae (7/7) and 97.8% with Escherichia coli (44/45), achieving an overall eradication rate of 92.4%. In mixed infections, the eradication rate was 85.7% (6/7). 5. No ototoxicity, nephrotoxicity or allergic reactions was observed. Abnormal laboratory findings observed were: GOT elevation in 3.1% of cases, GPT elevation in 3.9%, platelet increase in 1.5% and eosinophil increase in 0.8%, thus an overall rate of the appearance of abnormality was 5.6%. The above results indicate that an intravenous drip infusion of GM is a useful method for treating infections in pediatrics.

Adolescent↗
PubMed1988

[Clinical and pharmacokinetic studies of gentamicin in intravenous drip infusion to children].

Eighteen children with urinary tract infection were treated with intravenous drip infusion of gentamicin (GM), and clinical efficacy and pharmacokinetics were studied. Ages of the patients ranged from 2 months to 12 years. Doses of GM ranged 1.0 to 2.5 mg/kg every 8 to 12 hours, and treatment continued for 4 to 10 days. Among 18 patients treated, clinical results were excellent in 12, and good in 6. Values of BUN and creatinine remained within normal range in all patients during and after the GM treatment. One child had an eosinophilia. There were no cases that showed signs and symptoms of oto- and nephrotoxicity. Twenty eight time-serum level curves were studied in 16 patients during and after intravenous infusion of GM over 30 minutes. Doses were 1.0 mg/kg in 4, 1.9-2.0 mg/kg in 14, and 2.2-2.5 mg/kg in 10. Peak serum levels at 30 minutes after the start of infusion were 2.66-7.38 micrograms/ml (average 5.45 micrograms/ml) in cases receiving 1.0 mg/kg, 4.67-10.8 micrograms/ml (7.26 micrograms/ml) in 1.9-2.0 mg/kg, and 6.16-16.5 micrograms/ml (8.86 micrograms/ml) in 2.2-2.5 mg/kg. Elimination half-lives were 1.75-2.48 hours (average 2.10 hours) in cases with ages less than 1 year, 1.58-2.58 hours (2.01 hours) with 1 to 6 years, and 1.20-3.07 hours (1.66 hours) with 7 to 12 years who were given doses of 1.9-2.5 mg/kg. There were no significant differences in pharmacokinetic parameters between first and last administration in these patients, suggesting that no accumulation occurred with above mentioned doses. Urinary recovery of GM ranged from 21.9 to 99.2 percent (average 62.48%) within 6.5 hours after the initiation of drip infusion.

Child↗
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

Non-Alzheimer dementia with status spongiosus and neuronal cell loss showing unusual perineuronal structures and point mutation at 129 codon of prion protein.

The subject presented with intellectual decline followed by progressive muscle weakness of the bilateral upper limbs when he was 60 years old. He had a point mutation (methionin-valine) at 129 prion protein codon. He died at the age of 63 and necropsy revealed bilateral frontal lobe atrophy. The frontal cortex showed neuronal cell loss in layers II and III with spongiform change. Reusche silver impregnation technique for beta-peptide combined with ubiquitin immunostaining revealed perineuronal structures encircling degenerated neurons and ubiquitin-immunoreactive (IR) dot-like deposits. They were distributed particularly in the temporal neocortex and entorhinal cortex. They differed from either classic senile or diffuse plaque by the absence of amyloid core in the center and of amyloid fibrils. Ubiquitin-IR materials were also found as neuronal inclusions in the hippocampal granular cells. Nigral degeneration and neuronal loss in the hypoglossal nerve nucleus and in the anterior horn of the spinal cord were also found and spinal cord motoneurons had Bunina body inclusions. The clinical features and pathological findings were consistent with non-Alzheimer dementia with status spongiosus and neuronal cell loss. The unusual perineuronal structures found in our case might be a specific cellular pathology of dementia of the frontal lobe type.

Cell Death↗