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Biomedical subjects

S Kai

Publications and source records attributed to S Kai.

At least 109 records · Page 6Linked to original sources
PubMed1986

[Reproduction studies of VP 16-213 (II)--Oral administration to rats during the period of fetal organogenesis].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to pregnant Crj: CD (Sprague-Dawley) rats from day 7 through 17 of gestation at dose levels of 1, 3 and 10 mg/kg/day. The summarized results obtained are as follows: VP 10 mg/kg suppressed the maternal body weight increase from day 12 through 20 of gestation. VP 10 mg/kg brought the inhibition of fetal growth accompanied by the lowered values in body weight and body length. Furthermore, the elevated incidences of skeletal anomalies and unossified 5th and 6th sternums, as well as retarded ossification of thoracic vertebrae were also noted in this dose level. VP 10 mg/kg induced anophthalmia, microphthalmia and dilated lateral ventricles in fetuses (F1), as well as unilateral anophthalmia in offspring (F1). VP 10 mg/kg increased the days required for opening of eyelids and descending of testes in offspring (F1), but failed to affect their learning ability, motility, motor activity or emotional development. VP 10 mg/kg suppressed the growth of genital organs in F1 rats of both sexes, but failed to affect their reproductive ability or gestation period. As for F2 newborns derived from F1 rats whose dams had ever received VP 10 mg/kg during the period of fetal organogenesis, the number of implantations and survivors as well as birth indexes lowered due to changes in these items restricted to a few litters. Based on these results, the no-effect dose level of VP under the present experimental condition was estimated to be 3 mg/kg/day against dams and their offspring.

Administration, Oral↗
PubMed1986

[Reproduction studies of VP 16-213 (III)--Oral administration to rabbits during the period of fetal organogenesis].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to pregnant JW-NIBS rabbits from day 6 through 18 of gestation at dose levels of 0.3, 1, 3 and 10 mg/kg/day. The summarized results obtained are as follows: VP 3 and 10 mg/kg elevated the maternal mortality dose-responsively. VP 3 mg/kg and lower doses failed to affect the fetal growth and ossification processes, and did not induce drug-dependent external and visceral anomalies as well as skeletal variations and anomalies. Based on these results, the no-effect dose levels of VP under the present experimental condition were estimated to be 1 mg/kg/day against dams and 3 mg/kg/day against fetuses.

Administration, Oral↗
PubMed1986

[Reproduction studies of VP 16-213 (IV)--Oral administration to rats during the perinatal and lactation periods].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to female Crj: CD (Sprague-Dawley) rats from day 17 of gestation through postpartum day 20 at dose levels of 1, 3 and 10 mg/kg/day. The summarized results obtained are as follows: VP 10 mg/kg induced thymic atrophy in dams. VP failed to affect the parturition of dams. VP 10 mg/kg lowered the viability of newborns (F1) on postpartum day 3 and increased the days required for descending of testes, but failed to affect the growth of genital organs, learning ability, motility motor activity or emotional development. VP 10 mg/kg brought a transient suppression of body weight increase in pregnant F1 rats, but failed to affect their reproductive ability and parturition. F2 newborns derived from F1 rats whose dams had ever received VP during the prenatal and lactation periods showed no changes in observation items at birth. Long-term rearing F1 rats derived from VP-treated dams manifested no delayed toxicity including carcinogenicity. Based on these results, the no-effect dose level of VP under the present experimental condition was estimated to be 3 mg/kg/day against dams and their offspring.

Administration, Oral↗
PubMed1986

[Reproduction studies of VP 16-213 (V)--Intravenous administration to rats prior to and in the early stages of pregnancy].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered intravenously to male Crj: CD (Sprague-Dawley) rats for 61 days and to female rats of the same strain for 14 days prior to mating at dose levels of 0.05, 0.2 and 0.8 mg/kg/day. These animals were then mated under the consecutive administration of this drug and the females confirmed to be copulated were further dosed from day 0 through 7 of gestation. The summarized results obtained are as follows: Body weight increases were suppressed at the dose level of VP 0.8 mg/kg in males and females. VP 0.2 and 0.8 mg/kg decreased the thymic weight and 0.8 mg/kg decreased testicular and epididymal weight in males showing macroscopic atrophy of these organs, but these doses failed to affect the reproductive ability and so on in parent rats. As for fetuses, VP 0.8 mg/kg elevated the mortality, decreased the number of survivors and suppressed their growth. Furthermore, this dose raised the incidences of anophthalmia, microphthalmia, dilated lateral ventricles and unossified 5th and 6th sternums, as well as brought retarded ossification of sternums, cervical vertebrae, sacral and coccygeal vertebrae, metacarpus and thoracic vertebrae. Based on these results, the no-effect dose levels of VP under the present experimental condition were estimated to be 0.05 mg/kg/day against parent rats of both sexes and 0.2 mg/kg/day against their offspring.

Animals↗
PubMed1986

[Reproduction studies of VP 16-213 (VI)--Intravenous administration to rats during the perinatal and lactation periods].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered intravenously to female Crj: CD (Sprague-Dawley) rats from day 17 of gestation through postpartum day 20 at dose levels of 0.05, 0.2 and 0.8 mg/kg/day. The summarized results obtained are as follows: VP 0.2 and 0.8 mg/kg suppressed the body weight increase and brought thymic atrophy in dams. VP failed to affect the states of birth of newborns (F1). In F1 offspring, VP 0.8 mg/kg increased the days required for testicular descending and vaginal opening, and suppressed the body weight increase, but failed to affect the growth of genital organs, reproductive ability, learning ability, motility, motor activity or emotional development. F2 newborns derived from F1 rats whose dams had ever received VP during the prenatal and lactation periods showed no changes in observation items at birth. Based on these results, the no-effect dose level of VP under the present experimental condition was estimated to be 0.05 mg/kg/day against dams and 0.2 mg/kg/day against their offspring.

Animals↗
PubMed1986

[Toxicity studies of VP 16-213 (III)--Oral six-month chronic toxicity in rats].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to Crj : CD (Sprague-Dawley) rats of both sexes at dose levels of 1, 3, 10 and 30 mg/kg/day for six months with the object of examining its chronic toxicity and the reversibility of toxic effects. The summarized results obtained are as follows: VP 30 mg/kg suppressed body weight increase and feed intake, and brought transient diarrhea, anemia and depilation. Some animals receiving this dose died showing systemic debility, emaciation and ataxia. VP 3 mg/kg and higher predominantly decreased red blood cell count as well as white blood cell count accompanied with lowered lymphocyte fraction. VP 30 mg/kg lowered total serum protein content and elevated A/G ratio in males, and lowered serum alkaline phosphatase activity in females. VP 10 and 30 mg/kg predominantly induced thymic atrophy, testicular atrophy with suppression of spermatogenesis and tubular atrophy, a decrease in epididymal weight, and splenic erythropoiesis. Above-described changes excluding the findings on testis and epididymis in VP 30 mg/kg group were shown to be generally reversible. Based on these results, the non-effect dose level of VP under the present experimental condition was estimated to be 1 mg/kg/day against rats of both sexes.

Administration, Oral↗
PubMed1986

[Toxicity studies of VP 16-213 (IV)--Intravenous one-month subacute toxicity in rats].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered intravenously to Crj : CD (Sprague-Dawley) rats of both sexes at dose levels of 0.15, 0.50, 1.5 and 4.5 mg/kg/day for one month with the object of examining its subacute toxicity and the reversibility of toxic effects. For the purpose of comparison, vincristine (abbr. to VCR) was administered in the same manner at dose levels of 0.04 and 0.08 mg/kg/day. The summarized results obtained are as follows: VP 0.50 mg/kg and higher suppressed body weight increase and food intake dose-responsively. VP 4.5 mg/kg brought depilation and anemia, and some of male animals receiving this dose died showing systemic debility, emaciation and ataxia. VP 0.50 mg/kg and higher decreased white blood cell count accompanied with lowered lymphocyte fraction, and 1.5 and 4.5 mg/kg predominantly decreased red blood cell count. VP 1.5 and 4.5 mg/kg lowered total serum protein content and serum alkaline phosphatase activity, and elevated A/G ratio. VP 0.50 mg/kg and higher predominantly decreased testicular weight, and 1.5 and 4.5 mg/kg predominantly brought thymic atrophy, hypoplasia of bone marrow and testicular atrophy with suppression of spermatogenesis and tubular atrophy. VP 4.5 mg/kg induced atrophy of germinal centers and hemosiderosis in spleen, and epididymal atrophy with decrease of sperms in number and appearance of giant cells. Above-described changes excluding the findings on testis and epididymis were generally reversible. Most of the findings for a reference drug, VCR, were similar to those for VP, and their severities brought by VP 1.5 and 4.5 mg/kg were comparable to those by VCR 0.04 and 0.08 mg/kg, respectively. Based on these results, the non-effect dose level of VP under the present experimental condition was estimated to be 0.15 mg/kg/day against rats of both sexes.

Anemia↗
PubMed1986

Effects of flavonoids on xanthine oxidation as well as on cytochrome c reduction by milk xanthine oxidase.

That flavonoids inhibit xanthine oxidase from cow milk was confirmed by measuring oxygen consumption with an oxygen electrode. In contrast, flavonoids did not inhibit glucose oxidase, another oxygen consuming enzyme. Among the flavonoids tested, quercetin, kaempferol, myricetin, chrysin, quercitrin, and morin were potent inhibitors of xanthine oxidase; their inhibition rates (%) were 80, 70, 69, 62, 59, and 51 at 100 microM (except chrysin at 50 microM), respectively. The xanthine oxidase-inhibiting activities of the flavonoids were not always well correlated with the suppressive activities of the flavonoids on cytochrome c reduction by a xanthine-xanthine oxidase system. The inhibition of xanthine oxidase by quercetin was not affected by cupric ion. The partition rates of the flavonoids between n-butanol and a buffer solution seemed to account for some of the inhibition.

Animals↗
PubMed1985

Secondary correction of the cleft lip and nose deformity: a new technique for revision of whistling deformity.

Reconstruction of the continuity of the orbicularis oris is the main component in correction of the whistling deformity. However, many of the cases are associated with other deformities, such as conspicuous lip scars, an unnaturally wide central lip, flaring alae with wide nostril floors, and a short columella with a flat nasal tip. We report a technique that combines correction of such deformities with reconstruction of the orbicularis oris in a single operation.

Adolescent↗