Примери за използване на Skeletal variations на Английски и техните преводи на Български
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The incidence of skeletal variations and malformations e.g.
Findings included embryo-lethality,reduced foetal growth, and skeletal variations.
Soft tissue and skeletal variations in the foetuses were also observed at 10 and 20 mg/kg/day.
At≥60 mg/kg/day there were decreased foetal body weights, and minor skeletal variations.
The incidence of skeletal variations and malformations(e.g. sternal cleft) was increased at 0.3 and 0.9 mg/kg.
These findings included decreased foetal body weight,foetal oedema, and an increase in skeletal variations/ malformations, early intra-uterine deaths and still births.
In rabbits, decreased foetal weight and skeletal variations indicative of developmental delays were noted only in the presence of severe maternal toxicity, with a no-effect dose of 50 mg/kg(9-fold human exposure).
These findings included decreased foetal body weight,foetal oedema, and an increase in skeletal variations/malformations, early intra-uterine deaths and still births.
A slight increase in two foetal skeletal variations(misshapen sternebra, sternebra bipartite ossification) was observed in rabbits at an Neparvis dose of 4.9 mg sacubitril/5.1 mg valsartan/kg/day.
At 3600 mg/kg/day, in only one of the 2 EFD studies,there was a slight decrease in fetal weight associated with a marginal increase in skeletal variations/minor anomalies.
Effects on embryo-foetal development(embryo-foetal lethality and skeletal variations) were observed at 50 mg/kg/day(at low multiple of clinical exposure).
However, at systemic plasma exposures significantly below(rabbits) or not significantly higher(rat) than the expected human exposures during therapeutic dosing,a number of minor changes, including thymic elongation and minor skeletal variations were seen, indicating developmental delay.
Deferasirox was not teratogenic, butcaused increased frequency of skeletal variations and stillborn pups in rats at high doses that were severely toxic to the non-iron-overloaded mother.
In an embryo-foetal development study in rats, increased post-implantation loss, malformations(absence of caudal vertebrae andin some cases also of sacral vertebrae), skeletal variations and lower foetal body weights were observed.
In rabbits, decreased foetal weight and skeletal variations indicative of developmental delays were noted only in the presence of severe maternal toxicity, with a no-effect.
In rats and rabbits embryo-foetal toxicity(e.g. increased early resorptions, postimplantation loss, decreased viable foetuses)and signs of delayed development(increased skeletal variations) were found in the presence of maternal toxicity.
Deferasirox was not teratogenic, butcaused increased frequency of skeletal variations and stillborn pups in rats at high doses that were severely toxic to the non-iron-overloaded mother.
In rats, decreased foetal weights and increased skeletal variations including reduced ossification of the sternabrae, vertebrae, and skull were observed at the high dose of 15 mg/kg/day(6-fold the estimated human exposure based on AUCs) and were associated with maternal toxicity(reduced maternal body weights).
In pregnant rabbits, alectinib caused embryo-foetal loss,small fetuses and increased incidence of skeletal variations at exposures 2.9-fold of the human AUC exposure at the recommended dose.
In rabbits, the effects of saxagliptin were limited to minor skeletal variations observed only at maternally toxic doses(NOEL 158 and 224 times the human exposure for saxagliptin and the major metabolite, respectively at RHD).
Pregnant mice exposed to axitinib showed an increased occurrence of cleft palate malformations and skeletal variations, including delayed ossification, at exposure levels below the expected human exposure.
In rabbits, the effects of saxagliptin were limited to minor skeletal variations observed only at maternally toxic doses NOEL 158 and 224 times the human exposure for saxagliptin and the major metabolite, respectively, at.
In rats, embryofoetotoxicity(pregnancy loss, decreased foetal viability, decreased foetal body weights,increased frequency of skeletal variations) and postnatal developmental toxicity(decreased survival of pups) was observed at maternally toxic dosages.
Effects seen in the rabbit embryo-foetal development toxicity study(skeletal variations and incomplete ossificaton) are related to exaggerated pharmacology, and likely not relevant for patients.
Embryo-lethality and foetal effects(mainly decreased foetal weights, premature fusion of the facial bones(fused maxilla/zygomatic)visceral and skeletal variations) in rats and increased resorption of foetuses and skeletal variations in rabbits were present in the embryotoxicity studies.
At exposures lower than those obtained at therapeutic doses in humans,posaconazole caused skeletal variations and malformations, dystocia, increased length of gestation, reduced mean litter size and postnatal viability.
Embryo foetal lethality and increases in skeletal anomalies(extra sternabrae, extra ribs, increases in minor skeletal variations, delayed ossification and variations of the sternabrae) were seen above exposures corresponding to 0.25 of the human clinical AUC.
In pregnant rats, ibrutinib at a dose of 80 mg/ kg/ day was associated with increased post-implantation loss and increased visceral( heart and major vessels)malformations and skeletal variations with an exposure margin 14 times the AUC found in patients at a daily dose of 560 mg. At a dose of≥ 40 mg/ kg/ day, ibrutinib was associated with decreased foetal weights( AUC ratio of≥ 5.6 as compared to daily dose of 560 mg in patients).
Reduced foetal body weights were observed at a maternally toxic dose of 300 mg/kg/day in rats(3 times human clinical exposure based on AUC), andan increased incidence of skeletal variations, including small phalanges in the forelimb was observed at a maternally toxic dose of 20 mg/kg/day in rabbits(4 times human clinical exposure based on AUC).
An increased incidence of a skeletal variation(increased incidence of a rib present at the seventh cervical vertebra) at≥100 mg/kg/day was observed in rats.