Примери за използване на Maternally toxic на Английски и техните преводи на Български
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In ferrets, lomitapide was both maternally toxic and teratogenic at< 1 times the MRHD.
Produced a transient reduction in body weight in the offspring at a maternally toxic dose.
Following exposure to nicorandil at doses that were maternally toxic, embryotoxicity was observed in the rat and rabbit.
Pramipexole was not teratogenic in rats and rabbits butwas embryotoxic in the rat at maternally toxic doses.
Maternally toxic doses of anagrelide in rats and rabbits were associated with increased embryo resorption and foetal mortality.
In rabbits, developmental toxicity was observed only at maternally toxic doses(see section 5.3).
Only at maternally toxic doses, empagliflozin also caused bent limb bones in the rat and increased embryofetal loss in the rabbit.
Pramipexole was not teratogenic in rats and rabbits butwas embryotoxic in the rat at maternally toxic doses.
At a high maternally toxic dose(more than 40 times the recommended human dose), teratogenic effects were seen in the rat.
Administration of Rienso during organogenesis in rats at maternally toxic doses of 100 mg Fe/kg/day caused a decrease in foetal weights.
Maternally toxic doses of anagrelide(60 mg/ kg/ day and above) in rats and rabbits were associated with increased embryo resorption and foetal mortality.
Memantine was not teratogenic in rats and rabbits,even at maternally toxic doses, and no adverse effects of memantine were noted on fertility.
Fluticasone furoate was not teratogenic in rats or rabbits, butdelayed development in rats and caused abortion in rabbits at maternally toxic doses.
Studies in mice showed reduced oestrous cycling at maternally toxic doses, but did not indicate harmful effects with respect to fertility(see section 5.3).
However, tenofovir disoproxil reduced the viability index andweight of pups in a peri-postnatal toxicity study at maternally toxic doses.
Treatment of rats at maternally toxic doses1 mg/kg/day(0.3 times the human exposure) resulted in reduced numbers of live foetuses and/or reductions in foetal body weights.
In reproduction toxicity studies in rats and rabbits, decreased weight and viability of foetuses andoffspring were observed at maternally toxic doses.
Reproduction studies have shown minor embryotoxicity at doses close to maternally toxic ones(increased number of resorptions, pre-implantation and post-implantation losses).
Studies in animals did not indicate any teratogenic effects in rats or rabbits, butembryotoxicity was observed in rats at maternally toxic doses(see section 5.3).
Reproduction studies have shown minor embryotoxicity at doses close to maternally toxic ones(increased number of resorptions, pre-implantation and post-implantation losses).
In an embryo foetal developmental toxicity study with nasally administered ketamine in rabbits, skeletal malformations were observed andfoetal body weight was reduced at maternally toxic doses.
At maternally toxic doses, zidovudine given to rats during organogenesis resulted in an increased incidence of malformations, but no evidence of foetal abnormalities was observed at lower doses.
In rats, rabbits and dogs atorvastatin had no effect on fertility and was not teratogenic,however, at maternally toxic doses fetal toxicity was observed in rats and rabbits.
The maternally toxic dose(approximately 2.3 times the human clinical exposure based on AUC) also resulted in foetal growth retardation, including decreased foetal weights and delayed skeletal ossification.
It is teratogenic based on a low incidence of foetal hydrocephaly,associated with maternally toxic doses, which was observed in rabbits at an Neparvis dose of≥4.9 mg sacubitril/5.1 mg valsartan/kg/day.
At a maternally toxic dose in rats(250 mg/kg/day), lower foetal viability and a higher incidence of a visceral malformation were observed at maternal exposure that was 510 times the maximum clinical dose of 15 mg/day.
Developmental toxicity studies in the rat andrabbit have shown embryo-fetal lethality at maternally toxic doses, but no direct embryo-foetal toxicity below maternally toxic doses.
In a rabbit developmental toxicity study at the maternally toxic dose, there were foetal anomalies observed(fused sternebrae, and 2 foetuses had various visceral observations), and a slight decrease in foetal body weight.
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.
Intravenous(80 μg/kg/day) administration of filgrastim to rabbits during the period of organogenesis was maternally toxic and increased spontaneous abortion, post-implantation loss, and decreased mean live litter size and fetal weight were observed.