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1 e genetically inactivated Mfn-1 and Mfn-2 in midgestational and postnatal cardiac myocytes using a lo
2 nal data suggest that supplementing maternal midgestational calcium intake may lower offspring blood
4 similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neu
6 ether with its partner, RIP3 (RIPK3), drives midgestational death of caspase 8 (Casp8)-deficient embr
8 s of mdmx, a p53-binding protein, results in midgestational embryo lethality, a phenotype that is com
9 l ubiquitous overexpression of Cts8 leads to midgestational embryonic lethality caused by severe vasc
11 in redirecting trophoblast fate towards the midgestational expansion of the labyrinth region while m
12 as those observed in schizophrenia, whereas midgestational exposure causes selective elimination of
18 ity are required for adult but not early and midgestational hematopoiesis supports the notion that mu
19 ow-TF male mice had a 42% incidence of fatal midgestational hemorrhage (n = 41), whereas no fatal mid
20 tional hemorrhage (n = 41), whereas no fatal midgestational hemorrhages were observed in low-TF femal
24 ugh some EPCR(-/-) embryos were rescued from midgestational lethality, this regimen yielded no EPCR(-
26 Conversely, ectopic BDNF overexpression in midgestational mouse hearts results in an increase in ca
27 d the combined effects of in utero early- to midgestational nutrient restriction and postnatal obesit
29 s exploratory study used the Danish archived midgestational sera and their nationwide registers to se
33 ignificantly reduced viability and displayed midgestational vascular patterning defects analogous to
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