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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
3                                          For midgestational cases aged 20-24 postconceptional weeks (
4  similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neu
5 oth alleles of either Rip1 or Rip3 to rescue midgestational death of Casp8-deficient mice.
6 ether with its partner, RIP3 (RIPK3), drives midgestational death of caspase 8 (Casp8)-deficient embr
7 is, and placental hemorrhage, which leads to midgestational death of low-TF female mice.
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
10  infection during early pregnancy results in midgestational embryonic loss in naive C57BL/6 mice.
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
13 a1G T-type Ca(2+) channels are functional in midgestational fetal myocardium.
14                        The midbrains of five midgestational fetuses (19-26 gestational weeks) and six
15  ontogeny and first appears at low levels in midgestational FLC between days 13.5 and 14.5.
16          A critical event that occurs during midgestational heart development is the formation of the
17 ling pathways that control key events during midgestational heart development.
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
21                Primary outcome measures were midgestational indexes of utero-placental vascular-endot
22       Null mutations in mouse AML1 result in midgestational lethality with a complete lack of fetal l
23          Mice lacking Abi1 or alpha4 exhibit midgestational lethality with abnormalities in placental
24 ugh some EPCR(-/-) embryos were rescued from midgestational lethality, this regimen yielded no EPCR(-
25 17 linker-scanner mutations were analyzed in midgestational mouse embryos.
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
28                               Both early and midgestational radiation exposure diminished the surface
29 s exploratory study used the Danish archived midgestational sera and their nationwide registers to se
30 m of mice is established during the early to midgestational stage of development.
31                                           By midgestational stages, PACE4 mRNA is expressed in multip
32 placental insufficiency that is induced by a midgestational stress challenge.
33 ignificantly reduced viability and displayed midgestational vascular patterning defects analogous to

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