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The present study examined expression and cell-specific localization of nectins during mouse follicular development.
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To determine the functional relationship between the PTEN/PI3K signaling and the Tsc/mTORC1 signaling within the oocyte in regulating follicular activation, we crossed Oo Tsc1−/− mice with Oo Pten−/− mice and studied follicular development in progeny mice with concurrent loss of Tsc1 and Pten in oocytes (referred to as Oo Tsc1−/−; Pten−/− mice).
The study of Hu et al. (2002) examined how profound changes in androgen/estrogen ratio would affect mouse in vitro follicular development.
To study the functional contribution of PDK1 signaling in the excessive follicular activation in Oo Tsc1−/− ovaries, we crossed Oo Tsc1−/− mice with Oo Pdk1−/− mice (9) and studied follicular development in the progeny (referred to as Oo Tsc1−/−; Pdk1−/− mice).
To determine how the loss of Tsc1 from oocytes impedes mouse fertility, we compared the first wave of postnatal follicular development in Oo Tsc1−/− mice to that in Oo Tsc1+/+ mice.
For tracing the follicular development, 140 mice were sacrificed between 5 and 57 days after the first tamoxifen injection.
Objective: Our aim was to determine the impact of freezing, thawing, and subcutaneous transplantation on follicular development in grafted mouse ovaries.
To study the expression of plexin-B1 in the mouse ovary and its possible role in follicular development.
This together with previous report in mouse supports the possible role of miRNAs during follicular development and oocyte growth.
Using another mice strain, however, Gook et al. (2001) reported follicular development up to the antral stage after xenograft into non-hypogonadic SCID mice without exogenous gonadotrophin stimulation.
To stimulate follicular development, immature 23-day-old female mice were injected intraperitoneally with 5 IU of PMSG.
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