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To examine whether there exist any novel sodium channel subtype in cochlear hair cells, the sensory epithelia locating in premature mouse cochlea was carefully dissected and used for the identification of VGSCs in cochlear hair cells.
Goat anti-p55 (T-19) and anti-gelsolin (N-18) were purchased from Santa Cruz Biotechnology, Inc. Whole-mount immunostaining for mouse cochlea was performed as described (Kikkawa et al. 2005).
Induction of inflammation in the mouse cochlea was observed following antigen challenge to the inner ear.
Surgical access to the mouse cochlea was performed similarly to what was previously described for electrophysiological measurements [ 20, 21].
Complex IV activity in the mouse cochlea was suppressed by approximately 20% immediately after noise exposure in the noise-only group.
Similar(55)
At birth, however, the Igf1−/− mouse cochlea is the normal size with the expected complement of cell types in the organ of Corti.
Mouse cochlea were dissected and incubated with anti-prestin antibody (1 100 goat anti-prestin, Santa Cruz, CA) in incubation buffer overnight at 4°C.
A reference mouse cochlea is shown to demonstrate the normal cochlear architecture of three rows of outer hair cells and a single row of inner hair cells.
Because the bone surrounding the mouse cochlea is thinner than that of the guinea pig cochlea, we sought to use OCT to perform in vivo vibrometry of the unopened mouse cochlea.
Although the detatils of endolymphatic Ca2+ development are not known, it has been reported that a mature composition of endolymph in the mouse cochlea is reached around postnatal (P) day 8 (P8, where P0 indicates date of birth) [ 4].
Briefly, mouse cochleae were fixed with 4% paraformaldehyde in PBS for 2 hr at room temperature.
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