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In characterizing the phenotype of LMO4 deficient mice we noticed a structural defect in the eye.
In mice, we noticed that the frequency of observed seizure activity was not significantly different between deletion and Ube3a mutation mice [23].
In young mice we noticed a remarkable increase in TUNEL positive areas at 3 and 4 days post infection (Fig. 7B and C).
Comparing levels of Venus+ cells in the VLV with those in VV transgenic mice we noticed an overall similar pattern of transgene expression but a generally lower percentage of Venus+ cells in the VV strain (Fig. 4b).
At the same time when we observed a decline in dendritic spine density in the somatosensory cortex of 13 15 and 18 20 months-old 3xTg-AD mice, we noticed that some dendrites showed a dystrophic volume increase over time (Fig. 3A and 3B).
When we crossed our single transgenic VLV mice with the LacI repressor mice we noticed that reporter transgene expression was actually quite effectively silenced in the peripheral blood where only about 5% of cells scored as Venus+ by highly sensitive flow cytometry.
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As ankyrin-B mutant mice aged we noticed a consistent pattern of kyphosis, hair loss and general deterioration compared to their littermates.
Of particular interest, in our mouse model, we noticed, upon kanamycin treatment, a time-dependent down-regulation of prestin transcript prior to detectable apoptotic cell death observed in OHCs which becomes obvious on day 14.
During the course of maintaining the Neat1 KO mouse colony, we noticed that only a small number of offspring could be obtained from Neat1 KO females.
During long-time time lapse imaging of the steady-state mouse skin, we noticed the epidermis occasionally appear with bursts of ERK activation patterns, where ERK activation is propagated from cell to cell in a radial wave.
In our uninfected control mice, we also noticed that the normalized running distance was significantly higher in female mice (p = 0.021).
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