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Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels.
Since epidermal morphology varies at different body sites we chose to measure the effect of Setd8 deletion on mouse tail and back skin.
Briefly, a beam of light was focused on the dorsal surface of the mouse tail and the time until the tail flicked was monitored (tail-withdrawal latency) [ 32].
To screen large areas of the skin in a three-dimensional manner, epidermal whole mounts of mouse tail and back skin were analysed for YFP/LacZ+ cells (Braun et al, 2003).
In fact, retinol derivatives were thought to be useful for the treatment of photoaging after the observation that retinyl propionate induces epidermal thickening in mouse tail and promoted collagen formation in UV-irradiated mice (Green et al 1998).
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Primary fibroblast cultures from 11 mice1gt/gt mice and 12 wild type animals were established from mouse tails and propagated under standard conditions.
Genomic DNA was isolated from mouse tails and digested with EcoRI or PstI.
MSI testing was performed from microdissected normal intestinal or tumour tissue, compared with mouse tails and quantified by the number of mutations per marker (NMPM).
To confirm that the transgenic mice incorporated the human gene into the murine genome, we continually performed PCR specifically targeting human AVPR1A using genomic DNA isolated from mouse tails and the following primers: forward, 5′-GGCGCTGGCAACACAAG-3′; and reverse, 5′-AGCACATTTGCGGCAGCACCT-3′.
Offspring from intercrosses were genotyped by PCR analysis using mouse tail DNA and WT and KO allele-specific primers.
Venous blood samples were collected at 5, 15, 30, and 60 min p.i. via the mouse tail vein and further processed.
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