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Transplantation of the C26 tumor to a host mouse causes a significant loss of body weight and muscle mass and closely reproduces the clinical features of cancer-induced muscle wasting [7], [15].
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In the other cage, females were given the opportunity to take a daily blood feed on a vertebrate host (mouse and chicken) for a period of 10 days.
Thus, at 3 days after CTX injury, a robust, predominately mononuclear, inflammatory infiltrate was evident within injured muscle in all host mice receiving WT BM (Fig. 1 A, D ).
Notably, this stabilization occurs in the surface region of the protein that was identified as polymorphic between ROP5 alleles in T. gondii[ 37], and was recently shown to be the interface of an interaction with the host (mouse) immunity-related GTPase (IRG) protein [ 19].
Data were discarded if (a) changes in tumour pO2 were associated with reflex movements of the host mouse, (b) tumour pO2 did not drop to 0 mmHg after killing of the host mouse or (c) the probe calibration at the end of an experiment gave data that differed significantly from the precalibration data.
In our experience, despite achieving a near complete removal of MIF from both the B16-F10 tumour cells and the host mouse, we inhibited tumour growth by 43%.
After a while, Vacanti concluded that the cells had failed to form new tissues; the only tissues evident had clearly come from the host mouse.
(1) Day one: application of Kir4.1 (host rabbit); (2) Day two: application of secondary anti-rabbit antibodies and thereafter pp38 (host mouse); (3) Day three: application of secondary anti-mouse antibodies.
With sufficiently detailed protein sequence identifications, the observed protein changes can be attributed to either the host mouse or the human tumor cells.
Neo-regenerative tissues were completely fused with host mouse tissues.
Moreover, we found that transplanted human endometrial tissues contained blood vessels of the host mouse.
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