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Several reports have suggested that antivascular treatments could reduce body weight in mouse models of obesity [12], [13], [14], but whether antiangiogenic therapy by blockade of VEGFR1 or VEGFR2 can achieve this effect remains unknown.
Marker rs6212614 resides in Orgwq5 (organ weight QTL 5, chromosome 3), a QTL affecting organ weight in mouse [ 44].
To determine if genes affecting hippocampus weight in mouse also influence hippocampus volume in humans we used a protocol developed in R [ 55].
Treatment with DOPC-encapsulated siRNA via intravenous or intraperitoneal injections was highly effective in reducing both in vivo expression of target genes (e.g., EphA2, FAK, neuropilin-2, or IL-8) and tumor weight in mouse models of different human cancers [ 16– 16].
Among all these data only very few were in conflict with a protective effect of the omega-3 PUFA [ 127, 175], but in these cases extremely high doses of LC-omega-3 PUFA were administered (about 3 7 g EPA + DHA/kg body weight in mouse or 12 g EPA + DHA/kg body weight in rat; for the calculation used, see [ 216]).
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PFOS induced a loss of body weight in mice and an increase in the relative weight of the liver.
An increase in liver weight in mice fed the purified EPS was observed, but with no change in liver lipids.
Effective antiplasmodial doses of VD3 and 22-OCT resulted in a loss of body weight in mice.
In addition, the loss of body weight in mice accompanied the treatment with the free MMC in this study (Figure 8D) but was not found in the treatment with the hybrid PLA NPs/MMC-SPC.
The tumor volume and weight in mice treated with EGCG or ATRA alone did not differ from those in mice treated with the vehicle control.
In the current study, we used a single dose of CBD at 20 50 mg/kg body weight in mice, which showed significant efficacy in an acute inflammation model.
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