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Further support for this hypothesis comes from a study in mutant mice, which revealed that abolition of nNOS, but not inducible NOS (iNOS), reduced REMS in mice [39].
Our results are based on extensive breeding studies of Alkbh1 targeted mice, which revealed a dramatic effect on lethality and sex-ratio in adult mice.
In this approach, he performed an miRNA analysis of CD11b+ myeloid cells in the spleen of healthy and tumor bearing mice which revealed around 80 differentially expressed.
The group performed radiotelemetry in unanesthetized mice, which revealed tachycardia in heterozygotes without a change in blood pressure or baroreceptor sensitivity, consistent with studies of human NET A457P carriers.
This was supported by ex vivo length tension analyses of thoracic aortic segments from 13-month-old mice, which revealed a leftward shift in the relationship in segments harvested from Col1a1 r/r mice (P < 0.001; Fig. 3A).
To elaborate potential involvement of neuritin in neuritic atrophy, we measured mRNA level of neuritin in the hippocampi of 6-month-old Tg2576 mice, which revealed a decrease in neuritin mRNA when compared with that of WT littermate control (** P=0.0079, unpaired t-test; Figure 4a).
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The existence of non-HIF signalling functions of FIH is supported by studies of targeted FIH inactivation in mice, which reveal a metabolic phenotype that seems unrelated to the action of FIH on HIF [ 18].
In summary, we have found for the first time that the formation of A β-AGE exacerbates the toxicity of A β with the mechanisms involving activation of RAGE/GSK-3 pathway, and inhibition of AGEs including A β-AGE can restore the cognitive deficit in AD-like micel mice, which reveal that the underlying mechanism of T2D to be related to AD may be through increasing formation of A β-AGE.
Insight into the cellular mechanism(s) by which progesterone affects mammary morphogenesis has been disclosed by a new PR-LacZ knockin mouse, which revealed that PR's spatial expression pattern undergoes precise choreographed distributional changes that precede key stages in postnatal mammary development.
The regions, homologue to the two inversed fragments of non-rodent mammalians, are in opposite direction to those of mouse, which reveals both inversions occurred before the divergence of mouse and rat, and after the divergence of primates and rodents.
In the present study, we generated an AS160-knockout mouse model to study the effects of AS160 deletion on glucose homoeostasis in mouse, which reveals similarities and differences between the AS160-knockout mouse and the human patients bearing the AS160 truncation mutation [ 19].
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