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> > -wrap-foot> To further investigate the changes in the lipidome of SOD1(G86R) mice, we attributed hypothesis-based identifications to the significantly deregulated lipid species, according to their atomic masses in the HMDB database (29).
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This is much earlier than in APP.V717I mice and in bigenic biAT mice, which we attribute to the triple mutant APP.SLA in the current AAV model, which produces more Aβ42 than APP.V717I (Figure S2) expressed in our amyloid model [24], [29].
Finally, because TH is expressed in noradrenergic neurons of DD mice [24], [25], we attributed the small amount of TH seen in IHC of the BLA in DD mice to noradrenergic axons.
The commercial anti-vimentin antibody showed a somewhat weaker signal for vimentin in the M210B4 mouse cell line extract which we attributed to the lower reactivity of this antibody with rodent vimentin than with human vimentin as described previously for this antibody [47].
However, these treatments also increased reactivity in the WT hSOD1 mice and thus we attribute C4F6 reactivity in this case to relaxation of the WT SOD1 structure to loosen the tight bend in the backbone around amino acids 90 93.
We found that cholesterol and lipoproteins were preferentially reduced relative to triglycerides in serum from Mbtps1 wrt/wrt mice, an effect that we attribute to a more severe impairment of SREBP2 processing as compared with SREBP1 processing.
Over a time period of 3 weeks, we observed a significantly higher tumor growth rate in the Rag2−/− γc−/− mice (Fig. 6a), which we attribute to the influence of the immune system of the Balb/c mouse.
Because FGF21 is an important metabolic regulator, we next investigated whether the atherosclerosis-prone phenotype of DKO mice is attributed to impaired glucose or lipid metabolism.
Previously we established that increased O2- production in STZ-induced diabetic mice is attributed to eNOS uncoupling, which was significantly attenuated by Ang II signaling blockers [ 16].
However, growth retardation and late embryonic lethality in Rtl1-deleted mice are attributed to a placental defect (Sekita et al. 2008), and we saw no change in Rtl1 expression in TGPAT placentae.
We demonstrate that the increased number of γδ T cells in Id3−/− mice is attributed to the increase in SAP-dependent cells.
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