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Consequently, we set out to characterize the implications of the transient TRPC3 current for electrical and mechanical function of murine hearts using the isolated perfused Langendorff preparation.
We then proceeded to investigate the basis of these anti-arrhythmic effects of NS1643 and nicorandil in the hypokalaemic murine hearts using established arrhythmia provocation protocols.
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We explored the anti-arrhythmic efficacy of K+ channel activation in the hypokalaemic murine heart using NS1643 and nicorandil, compounds which augment IKr and IKATP respectively.
In conclusion, we have developed a highly reproducible method to isolate endothelial cells from murine heart using cell surface markers Sca-1+, CD31+ and CD45−.
Murine hearts were used in view of their potential utility in future atrial studies of the effects of genetic modifications.
Secondly, we quantified the anti-arrhythmic efficacy of NS1643 and nicorandil in the hypokalaemic murine heart by using an established clinical method of arrhythmia provocation.
Secondly, we quantified the anti-arrhythmic efficacy of NS1643 and nicorandil in the hypokalaemic murine heart by using the established arrhythmia provocation protocol of PES.
Since mPR59/B δ1 and mPR59/B δ3 are putatively novel, and to further confirm their existence, we performed a reverse transcription on NIH 3T3 and murine heart RNA using primer E3 annealing in the mPR59 3' UTR.
Total RNAs were extracted from hearts using the RNeasy fibrous tissue mini kit (Qiagen) and were reversed transcribed with Moloney murine leukemia virus reverse transcriptase (Invitrogen) and random hexamers (Promega) to generate cDNAs.
The present study provides a first direct quantitative comparison of volume-based evaluation of in vivo imaging data and in vitro data on the uptake of SPECT tracers in murine brain and heart using [I]IBZM and [99mTc]sestamibi, respectively.
To focus incident light on the intact open chest murine heart, we used a telecentric scan lens (SL, Thorlabs).
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