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To establish the age depth model, we expressed the depth as MTD-corrected depth.
In this model, we expressed regret as a fraction of the loss of potential utilities [ 24].
In order to incorporate uncertainty in the model, we expressed these probabilities as beta distributions [ 29, 30].
To test this model, we expressed the wild-type pak-1 A isoform cDNA behind the lag-2 promoter, which drives expression in DTCs but not surrounding cells (Blelloch et al. 1999).
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To get more physical insight into the model, we express scale factor in three useful forms [17, 18, 19, 20, 21, 22] (emergent, logamediate, and intermediate scenarios) under which the universe expands differently.
Similar as the energy arrival model, we express the state transition probability matrix between E t and (tilde {E}_{t}) as a policy matrix P with elements p i,j ∈{0,1},∀i,j denoting the event of using (i−j) unites of energy in state E t =i.
To further test this model, we ectopically expressed Esg in differentiated ECs using the EC-specific, temperature-inducible driver MyoIA-Gal4, UAS-GFP, tub-Gal80 ts (MyoIA ts ).
To generate a humanized CML model, we retrovirally expressed BCR-ABL1 in the cord blood CD34+ cells and transplanted these into NOD-SCID (non-obese diabetic/severe-combined immunodeficient) interleukin-2-receptor γ-deficient mice.
To create an optogenetic variant of Goddard's classical kindling model of epilepsy1, we expressed the high-efficiency E123T/T159C Channelrhodopsin-2 (ChR2) varinnt8 in M1 PCs using the CaMKIIα promoter, by bilateral stereotaxic injection of adeno-associated virus (AAV) in male P30 45 C57BL/6 mice (see Methods).
Using nuclei of mouse rods as an experimental model lacking peripheral heterochromatin, we expressed a LEMD2 transgene alone or in combination with lamin C in these cells and observed no restoration of peripheral heterochromatin in either case.
We expressed model outputs as probability distributions summarized by a mean point estimate with 90% credible intervals (CrIs).
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