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We performed the non-parametric tests with the cross-gene error model being inactive.
We used 6 replicates for each non-parametric tests with the global standard error model being inactive because more than five replicates were recommended for the tests.
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The remaining eight model boxes were "inactive", as their response was the result of the motions imposed by the active model boxes through the connection between boxes.
As comparison, it could be observed that the rats in model group were inactive and anorectic.
On the one hand, false dispensable predictions may indicate that alternate pathways present in the model are either inactive for the experimental conditions under observation or not present at all.
However, the core difference between the (direct) activation and the displacement model appears to be irreconcilable: in the activation model Bax and Bak are inactive unless receiving a stimulus from BH3-only proteins whereas in the displacement model they are active unless bound to anti-apoptotic proteins.
In this simplified model the core PGs are inactive and the interactions between the LSMGs as given in Fig. 1b in response to a generic differentiation stimulus a are considered.
We confirm model predictions experimentally that plasticity is inactive at stable states and that synaptic strength overshoots during recovery from visual deprivation.
Combined, these data support a model in which mitotic proteins are inactive due to improper post-translational modification conditions in the centrosome or incorporation into a protein complex that prevents access to substrates.
Although the K residue at site 106 may be necessary for catalysis if the small subunit is inactive, another model that explains the data would be one in which the wild-type large subunits (which have a T at site 106) require prior catalysis by the small subunit before they perform catalysis by themselves.
The most important finding of the present study was the peculiar pharmacological behaviour of IDN 5390 in in vivo systems, Indeed, IDN 5390 delivered according to an intermittent schedule, considered as an optimal regimen for PTX in preclinical models (Polizzi et al, 1999), was inactive against a responsive human ovarian carcinoma xenograft, the A2780/DDP, even at doses higher than those of PTX.
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Justyna Jupowicz-Kozak
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