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Complexes 1 and 2 did not appreciably inhibit HDAC activity when a cut-off of 50% inhibition was considered.
We found that treating A431neo cells with 1, 9 PA alone did not appreciably inhibit VEGF production compared to treating these cells with cetuximab alone; adding 1, 9 PA did not further lower the level of VEGF production that was inhibited by cetuximab (Figure 7C).
In mixing experiments, Ab-positive plasamplesples did not appreciably inhibit pegloticase enzymatic activity (that is, Ab were not neutralizing).
RO9021 thus did not appear to appreciably inhibit the JAK STAT pathway in the cell, further supporting the selectivity of the compound.
Remarkably, ML241 (20 μ m) did not appreciably inhibit labeling of any of the ∼170 kinases that were evaluated, whereas ML240 inhibited labeling of only three protein kinase domains by >50% when tested at 20 μ m: PIP5 K3 (a member of the phosphoinositide-3 kinase family), JAK1 JH2 (N-terminal pseudokinase domain of JAK1), and DNA-dependent protein kinase (DNAPK).
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The presence of other organic compounds in the background matrix appreciably inhibited the degradation of atrazine, while the effects of Cl−, CO2−3 and HCO−3 were comparatively negligible.
Cordyceps sinensis treatment appreciably inhibited the formation of protein carbonyls levels; P < 0.05) after exposure to hypoxia.
Some PI3K-inhibitors (PI-103 (13), NVP-BEZ235 (15)) selectively inhibit both PI3KC and TOR without appreciably inhibiting other protein kinases, including other PIKKs.
However, only nimodipine appreciably inhibited cardiac function when assayed at a concentration of 8.2 μM, causing a slowing of heart rate (but not cardiac arrest) in treated larvae.
Purified total IgG (17 μM) from a TTP patient with high titre (105% by comparison to reference plasma (18, 20)) anti-ADAMTS13 IgG directed against the N-terminal domains alone (#16 in Fig. 2B) appreciably inhibited VWF115 proteolysis, although specific cleavage products were still detected at this IgG concentration, suggesting that inhibition was not complete under these conditions.
ROS leads to bacteria death by inducing intracellular oxidation, membrane potential variation, and cellular contents release and the antibacterial ability of Ag-NPs@Ti is inhibited appreciably after adding ROS scavengers.
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