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The results suggest that biliary polycyclic aromatic hydrocarbon (PAH) metabolites were shown to better reflect the contamination gradients of PAHs than EROD activity.
These metabolites were shown to have anti-platelet effects mainly through inhibition of collagen and thromboxane-dependent aggregation for 12-HETE [1, 2], 13-hydroperoxy-9Z,11E octadecadienoic acid (13-HPODE) [3] and 13-HODE [4].
The logarithm of logP values of ADS-I and its metabolites were shown in Table 1, indicating that the logP values of ADS-I, M1 and M2 were −0.01, 0.95 ± 0.04, 1.57 ± 0.11 respectively.
The only significant non-zero pairwise partial correlation coefficients (α = 0.05) between metabolites were shown in network.
Previously defined as orphan receptors, key metabolites were shown to be the natural ligands of many nuclear receptors, including liver X receptors (LXRs) which respond to oxysterols and glucose [29], [30], farnesoid X receptor (FXR) which responds to bile acids [31], and the peroxisome proliferator-activated receptors (PPARs) which respond to fatty acids [32].
Over 50 identified metabolites were shown to differ significantly between the sample cohorts.
Similar(44)
Three examples of fermentations for primary metabolites are shown.
Data were collected by GCMS solution (Shimadzu), and identified metabolites are shown in Table 1.
Pharmacological data on bupropion and its metabolites are shown in the table.
These metabolites are shown in Table 2.
Groups of metabolites are shown in different colors.
More suggestions(16)
species were shown
metabolites were characterised
metabolites were confirmed
metabolites were suggested
metabolites were synthesized
metabolites were formed
metabolites were found
metabolites were produced
metabolites were analyzed
metabolites were increased
metabolites were identified
metabolites were targeted
metabolites were excreted
metabolites were extracted
metabolites were entered
metabolites were consumed
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