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These EF data strongly suggest that 5-OH-PCB95 was enantioselectively biotransformed, either by enzymatic reaction (e.g., formation of PCB95 sulfate compound/s) or by enzyme-complex formation and binding to cellular tissues (e.g., complexation with reduced glutathione, GSH), or both in the whole poplar plants.
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(A ) Lam4S2 binding to cellular lipids (see Figure 2A ).
This is due to some strong electrostatic bindings to cellular membranes.
†Lowest concentration showing binding to digestive tissues.
Similarly, trypsin treatment of the nanosensor coated with cellular membranes abolished AH peptide binding to the cellular membranes but did not affect the binding of a control lipid-binding peptide.
These properties are characteristic of signal transduction induced via ligand binding to the cellular receptor, lipoprotein receptor-related protein.
[18F]FE@SUPPY showed increased binding to tumor tissue (9.18 ± 2.38 fmol/mm2) compared to healthy tissue (3.50 ± 0.95 fmol/mm2).
Taken together, all these changes can ultimately lead to cellular and tissue injury and dysfunction [31].
The presumed function of these agonist drugs is through their binding to the natural cellular receptors of GABA within the neurons of the central nervous system that are located either in the spinal cord or within the brain tissue.
Furthermore, VDBP is essential for G-actin binding to inhibit uncontrolled intravascular G-actin polymerization after cellular tissue damage, and thus to inhibit microembolism and organ dysfunction after cellular necrosis.
Antibody binding to endothelium and subsequent cellular activation involving complement-dependent and -independent pathways leads to the recruitment of natural killer (NK) cells, polymorphonuclear neutrophils and macrophages, which contribute to capillaritis and eventual tissue injury 15– 15.
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