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Surprisingly, TLRs can either be activated by microbial compounds or cellular debris in the context of IR injury [ 42, 45– 45].
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Astrocytes have the ability to release harmful compounds (viral or cellular) or may influence neighbouring cells (like microglia) to produce harmful compounds which may damage neurons [ 4, 12, 13].
Biological electrophiles result from oxidative metabolism of exogenous compounds or endogenous cellular constituents, and they contribute to pathophysiologies such as toxicity and carcinogenicity.
But genomes encode a complex set of processes, and the most reasonable hypothesis for a given connection such as the exchange of pathogenesis genes between Escherichia coli and P. aeruginosa may not be the correct one; genetic affinities may instead reflect gene transfers related to respiration, metabolism of available compounds, or other cellular processes.
While other mechanisms, for instance chemical (volatile compounds) or acoustical (cellular vibrations) pathways, may provide an alternative explanation of the observed effects in certain experimental setups, none of the suggested mechanisms are able to provide a watertight explanation of the observed effects in all the setups.
Immunomodulating activity refers to biological or pharmacological effects of compounds on humoral or cellular aspects of the immune response.
To investigate the potential use of an extract, fractions or compounds, the cellular toxicity also has to be determined.
To gain insight into the role of PpHsp16.4 during different stress responses, we monitored transcript levels of the genes encoding this protein in moss gametophyte colonies exposed to different stress conditions or treated with various hormones or chemical compounds producing cellular stress.
Thus, it is unlikely that the effects of these compounds on cellular proliferation or biologic response in vivo in male or female rats involve binding interactions with either ER or type II sites.
Identification of unique recurrent single nucleotide variations (SNVs) or expression alterations that enable resistance can offer insights into the mechanism of action or cellular targets of compounds.
These results indicate caution when interpreting results using these compounds in cellular assays or in vivo because Nec-1 is not only a RIPK1 inhibitor but also a potent IDO inhibitor.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com