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This redox-mediated optimization process is most probably cell cycle regulated, given that the expression of canonical histone genes occurs only in the S-phase (also see below).
Most probably, cell wall-associated or soluble factors other than lipoglycans [e.g. heat shock proteins (Bulut et al., 2005)] stimulate TLR4 signaling in M. tuberculosis infection; while both live and 'heat-killed' M. tuberculosis activate cells via TLR2, only live M. tuberculosis induces TLR4-dependent activation excluding a major role for the heat-stable glycolipids (Means et al., 1999).
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Although these results are most probably cell-type dependent (as with the cleavage of talin), they show that calpain levels (which are represented by the additional species Z) play an important role in the regulation of focal adhesions through kindlins.
Scoring the different Pros+ cell type morphology, we found that the wild type larval AMC (TO and DO) was composed of 8 (± 1) large Pros+ cells (most probably accessory cells) and 40 (± 4.1) small Pros+ cells.
As both IL-1RI and MyD88 are essential for signal transduction on IL-1 binding, these results showed that nonhematopoieitic cells, most probably endothelial cells, are necessary to develop fully the inflammatory response to IL-1β.
PCR performed on single sorted cell and 5 sorted cells led to inconsistent amplification of the β-globin gene (data not shown); most probably revealing cell and/or DNA lost during the procedure.
In contrast, the human recombinant anti-TPO aAbs expressed in CHO cells (B4′) bound 90% of the monocyte population but only 40% of the lymphocyte population (most probably NK cell lymphocytes).
From these lines of evidence, we infer that cells constituting the blood brain barrier, most probably endothelial cells, cross-present parasite antigens during PbA infection, thus becoming targets for CD8+ T-cell cytolysis.
Double labeling with neuronal markers indicated that these cells are not neurons and are most probably glial cells (data not shown).
Based on data from suppression assays, most probably, Treg cells exert their suppressive activity over CD4+ T cells in a partial TGF- β dependent mechanism.
Conceptually, alarmins should be molecules present inside of cells sheltered from the immune system, and only released during tissue injury, most probably during cells necrosis or plasma membrane rupture [21].
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