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Epithelium may have been evolved to induce proinflammatory cytokines and chemokines to recruit immune cells to the site of infection in lieu of secreting anti-inflammatory cytokine such as IL-10 to dampen the inflammation on its own.
Hence we conclude that the gap gene network has evolved to induce a large number of attractors which correspond to various developmental states.
In response to DSBs and other types of DNA damage, eukaryotic cells have evolved to induce a complex network of DNA damage signaling, which coordinate cell cycle checkpoint with DNA repair to maintain genome stability.
Hence we infer that the gap gene network might have evolved to induce a large number of attractors (by increasing the number of mutual inhibitions) which correspond to various developmental states.
Similar(56)
Surprisingly, during a bacterial infection, different ER stress sensors are activated indicating that bacteria have evolved strategies to induce a particular UPR pathway.
It is therefore expected that retroviruses have evolved mechanisms to induce activation and cell-cycle entry of the target cells and facilitate infection.
These syndromes start with infection induced systemic inflammatory response syndrome (SIRS) and evolve to sepsis induced acute organ dysfunction and cardiovascular collapse.
CMT and DNMT3 evolved to target H3K9me2-heterochromatin, whiconsequentlytly induced the emergence of DRMs to function in euchromatin, which is depleted of H3K9me2 and enriched for H3K4me3.
Furthermore, viruses have evolved to enter cells by a variety of mechanisms, inducing a wide array of cellular responses.
Iron deficiency‐induced thrombocytosis may have evolved to maintain or increase the coagulation capacity in conditions with chronic bleeding.
We speculate that ID‐induced thrombocytosis may have evolved to maintain or increase the coagulation capacity in conditions with chronic bleeding.
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