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In summary, we showed that the PAR-2 agonist tryptase can modulate L6 myoblast proliferation which involves the modulation of COX-2 activity and possibly 15Δ-PGJ2 production.
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This underscores that tissue repair entails essentially tightly controlled proliferation as opposed to uncontrolled proliferation in cancer which involves similar factors [ 19].
We have previously shown that alterations in cholesterol levels in myoblasts induce changes in proliferation and differentiation, which involves activation of Wnt/beta-catenin signaling pathway.
These mutations appeared to occur early in the process of carcinogenesis, which involves proliferation of cells in terminal end buds (TEBs) and intraductal hyperplasia before carcinomas develop.
For non-melanoma skin cancer (NMSC), these changes are classically defined as occurring in stages: (a) initiation, involving DNA damage leading to mutations, (b) promotion, which involves proliferation and inflammation, and (c) progression, involving additional genetic mutations or structural genomic changes that result in malignancy.
First, innate immunity is dependent on the direct activation or recruitment of effector cells and consequently can be elicited more rapidly than the adaptive immune response, which involves cell proliferation by clonal expansion.
Interestingly, defensins play a role in epithelial wound repair, which involves migration, proliferation and EGFR activation [ 32].
Benign hyperplasia (BH), which involves the proliferation of epithelial cells, commonly develops with aging and may increase the risk of breast cancer [ 2].
Re-epithelialisation is the process of restoring an intact epidermis after cutaneous injury, which involves the migration, proliferation, stratification and differentiation of keratinocytes, and the gradual restoration of an intact basement membrane (BM) [8], [11] [13].
Recently, Yu et al. [6] showed that primary human alveolar type II (AT II) epithelial cells maintained in 3D Matrigel cultures undergo cystogenesis to form alveolar-like cysts (ALCs) by a different mechanism which involves neither cell proliferation nor death.
These finding collectively suggest the importance to DNA replication and repair mechanism during SE which involves active cell proliferation.
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