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For instance, interactions of inert and reactive bioactive assemblies and the consequent chemical reaction would free or slowly cross-link the biological molecules, and altered oxidative product may produce damaging molecules precipitating aging of the biological tissues.
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This approach, known as structural proteomics, will help with the design of new drugs, since many drugs work by fitting into spaces in protein molecules and altering the way those molecules behave.Another approach, known as functional proteomics, asks a different question.
This suggests the lipoprotein environment of circulating and sub-endothelial monocytes in Type 2 diabetes could promote altered shedding of membrane-bound cytokines, receptors and adhesion molecules and alter cell-cell interactions.
Down-regulated F-actin and CD54 adhesion molecule, and altered Rho A-ROCK signaling likely contributed to impaired macrophage function.
A number of immune dysfunctions have been reported in sepsis, including apoptosis of T lymphocytes and B lymphocytes, altered cellular cytokine production, increased levels of the anti-inflammatory IL-10, impaired phagocytosis, monocyte deactivation with diminished major histocompatibility class II molecule expression, and altered response to microbial products [ 17- 22].
One element of the generalized alterations in the vasculature in diabetes is endothelial dysfunction [ 3], characterized by increased permeability [ 4], increased expression of pro-inflammatory molecules [ 5], and altered vasomotoric responses [ 6].
Endothelial activation denotes a devastating key event in sepsis pathophysiology that is characterized by increased expression of luminal adhesion molecules, leukocyte recruitment, and altered vasomotor tone, resulting in vascular barrier breakdown [ 1- 3].
These results demonstrated that metal nanoparticles may influence fibroblast function by negatively modulating the deposition of extracellular matrix molecules (ECM) and altering the expression of ECM receptors, cytoskeletal reorganization, and cell migration.
Typically, small molecules bind and alter the function of specific transcriptional regulators that regulate transcription of genes encoding the cognate transporters and metabolic enzymes [1].
Moreover, considerations should be taken of drug resistance mechanisms, including reduced intracellular drug accumulation, increased detoxification of the drug by thiol-containing molecules, increased DNA damage repair, and altered cell signaling pathways and apoptosis mediators [ 13].
Interestingly, exosomes purified from mast cells [29] and neuronal cells [24] are enriched in mRNA molecules that stimulate and alter gene expression of recipient cells.
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