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Commensal microbial communities protect the host against invading pathogens, and disrupting beneficial microbiota may leave the host vulnerable to pathogenic fungal infections.
The lung, like the intestine, is vulnerable to pathogenic insult and is constantly exposed to potentially harmful substances.
For instance, the classical surgical meshes are used to bridge severe wounds and for tissue therapy, but it is highly vulnerable to pathogenic invasions.
Specifically we demonstrate that HDAC6 drives the deacetylation of KXGS motifs, leaving tau vulnerable to pathogenic mechanisms that promote hyperphosphorylation and polymerization.
In marsupials in particular, the newborn, which does not receive any passive immunity during foetal development, lacks a mature immune system and this renders them more vulnerable to pathogenic infections and therefore they are highly dependent on maternal immune source via milk for adequate protection [ 24, 25].
Using a site-specific antibody to detect acetylation of KXGS motifs, we demonstrate that these sites are hypoacetylated in patients with AD, as well as a mouse model of tauopathy, suggesting that loss of acetylation on KXGS motifs renders tau vulnerable to pathogenic insults.
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These observations accentuate the importance of cartilage stability; disrupted cartilage due to genetic disorders might be more accessible and vulnerable to autoimmune attack by pathogenic antibodies.
Second, their topological centrality and high biological cost could make hubs particularly vulnerable to a wide range of pathogenic factors.
Second, hubs are more biologically costly and therefore more vulnerable to a diverse range of pathogenic processes.
These findings accentuate the importance of cartilage stability; cartilage disrupted as a result of genetic disorders could be more accessible and vulnerable to an autoimmune attack by pathogenic antibodies.
Cartilage disrupted as a result of genetic disorders could be more accessible and vulnerable to an autoimmune attack by pathogenic antibodies, which was emphasized by the recent observations of enhanced cartilage-specific antibody binding and, thus, arthritis severity in mice with collagen type IX deficiency [ 55].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com