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Gene therapy approaches are particularly attractive for such therapeutic strategies, since local, long-term expression of therapeutic proteins in the colorectal system is potentially achievable.
Although the colorectal system is readily accessible externally, the presence of the mucous coat on the colonic epithelium and the dynamic fluidic properties of the colorectal system act as barriers for the access to the colonic tissue by viral vectors that are administered intracolonically.
Inflammatory bowel disease (IBD), consisting of two idiopathic inflammatory disorders, Crohn's disease and ulcerative colitis, is characterized by chronic intestinal inflammation, which causes severe destruction of the mucosa of the colorectal system [ 1- 4].
The ability to associate stably with target tissue may be particularly important for the transduction of the colorectal system, where the dynamic fluidic properties inhibit stable association of viral particles with colonic tissues.
Virus-mediated delivery of therapeutic transgenes to the inflamed colon holds a great potential to serve as an effective therapeutic strategy for inflammatory bowel disease, since local, long-term expression of the encoded therapeutic proteins in the colorectal system is potentially achievable.
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The Asia-Pacific Colorectal Screening System (APCS) score also is helpful in stratifying the risk for advanced neoplasia in the asymptomatic population.
Our assessment of inequity in the colorectal cancer care system further exemplifies the importance of a team approach.
Currently, there remains no widely accepted method of sub-classification; however, our data would lend support to the suggested incorporation of liver resectability status in a revised colorectal cancer-staging system (Nordlinger et al, 2007).
Take the controversy over ImClone Systems' colorectal cancer drug, Erbitux.
Therefore, these data provide a launchpad for further exploration of the molecular characterization of colorectal tumorigenesis using systems biology approaches.
In the present study, LiCl treatment enhanced GSK3 β Ser9 phosphorylation, increased PARP cleavage and PI-labelled apoptosis, thus indicating an anti-apoptotic role for GSK3 β in the colorectal epithelial model systems.
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