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Since we present evidence that in the brain of a human LD patient there is a clear induction of ER-stress markers, we suggest that differences between samples from mouse and human brains may account for this apparent contradiction.
Given the different polymorphism-detection principles of DArT, SSR and RFLP markers, we suggest that the centromeric clustering largely reflects centromeric suppression of recombination [ 33, 37].
To increase the accuracy of the recordings based on external markers, we suggest that virtual markers could be added to our model.
Given that egr-5 knockdown reduces both epidermal cell density as well as the expression of AGAT-1 and zpuf-6 markers, we suggest that egr-5 is responsible for both the maturation of epidermal progeny cells and the expression of progeny markers.
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Traditionally biomarkers are cell surface or intracellular molecular markers – here we suggest that the degree of leakiness of tumor blood vessels 'integrates' underlying tumor microenvironmental factors related to angiogenesis, and represents the underlying tumor pathomorphological status.
The markers and optimised protocols we suggest can help to improve cell therapy of cartilage defects and chondrocyte differentiation from stem cell sources.
Because these recombinants will be genotyped with several more markers in subsequent steps, we suggest extracting DNA from the leaf samples set aside earlier at −80°C (step 4b).
Because our study did not reveal significant predictive markers for early fatal outcomes, we suggest for the moment not to withhold concurrent chemo-radiotherapy based only on such a marker.
Given that retinal arteriolar abnormalities are markers for early microvascular damage, we suggest that DPN may arise, at least in part, from generalized systemic microvascular disease leading to damage of peripheral nerves.
We suggest that more markers should be genotyped in subsequent studies for a better mapping.
In this study we reported several markers that suggest that chronic oral dosing with eudragit-encapsulated rapamycin has little impact on the metabolic status of marmosets.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com