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In conclusion, the high significant correlations between PCI and ECW, in all the observed walking conditions, suggest that PCI is a valid outcome measure in subacute stroke patients.
These results suggest that PCI may have a useful role to play in the site specific activation of cytotoxic agents like gelonin, given at a dose level that has no effect in the absence of light.
These findings suggest that PCI may confer a long-term protective effect from dementia.
We proposed that PCI may augment the biological activity of many agents including tumor cell targeted therapeutics and fusion constructs.
The present systematic review indicates that PCI decreases brain metastases incidence and that PCI improves survival in SCLC patients.
These results confirm that PCI prevents and does not simply delay the emergence of brain metastases.
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Since changes in expression breadth tend to be mediated by tissue-specific differences in chromatin organization, these data support earlier analyses concluding that PCI-dependent effects on chromatin structure do not closely parallel methylation-dependent effects on transcription [24].
This implies that PCI+ genes feature higher transcription/repair or greater negative selection pressure than PCI- genes which remains consistent with the hypothesis that PCIs favor intron insertion via a separate chromatin effect.
Collectively, these results demonstrate that PCI-32765 directly inhibits Btk activity stimulated by BCR activation in primary B lymphocytes.
Furthermore, the results showed that PCI-bleomycin induced a higher level of DNA damage than bleomycin alone in all three cell lines), supporting increased import of bleomycin.
Following treatment, splenocytes from the mice were isolated and assayed to ensure that PCI-32765 was binding Btk as previously reported [ 17].
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