HIGHLIGHTS
SUMMARY
In this context, loss of the negative_feedback effect of LPA on ATX expression via induction of the ATX gene by inflammatory cytokines, allowing sustained elevation of ATX and LPA levels, has been proposed as a hallmark of chronic inflammatory disease, including cancer (reviewed by_[8]). In the present prospective clinical study, the authors have begun addressing the putative involvement of the ATX-LPA axis in CSDH by examining levels of ATX activity in CSDH fluid and have investigated the hypothesis that CSF is a potential source for ATX in CSDH by incorporating analysis of . . .
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