https://www.selleckchem.com/products/gdc-0068.html
019) and non-smoking (p less then 0.001) controls, also in the age- and sex- adjusted model (p less then 0.001). Plasma HA was not associated with AECOPD, airway-related hospitalizations in the previous year, or systemic inflammation in COPD. Arterial pulse wave velocity explained some of the variance ( less then 10%) in plasma HA (p = 0.006). Overall, these results indicate that expression of HYAL-2, but not plasma HA nor HAS-3, is enhanced in patients with COPD compared to (non)smoking controls. Furthermore, HA was not associate
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