While it remains uncertain whether early IT is associated with a reduction in cardiovascular endpoints, we find no evidence that such treatment adversely affects patient-reported outcomes early in the course of the disease.
Concerning the CEL volume as a secondary endpoint, we found a similar pattern: multivariate analysis revealed a significant reduction in CEL volume compared to baseline in the analyzable population as a whole (p = 0.008).
At study endpoint, we found 23 patients still in UWS based on behavioral assessment on at least two different occasions.
When using NHG as the endpoint we found a statistically significant association with T3 only in grade II.
By monitoring this endpoint, we found that TLR4 transcript levels increased during the first several hours of SMF exposure.
Although not a primary endpoint, we found an interesting and previously unreported association between hyponatremia and leukocyte count in these patients.
In analyzing our primary endpoint, we found that there was a secular trend associated with a natural decline of the time under MV (secular trend β1 = −0.055, P = 0.012).
In a secondary analysis using all cause mortality as the endpoint, we found a similar relation between systolic intensification threshold, time to intensification, time to follow-up, and all cause mortality (table 4).
In the cemented group of primary THAs, with revision due to deep infection as endpoint, we found the same pattern of gradual increase in revision risk over time (Table 2, Figures 1 and 2).
When we applied distant metastasis-free survival as an endpoint, we found that patients expressing high levels of ST3GAL2 had a worse outcome, confirming the involvement of SSEA4-positive cells in metastasis formation (Fig. 7c), as observed in the case of metastasis-derived PDXs.
