For example, the similar marker patterning for baseline caries, increment and incidence but different for progression (with a few and a dominant lactobacilli marker) may, hypothetically, reflect mechanistic differences between initiation and progression of lesions.
To investigate whether or not LV function had changed according to baseline BNP levels, we adjusted all models that assessed associations with markers of LV function for baseline values of these markers.
The relatively small number of patients in this trial precluded us from performing a detailed multivariate analysis, although the ALC remained a significant prognostic marker when we controlled for baseline LDH.
Subjects with higher levels of hs-CRP, sTNFR1, and sTNFR2 at 48 weeks had an increased odds of subsequent diabetes, after adjustment for baseline marker level, age, BMI at week 48, CD4 count at week 48 (< vs. >200 cells/mm), and indinavir use (all Ptrend ≤ 0.05).
After adjustment for baseline markers of LV diastolic dysfunction, 10−3 ⋅ kPa−1 lower distensibility coefficients of carotid, brachial, and femoral arteries remained significantly associated with a 0.29, 0.38, and 0.73 mL/m higher LA volume index, respectively.
These associations were attenuated after adjustment for baseline markers of LV systolic and diastolic dysfunction, but type 2 diabetes was still significantly associated with a higher LV mass index (3.41 g/m2.7) and E/e′ (1.43).
Random effects linear regression was used to estimate the effect of treatment and time on average post-baseline marker levels, while also adjusting for baseline (Day 0) levels.
We next compared secondary models formed from all influential biomarkers (n = 18 multimarkers), a five biomarker panel and a single lactobacilli marker, for ability to predict baseline caries (Table 1, Fig. 2A).
Significant differences for baseline inflammatory markers were found between WT and ABIN1[D485N] mice.
No significant differences between treatment groups were observed for baseline bone markers.
