There was no interaction by race/ethnicity; however, all associations varied by sex with men having lower muscle mass per unit increase in depressive symptoms (data not shown).
Adjustment for type 2 versus type 1 diabetes and differences in severity of neuropathy, insulin use, foot deformities, smoking status, and alcohol intake had no impact on these differences in painful symptoms (data not shown); i.e., these variables could not account for the disparity in symptoms between type 1 and type 2 diabetes.
In addition, the symptoms data are self-reported by the study participants.
In particular, we focus only on collecting one month of symptoms data in order to have a high participation rate from our study participants.
Of note, whole-body [F]fluoride scans additionally showed hotspots in the manubriosternal joints in both patients and in the left acromion-clavicular joint in one patient corresponding to clinical symptoms (data not shown in Table 2).
Thus, given a date t, we consider valid a time window of five days if the following conditions are satisfied: (i) mobility data for (t_{mathrm{hist}} in [0,2]), and (ii) symptoms data for the time (t_{mathrm{hor}}in [0,2]).
In addition to classical symptoms (data not shown), a total of 12 values (4 isolates X 3 biological replicates) were used to build the partial resistance index.
In terms of depressive symptoms, data extracted from three studies (106 patients treated with antidepressants and 108 with placebo) showed no statistically significant difference between antidepressants and placebo (mean difference –0.93, 95% CI –2.27 to 0.41) (Fig. 3).
To identify the different trajectory subtypes in terms of negative symptoms, data from 400 patients with complete 1-year PANSS negative subscale scores were fit to a sequential series of quadratic growth models that reflected one to five different trajectory latent classes.
