D Met/Met = two) and existing PTSD symptom severity (CAPS score) were entered in step 2. The genotype PTSD symptom severity interaction was entered in step 3. These models have been run separately for the adjusted volumes from the left and right hippocampus. The for significance was adjusted applying Bonferroni correction for the 2 hemispheres (p = 0.05 two = 0.025). To evaluate the part of additional possible confounders, like education (highest grade completed) and population stratification (see Appendix 1 for any detailed description), we ran post hoc analyses with all the prospective confounder added to step 1 of your 3-stage models as previously described. To examine regardless of whether sex influenced the results, we repeated the analyses immediately after removing the girls in the information set.ResultsSample characteristicsWe included 146 (90 male) white, non-Hispanic veterans in our analyses. Group demographic characteristics by Val158Met genotype are shown in Table 1. The groups did notRLLRFig. 1: Automated segmentation from the hippocampus. Coronal and sagittal views showing the right (red) and left (yellow) hippocampal regions of interest as defined by FreeSurfer.J Psychiatry Neurosci 2017;42(two)Hayes et al.differ significantly in age, sex, WTAR-estimated IQ, variety of lifetime mood issues or substance use diagnoses, CAPS score, duration of symptoms, or probable mild TBI. Nonetheless, the groups differed in education, using the Met homozygote group obtaining additional education than the Val/Met group (p = 0.032).Moderating effect of COMT Val158MetHierarchical linear regression showed no significant overall model effect in steps 1 and two for the left hippocampus (Table two). Just after entering the genotype PTSD symptom severity interaction inside the third step, the general model was substantial (F8,137 = two.IL-13 Protein site 69, p = 0.IGF-I/IGF-1 Protein manufacturer 009, R2 = 0.PMID:26446225 14), having a substantial F alter (F1,137 = 5.43, p = 0.022, R2 = 0.03). Further examination in the interaction term revealed that men and women homozygous for the Val allele showed decreased left hippocampal volume with escalating PTSD symptom severity ( = .49, p = 0.007; Fig. 2A). There was no association amongst leftTable 1: Sample characteristicshippocampal volume and PTSD symptom severity for either the Val/Met group ( = .03, p = 0.80; Fig. 2B) or the Met/ Met homozygous group ( = .01, p = 0.90; Fig. 2C). Working with a categorical PTSD variable did not modify the pattern of final results; the moderating effect of COMT Val158Met on the association involving PTSD and left hippocampal volume remained substantial. For the correct hippocampus, there had been no important major effects or an interaction effect. For Val/Val homozygotes, there was no association amongst PTSD symptom severity and proper hippocampal volume ( = .20, p = 0.27). This was also accurate for the Val/Met group ( = .09, p = 0.52) and Met/ Met homozygotes ( = .26, p = 0.16).Post hoc models for prospective confounding variablesNone on the post hoc models that incorporated further covariates modified the estimates with the main effects in step 2 or the genotype PTSD symptom severity interaction in step three.Group; mean SD or no. ( ) Characterisitc Age, yr Male sex Education, yr WTAR estimated IQ* CAPS total score Symptom duration, mo Lifetime mood disorder diagnosis Lifetime substance use diagnosis Probable TBI L hippocampal vol, mm3 R hippocampal vol, mm3 Total (n = 146) 31 8 135 (92.five) 14 two 103 11.5 44 28.six 58 60.five 48 (32.9) 93 (63.7) 69 (47) 4355 365 4456 389 Val/Val (n = 45) 32 8.1 43 (95.six) 14 two.three 104 ten.9 47 27.7 63 62.8 16 (35.6).
