Factor loading (λ) estimates for Beck Depression Inventory items for non-users and frequent-users of alcohol, nicotine, and cannabis, under the factorial invariance model.

<p>Factor loading (λ) estimates for Beck Depression Inventory items for non-users and frequent-users of alcohol, nicotine, and cannabis, under the factorial invariance model.</p

Types of Measurement Invariance.

<p>Types of measurement invariance, with parameters unable to be equated displayed in red and dashed. (A) Strict factorial invariance, with between group differences arising from different factor means and/or different factor variances. (B) Failure of metric invariance, with between group differences arising from different factor loadings. (C) Failure of configural invariance, with between group differences arising from different numbers of latent factors.</p

Likelihood ratio tests (χ² and p-value) for ordinal difference of means tests for Beck Depression Inventory items between non-users and frequent-users of alcohol, nicotine and cannabis.^*

<p>Likelihood ratio tests (χ² and p-value) for ordinal difference of means tests for Beck Depression Inventory items between non-users and frequent-users of alcohol, nicotine and cannabis.<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0152118#t002fn001" target="_blank">^*</a></p

Sample frequencies by parental relationship and race.

<p>Sample frequencies by parental relationship and race.</p

Indices of model fit to assess within-group genetic and environmental contributions and between-group racial heterogeneity.

<p>The table presents the following values: −2 times the log likelihood (-2LL), the number of free parameters in the model (<i>k</i>), an index of the balance between goodness of model fit and parsimony (Akaike's information criterion, or AIC), and the <i>p</i>-value significance result from the likelihood ratio test (distributed as a chi-square statistic). The fit of model 2 was compared to model 1 and all subsequent models were compared to model 2. Significant <i>p</i>-values indicate a significant reduction in model fit. AA =  African American, EA =  European American, <i>f</i>² =  fetal effect, <i>m</i>² =  maternal effect and <i>c</i>² =  shared environmental effect.</p

Expected covariance of gestational age expressed as variance components between pregnancy outcomes as a function of relationship between offspring.

<p><i>f</i>² = fetal genetic,</p><p><i>m</i>² = maternal genetic,</p><p><i>c</i>² = shared familial environment.</p><p><i>h</i> = parameter to allow for differences in half-sibling versus full-sibling shared environment.</p

Estimated variance components from model 2 with empirically derived 95% bootstrap confidence intervals adjusted for covariates (birth order, maternal age, fetal sex, source of care, smoking, maternal education).

<p>Estimated variance components from model 2 with empirically derived 95% bootstrap confidence intervals adjusted for covariates (birth order, maternal age, fetal sex, source of care, smoking, maternal education).</p

HCMV cross-reactivity potential of 77 SCT DRP from whole exome sequencing data using sliding window match analysis.

<p>HCMV cross-reactivity potential of 77 SCT DRP from whole exome sequencing data using sliding window match analysis.</p

Human-CMV short sequence homology in GVHD tissue specific peptide and gene distribution from GTEx analysis (n = 18).

<p>GVHD incidence denotes the specific organs affected in each patient; Peptides, lists the number of unique peptide-HLA complexes matched between human and CMV peptide library; the column, <i>Genes</i> lists the source genes for the aforementioned peptides; <i>GVHD tissue specific peptides</i> lists the number of peptides which bind HLA with an IC50 <500nM, and are expressed in tissues affected by GVHD; <i>GVHD tissue gene expression</i> denotes the number of genes expressed at an RPKM >10 corresponding to the GVHD tissue specific peptides. Note: *- All patients with an asterisk following their numeric representation experienced CMV reactivation prior to GVHD (except Patients 67 and 71, <i>de novo</i> CMV infected) and patients without an asterisk experienced GVHD prior to CMV reactivation. **- human peptides may have overlapping areas of homology yielding a higher number of matches. Immunogenic CMV genes in this context refer to the genes associated with HCMV ORF-specific CD8+ T memory cell responses measured in frequency among CMV seropositive patients previously [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178763#pone.0178763.ref036" target="_blank">36</a>].</p

GVHD tissue-specific immunogenic CMV peptide matches, CMV reactivation before GVHD patients.

<p>Patient-specific process of cross comparison along with the source genes, IC50 values to indicate inverse binding affinity and GVHD organ specific tissue involvement. *Note: Twelve patients with CMV reactivation/infection before GVHD onset exhibited previously identified immunogenic CMV peptide matches with gene expression specific to the tissues affected by GVHD (above); The filter of immunogenicity provides a connection to T cell reactivity shown <i>in vitro</i> to the listed CMV genes in a separate patient population [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178763#pone.0178763.ref036" target="_blank">36</a>]; Patient 79 with muscle/fascia GVHD showed no muscle-specific previously <i>known immunogenic</i> CMV peptide matches but still had three relevant CMV peptide matches expressed in the skeletal muscle (not shown); Tissues in parentheses were also affected by GVHD but without immunogenic matches/expression by patient; Patients 67 and 71 experienced <i>de novo</i> CMV infection; All 13 patients exhibited multiple CMV peptide matches with unknown immunogenicity.</p