The role of children’s negative attributions on depressive symptoms: an inherited characteristic or a product of the early environment?

Negative attributional style has been associated with depressive symptoms in children. Yet, it is unclear whether these cognitive biases reflect inherited characteristics of the broader depressive phenotype or are a product of children's environments. While existing data in adolescents show that negative attributions reflect a genetic predisposition, elevating depressive responses to stress, other data suggest that negative attributions in children are more likely to reflect early environmental experiences on symptoms. Here, we assess the degree to which negative attributional style and depressive symptoms arise from common genetic, shared and non-shared environmental influences in childhood. Monozygotic and dizygotic twins reported on attributional style and depressive symptoms at age 8 (n = 300 pairs) and at age 10 (n = 250 pairs). Two multivariate models with varying assumptions on the nature of the relationship between negative attributions and depressive symptoms within and across time were fit to the data. The Common Pathway model provided better fit than the Cholesky decomposition. A common, latent factor influenced both attributional style and depressive symptoms at both time-points in children. The only significant influences on this factor were shared and non-shared aspects of the environment. Placing the present findings with those of adolescents suggests possible developmental differences in the relationship between attributional style and depressive symptoms.</p

The role of children’s negative attributions on depressive symptoms: an inherited characteristic or a product of the early environment?

Negative attributional style has been associated with depressive symptoms in children. Yet, it is unclear whether these cognitive biases reflect inherited characteristics of the broader depressive phenotype or are a product of children's environments. While existing data in adolescents show that negative attributions reflect a genetic predisposition, elevating depressive responses to stress, other data suggest that negative attributions in children are more likely to reflect early environmental experiences on symptoms. Here, we assess the degree to which negative attributional style and depressive symptoms arise from common genetic, shared and non-shared environmental influences in childhood. Monozygotic and dizygotic twins reported on attributional style and depressive symptoms at age 8 (n = 300 pairs) and at age 10 (n = 250 pairs). Two multivariate models with varying assumptions on the nature of the relationship between negative attributions and depressive symptoms within and across time were fit to the data. The Common Pathway model provided better fit than the Cholesky decomposition. A common, latent factor influenced both attributional style and depressive symptoms at both time-points in children. The only significant influences on this factor were shared and non-shared aspects of the environment. Placing the present findings with those of adolescents suggests possible developmental differences in the relationship between attributional style and depressive symptoms.</p

Supervised analysis based on IGKV3-20 induction of immunology genes in different sub-groups.

<p>Heat map of immunology gene sets differentially modulated in PBMCs by IGKV3-20 or PBS (unstimulated). Genes up-regulated (red) and down-regulated (green) by IGKV3-20 are listed for each analysis. (<b>A</b>) 24 h HCV-negative; (<b>B</b>) 24 h HCV-positive; (<b>C</b>) 6 d HCV-negative; (<b>D</b>) 6 d HCV-positive.</p

Supervised analysis based on IGKV3-20 induction in different sub-groups.

<p>(<b>A–D</b>) Heat map of gene sets differentially modulated in PBMCs by IGKV3-20 or PBS (unstimulated) in the four identified sub-groups. (<b>E</b>) Venn diagram indicating the number of unique and common up-regulated genes in the four sub-groups.</p

Clinical parameters of enrolled subjects.

<p>Clinical parameters of enrolled subjects.</p

S. Šargunov, La nonna e la Facoltà di Giornalismo

<div><p>Hepatitis C virus (HCV) has been identified as one of the major risk factors for type II mixed cryoglobulinemia (MC), during the clinical evolution of chronic hepatitis, which may lead to development of B cell non-Hodgkin's lymphoma (NHL). We have previously shown that the candidate idiotype vaccine, based on the IGKV3-20 light chain protein, is able to induce activation and maturation of circulating antigen presenting cells (APCs) in both HCV-positive and HCV-negative healthy control subjects, with production of Th2-type cytokines. Here, the effect of the recombinant IGKV3-20 protein on human peripheral blood mononuclear cells (PBMCs) from HCV-positive subjects, with known blood levels of cryoglobulins, is shown via gene expression profiling analysis combined to multiparameter flow cytometry and multiplex analyses of cytokines.</p> </div

Supplementary Figure 1 from Prospective Evaluation of Cetuximab-Mediated Antibody-Dependent Cell Cytotoxicity in Metastatic Colorectal Cancer Patients Predicts Treatment Efficacy

Bland-Altman plot % increase in cetuximab-mediated ADCC: difference SRB assay-Cytotox96 vs average. By plotting the difference between the % ADCC increase determined by each of the methods against the mean of the two determinations it is possible to determine the concordance between both methods. The limits of agreement are also calculated to give a quantitative analysis of the differences between both methods.</p

Unsupervised hierarchical clustering.

<p>Heat map including all samples from 4 healthy controls (light blue) and 5 HCV-positive subjects (light red). Red indicates over-expression; green indicates under-expression; black indicates unchanged expression; gray indicates no detection of expression. Each row represents a single gene; each column represents a single sample. The dendrogram at the left of matrix indicates the degree of similarity among the genes examined by expression patterns. The dendrogram at the top of the matrix indicates the degree of similarity between samples.</p

Analysis of cytokine production in supernatants of PBMCs.

<p>Production of indicated cytokines was evaluated in supernatants of PBMCs from HCV-negative and positive subjects, induced by IGKV3-20 and LPS after 24 h and 6 d incubation.</p

Cytoscape analysis.

<p>Integrated analysis of immunology genes differentially modulated in PBMCs by IGKV3-20. Genes up-regulated are indicated in red and down-regulated are indicated in green. (<b>A</b>) 24 h HCV-negative; (<b>B</b>) 24 h HCV-positive; (<b>C</b>) 6 d HCV-negative; (<b>D</b>) 6 d HCV-positive.</p