Restricted Visual Scanpaths During Emotion Recognition in Childhood Social Anxiety Disorder.

Social anxiety disorder (SAD) has its typical onset in childhood and adolescence. Maladaptive processing of social information may contribute to the etiology and maintenance of SAD. During face perception, individuals execute a succession of visual fixations known as a scanpath which facilitates information processing.

Reduced left visual field bias for faces in adolescents with social anxiety disorder.

Individuals tend to explore the left side of a face first and for a longer time in comparison to the right side. This left visual field (LVF) bias is suggested to reflect right hemispheric dominance for face processing. Social anxiety disorder (SAD) is associated with maladaptive interpretations of facial expressions, but it is not known whether this is linked to an atypical LVF bias.

Correction: Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis.

[This corrects the article DOI: 10.1371/journal.pntd.

Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis.

Background: Melioidosis, caused by bioterror treat agent Burkholderia pseudomallei, is an important cause of community-acquired Gram-negative sepsis in Southeast Asia and Northern Australia. New insights into the pathogenesis of melioidosis may help improve treatment and decrease mortality rates from this dreadful disease. We hypothesized that changes in Von Willebrand factor (VWF) function should occur in melioidosis, based on the presence of endothelial stimulation by endotoxin, pro-inflammatory cytokines and thrombin in melioidosis, and investigated whether this impacted on outcome.

Frequent downregulation of the transcription factor Foxa2 in lung cancer through epigenetic silencing.

Purpose: We sought to determine the mechanisms of downregulation of the airway transcription factor Foxa2 in lung cancer and the expression status of Foxa2 in non-small-cell lung cancer (NSCLC).

Methods: A series of 25 lung cancer cell lines were evaluated for Foxa2 protein expression, FOXA2 mRNA levels, FOXA2 mutations, FOXA2 copy number changes and for evidence of FOXA2 promoter hypermethylation. In addition, 32 NSCLCs were sequenced for FOXA2 mutations and 173 primary NSCLC tumors evaluated for Foxa2 expression using an immunohistochemical assay.