The effect of perceptual information on output interference.

Retrieval from episodic memory has consequences (Malmberg, Lehman, Annis, Criss, & Shiffrin, The Psychology of Learning and Motivation, 61; 285-313, 2014). In some cases, the consequences are beneficial, as in the improvement in memory for items that were already retrieved (Izawa, 1970, Journal of Experimental Psychology, 83(2, Pt.1), 340-344; Izawa, Journal of Experimental Psychology, 89(1): 10-21, 1971; Roediger & Karpicke, Psychological Science, 17(3), 249-255, 2006).

Anxious behavior induces elevated hippocampal Cb receptor gene expression.

Anxiety is differentially expressed across a continuum of stressful/fearful intensity, influenced by endocannabinoid systems and receptors. The hippocampus plays important roles in the regulation of affective behavior, emotion, and anxiety, as well as memory. Location of Cb/Cb receptor action could be important in determining emotional valence, because while the dorsal hippocampus is involved in spatial memory and cognition, the ventral hippocampus has projections to the PFC, BNST, amygdala, and HPA axis, and is important for emotional responses to stress.

Opportunity for verbalization does not improve visual change detection performance: A state-trace analysis.

Evidence suggests that there is a tendency to verbally recode visually-presented information, and that in some cases verbal recoding can boost memory performance. According to multi-component models of working memory, memory performance is increased because task-relevant information is simultaneously maintained in two codes. The possibility of dual encoding is problematic if the goal is to measure capacity for visual information exclusively.

Intensity of anxiety is modified via complex integrative stress circuitries.

Escalation of anxious behavior while environmentally and socially relevant contextual events amplify the intensity of emotional response produces a testable gradient of anxiety shaped by integrative circuitries. Apprehension of the Stress-Alternatives Model apparatus (SAM) oval open field (OF) is measured by the active latency to escape, and is delayed by unfamiliarity with the passageway. Familiar OF escape is the least anxious behavior along the continuum, which can be reduced by anxiolytics such as icv neuropeptide S (NPS).

Nuance and behavioral cogency: How the Visible Burrow System inspired the Stress-Alternatives Model and conceptualization of the continuum of anxiety.

By creating the Visible Burrow System (VBS) Bob Blanchard found a way to study the interaction of genetics, physiology, environment, and adaptive significance in a model with broad validity. The VBS changed the way we think about anxiety and affective disorders by allowing the mechanisms which control them to be observed in a dynamic setting. Critically, Blanchard used the VBS and other models to show how behavioral systems like defense are dependent upon context and behavioral elements unique to the individual.

Dynamic memory searches: Selective output interference for the memory of facts.

The benefits of testing on later memory performance are well documented; however, the manner in which testing harms memory performance is less well understood. This research is concerned with the finding that accuracy decreases over the course of testing, a phenomena termed "output interference" (OI). OI has primarily been investigated with episodic memory, but there is limited research investigating OI in measures of semantic memory (i.

An R package for state-trace analysis.

State-trace analysis (Bamber, Journal of Mathematical Psychology, 19, 137-181, 1979) is a graphical analysis that can determine whether one or more than one latent variable mediates an apparent dissociation between the effects of two experimental manipulations. State-trace analysis makes only ordinal assumptions and so, is not confounded by range effects that plague alternative methods, especially when performance is measured on a bounded scale (such as accuracy). We describe and illustrate the application of a freely available GUI driven package, StateTrace, for the R language.

The design and analysis of state-trace experiments.

State-trace analysis (Bamber, 1979) addresses a question of interest in many areas of psychological research: Does 1 or more than 1 latent (i.e., not directly observed) variable mediate an interaction between 2 experimental manipulations? There is little guidance available on how to design an experiment suited to state-trace analysis, despite its increasing use, and existing statistical methods for state-trace analysis are problematic.

Proteomics of transformed lymphocytes from a family with familial pulmonary arterial hypertension.

Rationale: Not all family members with BMPR2 mutations develop pulmonary arterial hypertension (PAH), implying that additional modifier genes or proteins are necessary for full expression of the disease.

Objectives: To determine whether protein expression is altered in patients with familial PAH (FPAH) compared with obligate carriers and nondiseased control subjects.

Methods: Protein extracts from transformed blood lymphocytes from four patients with FPAH, three obligate carriers, and three married-in control subjects from one family with a known BMPR2 mutation (exon 3 T354G) were labeled with either Cy3 or Cy5.

High frequency of BMPR2 exonic deletions/duplications in familial pulmonary arterial hypertension.

Rationale: Previous studies have shown that approximately 55% of patients with familial pulmonary arterial hypertension (FPAH) have BMPR2 coding sequence mutations. However, direct sequencing does not detect other types of heterozygous mutations, such as exonic deletions/duplications.

Objective: To estimate the frequency of BMPR2 exonic deletions/duplications in FPAH.

Serotonin transporter polymorphisms in familial and idiopathic pulmonary arterial hypertension.

Rationale: Serotonin is a pulmonary vasoconstrictor and smooth muscle cell mitogen. The serotonin transporter (SERT) is abundant in pulmonary vascular smooth muscle. Compared with the short (S) allele, the long (L) SERT promoter allele is associated with increased SERT transcription and more severe pulmonary hypertension in a cohort of patients with chronic obstructive pulmonary disease, and was more prevalent in a cohort with idiopathic pulmonary arterial hypertension (IPAH), compared with control subjects.

Multilocus analysis of hypertension: a hierarchical approach.

While hypertension is a complex disease with a well-documented genetic component, genetic studies often fail to replicate findings. One possibility for such inconsistency is that the underlying genetics of hypertension is not based on single genes of major effect, but on interactions among genes. To test this hypothesis, we studied both single locus and multilocus effects, using a case-control design of subjects from Ghana.

Pulmonary veno-occlusive disease caused by an inherited mutation in bone morphogenetic protein receptor II.

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension in which the vascular changes originate in the small pulmonary veins and venules. The pathogenesis is unknown and any link with primary pulmonary hypertension (PPH) has been speculative. Mutations in the bone morphogenetic protein receptor II (BMPR2) gene have been identified in at least 50% of familial cases and in 25% of sporadic cases of PPH.

Heterozygosity for a surfactant protein C gene mutation associated with usual interstitial pneumonitis and cellular nonspecific interstitial pneumonitis in one kindred.

Familial pulmonary fibrosis is a heterogeneous group of interstitial lung diseases of unknown cause that is associated with multiple pathologic subsets. Mutations in the surfactant protein C (SP-C) gene (SFTPC) are associated with familial desquamative and nonspecific interstitial pneumonitis. Genetic studies in familial usual interstitial pneumonitis have been inconclusive.

An exon splice enhancer mutation causes autosomal dominant GH deficiency.

Familial isolated GH deficiency type II (IGHD II) is caused, in some cases, by heterogeneous IVS3 mutations that affect GH mRNA splicing. We report here our finding an A-->G transition of the fifth base of exon 3 (E3+ 5 A-->G) in affected individuals from an IGHD II family. This mutation disrupts a (GAA)(n) exon splice enhancer (ESE) motif immediately following the weak IVS2 3' splice site.