A restriction fragment length polymorphism (RFLP) map for barley (Hordeum vulgare L.) has been developed on the basis of a population of anther culture derived, doubled haploids from the F1 of cultivars 'Proctor' × 'Nudinka'. Wheat genomic, oat cDNA, and barley cDNA clones provided the major source of the probes. Additional clones included genomic clones from Aegilops squarrosa L. and barley, two dehydrin genes, a barley promoter, and a wheat ribosomal gene. In total, 155 RFLPs and two known genes (hulless and Mla12 powdery mildew resistance) have been placed on the linkage map. Clones were assigned to chromosomes using disomic wheat–barley chromosome addition lines. Chromosome arm orientation was done using 'Chinese Spring' wheat nullisomic–tetrasomic and ditelosomic aneuploid stocks. Markers have been located on all chromosome arms except 6S, and the total map length is 1096 centimorgans (cM). Considerations involved in RFLP mapping, including choice and number of restriction endonucleases, disturbed segregation ratios, and uneven distribution of markers in the genome are discussed as well as future improvements and applications of this map.Key words: restriction fragment length polymorphism, mapping, Hordeum vulgare L., Mla12.

Although genomic discovery provides the potential for population health benefit, the current knowledge base around implementation to turn this promise into a reality is severely limited. Current gaps in the literature demonstrate a need to apply implementation science principles to genomic medicine in order to deliver on the promise of precision medicine.Genet Med advance online publication 12 January 2017.

Background Collectively, functional neuroimaging studies implicate frontal-limbic dysfunction in the pathophysiology of posttraumatic stress disorder (PTSD), as reflected by altered amygdala reactivity and deficient prefrontal responses. These neural patterns are often elicited by social signals of threat (fearful/angry faces) and traumatic reminders (combat sounds, script-driven imagery). Although PTSD can be conceptualized as a disorder of emotion dysregulation, few studies to-date have directly investigated the neural correlates of volitional attempts at regulating negative affect in PTSD. Methods Using functional magnetic resonance imaging and a well-validated task involving cognitive regulation of negative affect via reappraisal and known to engage prefrontal cortical regions, the authors compared brain activation in veterans with PTSD (n=21) and without PTSD (n=21, combat-exposed controls/CEC), following military combat trauma experience during deployments in Afghanistan or Iraq. The primary outcome measure was brain activation during cognitive reappraisal (i.e., decrease negative affect) as compared to passive viewing (i.e., maintain negative affect) of emotionally-evocative aversive images. Results The subjects in both groups reported similar successful reduction in negative affect following reappraisal. The PTSD group engaged the dorsolateral prefrontal cortex during cognitive reappraisal, albeit to a lesser extent than the CEC group. Although the amygdala was engaged in both groups during passive viewing of aversive images, neither group exhibited attenuation of amygdala activation during cognitive reappraisal. Conclusions Veterans with combat-related PTSD showed less recruitment of the dorsolateral prefrontal cortex involved in cognitive reappraisal, suggesting focal and aberrant neural activation during volitional, self-regulation of negative affective states.

Increased error monitoring, as measured by the error-related negativity (ERN), has been shown to persist after treatment for obsessive-compulsive disorder in youth and adults; however, no previous studies have examined the ERN following treatment for related anxiety disorders. We used a flanker task to elicit the ERN in 28 youth and young adults (8–26 years old) with primary diagnoses of generalized anxiety disorder (GAD) or social anxiety disorder (SAD) and 35 healthy controls. Patients were assessed before and after treatment with cognitive-behavioral therapy (CBT) or selective serotonin reuptake inhibitors (SSRI), and healthy controls were assessed at a comparable interval. The ERN increased across assessments in the combined sample. Patients with SAD exhibited an enhanced ERN relative to healthy controls prior to and following treatment, even when analyses were limited to SAD patients who responded to treatment. Patients with GAD did not significantly differ from healthy controls at either assessment. Results provide preliminary evidence that enhanced error monitoring persists following treatment for SAD in youth and young adults, and support conceptualizations of increased error monitoring as a trait-like vulnerability that may contribute to risk for recurrence and impaired functioning later in life. Future work is needed to further evaluate the ERN in GAD across development, including whether an enhanced ERN develops in adulthood or is most apparent when worries focus on internal sources of threat.

The longitudinal relations between physiological markers of child emotion regulation and maternal parenting practices were examined from 2 to 4 years of age. At Time 1, cardiac vagal tone was assessed for one hundred four 2-year-olds (54 females); their mothers completed an assessment of parenting styles. Two years later, at Time 2, 84 of the original participants were reassessed on measures of cardiac vagal tone and parenting style. Results indicated both baseline cardiac vagal tone and maternal parenting practices to be stable from 2 to 4 years of age. Children's cardiac vagal tone predicted specific parenting practices from the toddler to preschool years. Further, child cardiac vagal tone moderated maternal restrictive-parenting practices from 2 to 4 years of age; mothers of children who were highly or moderately physiologically dysregulated were more likely to report restrictive parenting practices at both 2 and 4 years of age.

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Recent studies show decreased functional connectivity in the default mode network (DMN) in PTSD; however, few have directly examined combat trauma specifically. There is limited understanding of how combat itself may affect the DMN. Some literature suggests that trauma exposure, rather than PTSD, can disrupt the DMN. To further elucidate the effect of trauma and PTSD on the DMN, we investigated DMN functional connectivity during the resting-state in veterans with PTSD, combat-exposed controls, and never-traumatized healthy controls. Results revealed that DMN connectivity was reduced in veterans exposed to combat trauma with and without PTSD compared to healthy civilian controls. Specifically, both groups of veterans demonstrated weaker connectivity within a network involving the precuneus, medial prefrontal cortex (mPFC) and right superior parietal lobule regardless of whether the mPFC or precuneus was chosen as a seed region. Findings suggest that the experience of trauma, rather than the pathology of PTSD, may be related to DMN changes.

Background Cognitive behavioral therapy (CBT) is a well-established treatment for anxiety and depression; however, response to CBT is heterogeneous across patients and many remain symptomatic after therapy, raising the need to identify prospective predictors for treatment planning. Altered neural processing of reward has been implicated in both depression and anxiety, and improving hedonic capacity is a goal of CBT. However, little is known about how neural response to reward relates to CBT outcomes in depression and anxiety. The current study used the reward positivity (RewP) event-related potential (ERP) component to examine whether neural reactivity to reward would predict CBT response in a sample of patients with anxiety without depression (n = 30) and comorbid anxiety and depression (CAD, n = 22). Methods Participants completed a guessing reward ERP paradigm before completing 12 weeks of standard CBT. Results The majority of the sample (68%; 35 of 52 patients) responded to treatment, and those with a reduced RewP at baseline were more likely to respond to treatment. A reduced RewP was also associated with a greater pre-to-post CBT reduction in depressive symptoms among individuals with CAD, but not among individuals with pure anxiety. Conclusions CBT may be most beneficial in reducing depressive symptoms for individuals who demonstrate decreased reward reactivity prior to treatment. CBT may target reward brain function, leading to greater improvement in symptoms. These effects may be strongest, and therefore most meaningful, for individuals with reward processing deficits prior to treatment.