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Field trials were conducted in North Carolina in 2017 and Louisiana and Mississippi in 2018 to determine the effect of pretransplanting applications of diquat on sweetpotato crop tolerance, yield, and storage root quality. In North Carolina treatments consisted of two rates of diquat (560 or 1,120 g ai ha−1) alone or mixed with 107 g ai ha−1 flumioxazin and applied 1 d before transplanting (DBP), sequential applications of diquat (560 or 1,120 g ha−1) 1 and 17 DBP, 107 g ha−1 flumioxazin alone, and a nontreated check. In Louisiana and Mississippi treatments consisted of diquat (560 or 1,120 g ha−1) applied 1 DBP either alone or followed by (fb) rehipping rows or 107 g ha−1 flumioxazin immediately prior to transplanting. Additional treatments included 546 g ha−1 paraquat applied 1 DBP and a nontreated check. In North Carolina injury was ≤3% for all treatments through 23 d after transplanting (DAP), and no injury was observed after 23 DAP. Visual sweetpotato stunting pooled across the Mississippi and Louisiana trials ranged from 1% to 14%, 0% to 6%, and 0% to 3% at 2, 4, and 6 wk after planting (WAP), respectively, and no crop injury was observed after 6 WAP. Diquat applied 1 DBP and not fb rehipping resulted in greater crop injury (12%) than comparable treatments that were rehipped (2%). In North Carolina single and sequential diquat applications resulted in reduced No. 1 sweetpotato yield (24,230 and 24,280 kg ha−1, respectively) compared with the nontreated check, but No. 1 yield when diquat plus flumioxazin (26,330 kg ha−1) was used was similar to that of the nontreated check. No. 1 yield did not differ by treatment in Louisiana and Mississippi.
Field trials were conducted near Pontotoc, Mississippi; Chase, Louisiana; and Clinton, North Carolina, in 2017 and 2018 to determine the effect of pendimethalin rate and timing application on sweetpotato crop tolerance, yield, and storage root quality. Treatments consisted of five pendimethalin rates (266, 532, 1,065, 1,597, and 2,130 g ai ha−1) by two application timings (0 to 1 or 10 to 14 d after transplanting). Additionally, a nontreated check was included for comparison. Crop injury (stunting) was minimal (≤4%) through 6 wk after transplanting (WAP) and no injury was observed from 8 to 14 WAP, regardless of application timing or rate. The nontreated check yielded 6.6, 17.6, 5.5, and 32.1 × 103 kg ha−1 of canner, no. 1, jumbo, and total grades, respectively. Neither pendimethalin application timing nor rate influenced jumbo, no. 1, marketable, or total sweetpotato yield. Overall, these results indicate that pendimethalin will be a valuable addition to the toolkit of sweetpotato growers.
Externalizing disorders are known to be partly heritable, but the biological pathways linking genetic risk to the manifestation of these costly behaviors remain under investigation. This study sought to identify neural phenotypes associated with genomic vulnerability for externalizing disorders.
One-hundred fifty-five White, non-Hispanic veterans were genotyped using a genome-wide array and underwent resting-state functional magnetic resonance imaging. Genetic susceptibility was assessed using an independently developed polygenic score (PS) for externalizing, and functional neural networks were identified using graph theory based network analysis. Tasks of inhibitory control and psychiatric diagnosis (alcohol/substance use disorders) were used to measure externalizing phenotypes.
A polygenic externalizing disorder score (PS) predicted connectivity in a brain circuit (10 nodes, nine links) centered on left amygdala that included several cortical [bilateral inferior frontal gyrus (IFG) pars triangularis, left rostral anterior cingulate cortex (rACC)] and subcortical (bilateral amygdala, hippocampus, and striatum) regions. Directional analyses revealed that bilateral amygdala influenced left prefrontal cortex (IFG) in participants scoring higher on the externalizing PS, whereas the opposite direction of influence was observed for those scoring lower on the PS. Polygenic variation was also associated with higher Participation Coefficient for bilateral amygdala and left rACC, suggesting that genes related to externalizing modulated the extent to which these nodes functioned as communication hubs.
Findings suggest that externalizing polygenic risk is associated with disrupted connectivity in a neural network implicated in emotion regulation, impulse control, and reinforcement learning. Results provide evidence that this network represents a genetically associated neurobiological vulnerability for externalizing disorders.
Posttraumatic stress disorder (PTSD) and stress/trauma exposure are cross-sectionally associated with advanced DNA methylation age relative to chronological age. However, longitudinal inquiry and examination of associations between advanced DNA methylation age and a broader range of psychiatric disorders is lacking. The aim of this study was to examine if PTSD, depression, generalized anxiety, and alcohol-use disorders predicted acceleration of DNA methylation age over time (i.e. an increasing pace, or rate of advancement, of the epigenetic clock).
Genome-wide DNA methylation and a comprehensive set of psychiatric symptoms and diagnoses were assessed in 179 Iraq/Afghanistan war veterans who completed two assessments over the course of approximately 2 years. Two DNA methylation age indices (Horvath and Hannum), each a weighted index of an array of genome-wide DNA methylation probes, were quantified. The pace of the epigenetic clock was operationalized as change in DNA methylation age as a function of time between assessments.
Analyses revealed that alcohol-use disorders (p = 0.001) and PTSD avoidance and numbing symptoms (p = 0.02) at Time 1 were associated with an increasing pace of the epigenetic clock over time, per the Horvath (but not the Hannum) index of cellular aging.
This is the first study to suggest that posttraumatic psychopathology is longitudinally associated with a quickened pace of the epigenetic clock. Results raise the possibility that accelerated cellular aging is a common biological consequence of stress-related psychopathology, which carries implications for identifying mechanisms of stress-related cellular aging and developing interventions to slow its pace.
Field studies were conducted in 2011 and 2012 at the Horticultural Crops Research Station near Clinton, NC, to determine ‘Covington' sweetpotato tolerance to S-metolachlor rate and application timing. Treatments were a factorial arrangement of four S-metolachlor rates (0, 1.1, 2.2, or 3.4 kg ai ha−1) and six application timings (0, 2, 5, 7, 9, or 14 d after transplanting [DAP]). Immediately following application, 1.9 cm of irrigation was applied to individual plots. Sweetpotato injury was minimal for all treatments (≤ 10%). No. 1 grade sweetpotato yield displayed a negative linear response to S-metolachlor rate, and decreased from 25,110 to 20,100 kg ha−1 as S-metolachlor rate increased from 0 to 3.4 kg ha−1. Conversely, no. 1 sweetpotato yield displayed a positive linear response to S-metolachlor application timing and increased from 19,670 to 27,090 kg ha−1 as timing progressed from 0 to 14 DAP. Total marketable sweetpotato yield displayed a quadratic response to both S-metolachlor application rate and timing. Total marketable yield decreased from 44,950 to 30,690 kg ha−1 as S-metolachlor rate increased from 0 to 3.4 kg ha−1. Total marketable yield increased from 37,800 to 45,780 kg ha−1 as application timing was delayed from 0 to 14 DAP. At 1.1 kg ha−1 S-metolachlor, sweetpotato storage root length to width ratio displayed a quadratic relationship to application timing and increased from 1.87 to 2.23 for applications made 0 to 14 DAP. At 2.2 kg ha−1 of S-metolachlor, sweetpotato length to width ratio displayed a quadratic response to application timing, increased from 1.57 to 2.09 for 0 to 10 DAP, and decreased slightly from 2.09 to 2.03 for 10 to 14 DAP. Application timing did not influence length to width ratio of sweetpotato storage roots for those plots treated with S-metolachlor at either 0 or 3.4 kg ha−1.
Introduction
The study of individual differences in resilience to traumatic stress has received unprecedented attention in recent years from investigators in the field of post-traumatic stress disorder (PTSD) but there remains a lack of consensus regarding the definition, measurement, and conceptualization of the construct. Trait personality psychologists have grappled with similar issues since the seminal work of Jack Block (1961) on the construct of ego resilience over 50 years ago. In the process, they have developed comprehensive models of personality and psychometrically sophisticated tools for the measurement of its traits that can potentially inform and advance the study of resilience. The primary purpose of this chapter is to review the literature on personality factors involved in resilience to traumatic stress and to outline a model for conceptualizing this interface.
Contemporary models of personality aim to identify the structure and basis for behavioral traits – defined as individual differences in patterns of thoughts, feelings, and actions that are consistent across developmental periods and environmental contexts. Personality models differ considerably with regard to the factor structure, number, and definition of specific traits. Because of this, research on personality traits that confer risk or resilience to the development of post-traumatic psychopathology has yielded a complicated collection of studies examining disparate constructs and measures. To provide coherence and organization to this literature, this chapter will focus on three broadband personality dimensions described by Tellegen (1985, 2000) that are also represented with subtle definitional variations in most other contemporary trait models of personality. For this reason, they are known as the “big three” personality factors: positive emotionality/extraversion (PEM), negative emotionality/neuroticism (NEM), and constraint/impulsivity (CON).