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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.
To determine whether probiotic prophylaxes reduce the odds of Clostridium difficile infection (CDI) in adults and children.
Individual participant data (IPD) meta-analysis of randomized controlled trials (RCTs), adjusting for risk factors.
We searched 6 databases and 11 grey literature sources from inception to April 2016. We identified 32 RCTs (n=8,713); among them, 18 RCTs provided IPD (n=6,851 participants) comparing probiotic prophylaxis to placebo or no treatment (standard care). One reviewer prepared the IPD, and 2 reviewers extracted data, rated study quality, and graded evidence quality.
Probiotics reduced CDI odds in the unadjusted model (n=6,645; odds ratio [OR] 0.37; 95% confidence interval [CI], 0.25–0.55) and the adjusted model (n=5,074; OR, 0.35; 95% CI, 0.23–0.55). Using 2 or more antibiotics increased the odds of CDI (OR, 2.20; 95% CI, 1.11–4.37), whereas age, sex, hospitalization status, and high-risk antibiotic exposure did not. Adjusted subgroup analyses suggested that, compared to no probiotics, multispecies probiotics were more beneficial than single-species probiotics, as was using probiotics in clinical settings where the CDI risk is ≥5%. Of 18 studies, 14 reported adverse events. In 11 of these 14 studies, the adverse events were retained in the adjusted model. Odds for serious adverse events were similar for both groups in the unadjusted analyses (n=4,990; OR, 1.06; 95% CI, 0.89–1.26) and adjusted analyses (n=4,718; OR, 1.06; 95% CI, 0.89–1.28). Missing outcome data for CDI ranged from 0% to 25.8%. Our analyses were robust to a sensitivity analysis for missingness.
Moderate quality (ie, certainty) evidence suggests that probiotic prophylaxis may be a useful and safe CDI prevention strategy, particularly among participants taking 2 or more antibiotics and in hospital settings where the risk of CDI is ≥5%.
Metsulfuron is used for POST control of spotted spurge in many warm-season turfgrasses. A suspected resistant (R) biotype of spotted spurge was collected from turfgrass in Georgia with a history of exclusive metsulfuron use. Research was conducted to evaluate the resistance level of this biotype to metsulfuron, efficacy of other mechanisms of action for control, and the molecular basis for resistance. Compared with a susceptible (S) biotype, the R biotype required >90 and >135 times greater metsulfuron rates to reach 50% injury and reduce biomass 50% from the nontreated, respectively. The R biotype was also resistant to trifloxysulfuron but was injured equivalent to the S biotype from dicamba, glyphosate, and triclopyr. Gene sequencing of the R biotype revealed a Trp574 to Leu substitution that has conferred resistance to acetolactate synthase (ALS) inhibitors in previous research. This is the first report of ALS resistance in spotted spurge. More importantly, this is the first report of a herbicide-resistant broadleaf weed from a turfgrass system in the United States.
is the only known uranyl oxide hydrate mineral that contains U4+,
and it has been proposed that ianthinite may be an important Pu4+
-bearing phase during the oxidative dissolution of spent nuclear fuel. The
crystal structure of ianthinite, orthorhombic, a 7.178(2),
b 11.473(2), c. 30.39(1) Å,
V 2502.7 Å3, Z = 4, space
group P21cn, has been solved by direct methods and refined by
least-squares methods to an R index of 9.7 % and a
wR index of 12.6 % using 888 unique observed [ | F | ≥
5σ | F | ] reflections. The structure contains both U6+ and
U4+. The U6+ cations are present as roughly linear
(U6+O2)2+ uranyl ions (Ur) that are in
turn coordinated by five O2-and OH located at the equatorial
positions of pentagonal bipyramids. The U4+ cations are
coordinated by O2-, OH and H2O in a distorted
octahedral arrangement. The Urφ5 and
U4+φ6 (φ: O2-, OH, H2O)
polyhedra link by sharing edges to form two symmetrically distinct sheets at
z z ≈ 0.0 and z ≈ 0.25 that are parallel to (001). The
sheets have the β-U3O8 sheet anion-topology. There are
five symmetrically distinct H2O groups located at z ≈ 0.125
between the sheets of Uφn polyhedra, and the sheets of
Uφn polyhedra are linked together only by hydrogen bonding to
the intersheet H2O groups. The crystal-chemical requirements of
U4+ and Pu4+ are very similar, indicating that
extensive Pu4+ ↔ U4+ substitution can occur within the
sheets of Uφn polyhedra in the structure of ianthinite.
Ostracodes have a wide geographical distribution in the Ordovician of Scotland. They are known from the Southern Uplands, the Girvan district, the Highland Border region and the Inner Hebrides. Overall, more than forty species are recorded. They occur in clastic and carbonate rocks indicative of a range of shallow to deeper marine-shelf environments. Though many of the faunas are allochthonous, broad patterns of ostracode palaeoenvironmental distribution can be elucidated, and elements of the shallow marine Leperditella and open marineshelf Anisocyamus associations (previously recorded from N America) are present. Indigenous faunas are absent from the deep marine sediments of the Southern Uplands Northern Belt. Ostracodes are known from the Arenig, Llanvirn, Caradoc and Ashgill series in Scotland; those of the latter two series have widest biostratigraphical value. In the Girvan district the Caradoc species ‘Ctenobolbina’ ventrospinosa, Krausella variata, Balticella deckeri and Monoceratella teres have correlative value with N America, whilst the Ashgill species Kinnekullea comma appears to be a locum for the anceps graptolite Biozone in Britain, Ireland and possibly the eastern Baltic. The ostracodes are of typical Laurentian affinity, but show progressive generic links with the Baltic region during the late Llanvirn–Caradoc interval, and by Ashgill times display species-level links with southern Britain and Ireland. These distributional patterns suggest approaching geographical proximity for the early Palaeozoic continents of Laurentia, Baltica and Avalonia, and the ability of some Ordovician ostracodes to cross the Iapetus Ocean.