Biological embedding of maternal postpartum depressive symptoms: The potential role of cortisol and telomere length.

Although maternal postpartum depressive symptoms (PDS) are associated with child behavior problems, the underlying biological mechanisms are poorly understood. Thus, the current study focused on 193 healthy mother-child dyads and investigated child cortisol and telomere length as potential mediating factors. At 3 and 6 months postpartum, mothers reported on PDS. At age 6, children provided saliva and buccal swab samples. At age 10, mothers and children reported on child behavior problems. Structural equation modelling revealed (a) no association between PDS and child behavior problems and thus no possibility of mediation, but that (b) lower cortisol forecast more child-reported internalizing problems, and (c) shorter telomere length predicted more child-reported internalizing and externalizing problems. These findings raise mediational questions about the determinants of these biomarkers

Testing three hypotheses about effects of sensitive-insensitive parenting on telomeres.

Telomeres are the protective DNA-protein sequences appearing at the ends of chromosomes; they shorten with each cell division and are considered a biomarker of aging. Shorter telomere length and greater erosion have been associated with compromised physical and mental health and are hypothesized to be affected by early life stress. In the latter case, most work has relied on retrospective measures of early life stressors. The Dutch research (n = 193) presented herein tested 3 hypotheses prospectively regarding effects of sensitive-insensitive parenting during the first 2.5 years on telomere length at age 6, when first measured, and change over the following 4 years. It was predicted that (1) less sensitive parenting would predict shorter telomeres and greater erosion and that such effects would be most pronounced in children (2) exposed to prenatal stress and/or (3) who were highly negatively emotional as infants. Results revealed, only, that prenatal stress amplified parenting effects on telomere change-in a differential-susceptibility-related manner: Prenatally stressed children displayed more erosion when they experienced insensitive parenting and less erosion when they experienced sensitive parenting. Mechanisms that might initiate greater postnatal plasticity as a result of prenatal stress are highlighted and future work outlined. (PsycINFO Database Record (c) 2020 APA, all rights reserved)

Lie Algebras and Growth in Branch Groups

We compute the structure of the Lie algebras associated to two examples of branch groups, and show that one has finite width while the other, the ``Gupta-Sidki group'', has unbounded width. This answers a question by Sidki. More precisely, the Lie algebra of the Gupta-Sidki group has Gelfand-Kirillov dimension $\log3/\log(1+\sqrt2)$. We then draw a general result relating the growth of a branch group, of its Lie algebra, of its graded group ring, and of a natural homogeneous space we call "parabolic space", namely the quotient of the group by the stabilizer of an infinite ray. The growth of the group is bounded from below by the growth of its graded group ring, which connects to the growth of the Lie algebra by a product-sum formula, and the growth of the parabolic space is bounded from below by the growth of the Lie algebra. Finally we use this information to explicitly describe the normal subgroups of the "Grigorchuk group". All normal subgroups are characteristic, and the number of normal subgroups of index $2^n$ is odd and is asymptotically $n^{\log_2(3)}$

Beyond Time and Space:The Effect of a Lateralized Sustained Attention Task and Brain Stimulation on Spatial and Selective Attention

The Theory of Visual Attention (TVA) provides a mathematical formalisation of the “biased competition” account of visual attention. Applying this model to individual performance in a free recall task allows the estimation of 5 independent attentional parameters: visual short-term memory (VSTM) capacity, speed of information processing, perceptual threshold of visual detection; attentional weights representing spatial distribution of attention (spatial bias), and the top-down selectivity index. While the TVA focuses on selection in space, complementary accounts of attention describe how attention is maintained over time, and how temporal processes interact with selection. A growing body of evidence indicates that different facets of attention interact and share common neural substrates. The aim of the current study was to modulate a spatial attentional bias via transfer effects, based on a mechanistic understanding of the interplay between spatial, selective and temporal aspects of attention. Specifically, we examined here: (i) whether a single administration of a lateralized sustained attention task could prime spatial orienting and lead to transferable changes in attentional weights (assigned to the left vs right hemi-field) and/or other attentional parameters assessed within the framework of TVA (Experiment 1); (ii) whether the effects of such spatial-priming on TVA parameters could be further enhanced by bi-parietal high frequency transcranial random noise stimulation (tRNS) (Experiment 2). Our results demonstrate that spatial attentional bias, as assessed within the TVA framework, was primed by sustaining attention towards the right hemi-field, but this spatial-priming effect did not occur when sustaining attention towards the left. Furthermore, we show that bi-parietal high-frequency tRNS combined with the rightward spatial-priming resulted in an increased attentional selectivity. To conclude, we present a novel, theory-driven method for attentional modulation providing important insights into how the spatial and temporal processes in attention interact with attentional selection

The association of exposure, risk, and resiliency factors with PTSD among Jews and Arabs exposed to repeated acts of terrorism in Israel

Israel has faced ongoing terrorism since the beginning of the Al Aqsa Intifada in September 2000. The authors examined risk and resiliency factors associated with posttraumatic stress disorder (PTSD) among 1,117 Jews and 394 Arab adult citizens of Israel during August and September 2004 through telephone interviews. Probable PTSD was found among 6.6% of Jews and 18.0% of Arabs. Predictors of probable PTSD in a multivariate model for Jews were refusal to report income, being traditionally religious, economic and psychosocial resource loss, greater traumatic growth, and lower social support. For Arabs, predictors were low education and economic resource loss among those exposed to terrorism. Findings for only those directly exposed to terrorism were similar to those for the overall national sample.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/58032/1/20307_ftp.pd

Longitudinal changes of telomere length and epigenetic age related to traumatic stress and post-traumatic stress disorder

Several studies have reported an association between traumatic stress and telomere length suggesting that traumatic stress has an impact on ageing at the cellular level. A newly derived tool provides an additional means to investigate cellular ageing by estimating epigenetic age based on DNA methylation profiles. We therefore hypothesise that in a longitudinal study of traumatic stress both indicators of cellular ageing will show increased ageing. We expect that particularly in individuals that developed symptoms of post-traumatic stress disorder (PTSD) increases in these ageing parameters would stand out.From an existing longitudinal cohort study, ninety-six male soldiers were selected based on trauma exposure and the presence of symptoms of PTSD. All military personnel were deployed in a combat zone in Afghanistan and assessed before and 6 months after deployment. The Self-Rating Inventory for PTSD was used to measure the presence of PTSD symptoms, while exposure to combat trauma during deployment was measured with a 19-item deployment experiences checklist. These groups did not differ for age, gender, alcohol consumption, cigarette smoking, military rank, length, weight, or medication use. In DNA from whole blood telomere length was measured and DNA methylation levels were assessed using the Illumina 450K DNA methylation arrays. Epigenetic ageing was estimated using the DNAm age estimator procedure.The association of trauma with telomere length was in the expected direction but not significant (. B=. -10.2, p=. 0.52). However, contrary to our expectations, development of PTSD symptoms was associated with the reverse process, telomere lengthening (. B=. 1.91, p=. 0.018). In concordance, trauma significantly accelerated epigenetic ageing (. B=. 1.97, p=. 0.032) and similar to the findings in telomeres, development of PTSD symptoms was inversely associated with epigenetic ageing (. B=. -0.10, p=. 0.044). Blood cell count, medication and premorbid early life trauma exposure did not confound the results.Overall, in this longitudinal study of military personnel deployed to Afghanistan we show an acceleration of ageing by trauma. However, development of PTSD symptoms was associated with telomere lengthening and reversed epigenetic ageing. These findings warrant further study of a perhaps dysfunctional compensatory cellular ageing reversal in PTSD

Feline leukaemia virus: half a century since its discovery

In the early 1960s, Professor William (Bill) F.H. Jarrett was presented with a timeGÇôspace cluster of cats with lymphoma identified by a local veterinary practitioner, Harry Pfaff, and carried out experiments to find if the condition might be caused by a virus, similar to lymphomas noted previously in poultry and mice. In 1964, the transmission of lymphoma in cats and the presence of virus-like particles that resembled GÇÿthe virus of murine leukaemiasGÇÖ in the induced tumours were reported in Nature. These seminal studies initiated research on feline leukaemia virus (FeLV) and launched the field of feline retrovirology. This review article considers the way in which some of the key early observations made by Bill Jarrett and his coworkers have developed in subsequent years and discusses progress that has been made in the field since FeLV was first discovered

Neurobiological Mechanisms That Contribute to Stress-related Cocaine Use

The ability of stressful life events to trigger drug use is particularly problematic for the management of cocaine addiction due to the unpredictable and often uncontrollable nature of stress. For this reason, understanding the neurobiological processes that contribute to stress-related drug use is important for the development of new and more effective treatment strategies aimed at minimizing the role of stress in the addiction cycle. In this review we discuss the neurocircuitry that has been implicated in stress-induced drug use with an emphasis on corticotropin releasing factor actions in the ventral tegmental area (VTA) and an important pathway from the bed nucleus of the stria terminalis to the VTA that is regulated by norepinephrine via actions at beta adrenergic receptors. In addition to the neurobiological mechanisms that underlie stress-induced cocaine seeking, we review findings suggesting that the ability of stressful stimuli to trigger cocaine use emerges and intensifies in an intake-dependent manner with repeated cocaine self-administration. Further, we discuss evidence that the drug-induced neuroadaptations that are necessary for heightened susceptibility to stress-induced drug use are reliant on elevated levels of glucocorticoid hormones at the time of cocaine use. Finally, the potential ability of stress to function as a “stage setter” for drug use – increasing sensitivity to cocaine and drug-associated cues – under conditions where it does not directly trigger cocaine seeking is discussed. As our understanding of the mechanisms through which stress promotes drug use advances, the hope is that so too will the available tools for effectively managing addiction, particularly in cocaine addicts whose drug use is stress-driven