Childhood maltreatment and adulthood victimization:An evidence-based model

There is ample evidence showing that childhood maltreatment increases two to three fold the risk of victimization in adulthood. Various risk factors, including posttraumatic stress disorder (PTSD) symptoms, dissociation, self-blame, and alcohol abuse are related to revictimization. Although previous research examined associations between risk factors for revictimization, the evidence is limited and the proposed models mostly include a handful of risk factors. Therefore, it is critical to investigate a more comprehensive model explaining the link between childhood maltreatment and adulthood (re)victimization. Accordingly, this study tested a data-driven theoretical path model consisting of 33 variables (and their associations) that could potentially enhance understanding of factors explaining revictimization. Cross-sectional data derived from a multi-wave study were used for this investigation. Participants (N = 2156, age mean = 19.94, SD = 2.89) were first-year female psychology students in the Netherlands and New Zealand, who responded to a battery of questionnaires and performed two computer tasks. The path model created by structural equation modelling using modification indices showed that peritraumatic dissociation, PTSD symptoms, trauma load, loneliness, and drug use were important mediators. Attachment styles, maladaptive schemas, meaning in life, and sex motives connected childhood maltreatment to adulthood victimization via other factors (i.e., PTSD symptoms, risky sex behavior, loneliness, emotion dysregulation, and sex motives). The model indicated that childhood maltreatment was associated with cognitive patterns (e.g., anxious attachment style), which in turn were associated with emotional factors (e.g., emotion dysregulation), and then with behavioral factors (e.g., risky sex behavior) resulting in revictimization. The findings of the study should be interpreted in the light of the limitations. In particular, the cross-sectional design of the study hinders us from ascertaining that the mediators preceded the outcome variable. </p

Studying Millisecond Pulsars in X-rays

Millisecond pulsars represent an evolutionarily distinct group among rotation-powered pulsars. Outside the radio band, the soft X-ray range ($\sim 0.1$--10 keV) is most suitable for studying radiative mechanisms operating in these fascinating objects. X-ray observations revealed diverse properties of emission from millisecond pulsars. For the most of them, the bulk of radiation is of a thermal origin, emitted from small spots (polar caps) on the neutron star surface heated by relativistic particles produced in pulsar acceleration zones. On the other hand, a few other very fast rotating pulsars exhibit almost pure nonthermal emission generated, most probably, in pulsar magnetospheres. There are also examples of nonthermal emission detected from X-ray nebulae powered by millisecond pulsars, as well as from pulsar winds shocked in binary systems with millisecond pulsars as companions. These and other most important results obtained from X-ray observations of millisecond pulsars are reviewed in this paper, as well as results from the search for millisecond pulsations in X-ray flux of the radio-quite neutron star RX J1856.5-3754

Mutation of a single residue, β-glutamate-20, alters protein–lipid interactions of light harvesting complex II

It is well established that assembly of the peripheral antenna complex, LH2, is required for proper photosynthetic membrane biogenesis in the purple bacterium Rhodobacter sphaeroides. The underlying interactions are, as yet, not understood. Here we examined the relationship between the morphology of the photosynthetic membrane and the lipid–protein interactions at the LH2–lipid interface. The non-bilayer lipid, phosphatidylethanolamine, is shown to be highly enriched in the boundary lipid phase of LH2. Sequence alignments indicate a putative lipid binding site, which includes β-glutamate-20 and the adjacent carotenoid end group. Replacement of β-glutamate-20 with alanine results in significant reduction of phosphatidylethanolamine and concomitant raise in phosphatidylcholine in the boundary lipid phase of LH2 without altering the lipid composition of the bulk phase. The morphology of the LH2 housing membrane is, however, unaffected by the amino acid replacement. In contrast, simultaneous modification of glutamate-20 and exchange of the carotenoid sphaeroidenone with neurosporene results in significant enlargement of the vesicular membrane invaginations. These findings suggest that the LH2 complex, specifically β-glutamate-20 and the carotenoids' polar head group, contribute to the shaping of the photosynthetic membrane by specific interactions with surrounding lipid molecules

Conditioned fear and extinction learning performance and its association with psychiatric symptoms in active duty Marines

BACKGROUND: Posttraumatic Stress Disorder (PTSD) is a major public health concern, especially given the recent wars in Iraq and Afghanistan. Nevertheless, despite a sharp increase in the incidence of psychiatric disorders in returning veterans, empirically based prevention strategies are still lacking. To develop effective prevention and treatment strategies, it is necessary to understand the underlying biological mechanisms contributing to PTSD and other trauma related symptoms. METHODS: The “Marine Resiliency Study II” (MRS-II; October 2011–October 2013) Neurocognition project is an investigation of neurocognitive performance in Marines about to be deployed to Afghanistan. As part of this investigation, 1195 Marines and Navy corpsmen underwent a fear conditioning and extinction paradigm and psychiatric symptom assessment prior to deployment. The current study assesses (1) the effectiveness of the fear potentiated startle paradigm in producing fear learning and extinction and (2) the association of performance in the paradigm with baseline psychiatric symptom classes (healthy: n = 923, PTSD symptoms: n = 42, anxiety symptoms: n = 37, and depression symptoms: n = 12). RESULTS: Results suggest that the task was effective in producing differential fear learning and fear extinction in this cohort. Further, distinct patterns emerged differentiating the PTSD and anxiety symptom classes from both healthy and depression classes. During fear acquisition, the PTSD symptom group was the only group to show deficient discrimination between the conditioned stimulus (CS+) and safety cue (CS−), exhibiting larger startle responses during the safety cue compared to the healthy group. During extinction learning, the PTSD symptom group showed significantly less reduction in their CS+ responding over time compared to the healthy group, as well as reduced extinction of self-reported anxiety to the CS+ by the end of the extinction session. Conversely, the anxiety symptom group showed normal safety signal discrimination and extinction of conditioned fear, but exhibited increased baseline startle reactivity and potentiated startle to CS+, as well as higher self-reported anxiety to both cues. The depression symptom group showed similar physiological and self-report measures as the healthy group. DISCUSSION: These data are consistent with the idea that safety signal discrimination is a relatively specific marker of PTSD symptoms compared to general anxiety and depression symptoms. Further research is needed to determine if deficits in fear inhibition vs. exaggerated fear responding are separate biological “domains” across anxiety disorders that may predict differential biological mechanisms and possibly treatment needs. Future longitudinal analyses will examine whether poor learning of safety signals provides a marker of vulnerability to develop PTSD or is specific to symptom state

Method of Payment and Price, Overhead Rate : Lump Sum, December 16, 2008

In the aftermath of a traumatic event, many people suffer from psychological distress, but only a minority develops posttraumatic stress disorder (PTSD). Pre-trauma individual differences in fear conditioning, most notably reduced extinction learning, have been proposed as playing an important role in the etiology of PTSD. However, prospective data are lacking. In this study, we prospectively tested whether reduced extinction was a predictor for later posttraumatic stress. Dutch soldiers (N = 249) were administered a conditioning task before their four-month deployment to Afghanistan to asses individual differences in extinction learning. After returning home, posttraumatic stress was measured. Results showed that reduced extinction learning before deployment predicted subsequent PTSD symptom severity, over and beyond degree of pre-deployment stress symptoms, neuroticism, and exposure to stressors on deployment. The findings suggest that reduced extinction learning may play a role in the development of PTSD