Maladaptive trauma appraisals mediate the relation between attachment anxiety and PTSD symptom severity.

OBJECTIVE: In a large sample of community-dwelling older adults with histories of exposure to a broad range of traumatic events, we examined the extent to which appraisals of traumatic events mediate the relations between insecure attachment styles and posttraumatic stress disorder (PTSD) symptom severity. METHOD: Participants completed an assessment of adult attachment, in addition to measures of PTSD symptom severity, event centrality, event severity, and ratings of the A1 PTSD diagnostic criterion for the potentially traumatic life event that bothered them most at the time of the study. RESULTS: Consistent with theoretical proposals and empirical studies indicating that individual differences in adult attachment systematically influence how individuals evaluate distressing events, individuals with higher attachment anxiety perceived their traumatic life events to be more central to their identity and more severe. Greater event centrality and event severity were each in turn related to higher PTSD symptom severity. In contrast, the relation between attachment avoidance and PTSD symptoms was not mediated by appraisals of event centrality or event severity. Furthermore, neither attachment anxiety nor attachment avoidance was related to participants' ratings of the A1 PTSD diagnostic criterion. CONCLUSION: Our findings suggest that attachment anxiety contributes to greater PTSD symptom severity through heightened perceptions of traumatic events as central to identity and severe. (PsycINFO Database Record

Leaf Traits, Neighbors, and Abiotic Factors: Ways That Context Can Mediate the Impact of Invasive Species on Nitrogen Cycling

Species invasions are more prevalent than ever before. While the addition of a species can dramatically change critical ecosystem processes, factors that mediate the direction and magnitude of those impacts have received less attention. A better understanding of the factors that mediate invasion impacts on ecosystem functioning is needed in order to target which exotic species will be most harmful and which systems are most vulnerable. The role of invasion on nitrogen (N) cycling is particularly important since N cycling controls ecosystem services that provision human health, e.g. nutrient retention and water quality.

We conducted a meta-analysis and in-depth studies focused on the invasive grass species, Microstegium vimineum, to better understand how (i) plant characteristics, (ii) invader abundance and neighbor identity, and (iii) environmental conditions mediate the impacts of invasion on N pools and fluxes. The results of our global meta-analysis support the concept that invasive species and reference community traits such as leaf %N and leaf C:N are useful for understanding invasion impacts on soil N cycling, but that trait dissimilarities between invaded and reference communities are most informative. Regarding the in-depth studies of Microstegium, we did not find evidence to suggest that invasion increases net nitrification as other studies have shown. Instead, we found that an interaction between its abundance and the neighboring plant identify were important for determining soil nitrate concentrations and net nitrification rates in the greenhouse. In field, we found that variability in environmental conditions mediated the impact of Microstegium invasion on soil N pools and fluxes, primarily net ammonification, between sites through direct, indirect, and interactive pathways. Notably, we detected a scenario in which forest openness has a negative direct effect and indirect positive effect on ammonification in sites with high soil moisture and organic matter. Collectively, our findings suggest that dissimilarity in plant community traits, neighbor identity, and environmental conditions can be important drivers of invasion impacts on ecosystem N cycling and should be considered when evaluating the ecosystem impacts of invasive species across heterogeneous landscapes.

The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease.

Thymic graft-versus-host disease (tGVHD) can contribute to profound T cell deficiency and repertoire restriction after allogeneic BM transplantation (allo-BMT). However, the cellular mechanisms of tGVHD and interactions between donor alloreactive T cells and thymic tissues remain poorly defined. Using clinically relevant murine allo-BMT models, we show here that even minimal numbers of donor alloreactive T cells, which caused mild nonlethal systemic graft-versus-host disease, were sufficient to damage the thymus, delay T lineage reconstitution, and compromise donor peripheral T cell function. Furthermore, to mediate tGVHD, donor alloreactive T cells required trafficking molecules, including CCR9, L selectin, P selectin glycoprotein ligand-1, the integrin subunits alphaE and beta7, CCR2, and CXCR3, and costimulatory/inhibitory molecules, including Ox40 and carcinoembryonic antigen-associated cell adhesion molecule 1. We found that radiation in BMT conditioning regimens upregulated expression of the death receptors Fas and death receptor 5 (DR5) on thymic stromal cells (especially epithelium), while decreasing expression of the antiapoptotic regulator cellular caspase-8-like inhibitory protein. Donor alloreactive T cells used the cognate proteins FasL and TNF-related apoptosis-inducing ligand (TRAIL) (but not TNF or perforin) to mediate tGVHD, thereby damaging thymic stromal cells, cytoarchitecture, and function. Strategies that interfere with Fas/FasL and TRAIL/DR5 interactions may therefore represent a means to attenuate tGVHD and improve T cell reconstitution in allo-BMT recipients.

HIV/AIDS-related institutional mistrust among multiethnic men who have sex with men: effects on HIV testing and risk behaviors.

OBJECTIVE: To investigate relationships between institutional mistrust (systematic discrimination, organizational suspicion, and conspiracy beliefs), HIV risk behaviors, and HIV testing in a multiethnic sample of men who have sex with men (MSM), and to test whether perceived susceptibility to HIV mediates these relationships for White and ethnic minority MSM. METHOD: Participants were 394 MSM residing in Central Arizona (M age = 37 years). Three dimensions of mistrust were examined, including organizational suspicion, conspiracy beliefs, and systematic discrimination. Assessments of sexual risk behavior, HIV testing, and perceived susceptibility to HIV were made at study entry (T1) and again 6 months later (T2). RESULTS: There were no main effects of institutional mistrust dimensions or ethnic minority status on T2 risk behavior, but the interaction of systematic discrimination and conspiracy beliefs with minority status was significant such that higher levels of systematic discrimination and more conspiracy beliefs were associated with increased risk only among ethnic minority MSM. Higher levels of systematic discrimination were significantly related to lower likelihood for HIV testing, and the interaction of organizational suspicion with minority status was significant such that greater levels of organizational suspicion were related to less likelihood of having been tested for HIV among ethnic minority MSM. Perceived susceptibility did not mediate these relationships. CONCLUSION: Findings suggest that it is important to look further into the differential effects of institutional mistrust across marginalized groups, including sexual and ethnic minorities. Aspects of mistrust should be addressed in HIV prevention and counseling efforts.

Peer rejection and social information-processing factors in the development of aggressive behavior problems in children.

The relation between social rejection and growth in antisocial behavior was investigated. In Study 1,259 boys and girls (34% African American) were followed from Grades 1 to 3 (ages 6-8 years) to Grades 5 to 7 (ages 10-12 years). Early peer rejection predicted growth in aggression. In Study 2,585 boys and girls (16% African American) were followed from kindergarten to Grade 3 (ages 5-8 years), and findings were replicated. Furthermore, early aggression moderated the effect of rejection, such that rejection exacerbated antisocial development only among children initially disposed toward aggression. In Study 3, social information-processing patterns measured in Study 1 were found to mediate partially the effect of early rejection on later aggression. In Study 4, processing patterns measured in Study 2 replicated the mediation effect. Findings are integrated into a recursive model of antisocial development.

How Locally Designed Access and Use Controls Can Prevent the Tragedy of the Commons in a Mexican Small-Scale Fishing Community

The Seri people, a self-governed community of small-scale fishermen in the Gulf of California, Mexico, have ownership rights to fishing grounds where they harvest highly valuable commercial species of bivalves. Outsiders are eager to gain access, and the community has devised a set of rules to allow them in. Because Seri government officials keep all the economic benefits generated from granting this access for themselves, community members create alternative entry mechanisms to divert those benefits to themselves. Under Hardin’s model of the tragedy of the commons, this situation would eventually lead to the overexploitation of the fishery. The Seri people, however, are able to simultaneously maintain access and use controls for the continuing sustainability of their fishing grounds. Using insights from common- pool resources theory, I discuss how Seri community characteristics help mediate the conflict between collective action dilemmas and access and use controls.

The role of β-arrestins in the termination and transduction of G-protein-coupled receptor signals

β-arrestins are versatile adapter proteins that form complexes with most G-protein-coupled receptors (GPCRs) following agonist binding and phosphorylation of receptors by G-protein-coupled receptor kinases (GRKs). They play a central role in the interrelated processes of homologous desensitization and GPCR sequestration, which lead to the termination of G protein activation. β-arrestin binding to GPCRs both uncouples receptors from heterotrimeric G proteins and targets them to clathrincoated pits for endocytosis. Recent data suggest that β-arrestins also function as GPCR signal transducers. They can form complexes with several signaling proteins, including Src family tyrosine kinases and components of the ERK1/2 and JNK3 MAP kinase cascades. By recruiting these kinases to agonist-occupied GPCRs, β-arrestins confer distinct signaling activities upon the receptor. β-arrestin-Src complexes have been proposed to modulate GPCR endocytosis, to trigger ERK1/2 activation and to mediate neutrophil degranulation. By acting as scaffolds for the ERK1/2 and JNK3 cascades, β-arrestins both facilitate GPCR-stimulated MAP kinase activation and target active MAP kinases to specific locations within the cell. Thus, their binding to GPCRs might initiate a second wave of signaling and represent a novel mechanism of GPCR signal transduction.

Love is in the air: Sociality and pair bondedness influence sifaka reproductive signalling

© 2013 The Association for the Study of Animal Behaviour.Social complexity, often estimated by group size, is seen as driving the complexity of vocal signals, but its relation to olfactory signals, which arguably arose to function in nonsocial realms, remains underappreciated. That olfactory signals also may mediate within-group interaction, vary with social complexity and promote social cohesion underscores a potentially crucial link with sociality. To examine that link, we integrated chemical and behavioural analyses to ask whether olfactory signals facilitate reproductive coordination in a strepsirrhine primate, the Coquerel's sifaka, Propithecus coquereli. Belonging to a clade comprising primarily solitary, nocturnal species, the diurnal, group-living sifaka represents an interesting test case. Convergent with diurnal, group-living lemurids, sifakas expressed chemically rich scent signals, consistent with the social complexity hypothesis for communication. These signals minimally encoded the sex of the signaller and varied with female reproductive state. Likewise, sex and female fertility were reflected in within-group scent investigation, scent marking and overmarking. We further asked whether, within breeding pairs, the stability or quality of the pair's bond influences the composition of glandular signals and patterns of investigatory or scent-marking behaviour. Indeed, reproductively successful pairs tended to show greater similarity in their scent signals than did reproductively unsuccessful pairs, potentially through chemical convergence. Moreover, scent marking was temporally coordinated within breeding pairs and was influenced by past reproductive success. That olfactory signalling reflects social bondedness or reproductive history lends support to recent suggestions that the quality of relationships may be a more valuable proxy than group size for estimating social complexity. We suggest that olfactory signalling in sifakas is more complex than previously recognized and, as in other socially integrated species, can be a crucial mechanism for promoting group cohesion and maintaining social bonds. Thus, the evolution of sociality may well be reflected in the complexity of olfactory signalling.

Nutritional Control of L1 Arrest and Recovery in Caenorhabditis elegans by Insulin-like Peptides and Signaling

Animals must coordinate development with fluctuating nutrient availability. Nutrient availability governs post-embryonic development in Caenorhabditis elegans: larvae that hatch in the absence of food do not initiate post-embryonic development but enter "L1 arrest" (or "L1 diapause") and can survive starvation for weeks, while rapidly resume normal development once get fed. Insulin-like signaling (IIS) has been shown to be a key regulator of L1 arrest and recovery. However, the C. elegans genome encodes 40 insulin-like peptides (ILPs), and it is unknown which peptides participate in nutritional control of L1 arrest and recovery. Work in other contexts has identified putative receptor agonists and antagonists, but the extent of specificity versus redundancy is unclear beyond this distinction.

We measured mRNA expression dynamics with high temporal resolution for all 40 insulin-like genes during entry into and recovery from L1 arrest. Nutrient availability influences expression of the majority of insulin-like genes, with variable dynamics suggesting complex regulation. We identified 13 candidate agonists and 8 candidate antagonists based on expression in response to nutrient availability. We selected ten candidate agonists (daf-28, ins-3, ins-4, ins-5, ins-6, ins-7, ins-9, ins-26, ins-33 and ins-35) for further characterization in L1 stage larvae. We used destabilized reporter genes to determine spatial expression patterns. Expression of candidate agonists was largely overlapping in L1 stage larvae, suggesting a role of the intestine, chemosensory neurons ASI and ASJ, and the interneuron PVT in systemic control of L1 development. Transcriptional regulation of candidate agonists was most significant in the intestine, as if nutrient uptake was a more important influence on transcription than sensory perception. Scanning in the 5' upstream promoter region of these 40 ILPs, We found that transcription factor PQM-1 and GATA putative binding sites are depleted in the promoter region of antagonists. A novel motif was also found to be over-represented in ILPs.

Phenotypic analysis of single and compound deletion mutants did not reveal effects on L1 recovery/developmental dynamics, though simultaneous disruption of ins-4 and daf-28 extended survival of L1 arrest without enhancing thermal tolerance, while overexpression of ins-4, ins-6 or daf-28 shortened L1 survival. Simultaneous disruption of several ILPs showed a temperature independent, transient dauer phenotype. These results revealed the relative redundancy and specificity among agonistic ILPs.

TGF- β and steroid hormone (SH) signaling have been reported to control the dauer formation along with IIS. Our preliminary results suggest they may also mediate the IIS control of L1 arrest and recovery, as the expression of several key components of TGF-β and SH signaling pathway genes are negatively regulated by DAF-16, and loss-of-function of these genes partially represses daf-16 null phenotype in L1 arrest, and causes a retardation in L1 development.

In summary, my dissertation study focused on the IIS, characterized the dynamics and sites of ILPs expression in response to nutrient availability, revealed the function of specific agonistic ILPs in L1 arrest, and suggested potential cross-regulation among IIS, TGF-β signaling and SH signaling in controlling L1 arrest and recovery. These findings provide insights into how post-embryonic development is governed by insulin-like signaling and nutrient availability.

The spatiotemporal dynamics of autobiographical memory: neural correlates of recall, emotional intensity, and reliving.

We sought to map the time course of autobiographical memory retrieval, including brain regions that mediate phenomenological experiences of reliving and emotional intensity. Participants recalled personal memories to auditory word cues during event-related functional magnetic resonance imaging (fMRI). Participants pressed a button when a memory was accessed, maintained and elaborated the memory, and then gave subjective ratings of emotion and reliving. A novel fMRI approach based on timing differences capitalized on the protracted reconstructive process of autobiographical memory to segregate brain areas contributing to initial access and later elaboration and maintenance of episodic memories. The initial period engaged hippocampal, retrosplenial, and medial and right prefrontal activity, whereas the later period recruited visual, precuneus, and left prefrontal activity. Emotional intensity ratings were correlated with activity in several regions, including the amygdala and the hippocampus during the initial period. Reliving ratings were correlated with activity in visual cortex and ventromedial and inferior prefrontal regions during the later period. Frontopolar cortex was the only brain region sensitive to emotional intensity across both periods. Results were confirmed by time-locked averages of the fMRI signal. The findings indicate dynamic recruitment of emotion-, memory-, and sensory-related brain regions during remembering and their dissociable contributions to phenomenological features of the memories.

The liver kinase B1 is a central regulator of T cell development, activation, and metabolism.

T cell activation leads to engagement of cellular metabolic pathways necessary to support cell proliferation and function. However, our understanding of the signal transduction pathways that regulate metabolism and their impact on T cell function remains limited. The liver kinase B1 (LKB1) is a serine/threonine kinase that links cellular metabolism with cell growth and proliferation. In this study, we demonstrate that LKB1 is a critical regulator of T cell development, viability, activation, and metabolism. T cell-specific ablation of the gene that encodes LKB1 resulted in blocked thymocyte development and a reduction in peripheral T cells. LKB1-deficient T cells exhibited defects in cell proliferation and viability and altered glycolytic and lipid metabolism. Interestingly, loss of LKB1 promoted increased T cell activation and inflammatory cytokine production by both CD4(+) and CD8(+) T cells. Activation of the AMP-activated protein kinase (AMPK) was decreased in LKB1-deficient T cells. AMPK was found to mediate a subset of LKB1 functions in T lymphocytes, as mice lacking the α1 subunit of AMPK displayed similar defects in T cell activation, metabolism, and inflammatory cytokine production, but normal T cell development and peripheral T cell homeostasis. LKB1- and AMPKα1-deficient T cells each displayed elevated mammalian target of rapamycin complex 1 signaling and IFN-γ production that could be reversed by rapamycin treatment. Our data highlight a central role for LKB1 in T cell activation, viability, and metabolism and suggest that LKB1-AMPK signaling negatively regulates T cell effector function through regulation of mammalian target of rapamycin activity.

The origin and evolution of phototropins.

Plant phototropism, the ability to bend toward or away from light, is predominantly controlled by blue-light photoreceptors, the phototropins. Although phototropins have been well-characterized in Arabidopsis thaliana, their evolutionary history is largely unknown. In this study, we complete an in-depth survey of phototropin homologs across land plants and algae using newly available transcriptomic and genomic data. We show that phototropins originated in an ancestor of Viridiplantae (land plants + green algae). Phototropins repeatedly underwent independent duplications in most major land-plant lineages (mosses, lycophytes, ferns, and seed plants), but remained single-copy genes in liverworts and hornworts-an evolutionary pattern shared with another family of photoreceptors, the phytochromes. Following each major duplication event, the phototropins differentiated in parallel, resulting in two specialized, yet partially overlapping, functional forms that primarily mediate either low- or high-light responses. Our detailed phylogeny enables us to not only uncover new phototropin lineages, but also link our understanding of phototropin function in Arabidopsis with what is known in Adiantum and Physcomitrella (the major model organisms outside of flowering plants). We propose that the convergent functional divergences of phototropin paralogs likely contributed to the success of plants through time in adapting to habitats with diverse and heterogeneous light conditions.