IDENTIFICATION AND RETROSPECTIVE EVALUATION OF A FILARIOID NEMATODE SPECIES IN MANAGED GRASSHOPPER SPARROWS (AMMODRAMUS SAVANNARUM).

The grasshopper sparrow (Ammodramus savannarum) is a species of ground-dwelling passerine bird with 12 different subspecies. The Florida subspecies (Ammodramus savannarum floridanus) is classified as federally endangered, with the most common threats including habitat loss, nest predation, and floods. A managed breeding program was established at White Oak Conservation (Yulee, FL) in 2015 with eastern grasshopper sparrows (Ammodramus savannarum pratensis) as a model for breeding Florida grasshopper sparrows as part of an assurance colony. A filarioid parasite species (Aproctella sp.) was characterized by PCR after identification by blood films and postmortem examinations of both subspecies housed at White Oak Conservation. This Aproctella species was distinct from others with available sequence. Records from 157 eastern and Florida grasshopper sparrows were reviewed, and correlations between presence of filariasis and subspecies, sex, body condition score, and presence of systemic isosporosis, squamous metaplasia, coelomitis, airsacculitis, or a combination of conditions were investigated. Twenty-nine (18.5%) birds (13 of 71 Florida grasshopper sparrows; 16 of 86 eastern grasshopper sparrows) were positive for filariasis by blood film review, grossly or by tissue imprint at postmortem examination, or histologically. Filariasis was significantly correlated with systemic isosporosis, coelomitis, and airsacculitis; was not correlated with subspecies, sex, or squamous metaplasia; and had a questionable correlation with body condition score. This report provides evidence that this Aproctella species has potential to contribute to morbidity and mortality in the grasshopper sparrow. This information will be helpful for implementing effective measures against suspected vectors and for the development of best practice strategies for the health management of the species in breeding programs.

Fungi form interkingdom microbial communities in the primordial human gut that develop with gestational age.

Fungal and bacterial commensal organisms play a complex role in the health of the human host. Expansion of commensal ecology after birth is a critical period in human immune development. However, the initial fungal colonization of the primordial gut remains undescribed. To investigate primordial fungal ecology, we performed amplicon sequencing and culture-based techniques of first-pass meconium, which forms in the intestine prior to birth, from a prospective observational cohort of term and preterm newborns. Here, we describe fungal ecologies in the primordial gut that develop complexity with advancing gestational age at birth. Our findings suggest homeostasis of fungal commensals may represent an important aspect of human biology present even before birth. Unlike bacterial communities that gradually develop complexity, the domination of the fungal communities of some preterm infants by Saccromycetes, specifically Candida, may suggest a pathologic association with preterm birth.-Willis, K. A., Purvis, J. H., Myers, E. D., Aziz, M. M., Karabayir, I., Gomes, C. K., Peters, B. M., Akbilgic, O., Talati, A. J., Pierre, J. F. Fungi form interkingdom microbial communities in the primordial human gut that develop with gestational age.

The status-signaling property of self-esteem: the role of self-reported self-esteem and perceived self-esteem in personality judgments.

OBJECTIVE: The provision of information appears to be an important feature of self-esteem. The present studies examined whether self-esteem possesses a status-signaling property such that an individual's level of self-esteem is associated with how the individual is perceived by others. METHOD: In Study 1, trained judges watched brief videos of 157 participants and rated targets as having higher levels of self-esteem when the targets were believed to possess more positive personality characteristics. Study 2 found that participants (357 targets) were rated as having higher levels of self-esteem when they were given more positive personality evaluations by their friends and family members (1,615 perceivers). RESULTS: Consistent with the proposed status-signaling model, high levels of self-esteem were generally associated with the perception of positive personality characteristics. CONCLUSIONS: These findings are discussed in the context of an extended informational model of self-esteem consisting of both the status-tracking and status-signaling properties of self-esteem.

The fungal intestinal microbiota predict the development of bronchopulmonary dysplasia in very low birthweight newborns.

RATIONALE: Bronchopulmonary dysplasia (BPD) is the most common morbidity affecting very preterm infants. Gut fungal and bacterial microbial communities contribute to multiple lung diseases and may influence BPD pathogenesis. METHODS: We performed a prospective, observational cohort study comparing the multikingdom fecal microbiota of 144 preterm infants with or without moderate to severe BPD by sequencing the bacterial 16S and fungal ITS2 ribosomal RNA gene. To address the potential causative relationship between gut dysbiosis and BPD, we used fecal microbiota transplant in an antibiotic-pseudohumanized mouse model. Comparisons were made using RNA sequencing, confocal microscopy, lung morphometry, and oscillometry. RESULTS: We analyzed 102 fecal microbiome samples collected during the second week of life. Infants who later developed BPD showed an obvious fungal dysbiosis as compared to infants without BPD (NoBPD, p = 0.0398, permutational multivariate ANOVA). Instead of fungal communities dominated by Candida and Saccharomyces, the microbiota of infants who developed BPD were characterized by a greater diversity of rarer fungi in less interconnected community architectures. On successful colonization, the gut microbiota from infants with BPD augmented lung injury in the offspring of recipient animals. We identified alterations in the murine intestinal microbiome and transcriptome associated with augmented lung injury. CONCLUSIONS: The gut fungal microbiome of infants who will develop BPD is dysbiotic and may contribute to disease pathogenesis.

Congenital Disorders of Red Blood Cells.

See Bonus NeoBriefs videos and downloadable teaching slides Understanding the physiologic process of red blood cell development in utero and subsequent erythropoiesis in the neonate is crucial as this determines red blood cell structure and therefore function, which is vital to neonatal health. Infants frequently experience anemia, and special consideration must be given to the evaluation of these infants to determine the correct etiology. Traditionally, anemia is conceptualized in terms of inadequate red blood cell production, increased red blood cell destruction, or whole blood loss. This framework translates well to inherited red blood cell defects, which include genetic abnormalities in bone marrow productivity or structure of the red blood cell membrane, enzymes, or hemoglobin. This article highlights fetal and neonatal erythropoiesis and the underlying etiologies of the inherited red blood cell disorders, as well as reviews the appropriate diagnostic evaluation and next steps in management. It is imperative that neonatal clinicians remain informed about these disorders to enable early recognition and treatment, and ultimately to improve outcomes in affected infants.

Differential requirement for LAT and SLP-76 in GPVI versus T cell receptor signaling.

Mice deficient in the adaptor Src homology 2 domain-containing leukocyte phosphoprotein of 76 kD (SLP-76) exhibit a bleeding disorder and lack T cells. Linker for activation of T cells (LAT)-deficient mice exhibit a similar T cell phenotype, but show no signs of hemorrhage. Both SLP-76 and LAT are important for optimal platelet activation downstream of the collagen receptor, GPVI. In addition, SLP-76 is involved in signaling mediated by integrin alphaIIbbeta3. Because SLP-76 and LAT function coordinately in T cell signal transduction, yet their roles appear to differ in hemostasis, we investigated in detail the functional consequences of SLP-76 and LAT deficiencies in platelets. Previously we have shown that LAT(-/-) platelets exhibit defective responses to the GPVI-specific agonist, collagen-related peptide (CRP). Consistent with this, we find that surface expression of P-selectin in response to high concentrations of GPVI ligands is reduced in both LAT- and SLP-76-deficient platelets. However, platelets from LAT(-/-) mice, but not SLP-76(-/-) mice, aggregate normally in response to high concentrations of collagen and convulxin. Additionally, unlike SLP-76, LAT is not tyrosine phosphorylated after fibrinogen binding to integrin alphaIIbbeta3, and collagen-stimulated platelets deficient in LAT spread normally on fibrinogen-coated surfaces. Together, these findings indicate that while LAT and SLP-76 are equally required for signaling via the T cell antigen receptor (TCR) and pre-TCR, platelet activation downstream of GPVI and alphaIIbbeta3 shows a much greater dependency on SLP-76 than LAT.

Commentary - The Climate Change and Health Adaptation Program: Indigenous Climate Leaders' Championing Adaptation Effort. / Commentaire - Le Programme sur le changement climatique et l'adaptation du secteur de la santé : mesures d'adaptation mises en avant par les chefs de file autochtones en matière de climat.

The Climate Change and Health Adaptation Program (CCHAP) is a program within the First Nations Inuit Health Branch of Indigenous Services Canada (which was previously under the responsibility of Health Canada). The CCHAP supports Inuit and First Nation communities in mitigating and adapting to the health impacts of climate change. The impacts of climate change on Indigenous health can be observed in multiple areas including, but not limited to, food security, cultural medicines, mental health and landbased practices. This program seeks to address the needs of climate change and health in First Nation and Inuit communities to support resiliency and adaptation to a changing climate both now and in the future through its emphasis on youth and capacity building. The commentary is based on the Program's eleven years of experience working with and for Indigenous communities and provides an overview of the CCHAP model and the work it has and continues to support. This paper demonstrates three examples of community-based projects to mitigate and adapt to the health impacts of climate change to demonstrate climate change resiliency within Indigenous communities.

The Climate Change and Health Adaptation Program (CCHAP) for First Nations South of 60N directly supports First Nations communities to develop and undertake adaptation and mitigation projects to build upon their needs within a changing climate. This commentary outlines the CCHAP's work and history, and highlights three cases, in Selkirk First Nation, Arviat and The Mi'kmaw Climate Action, which demonstrate the work these communities have undertaken with support from the Program.

Le Programme sur le changement climatique et l'adaptation du secteur de la santé (PCCASS) pour les Premières Nations au nord du 60e parallèle apporte un soutien direct aux communautés des Premières Nations dans l'élaboration et la mise en oeuvre de projets d'adaptation et d'atténuation pour subvenir à leurs besoins dans le cadre d'un climat en mutation. Ce commentaire fournit un aperçu du travail et de l'historique du PCCASS et présente trois projets, sur le territoire de la Première Nation de Selkirk, à Arviat et sur le territoire Mi'kmaq, qui illustrent le travail entrepris par ces communautés avec le soutien du Programme.

Transmission probabilities of mouse parvovirus 1 to sentinel mice chronically exposed to serial dilutions of contaminated bedding.

Intermittent serodetection of mouse parvovirus (MPV) infections in animal facilities occurs frequently when soiled bedding sentinel mouse monitoring systems are used. We evaluated induction of seroconversion in naïve single-caged weanling ICR mice (n = 10 per group) maintained on 5-fold serially diluted contaminated bedding obtained from SCID mice persistently shedding MPV1e. Soiled bedding from the infected SCID mice was collected, diluted, and redistributed weekly to cages housing ICR mice to represent chronic exposure to MPV at varying prevalence in a research colony. Sera was collected every other week for 12 wk and evaluated for reactivity to MPV nonstructural and capsid antigens by multiplex fluorescent immunoassay. Mice were euthanized after seroconversion, and DNA extracted from lymph node and spleen was evaluated by quantitative PCR. Cumulative incidence of MPV infection for each of the 7 soiled bedding dilution groups (range, 1:5 to 1:78125 [v/v]) was 100%, 100%, 90%, 20%, 70%, 60%, and 20%, respectively. Most seropositive mice (78%) converted within the first 2 to 3 wk of soiled bedding exposure, correlating to viral exposure when mice were 4 to 7 wk of age. Viral DNA was detected in lymphoid tissues collected from all mice that were seropositive to VP2 capsid antigen, whereas viral DNA was not detected in lymphoid tissue of seronegative mice. These data indicate seroconversion occurs consistently in young mice exposed to high doses of virus equivalent to fecal MPV loads observed in acutely infected mice, whereas seroconversion is inconsistent in mice chronically exposed to lower doses of virus.

Quantitative genetics of plastron shape in slider turtles (Trachemys scripta).

Shape variation is widespread in nature and embodies both a response to and a source for evolution and natural selection. To detect patterns of shape evolution, one must assess the quantitative genetic underpinnings of shape variation as well as the selective environment that the organisms have experienced. Here we used geometric morphometrics to assess variation in plastron shell shape in 1314 neonatal slider turtles (Trachemys scripta) from 162 clutches of laboratory-incubated eggs from two nesting areas. Multivariate analysis of variance indicated that nesting area has a limited role in describing plastron shape variation among clutches, whereas differences between individual clutches were highly significant, suggesting a prominent clutch effect. The covariation between plastron shape and several possible maternal effect variables (yolk hormone levels and egg dimensions) was assessed for a subset of clutches and found to be negligible. We subsequently employed several recently proposed methods for estimating heritability from shape variables, and generalized a univariate approach to accommodate unequal sample sizes. Univariate estimates of shape heritability based on Procrustes distances yielded large values for both nesting populations (h2 approximately 0.86), and multivariate estimates of maximal additive heritability were also large for both nesting populations (h2max approximately 0.57). We also estimated the dominant trend in heritable shape change for each nesting population and found that the direction of shape evolution was not the same for the two sites. Therefore, although the magnitude of shape evolution was similar between nesting populations, the manner in which plastron shape is evolving is not. We conclude that the univariate approach for assessing quantitative genetic parameters from geometric morphometric data has limited utility, because it is unable to accurately describe how shape is evolving.

Ortho-quinones of benzene and estrogens induce hyperproliferation of human peripheral blood mononuclear cells.

Benzene is a known leukemogen. It has been hypothesized that benzene and natural estrogens initiate cancer by forming ortho-quinones (catechol quinones) that react with DNA in cells. These quinones form depurinating DNA adducts that generate the mutations leading to cancer. This study examined whether the treatment of normal human peripheral blood mononuclear cells with the ortho-quinones of benzene or estradiol would form DNA adducts and elicit an alteration in the proliferation of these cells. Both estradiol-3,4-quinone and benzene ortho-quinone formed depurinating DNA adducts and significantly increased the mitogen-induced proliferation of normal blood mononuclear cells. Immunophenotyping of the estradiol-3,4-quinone-treated blood cells indicated that monocyte/macrophage, natural killer and T-cells were particularly prone to hyperproliferation. Thus, DNA damage induced by the ortho-quinones of benzene and estradiol may promote the growth of human blood mononuclear cells, including those that appear in large numbers in leukemia and lymphoma.

Genetic influences on dynamic complexity of brain oscillations.

Human electroencephalogram (EEG) consists of complex aperiodic oscillations that are assumed to indicate underlying neural dynamics such as the number and degree of independence of oscillating neuronal networks. EEG complexity can be estimated using measures derived from nonlinear dynamic systems theory. Variations in such measures have been shown to be associated with normal individual differences in cognition and some neuropsychiatric disorders. Despite the increasing use of EEG complexity measures for the study of normal and abnormal brain functioning, little is known about genetic and environmental influences on these measures. Using the pointwise dimension (PD2) algorithm, this study assessed heritability of EEG complexity at rest in a sample of 214 young female twins consisting of 51 monozygotic (MZ) and 56 dizygotic (DZ) pairs. In MZ twins, intrapair correlations were high and statistically significant; in DZ twins, correlations were substantially smaller. Genetic analyses using linear structural equation modeling revealed high and significant heritability of EEG complexity: 62-68% in the eyes-closed condition, and 46-60% in the eyes-open condition. Results suggest that individual differences in the complexity of resting electrocortical dynamics are largely determined by genetic factors. Neurophysiological mechanisms mediating genetic variation in EEG complexity may include the degree of structural connectivity and functional differentiation among cortical neuronal assemblies.

Genetic and environmental influences on frontal EEG asymmetry: a twin study.

Research suggests that frontal EEG asymmetry (FA) is a relatively stable trait associated with individual differences in dispositional affect (affective style) and liability to mood disorders. If FA is genetically determined, it can potentially serve as an endophenotype in genetic studies of temperament and mood disorders. The purpose of this study was to assess heritability of FA as well as alpha band EEG power measured at different frontal recording sites. Resting EEG data from a population-based sample of 246 young adult female twins including 73 monozygotic (MZ) and 50 dizygotic (DZ) pairs were analyzed using linear structural equation modeling. FA measured at mid-frontal locations (F3 and F4) showed low but significant heritability, suggesting that 27% of the observed variance can be accounted for by genetic factors. There was no evidence for genetic influences on FA measured at lateral-frontal (F7 and F8) locations. In contrast, alpha band power was highly heritable at all four frontal sites (85-87%). These findings suggest that: (1) genetic influences on FA are very modest and therefore FA has a limited utility as an endophenotype for genetic studies of mood disorders and (2) prefrontal neural circuitry underlying individual differences in affective style is characterized by high developmental plasticity.

Macrophage activation and Fcgamma receptor-mediated signaling do not require expression of the SLP-76 and SLP-65 adaptors.

The Src-homology 2 domain-containing, leukocyte-specific phosphoprotein of 76 kDa (SLP-76) is a hematopoietic adaptor that plays a central role during immunoreceptor-mediated activation of T lymphocytes and mast cells and collagen receptor-induced activation of platelets. Despite similar levels of expression in macrophages, SLP-76 is not required for Fc receptor for immunoglobulin G (IgG; FcgammaR)-mediated activation. We hypothesized that the related adaptor SLP-65, which is also expressed in macrophages, may compensate for the loss of SLP-76 during FcgammaR-mediated signaling and functional events. To address this hypothesis, we examined bone marrow-derived macrophages (BMM) from wild-type (WT) mice or mice lacking both of these adaptors. Contrary to our expectations, SLP-76(-/-) SLP-65(-/-) BMM demonstrated normal FcgammaR-mediated activation, including internalization of Ig-coated sheep red blood cells and production of reactive oxygen intermediates. FcgammaR-induced biochemical events were normal in SLP-76(-/-) SLP-65(-/-) BMM, including phosphorylation of phospholipase C and the extracellular signaling-regulated kinases 1 and 2. To determine whether macrophages functioned normally in vivo, we infected WT and SLP-76(-/-) SLP-65(-/-) mice with sublethal doses of Listeria monocytogenes (LM), a bacterium against which the initial host defense is provided by activated macrophages. WT and SLP-76(-/-) SLP-65(-/-) mice survived acute, low-dose infection and showed no difference in the number of liver or spleen LM colony-forming units, a measure of the total body burden of this organism. Taken together, these data suggest that neither SLP-76 nor SLP-65 is required during FcgammaR-dependent signaling and functional events in macrophages.

Genetics, prefrontal cortex, and cognitive control: a twin study of event-related brain potentials in a response inhibition task.

Inhibition of prepotent responses plays a key role in cognitive executive control of goal-directed behavior. Response inhibition in Go/No-Go tasks elicits a distinct midfrontal ERP component, the N2, localized in previous studies to the anterior cingulate cortex. We assessed heritability of the No-Go N2 and the succeeding positive P3 component in 194 young female twins (52 monozygotic and 45 dizygotic pairs) who completed a cued version of the Continuous Performance Test. Genetic model-fitting analysis showed that about 60% of the variance in N2 and P3 amplitudes can be attributed to genetic factors, suggesting that frontal No-Go N2 and P3 components may index genetically transmitted individual differences in brain activity related to conflict processing and can potentially serve as endophenotypes for genetic studies of disorders characterized by neurobehavioral disinhibition.

Genetic influences on prepulse inhibition of startle reflex in humans.

Prepulse inhibition (PPI) is a suppression of the startle reflex that occurs when an intense startling stimulus is preceded by a weaker 'prepulse' stimulus. PPI deficits have been implicated in the biological bases of schizophrenia and some other neuropsychiatric disorders and proposed as a possible biological marker (endophenotype) for genetic studies. However, little is known about the genetic determination of PPI in humans. We examined acoustic eye-blink startle reflex and PPI in 142 young female twins (40 monozygotic and 31 dizygotic pairs) and conducted a biometrical genetic analysis using structural equation modeling. PPI showed significant heritability suggesting that over 50% of PPI variance in this sample can be attributed to genetic factors. Baseline startle magnitude showed higher heritability (about 70%).

Multifaceted, cross-generational costs of hybridization in sibling Drosophila species.

Maladaptive hybridization, as determined by the pattern and intensity of selection against hybrid individuals, is an important factor contributing to the evolution of prezygotic reproductive isolation. To identify the consequences of hybridization between Drosophila pseudoobscura and D. persimilis, we estimated multiple fitness components for F1 hybrids and backcross progeny and used these to compare the relative fitness of parental species and their hybrids across two generations. We document many sources of intrinsic (developmental) and extrinsic (ecological) selection that dramatically increase the fitness costs of hybridization beyond the well-documented F1 male sterility in this model system. Our results indicate that the cost of hybridization accrues over multiple generations and reinforcement in this system is driven by selection against hybridization above and beyond the cost of hybrid male sterility; we estimate a fitness loss of >95% relative to the parental species across two generations of hybridization. Our findings demonstrate the importance of estimating hybridization costs using multiple fitness measures from multiple generations in an ecologically relevant context; so doing can reveal intense postzygotic selection against hybridization and thus, an enhanced role for reinforcement in the evolution of populations and diversification of species.

Community-based participatory process--climate change and health adaptation program for Northern First Nations and Inuit in Canada.

OBJECTIVES: Health Canada's Program for Climate Change and Health Adaptation in Northern First Nation and Inuit Communities is unique among Canadian federal programs in that it enables community-based participatory research by northern communities. STUDY DESIGN: The program was designed to build capacity by funding communities to conduct their own research in cooperation with Aboriginal associations, academics, and governments; that way, communities could develop health-related adaptation plans and communication materials that would help in adaptation decision-making at the community, regional, national and circumpolar levels with respect to human health and a changing environment. METHODS: Community visits and workshops were held to familiarize northerners with the impacts of climate change on their health, as well as methods to develop research proposals and budgets to meet program requirements. RESULTS: Since the launch of the Climate Change and Health Adaptation Program in 2008, Health Canada has funded 36 community projects across Canada's North that focus on relevant health issues caused by climate change. In addition, the program supported capacity-building workshops for northerners, as well as a Pan-Arctic Results Workshop to bring communities together to showcase the results of their research. Results include: numerous films and photo-voice products that engage youth and elders and are available on the web; community-based ice monitoring, surveillance and communication networks; and information products on land, water and ice safety, drinking water, food security and safety, and traditional medicine. CONCLUSIONS: Through these efforts, communities have increased their knowledge and understanding of the health effects related to climate change and have begun to develop local adaptation strategies.

Time in a bottle: the evolutionary fate of species discrimination in sibling Drosophila species.

Disadvantageous hybridization favors the evolution of prezygotic isolating behaviors, generating a geographic pattern of interspecific mate discrimination where members of different species drawn from sympatric populations exhibit stronger preference for members of their own species than do individuals drawn from allopatric populations. Geographic shifts in species' boundaries can relax local selection against hybridization; under such scenarios the fate of enhanced species preference is unknown. Lineages established from populations in the region of sympatry that have been maintained as single-species laboratory cultures represent cases where allopatry has been produced experimentally. Using such cultures dating from the 1950s, we assess how Drosophila pseudoobscura and D. persimilis mate preferences respond to relaxed natural selection against hybridization. We found that the propensity to hybridize generally declines with increasing time in experimental allopatry, suggesting that maintaining enhanced preference for conspecifics may be costly. However, our data also suggest a strong role for drift in determining mating preferences once secondary allopatry has been established. Finally, we discuss the interplay between populations in establishing the presence or absence of patterns consistent with reinforcement.

An implicit theory of self-esteem: the consequences of perceived self-esteem for romantic desirability.

The provision of information appears to be an important property of self-esteem as evidenced by previous research concerning the status-tracking and status-signaling models of self-esteem. The present studies examine whether there is an implicit theory of self-esteem that leads individuals to assume targets with higher levels of self-esteem possess more desirable characteristics than those with lower levels of self-esteem. Across 6 studies, targets with ostensibly higher levels of self-esteem were generally rated as more attractive and as more desirable relationship partners than those with lower levels of self- esteem. It is important to note, however, that this general trend did not consistently emerge for female targets. Rather, female targets with high self-esteem were often evaluated less positively than those with more moderate levels of self-esteem. The present findings are discussed in the context of an extended informational model of self-esteem consisting of both the status-tracking and status-signaling properties of self-esteem.