1,323 research outputs found

    Making sense of social pretense: The effect of the dyad, sex and language ability in a large observational study of children’s behaviors in a social pretend play context

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    Pretend play with peers is purportedly an important driver of social development in the preschool period, however, fundamental questions regarding the features of children’s pretend play with a peer, and the effect of the dyad for pretend play, have been overlooked. The current study undertook detailed behavioral coding of social pretend play in 134 pairs of 5-year-old children (54% boys) in order to address three main aims: (i) describe the duration and proportion of children engaging in key social pretend play behaviors, namely, calls for attention, negotiation (comprising role assignment and joint proposals) and enactment of pretend play, (ii) examine the effect of the dyad in influencing the occurrence of different social pretend play behaviors, and (iii) assess the independent and combined effect of individual child characteristics (i.e., language ability and sex) that may influence social pretend play behaviors beyond the influence of the dyad. Results demonstrated the overwhelming effect of the dyad in shaping children’s social pretend play behaviors, with language ability and sex explaining relatively little of the total variability in play behaviors. Results are discussed considering the contribution that this type of study can make to theories of associations between children’s social development and social pretend play.LEGO Foundatio

    Impaired Competence for Pretense in Children with Autism: Exploring Potential Cognitive Predictors.

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    Lack of pretense in children with autism has been explained by a number of theoretical explanations, including impaired mentalising, impaired response inhibition, and weak central coherence. This study aimed to empirically test each of these theories. Children with autism (n=60) were significantly impaired relative to controls (n=65) when interpreting pretense, thereby supporting a competence deficit hypothesis. They also showed impaired mentalising and response inhibition, but superior local processing indicating weak central coherence. Regression analyses revealed that mentalising significantly and independently predicted pretense. The results are interpreted as supporting the impaired mentalising theory and evidence against competing theories invoking impaired response inhibition or a local processing bias. The results of this study have important implications for treatment and intervention

    Interaction between oxytocin receptor DNA methylation and genotype is associated with risk of postpartum depression in women without depression in pregnancy

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    Postpartum depression (PPD) affects up to 19% of women, negatively impacting maternal and infant health. Reductions in plasma oxytocin levels have been associated with PPD and heritability studies have established a genetic contribution. Epigenetic regulation of the oxytocin receptor gene (OXTR) has been demonstrated and we hypothesized that individual epigenetic variability at OXTR may impact the development of PPD and that such variability may be central to predicting risk. This case-control study is nested within the Avon Longitudinal Study of Parents and Children and included 269 cases with PPD and 276 controls matched on age group, parity, and presence or absence of depressive symptoms in pregnancy as assessed by the Edinburgh Postnatal Depression Scale. OXTR DNA methylation (CpG site -934) and genotype (rs53576 and rs2254298) were assayed from DNA extracted from blood collected during pregnancy. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for the association of elevated symptoms of PPD with genotype, methylation, and their interaction adjusted for psychosocial factors (n=500). There was evidence of an interaction between rs53576 and methylation in the OXTR gene amongst women who did not have depression prenatally but developed PPD (p interaction=0.026, adjusted for covariates, n=257). Those women with GG genotype showed 2.63 greater odds of PPD for every 10% increase in methylation level (95% CI: 1.37, 5.03), whereas methylation was unrelated to PPD amongst A carriers (OR=1.00, 95%CI: 0.58, 1.73). There was no such interaction among women with PPD and prenatal depression. These data indicate that epigenetic variation that decreases expression of OXTR in a susceptible genotype may play a contributory role in the etiology of postpartum depression

    CCL5 regulation of mucosal chlamydial immunity and infection

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    <p>Abstract</p> <p>Background</p> <p>Following genital chlamydial infection, an early T helper type 1 (Th1)-associated immune response precedes the activation and recruitment of specific Th1 cells bearing distinct chemokine receptors, subsequently leading to the clearance of <it>Chlamydia</it>. We have shown that CCR5, a receptor for CCL5, is crucial for protective chlamydial immunity. Our laboratory and others have also demonstrated that CCL5 deficiencies found in man and animals can increase the susceptibility and progression of infectious diseases by modulating mucosal immunity. These findings suggest the CCR5-CCL5 axis is necessary for optimal chlamydial immunity. We hypothesized CCL5 is required for protective humoral and cellular immunity against <it>Chlamydia</it>.</p> <p>Results</p> <p>The present study revealed that CCR5 and CCL5 mRNAs are elevated in the spleen, iliac lymph nodes (ILNs), and genital mucosa following <it>Chlamydia muriduram </it>challenge. Antibody (Ab)-mediated inhibition of CCL5 during genital chlamydial infection suppressed humoral and Th1 > Th2 cellular responses by splenic-, ILN-, and genital mucosa-derived lymphocytes. Antigen (Ag)-specific proliferative responses of CD4<sup>+ </sup>T cells from spleen, ILNs, and genital organs also declined after CCL5 inhibition.</p> <p>Conclusion</p> <p>The suppression of these responses correlated with delayed clearance of <it>C. muriduram</it>, which indicate chlamydial immunity is mediated by Th1 immune responses driven in part by CCL5. Taken together with other studies, the data show that CCL5 mediates the temporal recruitment and activation of leukocytes to mitigate chlamydial infection through enhancing adaptive mucosal humoral and cellular immunity.</p

    RPPA-based proteomics recognizes distinct epigenetic signatures in chronic lymphocytic leukemia with clinical consequences

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    The chronic lymphocytic leukemia (CLL) armamentarium has evolved significantly, with novel therapies that inhibit Bruton Tyrosine Kinase, PI3K delta and/or the BCL2 protein improving outcomes. Still, the clinical course of CLL patients is highly variable and most previously recognized prognostic features lack the capacity to predict response to modern treatments indicating the need for new prognostic markers. In this study, we identified four epigenetically distinct proteomic signatures of a large cohort of CLL and related diseases derived samples (n = 871) using reverse phase protein array technology. These signatures are associated with clinical features including age, cytogenetic abnormalities [trisomy 12, del(13q) and del(17p)], immunoglobulin heavy-chain locus (IGHV) mutational load, ZAP-70 status, Binet and Rai staging as well as with the outcome measures of time to treatment and overall survival. Protein signature membership was identified as predictive marker for overall survival regardless of other clinical features. Among the analyzed epigenetic proteins, EZH2, HDAC6, and loss of H3K27me3 levels were the most independently associated with poor survival. These findings demonstrate that proteomic based epigenetic biomarkers can be used to better classify CLL patients and provide therapeutic guidance

    A Study of Time-Dependent CP-Violating Asymmetries and Flavor Oscillations in Neutral B Decays at the Upsilon(4S)

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    We present a measurement of time-dependent CP-violating asymmetries in neutral B meson decays collected with the BABAR detector at the PEP-II asymmetric-energy B Factory at the Stanford Linear Accelerator Center. The data sample consists of 29.7 fb−1{\rm fb}^{-1} recorded at the ΄(4S)\Upsilon(4S) resonance and 3.9 fb−1{\rm fb}^{-1} off-resonance. One of the neutral B mesons, which are produced in pairs at the ΄(4S)\Upsilon(4S), is fully reconstructed in the CP decay modes J/ψKS0J/\psi K^0_S, ψ(2S)KS0\psi(2S) K^0_S, χc1KS0\chi_{c1} K^0_S, J/ψK∗0J/\psi K^{*0} (K∗0→KS0π0K^{*0}\to K^0_S\pi^0) and J/ψKL0J/\psi K^0_L, or in flavor-eigenstate modes involving D(∗)π/ρ/a1D^{(*)}\pi/\rho/a_1 and J/ψK∗0J/\psi K^{*0} (K∗0→K+π−K^{*0}\to K^+\pi^-). The flavor of the other neutral B meson is tagged at the time of its decay, mainly with the charge of identified leptons and kaons. The proper time elapsed between the decays is determined by measuring the distance between the decay vertices. A maximum-likelihood fit to this flavor eigenstate sample finds Δmd=0.516±0.016(stat)±0.010(syst)ps−1\Delta m_d = 0.516\pm 0.016 {\rm (stat)} \pm 0.010 {\rm (syst)} {\rm ps}^{-1}. The value of the asymmetry amplitude sin⁥2ÎČ\sin2\beta is determined from a simultaneous maximum-likelihood fit to the time-difference distribution of the flavor-eigenstate sample and about 642 tagged B0B^0 decays in the CP-eigenstate modes. We find sin⁥2ÎČ=0.59±0.14(stat)±0.05(syst)\sin2\beta=0.59\pm 0.14 {\rm (stat)} \pm 0.05 {\rm (syst)}, demonstrating that CP violation exists in the neutral B meson system. (abridged)Comment: 58 pages, 35 figures, submitted to Physical Review

    Measurement of the Branching Fraction for B- --> D0 K*-

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    We present a measurement of the branching fraction for the decay B- --> D0 K*- using a sample of approximately 86 million BBbar pairs collected by the BaBar detector from e+e- collisions near the Y(4S) resonance. The D0 is detected through its decays to K- pi+, K- pi+ pi0 and K- pi+ pi- pi+, and the K*- through its decay to K0S pi-. We measure the branching fraction to be B.F.(B- --> D0 K*-)= (6.3 +/- 0.7(stat.) +/- 0.5(syst.)) x 10^{-4}.Comment: 7 pages, 1 postscript figure, submitted to Phys. Rev. D (Rapid Communications

    Evidence for the Rare Decay B -> K*ll and Measurement of the B -> Kll Branching Fraction

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    We present evidence for the flavor-changing neutral current decay B→K∗ℓ+ℓ−B\to K^*\ell^+\ell^- and a measurement of the branching fraction for the related process B→Kℓ+ℓ−B\to K\ell^+\ell^-, where ℓ+ℓ−\ell^+\ell^- is either an e+e−e^+e^- or ÎŒ+Ό−\mu^+\mu^- pair. These decays are highly suppressed in the Standard Model, and they are sensitive to contributions from new particles in the intermediate state. The data sample comprises 123×106123\times 10^6 ΄(4S)→BBˉ\Upsilon(4S)\to B\bar{B} decays collected with the Babar detector at the PEP-II e+e−e^+e^- storage ring. Averaging over K(∗)K^{(*)} isospin and lepton flavor, we obtain the branching fractions B(B→Kℓ+ℓ−)=(0.65−0.13+0.14±0.04)×10−6{\mathcal B}(B\to K\ell^+\ell^-)=(0.65^{+0.14}_{-0.13}\pm 0.04)\times 10^{-6} and B(B→K∗ℓ+ℓ−)=(0.88−0.29+0.33±0.10)×10−6{\mathcal B}(B\to K^*\ell^+\ell^-)=(0.88^{+0.33}_{-0.29}\pm 0.10)\times 10^{-6}, where the uncertainties are statistical and systematic, respectively. The significance of the B→Kℓ+ℓ−B\to K\ell^+\ell^- signal is over 8σ8\sigma, while for B→K∗ℓ+ℓ−B\to K^*\ell^+\ell^- it is 3.3σ3.3\sigma.Comment: 7 pages, 2 postscript figues, submitted to Phys. Rev. Let

    Study of e+e- --> pi+ pi- pi0 process using initial state radiation with BABAR

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    The process e+e- --> pi+ pi- pi0 gamma has been studied at a center-of-mass energy near the Y(4S) resonance using a 89.3 fb-1 data sample collected with the BaBar detector at the PEP-II collider. From the measured 3pi mass spectrum we have obtained the products of branching fractions for the omega and phi mesons, B(omega --> e+e-)B(omega --> 3pi)=(6.70 +/- 0.06 +/- 0.27)10-5 and B(phi --> e+e-)B(phi --> 3pi)=(4.30 +/- 0.08 +/- 0.21)10-5, and evaluated the e+e- --> pi+ pi- pi0 cross section for the e+e- center-of-mass energy range 1.05 to 3.00 GeV. About 900 e+e- --> J/psi gamma --> pi+ pi- pi0 gamma events have been selected and the branching fraction B(J/psi --> pi+ pi- pi0)=(2.18 +/- 0.19)% has been measured.Comment: 21 pages, 37 postscript figues, submitted to Phys. Rev.
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