20 research outputs found

    Never Let Them See You Cry: Self-Presentation as a Moderator of the Relationship Between Exclusion and Self-Esteem

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    A debate exists concerning whether exclusion harms self-esteem. We hypothesized that social exclusion does harm self-esteem, but that this effect is evident only when self-presentational concerns to appear fine are minimal or people are unable to alter their report of self-esteem. In the first three studies, participants\u27 explicit and implicit self-esteem were measured following an exclusion or comparison condition where self-presentational pressures were likely high. Because respondents can easily control their reports on explicit measures, but not on implicit ones, we hypothesized that exclusion would result in lower self-esteem only when implicit measures were used. Results confirmed this hypothesis. In the final study, self-presentational concerns were directly manipulated. When self-presentational concerns were high, only implicit self-esteem was lowered by exclusion. But, when such concerns were low, this impact on self-esteem was seen on implicit and explicit measures. Implications for the sociometer hypothesis and the recent self-esteem debate are discussed

    Time course of the MuRF1-hiLUCs reporter induction and extent of muscle atrophy following dexamethasone treatment.

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    <p>(<b>A</b>) MuRF1-hiLUCs reporter rats were given either 600 ug/kg of dexamethasone or saline via i.p. for three consecutives days. <i>In vivo</i> images of ventral and right lateral views were acquired before treatments (baseline) and then daily thereafter, starting 24 hours after the first dose, until day 7. Shown are the ventral and lateral images of a representative rat from day 1- day 5. (<b>B</b>) Quantitation of the fold induction of luminescent intensity of the MuRF1-hiLUCs reporter during the time course of the dexamethasone (n = 10 for day 1–5, n = 9 for day 7) or saline (n = 8) treatment. Five distinct ROIs were chosen for the quantitation. Fold inductions were calculated over baseline values. Data are presented as means (symbols) <u>+</u> SEM (lines). Statistics were performed using ordinary two-way ANOVA with Dunnett's multiple comparisons test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. (<b>C</b>) Induction of the MuRF1-hiLUCs reporter in dissected skeletal muscles after dexamethasone treatment. MuRF1-hiLUCs reporter rats treated identically as indicated above but then sacrificed on day 3, one day after the last dosing. Skeletal muscles and otherwise indicated tissues were dissected out immediately after the luciferin injection and placed in a 6-well dish for visualization. The experiment shown is representative of three independent experiments. (<b>D</b>) Quantitation of the extent of hindlimb muscle atrophy in MuRF1-hiLUCs reporter rat after 7 days of dexamethasone treatment. All muscle weights were normalized to body weights and presented as percent of normalized muscle weights from control rats. CSA analysis for the tibialis anterior muscle was performed as described in the methods. Data are presented as mean (symbols) <u>+</u> SEM (lines). Statistics were performed using one-way or 2way ANOVA with Tukey's multiple comparisons test. **P<0.01, ***P<0.001, ****P<0.0001.</p

    Targeted insertion strategy for creating the MuRF1-hiLUCs knockin rat.

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    <p>An HCV-IRES-Luciferase-2A-SEAP reporter was inserted into the last intron of the endogenous MuRF1 gene via ZFN targeting (exons green with white numbers). In order to preserve the MuRF1 endogenous coding sequence and properly align the reporter ORF, a reconstructed last exon (exon 9) of the MuRF1 gene was included in the insertion cassette. This resulted in the shifting down of the original genomic exon 9 after knockin of the reporter cassette while leaving the 3′UTR intact. Founder #30 and two other founders were identified as valid MuRF1-hiLUCs knockin founder lines.</p

    Noninvasive Imaging of <i>In Vivo</i> MuRF1 Expression during Muscle Atrophy

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    <div><p>Numerous human diseases can lead to atrophy of skeletal muscle, and loss of this tissue has been correlated with increased mortality and morbidity rates. Clinically addressing muscle atrophy remains an unmet medical need, and the development of preclinical tools to assist drug discovery and basic research in this effort is important for advancing this goal. In this report, we describe the development of a bioluminescent gene reporter rat, based on the zinc finger nuclease-targeted insertion of a bicistronic luciferase reporter into the 3′ untranslated region of a muscle specific E3 ubiquitin ligase gene, MuRF1 (Trim63). In longitudinal studies, we noninvasively assess atrophy-related expression of this reporter in three distinct models of muscle loss (sciatic denervation, hindlimb unloading and dexamethasone-treatment) and show that these animals are capable of generating refined detail on <i>in vivo</i> MuRF1 expression with high temporal and anatomical resolution.</p></div
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