91 research outputs found

    Reliability of Transcriptional Cycles and the Yeast Cell-Cycle Oscillator

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    A recently published transcriptional oscillator associated with the yeast cell cycle provides clues and raises questions about the mechanisms underlying autonomous cyclic processes in cells. Unlike other biological and synthetic oscillatory networks in the literature, this one does not seem to rely on a constitutive signal or positive auto-regulation, but rather to operate through stable transmission of a pulse on a slow positive feedback loop that determines its period. We construct a continuous-time Boolean model of this network, which permits the modeling of noise through small fluctuations in the timing of events, and show that it can sustain stable oscillations. Analysis of simpler network models shows how a few building blocks can be arranged to provide stability against fluctuations. Our findings suggest that the transcriptional oscillator in yeast belongs to a new class of biological oscillators

    Being Mumā€™s Confidant, a Boon or Bane? Examining Gender Differences in the Association of Maternal Disclosure with Adolescentsā€™ Depressive Feelings

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    This article reports on a longitudinal study investigating gender differences in the association between maternal disclosure and adolescentsā€™ depressive symptoms. Little research has examined the relationship of parental disclosure to adolescentsā€™ depressive symptoms and research on sex differences is particularly lacking. In a sample of 428 families with a mean age of 13.36 (52% female) of the target adolescents, maternal and childrenā€™s disclosure and depressive symptoms were assessed twice with an interval of 4Ā years. Controlling for the quality of the parentā€“child relationship and levels of maternal depressive symptoms, the analyses revealed an interaction effect for childā€™s gender, moderating the effect of maternal disclosure on adolescentsā€™ depressive symptoms. Higher levels of maternal disclosure were accompanied by lower levels of depressive symptoms in girls and higher levels of depressive symptoms in boys. Gender differences in socialization, communication, individuation and social networks might explain why daughters and sons are differently affected by maternal disclosure

    Isolation in Globalizing Academic Fields: A Collaborative Autoethnography of Early Career Researchers

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    This study examines academic isolation ā€“ an involuntary perceived separation from the academic field to which one aspires to belong, associated with a perceived lack of agency in terms of oneā€™s engagement with the field ā€“ as a key challenge for researchers in increasingly globalized academic careers. While prior research describes early career researchersā€™ isolation in their institutions, we theorize early career researchersā€™ isolation in their academic fields and reveal how they attempt to mitigate isolation to improve their career prospects. Using a collaborative autoethnographic approach, we generate and analyze a dataset focused on the experiences of ten early career researchers in a globalizing business academic field known as Consumer Culture Theory. We identify bricolage practices, polycentric governance practices, and integration mechanisms that work to enhance early career researchersā€™ perceptions of agency and consequently mitigate their academic isolation. Our findings extend discussions on isolation and its role in new academic careers. Early career researchers, in particular, can benefit from a deeper understanding of practices that can enable them to mitigate isolation and reclaim agency as they engage with global academic fields

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    Protein Kinase C BetaII Peptide Inhibitor Exerts Cardioprotective Effects in Rat Cardiac Ischemia/Reperfusion Injury

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    Ischemia followed by reperfusion (I/R) in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. A cell-permeable protein kinase C (PKC) betaII peptide inhibitor was used to test the hypothesis that PKC betaII inhibition could attenuate PMN-induced cardiac dysfunction by suppression of superoxide production from PMNs and increase NO release from vascular endothelium. The effects of the PKC betaII peptide inhibitor were examined in isolated ischemic (20 min) and reperfused (45 min) rat hearts with PMNs. The PKC betaII inhibitor (10 microM; n = 7) significantly attenuated PMN-induced cardiac dysfunction compared with I/R hearts (n = 9) receiving PMNs alone in left ventricular developed pressure (LVDP) and the maximal rate of LVDP (+dP/dt(max)) cardiac function indices (p \u3c 0.01). The PKC betaII inhibitor at 10 microM significantly increased endothelial NO release from a basal value of 1.85 +/- 0.18 pmol NO/mg tissue to 3.49 +/- 0.62 pmol NO/mg tissue from rat aorta. It also significantly inhibited superoxide release (i.e., absorbance) from N-formyl-L-methionyl-L-leucyl-L-phenylalanine-stimulated rat PMNs from 0.13 +/- 0.01 to 0.02 +/- 0.004 (p \u3c 0.01) at 10 microM. Histological analysis of the left ventricle of representative rat hearts from each group showed that the PKC betaII peptide inhibitor-treated hearts experienced a marked reduction in PMN vascular adherence and infiltration into the postreperfused cardiac tissue compared with I/R + PMN hearts (p \u3c 0.01). These results suggest that the PKC betaII peptide inhibitor attenuates PMN-induced post-I/R cardiac contractile dysfunction by increasing endothelial NO release and by inhibiting superoxide release from PMNs

    Protein kinase C ƟII peptide inhibitor exerts cardioprotective effects in rat cardiac ischemia/reperfusion injury

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    Ischemia followed by reperfusion (I/R) in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. A cell-permeable protein kinase C (PKC) ƟII peptide inhibitor was used to test the hypothesis that PKC ƟII inhibition could attenuate PMN-induced cardiac dysfunction by suppression of superoxide production from PMNs and increase NO release from vascular endothelium. The effects of the PKC ƟII peptide inhibitor were examined in isolated ischemic (20 min) and reperfused (45 min) rat hearts with PMNs. The PKC ƟII inhibitor (10 ĀµM; n = 7) significantly attenuated PMN-induced cardiac dysfunction compared with I/R hearts (n = 9) receiving PMNs alone in left ventricular developed pressure (LVDP) and the maximal rate of LVDP (+dP/dtmax) cardiac function indices (p \u3c 0.01). The PKC ƟII inhibitor at 10 ĀµM significantly increased endothelial NO release from a basal value of 1.85 Ā± 0.18 pmol NO/mg tissue to 3.49 Ā± 0.62 pmol NO/mg tissue from rat aorta. It also significantly inhibited superoxide release (i.e., absorbance) from N-formyl-L-methionyl-L-leucyl-L-phenylalanine-stimulated rat PMNs from 0.13 Ā± 0.01 to 0.02 Ā± 0.004 (p \u3c 0.01) at 10 ĀµM. Histological analysis of the left ventricle of representative rat hearts from each group showed that the PKC ƟII peptide inhibitor-treated hearts experienced a marked reduction in PMN vascular adherence and infiltration into the postreperfused cardiac tissue compared with I/R + PMN hearts (p \u3c 0.01). These results suggest that the PKC ƟII peptide inhibitor attenuates PMN-induced post-I/R cardiac contractile dysfunction by increasing endothelial NO release and by inhibiting superoxide release from PMNs
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