298 research outputs found

    Meeting Couple and Coparenting Relationship Needs of Foster Caregivers: Perceptions of Georgia Child Welfare County Directors

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    Foster caregivers face many unique challenges that may cause strain on their couple/coparenting relationships. Though foster caregivers receive training to help them navigate certain challenges of fostering, there is a lack of resources dedicated to supporting their couple/coparenting relationships. In the study described in this article, we examined the perceptions of Georgia Division of Family and Children Services (DFCS) county directors regarding potential effects of providing healthy marriage and relationship education (HMRE) to foster caregivers. Findings suggest that DFCS directors are in favor of providing HMRE to foster parents but that barriers to doing so must be addressed

    Going it Alone: The Social and Emotional Life of Disconnected Youth

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    This study presents patterns across multiple dimensions of social isolation among a sample of military youth, and describes how these patterns are related to preceding risk factors and distal outcomes. The presentation will be of interest to professionals interested in strategies for fostering positive outcomes by developing and enhancing family and community support for at-risk youth populations

    Expanding Efficiency: Women\u27s Communication in Engineering

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    As engineering fields strive to be more inclusive of women, focusing on perceptions of women\u27s work is vital to understanding how women can succeed and the limitations they may face. One area in need of more attention is the connection between communication and women\u27s experiences in engineering. This article examines the gendered nature of writing labor in engineering, focusing on case studies of three women who were able to use writing effectively, yet how communication emerged as a gendered form of labor subject to gendered perceptions. While these women\u27s communication skills led to professional success, their association with writing echoes a historical division, where writing is viewed as less valuable than technical knowledge. This division has the potential to disadvantage women who are asked to take on more writing-related tasks. In addition, their writing and communication are subject to gendered perceptions of being ‘chatty’ or blunt rather than effective or efficient. Articulating these perceptions and attitudes can lead to a breakdown of the binary between writing and technical labor as well as appropriately valuing the contributions women make in engineering through writing

    A Monoclonal Antibody against p53 Cross-Reacts with Processing Bodies

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    The p53 tumor suppressor protein is an important regulator of cell proliferation and apoptosis. p53 can be found in the nucleus and in the cytosol, and the subcellular location is key to control p53 function. In this work, we found that a widely used monoclonal antibody against p53, termed Pab 1801 (Pan antibody 1801) yields a remarkable punctate signal in the cytoplasm of several cell lines of human origin. Surprisingly, these puncta were also observed in two independent p53-null cell lines. Moreover, the foci stained with the Pab 1801 were present in rat cells, although Pab 1801 recognizes an epitope that is not conserved in rodent p53. In contrast, the Pab 1801 nuclear staining corresponded to genuine p53, as it was upregulated by p53-stimulating drugs and absent in p53-null cells. We identified the Pab 1801 cytoplasmic puncta as P Bodies (PBs), which are involved in mRNA regulation. We found that, in several cell lines, including U2OS, WI38, SK-N-SH and HCT116, the Pab 1801 puncta strictly colocalize with PBs identified with specific antibodies against the PB components Hedls, Dcp1a, Xrn1 or Rck/p54. PBs are highly dynamic and accordingly, the Pab 1801 puncta vanished when PBs dissolved upon treatment with cycloheximide, a drug that causes polysome stabilization and PB disruption. In addition, the knockdown of specific PB components that affect PB integrity simultaneously caused PB dissolution and the disappearance of the Pab 1801 puncta. Our results reveal a strong cross-reactivity of the Pab 1801 with unknown PB component(s). This was observed upon distinct immunostaining protocols, thus meaning a major limitation on the use of this antibody for p53 imaging in the cytoplasm of most cell types of human or rodent origin

    Constitutively elevated levels of SOCS1 suppress innate responses in DF-1 immortalised chicken fibroblast cells.

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    The spontaneously immortalised DF-1 cell line is rapidly replacing its progenitor primary chicken embryo fibroblasts (CEFs) for studies on avian viruses such as avian influenza but no comprehensive study has as yet been reported comparing their innate immunity phenotypes. We conducted microarray analyses of DF-1 and CEFs, under both normal and stimulated conditions using chicken interferon-α (chIFN-α) and the attenuated infectious bursal disease virus vaccine strain PBG98. We found that DF-1 have an attenuated innate response compared to CEFs. Basal expression levels of Suppressor of Cytokine Signalling 1 (chSOCS1), a negative regulator of cytokine signalling in mammals, are 16-fold higher in DF-1 than in CEFs. The chSOCS1 “SOCS box” domain (which in mammals, interacts with an E3 ubiquitin ligase complex) is not essential for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1. Overexpression of SOCS1 in chIFN-α-stimulated DF-1 led to a relative decrease in expression of interferon-stimulated genes (ISGs; MX1 and IFIT5) and increased viral yield in response to PBG98 infection. Conversely, knockdown of SOCS1 enhanced induction of ISGs and reduced viral yield in chIFN-α-stimulated DF-1. Consequently, SOCS1 reduces induction of the IFN signalling pathway in chicken cells and can potentiate virus replication

    Cyclin-Dependent Kinase Activity Controls the Onset of the HCMV Lytic Cycle

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    The onset of human cytomegalovirus (HCMV) lytic infection is strictly synchronized with the host cell cycle. Infected G0/G1 cells support viral immediate early (IE) gene expression and proceed to the G1/S boundary where they finally arrest. In contrast, S/G2 cells can be infected but effectively block IE gene expression and this inhibition is not relieved until host cells have divided and reentered G1. During latent infection IE gene expression is also inhibited, and for reactivation to occur this block to IE gene expression must be overcome. It is only poorly understood which viral and/or cellular activities maintain the block to cell cycle or latency-associated viral IE gene repression and whether the two mechanisms may be linked. Here, we show that the block to IE gene expression during S and G2 phase can be overcome by both genotoxic stress and chemical inhibitors of cellular DNA replication, pointing to the involvement of checkpoint-dependent signaling pathways in controlling IE gene repression. Checkpoint-dependent rescue of IE expression strictly requires p53 and in the absence of checkpoint activation is mimicked by proteasomal inhibition in a p53 dependent manner. Requirement for the cyclin dependent kinase (CDK) inhibitor p21 downstream of p53 suggests a pivotal role for CDKs in controlling IE gene repression in S/G2 and treatment of S/G2 cells with the CDK inhibitor roscovitine alleviates IE repression independently of p53. Importantly, CDK inhibiton also overcomes the block to IE expression during quiescent infection of NTera2 (NT2) cells. Thus, a timely block to CDK activity not only secures phase specificity of the cell cycle dependent HCMV IE gene expression program, but in addition plays a hitherto unrecognized role in preventing the establishment of a latent-like state

    Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor

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    Cellular senescence suppresses cancer by arresting cell proliferation, essentially permanently, in response to oncogenic stimuli, including genotoxic stress. We modified the use of antibody arrays to provide a quantitative assessment of factors secreted by senescent cells. We show that human cells induced to senesce by genotoxic stress secrete myriad factors associated with inflammation and malignancy. This senescence-associated secretory phenotype (SASP) developed slowly over several days and only after DNA damage of sufficient magnitude to induce senescence. Remarkably similar SASPs developed in normal fibroblasts, normal epithelial cells, and epithelial tumor cells after genotoxic stress in culture, and in epithelial tumor cells in vivo after treatment of prostate cancer patients with DNA-damaging chemotherapy. In cultured premalignant epithelial cells, SASPs induced an epithelial–mesenchyme transition and invasiveness, hallmarks of malignancy, by a paracrine mechanism that depended largely on the SASP factors interleukin (IL)-6 and IL-8. Strikingly, two manipulations markedly amplified, and accelerated development of, the SASPs: oncogenic RAS expression, which causes genotoxic stress and senescence in normal cells, and functional loss of the p53 tumor suppressor protein. Both loss of p53 and gain of oncogenic RAS also exacerbated the promalignant paracrine activities of the SASPs. Our findings define a central feature of genotoxic stress-induced senescence. Moreover, they suggest a cell-nonautonomous mechanism by which p53 can restrain, and oncogenic RAS can promote, the development of age-related cancer by altering the tissue microenvironment

    Ecology of Juvenile Salmon in Shallow Tidal Freshwater Habitats of the Lower Columbia River, 2007?2010

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    The TFM study was designed to investigate the ecology and early life history of juvenile salmonids within shallow (<5 m) tidal freshwater habitats of the LCRE. We started collecting field data in June 2007. Since then, monthly sampling has occurred in the vicinity of the Sandy River delta (rkm 192–208) and at other sites and times in lower river reaches of tidal freshwater (rkm 110 to 141). This report provides a comprehensive synthesis of data covering the field period from June 2007 through April 2010
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