John Mendelsohn: The Passing Paintings Brochure

Brochure for John Mendelsohn: The Passing Paintings at the Thomas J. Walsh Art Gallery, December 2, 2014 - February 27, 2015.https://digitalcommons.fairfield.edu/mendelsohn-ephemera/1000/thumbnail.jp

Nuclear targeting of Bax during apoptosis in human colorectal cancer cells

Homeostasis in colonic epithelial cells is regulated by the balance between proliferative activity and cell loss by apoptosis. Because epithelial cells at the apex of colonic crypts undergo apoptosis and proliferative activity is usually restricted to the base of the crypts, it has been proposed that the limited availability of growth factor-signals at the upper portions of the crypts may trigger apoptosis. In the present studies, we investigate the mechanism of apoptosis mediated by growth factor deprivation in colorectal carcinoma cells by delineating the possible involvement of Bax and its subcellular localization. We report that inhibition of Epidermal Growth Factor Receptor (EGFR) tyrosine kinase activity and downregulation of EGFR by anti-EGFR mAb 225 induces apoptosis in human colorectal carcinoma DiFi and FET cells. Induction of apoptosis was preceded by enhanced expression of newly synthesized Bax protein, and required protein synthesis. In the mAb 225-treated cells, Bax was redistributed from the cytosol to the nucleus and subsequently, to the nuclear membranes. The observed induction of Bax expression by mAb 225 was not associated with p53 induction. However, mAb 225 treatment also triggered relocalization of p53 from the cytosol to a nuclear membrane-bound form. Induction of Bax and its redistribution to the nucleus of DiFi cells during apoptosis was also demonstrated in response to butyrate, a physiological relevant molecule in colonic epithelial cells as it is the principal short-chain fatty acid produced by bacterial fermentation of dietary fiber in colonic epithelium. Using immunofluorescence and confocal microscopy, we observed that Bax is predominantly localized in the cytosol, but during apoptosis it is localized both inside and along the nuclear membrane. Taken together, these findings suggest that apoptosis induced by growth factor-deprivation or butyrate may involve the subcellular redistribution of Bax in human colorectal carcinoma cells

Histoire des " Big Five " : OCEAN des cinq grands facteurs de la personnalité. Introduction du Big Five Inventory français ou BFI-FR

International audienceLa description de la personnalité a été conçue à partir d'une variété de points de vue théoriques et à différents niveaux d'abstraction. Dans l'étude de la personnalité, l'unité la plus fréquemment utilisée pour mesurer les différences individuelles a été le trait. Un consensus semble se dégager actuellement sur une taxonomie générale des traits de la personnalité, les cinq facteurs de la personnalité, connus sous le nom des " Big Five ", expression introduite par Goldberg. Le but de cet article est de resituer l'élaboration de la version originale du Big Five Inventory (BFI) de John, Donahue et Kentle (1991) dans son histoire, et parmi les autres tests disponibles le " TDA ou trait descriptive adjective " de Goldberg et le " NEO PI-R ou NEO personality inventory revised " de Costa et McCrae. La revue reprend les différents stades de conceptualisation des catégories qui furent élaborées à partir d'une sélection d'adjectifs de dictionnaires permettant de différencier un individu d'un autre. Seuls les traits seront utilisés pour l'élaboration des trois tests mentionnés. Les " Big Five " retrouvés à partir d'analyses factorielles peuvent se résumer en cinq facteurs réplicables connus sous le nom de OCEAN ou CANOE de la personnalité, moyen mnémotechnique pour E (Extraversion, Énergie, Enthousiasme) ; A (Agréabilité, Altruisme, Affection) ; C (Conscience, Contrôle, Contrainte) ; N (Émotions Négatives, Névrosisme, Nervosité) ; O (Ouverture, Originalité, Ouverture d'esprit), ordre établi par les auteurs du BFI. La structure des " Big Five " regroupe à un haut niveau d'abstraction les points communs de la plupart des systèmes existant sur la description de la personnalité et met à disposition un modèle descriptif intégré pour des recherches sur la personnalité

Creating a Culture of Mentoring @ Your Library

The need to find and retain high quality leadership for libraries is one of the top seven issues for academic libraries. With a significant percentage of librarians planning to retire in the next decade, retaining professionals is imperative. Librarians must not only be retained, but mentored and developed for future leadership roles in the academic library community (Hisle, 2002). Creating a “culture of mentoring” helps the organization, individuals in the organization, and those with whom they interact. This culture provides integrity (accountability) throughout the organization, and opportunities for learning, for feedback and for improvement of performance throughout the organization. Libraries are using mentoring to orient new librarians, to assist them through the promotion and tenure process, and to provide information to librarians interested in advancement

Growth factors regulate heterogeneous nuclear ribonucleoprotein K expression and function

Epidermal Growth Factor (EGF) family of growth factors and their receptors regulate normal and cancerous epithelial cell proliferation, a process that can be suppressed by antireceptor blocking antibodies. To identify genes whose expression may be modulated by antireceptor blocking antibodies, we performed a differential display screen with cells grown in the presence or absence of antireceptor blocking antibodies; isolates from one cDNA clone were 100% identical to human heterogeneous nuclear ribonucleoprotein K (hnRNP K), a protein with a conserved KH motif and RGG boxes, has been implicated in such functions as sequence-specific DNA binding, transcription, RNA binding and nucleocytoplasmic shuttling. Both EGF and heregulin-β1 induced expression of hnRNP K mRNA and protein in human breast cancer cells. This growth factor-mediated hnRNP K expression was effectively blocked by pretreatment of cultures with humanized anti-EGF Receptor (EGFR) antibody C225, or anti-human epidermal growth factor receptor-2 (HER2) antibody. Anti-EGFR monoclonal antibody also caused regression of human tumor xenografts and reduction in hnRNP K levels in athymic mice. Samples from grade III human breast cancer contained more hnRNP K protein than samples from grade II cancer. Finally, overexpression of hnRNP K in breast cancer cells significantly increased target c-myc promoter activity and c-Myc protein, hnRNP K protein levels, and enhanced breast cancer cell proliferation and growth in an anchorage-independent manner. These results suggested that the activity of human EGF receptor family members regulates hnRNP K expression by extracellular growth promoting signals and that therapeutic humanized antibodies against EGFR and HER2 can effectively block this function

Functional consequence of the MET-T1010I polymorphism in breast cancer.

Major breast cancer predisposition genes, only account for approximately 30% of high-risk breast cancer families and only explain 15% of breast cancer familial relative risk. The HGF growth factor receptor MET is potentially functionally altered due to an uncommon germline single nucleotide polymorphism (SNP), MET-T1010I, in many cancer lineages including breast cancer where the MET-T1010I SNP is present in 2% of patients with metastatic breast cancer. Expression of MET-T1010I in the context of mammary epithelium increases colony formation, cell migration and invasion in-vitro and tumor growth and invasion in-vivo. A selective effect of MET-T1010I as compared to wild type MET on cell invasion both in-vitro and in-vivo suggests that the MET-T1010I SNP may alter tumor pathophysiology and should be considered as a potential biomarker when implementing MET targeted clinical trials

Inhibition of EGFR Signaling: All Mutations Are Not Created Equal

Gazdar and Minna discuss the context and implications of a research article that examines the transformation potential and response to inhibitors of specific EGFR mutations found in lung cancer