45 research outputs found
Emeline Renz, CSCJ Supplemental Assignments, Spring 2020
No full textCSCJ Supplemental Assignments, Spring 2020. Submitted by Emeline Renz, GIS Coordinator, Sociology and Criminal Justice Department, Clark Atlanta University
Emeline Renz, Clark Atlanta University, April 20, 2020
No full textStatement submitted by Emeline Renz, GIS Coordinator (Faculty/Staff), Sociology and Criminal Justice Department, Clark Atlanta University
SprG1/SprF1, un système toxine-antitoxine de staphylococcus aureus : caractérisation, analyse du targetome de l’antitoxine SprF1 et lien avec la tolérance aux antibiotiques
No full textSlow-growing bacteria, referred as tolerant and persistent, are able to survive antibiotics, which contributes to treatment failures and relapsing infections. Among others, type I toxin-antitoxin (TA) systems have been linked to slow-growing bacteria formation. In Staphylococcus aureus, a major human pathogen, the SprF1 RNA antitoxin belonging to the type I SprG1/SprF1 TA system, can bind ribosomes to inhibit global translation and promote persister cells formation. To better understand the role of SprF1 in S. aureus antibiotic adaptation, we studied the regulation of the SprG1/SprF1 system and deciphered the SprF1 targetome. Using in silico analyses and MAPS (MS2 Affinity Purification coupled with RNA Sequencing), we uncovered 12 SprF1 mRNA targets, including sprG1 mRNA. Then, we demonstrated that SprF1 interacts, in vitro, with the yidC and rpmE2 mRNAs, the former encoding a protein insertase and the latter the ribosomal protein L31, and that this interaction can modulate YidC and RpmE2 protein expression. Subsequently, we observed that rpmE2 overexpression promotes antibiotic tolerance, which could contribute to the persistence phenotype induced by SprF1. Altogether, these findings highlight that some type I RNA antitoxins behave like typical regulatory RNAs, by interacting with several targets to participate in bacteria adaptation to their environment.Les bactéries au métabolisme ralenti (tolérantes et persistantes) sont capables de survivre aux antibiotiques ce qui contribue à l’échec des traitements et à la rechute des infections. Les systèmes toxine-antitoxine (TA) font partie des mécanismes participant à la formation des bactéries tolérantes/persistantes. Chez Staphylococcus aureus, un pathogène humain majeur, l’antitoxine ARN SprF1 appartenant au système TA de type I SprG1/SprF1, peut se fixer sur les ribosomes ce qui entraine une atténuation de la traduction et favorise la formation des bactéries persistantes. Afin de mieux comprendre le rôle de SprF1 dans l’adaptation de S. aureus aux antibiotiques, nous nous sommes intéressés à l’étude de la régulation du système SprG1/SprF1 et à l’identification du targetome de SprF1. Par des approches in silico et par la technique MAPS (MS2 Affinity Purification coupled with RNA Sequencing), nous avons mis en évidence 12 cibles ARNm de SprF1, dont l’ARNm sprG1. Nous avons ensuite démontré que SprF1 interagi, in vitro, avec les ARNm yidC et rpmE2, le premier codant une protéine insertase et le second la protéine ribosomale L31, et que cette interaction entraîne une modulation de l’expression des protéines YidC et RpmE2. Par la suite, nous avons observé que la surexpression de rpmE2 favorise la tolérance aux antibiotiques ce qui pourrait contribuer au phénotype de persistance induit par SprF1. Les résultats présentés dans ce travail de thèse montrent donc que certaines antitoxines de type I agissent comme des ARN régulateurs typiques qui, en interagissant avec plusieurs cibles, ont un rôle dans l’adaptation des bactéries à leur environnement
SprG1/SprF1, a Staphylococcus aureus toxin-antitoxin system : characterization, deciphering of the SprF1 antitoxin targetome and link to antibiotic tolerance
No full textLes bactéries au métabolisme ralenti (tolérantes et persistantes) sont capables de survivre aux antibiotiques ce qui contribue à l’échec des traitements et à la rechute des infections. Les systèmes toxine-antitoxine (TA) font partie des mécanismes participant à la formation des bactéries tolérantes/persistantes. Chez Staphylococcus aureus, un pathogène humain majeur, l’antitoxine ARN SprF1 appartenant au système TA de type I SprG1/SprF1, peut se fixer sur les ribosomes ce qui entraine une atténuation de la traduction et favorise la formation des bactéries persistantes. Afin de mieux comprendre le rôle de SprF1 dans l’adaptation de S. aureus aux antibiotiques, nous nous sommes intéressés à l’étude de la régulation du système SprG1/SprF1 et à l’identification du targetome de SprF1. Par des approches in silico et par la technique MAPS (MS2 Affinity Purification coupled with RNA Sequencing), nous avons mis en évidence 12 cibles ARNm de SprF1, dont l’ARNm sprG1. Nous avons ensuite démontré que SprF1 interagi, in vitro, avec les ARNm yidC et rpmE2, le premier codant une protéine insertase et le second la protéine ribosomale L31, et que cette interaction entraîne une modulation de l’expression des protéines YidC et RpmE2. Par la suite, nous avons observé que la surexpression de rpmE2 favorise la tolérance aux antibiotiques ce qui pourrait contribuer au phénotype de persistance induit par SprF1. Les résultats présentés dans ce travail de thèse montrent donc que certaines antitoxines de type I agissent comme des ARN régulateurs typiques qui, en interagissant avec plusieurs cibles, ont un rôle dans l’adaptation des bactéries à leur environnement.Slow-growing bacteria, referred as tolerant and persistent, are able to survive antibiotics, which contributes to treatment failures and relapsing infections. Among others, type I toxin-antitoxin (TA) systems have been linked to slow-growing bacteria formation. In Staphylococcus aureus, a major human pathogen, the SprF1 RNA antitoxin belonging to the type I SprG1/SprF1 TA system, can bind ribosomes to inhibit global translation and promote persister cells formation. To better understand the role of SprF1 in S. aureus antibiotic adaptation, we studied the regulation of the SprG1/SprF1 system and deciphered the SprF1 targetome. Using in silico analyses and MAPS (MS2 Affinity Purification coupled with RNA Sequencing), we uncovered 12 SprF1 mRNA targets, including sprG1 mRNA. Then, we demonstrated that SprF1 interacts, in vitro, with the yidC and rpmE2 mRNAs, the former encoding a protein insertase and the latter the ribosomal protein L31, and that this interaction can modulate YidC and RpmE2 protein expression. Subsequently, we observed that rpmE2 overexpression promotes antibiotic tolerance, which could contribute to the persistence phenotype induced by SprF1. Altogether, these findings highlight that some type I RNA antitoxins behave like typical regulatory RNAs, by interacting with several targets to participate in bacteria adaptation to their environment
SprG1/SprF1, un système toxine-antitoxine de staphylococcus aureus : caractérisation, analyse du targetome de l’antitoxine SprF1 et lien avec la tolérance aux antibiotiques
No full textSlow-growing bacteria, referred as tolerant and persistent, are able to survive antibiotics, which contributes to treatment failures and relapsing infections. Among others, type I toxin-antitoxin (TA) systems have been linked to slow-growing bacteria formation. In Staphylococcus aureus, a major human pathogen, the SprF1 RNA antitoxin belonging to the type I SprG1/SprF1 TA system, can bind ribosomes to inhibit global translation and promote persister cells formation. To better understand the role of SprF1 in S. aureus antibiotic adaptation, we studied the regulation of the SprG1/SprF1 system and deciphered the SprF1 targetome. Using in silico analyses and MAPS (MS2 Affinity Purification coupled with RNA Sequencing), we uncovered 12 SprF1 mRNA targets, including sprG1 mRNA. Then, we demonstrated that SprF1 interacts, in vitro, with the yidC and rpmE2 mRNAs, the former encoding a protein insertase and the latter the ribosomal protein L31, and that this interaction can modulate YidC and RpmE2 protein expression. Subsequently, we observed that rpmE2 overexpression promotes antibiotic tolerance, which could contribute to the persistence phenotype induced by SprF1. Altogether, these findings highlight that some type I RNA antitoxins behave like typical regulatory RNAs, by interacting with several targets to participate in bacteria adaptation to their environment.Les bactéries au métabolisme ralenti (tolérantes et persistantes) sont capables de survivre aux antibiotiques ce qui contribue à l’échec des traitements et à la rechute des infections. Les systèmes toxine-antitoxine (TA) font partie des mécanismes participant à la formation des bactéries tolérantes/persistantes. Chez Staphylococcus aureus, un pathogène humain majeur, l’antitoxine ARN SprF1 appartenant au système TA de type I SprG1/SprF1, peut se fixer sur les ribosomes ce qui entraine une atténuation de la traduction et favorise la formation des bactéries persistantes. Afin de mieux comprendre le rôle de SprF1 dans l’adaptation de S. aureus aux antibiotiques, nous nous sommes intéressés à l’étude de la régulation du système SprG1/SprF1 et à l’identification du targetome de SprF1. Par des approches in silico et par la technique MAPS (MS2 Affinity Purification coupled with RNA Sequencing), nous avons mis en évidence 12 cibles ARNm de SprF1, dont l’ARNm sprG1. Nous avons ensuite démontré que SprF1 interagi, in vitro, avec les ARNm yidC et rpmE2, le premier codant une protéine insertase et le second la protéine ribosomale L31, et que cette interaction entraîne une modulation de l’expression des protéines YidC et RpmE2. Par la suite, nous avons observé que la surexpression de rpmE2 favorise la tolérance aux antibiotiques ce qui pourrait contribuer au phénotype de persistance induit par SprF1. Les résultats présentés dans ce travail de thèse montrent donc que certaines antitoxines de type I agissent comme des ARN régulateurs typiques qui, en interagissant avec plusieurs cibles, ont un rôle dans l’adaptation des bactéries à leur environnement
Susan Glaspell’s Poetics and Politics of Rebellion, Iowa City, University of Iowa Press, 2017, 258 p
No full textInternational audience“In Susan Glaspell’s Poetics and Politics of Rebellion, Emeline Jouve has cleared away what Lawrence Langer once called Glaspell’s ‘old lace’ to reveal the ‘steel lining beneath the tender surface’—the politics and, really, outrage at injustice and belief in democratic idealism that are at the center of Glaspell’s dramaturgy—and her raison d’être as a writer.”—Drew Eisenhauer, Coventry UniversityA pioneer of American modern drama and founding member of the Provincetown Players, Susan Glaspell (1876–1948) wrote plays of a kind that Robert Brustein defines as a “drama of revolt,” an expression of the dramatists’ discontent with the prevailing social, political, and artistic order. Her works display her determination to put an end to the alienating norms that, in her eyes and those of her bohemian peers, were stifling American society. This determination both to denounce infringements on individual rights and to reform American life through the theatre shapes the political dimension of her drama of revolt.Analyzing plays from the early Trifles (1916) through Springs Eternal (1943) and the undated, incomplete Wings, author Emeline Jouve illustrates the way that Glaspell’s dramas addressed issues of sexism, the impact of World War I on American values, and the relationship between individuals and their communities, among other concerns. Jouve argues that Glaspell turns the playhouse into a courthouse, putting the hypocrisy of American democracy on trial. In staging rebels fighting for their rights in fictional worlds that reflect her audience’s extradiegetic reality, she explores the strategies available to individuals to free themselves from oppression. Her works envisage a better future for both her fictive insurgents and her spectators, whom she encourages to consider which modes of revolt are appropriate and effective for improving the society they live in. The playwright defines social reform in terms of collaboration, which she views as an alternative to the dominant, alienating social and political structures. Not simply accusing but proposing solutions in her plays, she wrote dramas that enacted a positive revolt.A must for students of Glaspell and her contemporaries, as well as scholars of American theatre and literature of the first half of the twentieth century
D. Stuttard (ed.), Looking at Medea: Essays and a translation of Euripides’ tragedy
No full text"Euripides’ Medea is one of the most often read, studied and performed of all Greek tragedies": such an introduction of the great Greek classics by Bloomsbury, the publisher of Looking at Medea. Essays and a translation of Euripides’ tragedy raises great expectations. Is it possible, in 2014, to offer new significant insights into Euripides’ most discussed play? Founder of the theatre company Actors of Dionysus, editor or author of several books on Ancient Greek drama and translator, David St..
Integrating somatics and meditation into dance curriculum
No full textIt can feel impossible to find time to add moments of healthful relaxation to an already crowded dance schedule, but it's something that can enhance a dancer's body and mind. Many universities offer a few courses in somatic techniques, but often they are minimal. The author proposes series of daily classes be offered to dance majors, consisting of Improvisation or Gaga Technique, Stretch and Conditioning, Mindful Meditation, Yoga, and Foam Roller coupled with Self and Partner Massage
Exercise training to reduce cardiovascular risk in patients with metabolic syndrome and type 2 diabetes mellitus: How does it work?
No full textMetabolic syndrome (MetS) – a clustering of pathological conditions, including abdominal obesity, hypertension, dyslipidemia and hyperglycaemia – is closely associated with the development of type 2 diabetes mellitus (T2DM) and a high risk of cardiovascular disease.
A combination of multigenetic predisposition and lifestyle choices accounts for the varying inter-individual risk to develop MetS and T2DM, as well as for the individual amount of the increase in cardiovascular risk in those patients. A physically active lifestyle can offset about half of the genetically mediated cardiovascular risk. Yet, the extent to which standardized exercise programmes can reduce cardiovascular risk differs between patients. Exercise parameters, such as frequency, intensity, type and duration or number of repetitions, differentially target metabolic function, vascular health and physical fitness. In addition, exercise-induced molecular mechanisms are modulated by other patient-specific variables, such as age, diet and medication.
This review discusses the molecular and cellular mechanisms underlying the effects of exercise training on cardiovascular risk specifically in patients with MetS and T2DM.The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: NK, MB and MD are supported by the German Centre for Cardiovascular Research (DZHK, partner sites Berlin (NK) and Greifswald (MB, MD)). EMVC is supported by the Fund for Scientific Research Flanders
Chemical literature and its use : notes of twelve Lectures, in chemistry 92, required of third year students in chemistry and chemical engineering, University of Illinois.
No full textMode of access: Internet
