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See detailJL 13, an atypical antipsychotic: A preclinical review
Ellenbroek, B. A.; Liégeois, Jean-François ULg

in Cns Drug Reviews (2003), 9(1, Spring), 41-56

The extensive pharmacological evaluation of JL 13 as an atypical antipsychotic drug has revealed a close similarity to clozapine, however with some major advantages. JL 13 was characterized as a weak D-2 ... [more ▼]

The extensive pharmacological evaluation of JL 13 as an atypical antipsychotic drug has revealed a close similarity to clozapine, however with some major advantages. JL 13 was characterized as a weak D-2 antagonist, both in vitro and in vivo, with a strong affinity for the D-4 and the 5-HT2A receptors. It has no affinity for the 5-HT2C receptor. In vivo microdialysis experiments in rat showed that JL 13, like clozapine, preferentially increased extracellular dopamine concentrations in the prefrontal cortex compared to nucleus accumbens or striatum. Behavioral studies showed that JL 13, like clozapine, has the profile of an atypical antipsychotic. Thus, JL 13 did not antagonize apomorphine-induced stereotypy nor did it produce catalepsy, but it antagonized apomorphine-induced climbing in rodents. It was inactive against d-amphetamine-induced stereotypy but antagonized d-amphetamine-induced hyperactivity in the mouse. Likewise, in the paw test, it was more effective in prolonging hindlimb retraction time than prolonging forelimb retraction time. Like other antipsychotic drugs, JL 13 reversed the apomorphine- and amphetamine-induced disruption of prepulse inhibition. In a complex temporal regulation schedule in the dog, JL 13 showed a high resemblance with clozapine without inducing sialorrhea, palpebral ptosis or any significant motor side effects. In rats and squirrel monkeys JL 13 induced a high degree of generalization (70%) to clozapine. Regarding behavioral toxicology, JL 13 did not produce dystonia or Parkinsonian symptoms in haloperidol-sensitized monkeys. After acute administration, again like clozapine, JL 13 induced only a transient increase in circulating prolactin. Last but not the least, regarding a possible hematological toxicity, unlike clozapine, JL 13 did not present sensitivity to peroxidase-induced oxidation. Moreover, its electrooxidation potential was close to that of loxapine and far from that of clozapine. Taking all these preclinical data into account, it appears that JL 13 is a promising atypical antipsychotic drug. [less ▲]

Detailed reference viewed: 39 (3 ULg)
See detailJNK/ROS Signaling Pathway Is Responsible for Induction of Autophagy in HDAC5 depleted Cancer Cells
Hendrick, Elodie ULg; Mathéus, Nicolas; Peixoto, Paul ULg et al

Conference (2013, January 29)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

Detailed reference viewed: 7 (0 ULg)
See detailJNK/ROS signaling pathway is responsible for induction of autophagy in HDAC5 depleted cancer cells
Hendrick, Elodie ULg; Mathéus, Nicolas; Peixoto, Paul ULg et al

Poster (2013, February 02)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

Detailed reference viewed: 7 (1 ULg)
See detailJNK/ROS signaling pathway is responsible for induction of autophagy in HDAC5 depleted cancer cells
Hendrick, Elodie ULg; Mathéus, Nicolas; Peixoto, Paul ULg et al

Poster (2013, January 28)

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure ... [more ▼]

Introduction: Histone deacetylases (HDAC) is a family of eighteen enzymes which modulates the acetylation level of histones and non-histone proteins to regulate gene expression and chromatin structure. Broad spectrum inhibitors of these enzymes such as SAHA can inhibit tumor growth both in vitro and in vivo and are currently used as anti-cancer agents in clinic. For many years, we are investigating the specific role of individual HDAC members in cancer biology and we have recently demonstrated that depletion of HDAC5 using siRNA technology triggered cancer cells to both autophagy and apoptosis (ref papier). The study of autophagy in cancer is a new research field that has recently generated tremendous attention due to the recognition that autophagy can have either pro-survival or pro-death functions depending on its level of activation. In addition, more and more studies indicate that a complex relationship exists between autophagy and apoptosis, and that the interplay between these two processes determines whether a cell will live or die. Aims: The goal of this study is to further understand the role of autophagy induced by HDAC5 depletion. Current investigations include determining the molecular mechanisms by which HDAC5 depletion induces autophagy and exploring regulatory relationship between autophagy and apoptosis on cancer cell death in absence of HDAC5. Results: The set up of the autophagy in absence of HDAC5 was demonstrated by the conversion of LC3 and development of autophagosomes by electronic microscopy. Transcriptomic study demonstrated a deregulation of a set of genes involved in ROS detoxification in HDAC5 depleted cancer cells leading to significant increase of ROS levels. Further investigations showed that pretreatment with NAC, a ROS scavenger, effectively blocked the accumulation of ROS and autopahgy triggered by HDAC5 silencing. Moreover, HDAC5 depletion induces activation of JNK, and knockdown of JNK by siRNA inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by HDAC5 depletion indicating that JNK activation may be a upstream signaling of ROS and should be a core component in HDAC5 silencing-induced autophagic signaling pathway. Finally, blocking of autophagy induced by HDAC5 silencing with NAC or chloroquine and bafilomycin enhanced pro-apoptotic effect. Conclusion: Autophagy functions as a prosurvival mechanism to mitigate HDAC5 depletion-induced apoptotic cell death, suggesting that targeting autophagy might improve the therapeutic effects of specific HDAC5 inhibition. [less ▲]

Detailed reference viewed: 3 (2 ULg)
Peer Reviewed
See detailJob characteristics and work engagement: multiple-group analyses of flexibility practices
Travaglianti, Fabrice ULg; De Zanet, Fabrice ULg; Vandenberghe, Christian et al

Poster (2014, May 16)

Detailed reference viewed: 61 (28 ULg)
See detailJob control in changing work environments
Hansez, Isabelle ULg; De Keyser, Véronique ULg

in Avallone, F.; Caetano, A.; Sinangil, H. (Eds.) Identity and diversity in organizations (2003)

Detailed reference viewed: 7 (1 ULg)
See detailjob day
Bruyère, Eric ULg

Speech/Talk (2013)

Detailed reference viewed: 16 (1 ULg)
See detailjob day
Bruyère, Eric ULg

Speech/Talk (2012)

Detailed reference viewed: 22 (0 ULg)
See detailjob day ulg
Bruyère, Eric ULg

Diverse speeche and writing (2014)

Detailed reference viewed: 14 (1 ULg)
Peer Reviewed
See detailThe job Demands-Resources Model and management commitment to safety applied to safe behaviour.
Hansez, Isabelle ULg; Chmiel, N.

Conference (2007, May 12)

Detailed reference viewed: 9 (0 ULg)
Full Text
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See detailJob satisfaction and self-efficacy to manage dementia in home caregivers: Effects of a three-day intervention
Marquet, Manon ULg; Missotten, Pierre ULg; Charlot, Valentine ULg et al

Poster (2013, July)

There is a growing need for interventions designed to help professionals who care for people with dementia. Nevertheless, most existing programs are developed for professionals working in institutional ... [more ▼]

There is a growing need for interventions designed to help professionals who care for people with dementia. Nevertheless, most existing programs are developed for professionals working in institutional settings. Thus, the objectives of our study are to evaluate the effectiveness of a three-day program aimed at training home help services (n=19). This intervention is targeted to enhance knowledge about dementia and help professionals to develop problem-solving strategies applicable to their everyday practice. Statistical analyses were based on self-report questionnaires administered before and after the intervention. Results indicate that participants find focused-problem coping to be more helpful after training and have better knowledge about dementia. Moreover, the program produces enhancement of job satisfaction and lower ageism scores. These findings are promising and suggest that a brief program can be effective to help caregivers of home-based services dealing with dementia problems. [less ▲]

Detailed reference viewed: 54 (14 ULg)
See detailLa "Joconde" de Léonard de Vinci et sa description par Giorgio Vasari
Fagnart, Laure ULg

Conference (2008, August 28)

Detailed reference viewed: 82 (1 ULg)
Full Text
See detailLa "Joconde", plus divine qu'humaine ?
Fagnart, Laure ULg

in Catalogue de l'exposition La passion Léonard, comprendre et créer (Réfectoire des Cordeliers) (2007)

Detailed reference viewed: 47 (12 ULg)
Full Text
See detailLa "Joconde", une histoire, un parcours
Fagnart, Laure ULg

in Fagnart, Laure (Ed.) Catalogue de l'exposition La Joconde inattendue (Château du Clos Lucé) (2007)

Detailed reference viewed: 73 (18 ULg)
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Peer Reviewed
See detailJoe G. Pinelli, dans le no man’s land de la bande dessinée
Paques, Frédéric ULg

in Textyles : Revue des Lettres Belges de Langue Française (2010), 36-37

Detailed reference viewed: 57 (16 ULg)
See detailJohann Wolfgang Goethe: Gedichte
Witte, Bernd; Viehöver, Vera ULg; Reinlein, Tanja

Book published by Reclam (2001)

Edition critique de 365 poèmes de Johann Wolfgang Goethe

Detailed reference viewed: 8 (1 ULg)
See detailJohann Wolfgang Goethe: Gedichte. Studienausgabe
Witte, Bernd; Reinlein, Tanja; Viehöver, Vera ULg

Book published by Reclam - 2. Auflage (2008)

Detailed reference viewed: 9 (0 ULg)
Full Text
See detailJohannes Arnoldus Bergellanus, De chalcographiae inventione poema encomiasticum
Adam, Renaud ULg

in De Schepper, Marcus; Kelders, Ann; Pauwels, Jan (Eds.) In de ban van boeken. Grote verzamelaars uit de negentiende eeuw in de Koninklijke Bibliotheek van België (2008)

Detailed reference viewed: 16 (0 ULg)
Full Text
See detailJohannes Arnoldus Bergellanus, De chalcographiae inventione poema encomiasticum
Adam, Renaud ULg

in De Schepper, Marcus; Kelders, Ann; Pauwels, Jan (Eds.) Les seigneurs du livre. Les grands collectionneurs du XIXème siècle à la Bibliothèque royale de Belgique (2008)

Detailed reference viewed: 16 (1 ULg)