Executive Coaching In Morocco: Simple Trend Or A Really Impactful Process?

Nowadays, organizations present an environment leading people to greater competitiveness and individual performance in the workplace. In order to better serve its interests and objectives, business community use different forms of support of their managers, namely the executive coaching, object of our study. This approach is applied as a managers’ performance development strategy (Grant & Greene, 2004; Moën & Federici, 2012; Moën & Skaalvik, 2009). Since the last 90’s, executive coaching is gaining progressive popularity in Morocco, thanks to the emergence of different coaching programs and institutions. The aim of the present study is to highlight the main reasons explaining the resort to this strategy, and to bring valuable insights about its success factors and its impacts on managers’ performance. Is executive coaching in Morocco just an observable trend or a real difference making process? Through semi-structured interviews, conducted with Moroccan coaches, coachees and a HR Manager, we will analysis this research question.Nowadays, organizations present an environment leading people to greater competitiveness and individual performance in the workplace. In order to better serve its interests and objectives, business community use different forms of support of their managers, namely the executive coaching, object of our study. This approach is applied as a managers’ performance development strategy (Grant & Greene, 2004; Moën & Federici, 2012; Moën & Skaalvik, 2009). Since the last 90’s, executive coaching is gaining progressive popularity in Morocco, thanks to the emergence of different coaching programs and institutions. The aim of the present study is to highlight the main reasons explaining the resort to this strategy, and to bring valuable insights about its success factors and its impacts on managers’ performance. Is executive coaching in Morocco just an observable trend or a real difference making process? Through semi-structured interviews, conducted with Moroccan coaches, coachees and a HR Manager, we will analysis this research question

Analyse de la pratique du coaching exécutif au Maroc

In the current context, the organizational climate presents an environment that leads managers to greater competitiveness and individual performance in order to better serve the interests and objectives of their organizations.  This leads them to resort to different forms of support, including coaching, considered as a strategy to develop the performance of managers. Since the end of the 90s, executive coaching has been gradually gaining popularity in Morocco, thanks to the emergence of various coaching programs and institutions. This article aims to analyze the practice of executive coaching in Morocco and to answer the following research question: Is executive coaching in Morocco just a fad or a real process with a real impact? The results of semi-structured interviews conducted with six coaches, three coachees and one HRD show that the practice of coaching in Morocco has gone beyond the stage of fashion, and that the characteristics of each of the participants have a direct impact on the effectiveness of the coaching process.   Keywods: Executive coaching Process Factors of success Effects JEL Classification: O15 Paper Type: Empircal ResearchDans le contexte actuel, le climat organisationnel présente un environnement conduisant les managers à une plus grande compétitivité et à une meilleure performance individuelle, afin de mieux servir les intérêts et les objectifs de leurs organisations.  Cela conduit ces dernières au recours à différentes formes d’accompagnement, dont le coaching, considéré comme étant une stratégie de développement de la performance des managers. Depuis la fin des années 90, le coaching exécutif gagne progressivement en popularité au Maroc, grâce notamment à l'émergence de différents programmes et institutions de coaching. Le présent article a pour objectif d’analyser la pratique du coaching exécutif au Maroc et de répondre à la question de recherche suivante : est-ce que le coaching exécutif au Maroc est juste un effet de mode ou bien un véritable processus avec un réel impact ? Les résultats d’entretiens semi-directifs menés auprès de six coachs, trois coachés et un DRH montrent que la pratique du coaching au Maroc a dépassé le stade de la mode, et que les caractéristiques liées à chacun des intervenants ont un impact direct sur l'efficacité du processus de coaching.   Mots clés : Coaching des cadres Processus Facteurs de réussite Effets Classification JEL : O15 Type de papier : Recherche empiriqu

Minimal information for studies of extracellular vesicles 2018 (MISEV2018):a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines

The last decade has seen a sharp increase in the number of scientific publications describing physiological and pathological functions of extracellular vesicles (EVs), a collective term covering various subtypes of cell-released, membranous structures, called exosomes, microvesicles, microparticles, ectosomes, oncosomes, apoptotic bodies, and many other names. However, specific issues arise when working with these entities, whose size and amount often make them difficult to obtain as relatively pure preparations, and to characterize properly. The International Society for Extracellular Vesicles (ISEV) proposed Minimal Information for Studies of Extracellular Vesicles (“MISEV”) guidelines for the field in 2014. We now update these “MISEV2014” guidelines based on evolution of the collective knowledge in the last four years. An important point to consider is that ascribing a specific function to EVs in general, or to subtypes of EVs, requires reporting of specific information beyond mere description of function in a crude, potentially contaminated, and heterogeneous preparation. For example, claims that exosomes are endowed with exquisite and specific activities remain difficult to support experimentally, given our still limited knowledge of their specific molecular machineries of biogenesis and release, as compared with other biophysically similar EVs. The MISEV2018 guidelines include tables and outlines of suggested protocols and steps to follow to document specific EV-associated functional activities. Finally, a checklist is provided with summaries of key points

Minimal information for studies of extracellular vesicles (MISEV2023): From basic to advanced approaches

Extracellular vesicles (EVs), through their complex cargo, can reflect the state of their cell of origin and change the functions and phenotypes of other cells. These features indicate strong biomarker and therapeutic potential and have generated broad interest, as evidenced by the steady year-on-year increase in the numbers of scientific publications about EVs. Important advances have been made in EV metrology and in understanding and applying EV biology. However, hurdles remain to realising the potential of EVs in domains ranging from basic biology to clinical applications due to challenges in EV nomenclature, separation from non-vesicular extracellular particles, characterisation and functional studies. To address the challenges and opportunities in this rapidly evolving field, the International Society for Extracellular Vesicles (ISEV) updates its 'Minimal Information for Studies of Extracellular Vesicles', which was first published in 2014 and then in 2018 as MISEV2014 and MISEV2018, respectively. The goal of the current document, MISEV2023, is to provide researchers with an updated snapshot of available approaches and their advantages and limitations for production, separation and characterisation of EVs from multiple sources, including cell culture, body fluids and solid tissues. In addition to presenting the latest state of the art in basic principles of EV research, this document also covers advanced techniques and approaches that are currently expanding the boundaries of the field. MISEV2023 also includes new sections on EV release and uptake and a brief discussion of in vivo approaches to study EVs. Compiling feedback from ISEV expert task forces and more than 1000 researchers, this document conveys the current state of EV research to facilitate robust scientific discoveries and move the field forward even more rapidly

Modulation of Pro-Inflammatory IL-6 Trans-Signaling Axis by Splice Switching Oligonucleotides as a Therapeutic Modality in Inflammation

Interleukin-6 (IL-6) is a pleiotropic cytokine that plays a crucial role in maintaining normal homeostatic processes under the pathogenesis of various inflammatory and autoimmune diseases. This context-dependent effect from a cytokine is due to two distinctive forms of signaling: cis-signaling and trans-signaling. IL-6 cis-signaling involves binding IL-6 to the membrane-bound IL-6 receptor and Glycoprotein 130 (GP130) signal-transducing subunit. By contrast, in IL-6 trans-signaling, complexes of IL-6 and the soluble form of the IL-6 receptor (sIL-6R) signal via membrane-bound GP130. Various strategies have been employed in the past decade to target the pro-inflammatory effect of IL-6 in numerous inflammatory disorders. However, their development has been hindered since these approaches generally target global IL-6 signaling, also affecting the anti-inflammatory effects of IL-6 signaling too. Therefore, novel strategies explicitly targeting the pro-inflammatory IL-6 trans-signaling without affecting the IL-6 cis-signaling are required and carry immense therapeutic potential. Here, we have developed a novel approach to specifically decoy IL-6-mediated trans-signaling by modulating alternative splicing in GP130, an IL-6 signal transducer, by employing splice switching oligonucleotides (SSO), to induce the expression of truncated soluble isoforms of the protein GP130. This isoform is devoid of signaling domains but allows for specifically sequestering the IL-6/sIL-6R receptor complex with high affinity in serum and thereby suppressing inflammation. Using the state-of-the-art Pip6a cell-penetrating peptide conjugated to PMO-based SSO targeting GP130 for efficient in vivo delivery, reduced disease phenotypes in two different inflammatory mouse models of systemic and intestinal inflammation were observed. Overall, this novel gene therapy platform holds great potential as a refined therapeutic intervention for chronic inflammatory diseases

Multiparametric Profiling of Single Nanoscale Extracellular Vesicles by Combined Atomic Force and Fluorescence Microscopy : Correlation and Heterogeneity in Their Molecular and Biophysical Features

Being a key player in intercellular communications, nanoscale extracellular vesicles (EVs) offer unique opportunities for both diagnostics and therapeutics. However, their cellular origin and functional identity remain elusive due to the high heterogeneity in their molecular and physical features. Here, for the first time, multiple EV parameters involving membrane protein composition, size and mechanical properties on single small EVs (sEVs) are simultaneously studied by combined fluorescence and atomic force microscopy. Furthermore, their correlation and heterogeneity in different cellular sources are investigated. The study, performed on sEVs derived from human embryonic kidney 293, cord blood mesenchymal stromal and human acute monocytic leukemia cell lines, identifies both common and cell line-specific sEV subpopulations bearing distinct distributions of the common tetraspanins (CD9, CD63, and CD81) and biophysical properties. Although the tetraspanin abundances of individual sEVs are independent of their sizes, the expression levels of CD9 and CD63 are strongly correlated. A sEV population co-expressing all the three tetraspanins in relatively high abundance, however, having average diameters of <100 nm and relatively low Young moduli, is also found in all cell lines. Such a multiparametric approach is expected to provide new insights regarding EV biology and functions, potentially deciphering unsolved questions in this field

Functional characterization of germline mutations in PDGFB and PDGFRB in primary familial brain calcification

Primary Familial Brain Calcification (PFBC), a neurodegenerative disease characterized by progressive pericapillary calcifications, has recently been linked to heterozygous mutations in PDGFB and PDGFRB genes. Here, we functionally analyzed several of these mutations in vitro. All six analyzed PDGFB mutations led to complete loss of PDGF-B function either through abolished protein synthesis or through defective binding and/or stimulation of PDGF-Rβ. The three analyzed PDGFRB mutations had more diverse consequences. Whereas PDGF-Rβ autophosphorylation was almost totally abolished in the PDGFRB L658P mutation, the two sporadic PDGFRB mutations R987W and E1071V caused reductions in protein levels and specific changes in the intensity and kinetics of PLCγ activation, respectively. Since at least some of the PDGFB mutations were predicted to act through haploinsufficiency, we explored the consequences of reduced Pdgfb or Pdgfrb transcript and protein levels in mice. Heterozygous Pdgfb or Pdgfrb knockouts, as well as double Pdgfb+/-;Pdgfrb+/- mice did not develop brain calcification, nor did Pdgfrbredeye/redeye mice, which show a 90% reduction of PDGFRβ protein levels. In contrast, Pdgfbret/ret mice, which have altered tissue distribution of PDGF-B protein due to loss of a proteoglycan binding motif, developed brain calcifications. We also determined pericyte coverage in calcification-prone and non-calcification-prone brain regions in Pdgfbret/ret mice. Surprisingly and contrary to our hypothesis, we found that the calcification-prone brain regions in Pdgfbret/ret mice model had a higher pericyte coverage and a more intact blood-brain barrier (BBB) compared to non-calcification-prone brain regions. While our findings provide clear evidence that loss-of-function mutations in PDGFB or PDGFRB cause PFBC, they also demonstrate species differences in the threshold levels of PDGF-B/PDGF-Rβ signaling that protect against small-vessel calcification in the brain. They further implicate region-specific susceptibility factor(s) in PFBC pathogenesis that are distinct from pericyte and BBB deficiency

Conditioned medium from mutant <i>PDGFB</i>-transfected HEK cells fails to induce membrane ruffles in human brain pericytes.

<p>After overnight serum starvation, human brain pericytes (HBP) were cooled on ice and exposed to cooled conditioned medium from HEK cells (described in Fig <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0143407#pone.0143407.g001" target="_blank">1B and 1C</a>) for 15 minutes, then warmed up in at 37°C for 30 min and fixed for phalloidin staining. A low concentration of exogenous PDGF-BB (2 ng/ml) in serum-free pericyte medium (A) and conditioned medium from wild-type <i>PDGFB-</i>transfected HEKs (B) were used as a positive controls. Supernatant from pcDNA-transfected HEKs was used as a negative control (C). The first two conditions induced widespread circular ruffles (arrowheads), which were absent in the negative control. Likewise, HBP treated with conditioned medium from mutant <i>PDGFB</i> transfected HEKs did not show any ruffles: (D) *242Yext*89 mutation, (E) M1? mutation and (F) L9R mutation. Cyan: DAPI. Green: Alexa 488 conjugated phalloidin. Scale bar: 30 μm.</p

Expression and autophosphorylation of PDGF-Rβ mutants in PAE cells.

<p>PAE cells were stably transfected with vectors expressing the different PFBC mutations found in <i>PDGFRB</i>. (<u>A</u>) After mRNA extraction, the total expression of human <i>PDGFRB</i> was detected with qPCR. Error bars indicate standard deviation between 3 independent experiments. ND: Not detected. (<u>B</u>) Immunoblot demonstrating the protein expression levels of the different <i>PDGFRB</i> mutants. Stable clones of mutant <i>PDGFRB</i> expressing PAE cells were treated with a proteasomal inhibitor (MG-132), lysosomal inhibitor (chloroquine) or vehicle for 4 hours before lysis. Total levels of PDGF-Rβ were visualized with anti-total PDGF-Rβ (28E1) antibody. The graphs indicate relative expression level of the inhibitor-treated conditions <i>vs</i> control condition for three individual experiments. Error bars indicate standard deviation. *<i>p</i><0.05 compared to basal wild type (WT) expression, ^#<i>p</i><0.05 when comparing inhibitor-treated <i>vs</i> control condition for each mutant. (CD) Autophosphorylation of the PDGF-Rβ mutants. PAE cells stably expressing mutant PDGF-Rβ were exposed to 40 ng/ml of exogenous PDGF-BB for 60 minutes after cooling on ice. A wild-type <i>PDGFRB</i>-expressing construct was used as a positive control, while a kinase dead (KD) variant was used as a negative control. Cell lysates were adjusted to yield a comparable amount of PDGF-Rβ signal. (C) Representative western blot demonstrating autophosphorylation of the different mutants on four residues. (D) Quantification of PDGF-Rβ autophosphorylation signal from tyrosine residues 751, 771, 1009 and 1021 using phospho-specific antibodies. Signals were normalized over total levels of PDGF-Rβ protein, and expressed as a percentage of wild-type PDGF-Rβ autophosphorylation. The graph represents the averaged results from the 4 tyrosine residues that were assessed in three independent experiments. *<i>p</i><0,05 when compared to the positive control (WT PDGF-Rβ).</p

Effect of <i>PDGFRB</i> mutations on PDGF-B signaling.

<p>(A) Western blot for known downstream targets of PDGF-B signaling. PAE cells were stimulated with 40 ng/ml PDGF-BB for the indicated time periods. Autophosphorylation of PDGF-Rβ mutants was investigated with a phosphospecific antibody raised against tyrosine 771, while downstream PDGF-BB signaling was assessed with antibodies directed against phosphorylated activated forms of ERK 1/2, Akt and PLCγ. β-actin was used as a loading control. (B). To quantify ERK 1/2, Akt and PLCγ activations over time, the signals were normalized over β-actin levels and plotted against time. Error bars indicate the standard deviation of three independent experiments. *<i>p</i>˂0,05 when compared to wild-type PDGFRβ (red), with the color of the star indicating the mutant PDGFRβ that is being compared to wild-type PDGFRβ (blue: L658P, yellow: R987W, brown: E1071V).</p