Democratic dialogue and collective learning in the context of self-managed teams

This paper provides a longitudinal, empirical view of the multifaceted and reciprocal processes of organizational learning in a context of self-managed teams. Organizational learning is seen as a social construction between people and actions in a work setting. The notion of learning as situated (Brown & Duguid 1989, Lave& Wenger 1991, Gherardi & al. 1998, Easterby-Smith & Araujo 1999, Abma 2003) opens up the possibility for placing the focus of research on learning in the community rather than in individual learning processes. Further, in studying processes in their social context, we cannot avoid taking power relations into consideration (Contu & Willmott 2003). The study is based on an action research with a methodology close to the ‘democratic dialogue’ presented by Gustavsen (2001). This gives a ground for research into how the learning discourse developed in the case study organization over a period of 5 years, during which time the company abandoned a middle management level of hierarchy and the teams had to figure out how to work as self-managed units. This paper discusses the (re)construction of power relations and its role in organizational learning. Power relations are discussed both in vertical and horizontal work relations. A special emphasis is placed on the dialectic between managerial aims and the space for reflection on the side of employees. I argue that learning is crucial in the search for the limits for empowerment and that these limits are negotiated both in actions and speech. This study unfolds a purpose-oriented learning process, constructing an open dialogue, and describes a favourable context for creative, knowledge building communities.

Glia-Motoneuron dialogue in ALS onset and progression in SOD1G93A-mice model

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the pro-gressive loss of motoneurons (MN). Increasing evidence points glial cells as key players for ALS onset and progression. Indeed, MN-glia signalling pathways involving either neuroprotection or inflammation are likely to be altered in ALS. We aimed to study the molecules related with glial function and/or reactivity by evaluating glial markers and hemichannels, mainly present in astrocytes. We also studied molecules involved in mi-croglia-MN dialogue (CXCR3/CCL21; CX3CR1/CX3CL1; MFG-E8), as well as proliferation (Ki-67) and inflammatory-related molecules (TLR2/4, NLRP3; IL-18) and alarming/calming signals (HMGB1/autotaxin). We used lumbar spinal cord (SC) homogenates from mice expressing a mutant human-SOD1 protein (mSOD1) at presymptomatic and late-symptomatic ALS stages. SJL (WT) mice at same ages were used as controls. We observed decreased expression of genes associated with astrocytic (GFAP and S100B) and microglial (CD11b) markers in mSOD1 at the presymptomatic phase, as well as diminished levels of gap junction components pannexin1 and connexin43 and expression of Ki-67 and decreased autotax-in. In addition, microglial-MN communication was negatively affected in mSOD1 mice as well as in-flammatory response. Interestingly, we observed astrocytic (S100B) and microglial (CD11b) reactivity, increased proliferation (Ki-67) and increased autotaxin expression in symptomatic mSOD1 mice. In-creased MN-microglial dialogue (CXCR3/CCL21; CX3CR1/CX3CL1; MFG-E8) and hemichannel activ-ity, namely connexin43 and pannexin1, were also observed in mSOD1 at the symptomatic phase, along with an elevated inflammatory response as indicated by increased levels of HMGB1 and NLRP3. Our results suggest that decreased autotaxin expression is a feature of the presymptomatic stage, and precede the network of pro-inflammatory-related symptomatic determinants, including HMGB1, CCL21, CX3CL1, and NLRP3. The identification of the molecules and signaling pathways that are dif-ferentially activated along ALS progression will contribute for a better design of therapeutic strategies for disease onset and progression.