Coding by Choice: A Transitional Analysis of Social Participation Patterns and Programming Contributions in the Online Scratch Community

While massive online communities have drawn the attention of researchers and educators on their potential to support active collaborative work, knowledge sharing, and user-generated content, few studies examine participation in these communities at scale. The little research that does exist attends almost solely to adults rather than communities to support youths’ learning and identity development. In this chapter, we tackle two challenges related to understanding social practices that support learning in massive social networking forums where users engage in design. We examined a youth programmer community, called Scratch.mit.edu, that garners the voluntary participation of millions of young people worldwide. We report on site-wide distributions and patterns of participation that illuminate the relevance of different online social practices to ongoing involvement in the online community. Drawing on a random sample of more than 5000 active users of Scratch.mit.edu over a 3-month time period in early 2012, we examine log files that captured the frequency of three types of social practices that contribute to enduring participation: DIY participatory activities, socially supportive actions, and socially engaging interactions. Using latent transition analysis, we found (1) distinct patterns of participation (classes) across three time points (e.g., high networkers who are generally active, commenters who focus mainly on social participation, downloaders engaging in DIY participatory activities), (2) unique migration changes in class membership across time, (3) relatively equal gender representation across these classes, and (4) importance of membership length (or age) in terms of class memberships. In the discussion, we review our approach to analysis and outline implications for the design and study of online communities and tools for youth

Wallerian-Like Degeneration of Central Neurons After Synchronized and Geometrically Registered Mass Axotomy in a Three-Compartmental Microfluidic Chip

Degeneration of central axons may occur following injury or due to various diseases and it involves complex molecular mechanisms that need to be elucidated. Existing in vitro axotomy models are difficult to perform, and they provide limited information on the localization of events along the axon. We present here a novel experimental model system, based on microfluidic isolation, which consists of three distinct compartments, interconnected by parallel microchannels allowing axon outgrowth. Neurons cultured in one compartment successfully elongated their axons to cross a short central compartment and invade the outermost compartment. This design provides an interesting model system for studying axonal degeneration and death mechanisms, with a previously impossible spatial and temporal control on specific molecular pathways. We provide a proof-of-concept of the system by reporting its application to a well-characterized experimental paradigm, axotomy-induced Wallerian degeneration in primary central neurons. Using this model, we applied localized central axotomy by a brief, isolated flux of detergent. We report that mouse embryonic cortical neurons exhibit rapid Wallerian-like distal degeneration but no somatic death following central axotomy. Distal axons show progressive degeneration leading to axonal beading and cytoskeletal fragmentation within a few hours after axotomy. Degeneration is asynchronous, reminiscent of in vivo Wallerian degeneration. Axonal cytoskeletal fragmentation is significantly delayed with nicotinamide adenine dinucleotide pretreatment, but it does not change when distal calpain or caspase activity is inhibited. These findings, consistent with previous experiments in vivo, confirm the power and biological relevance of this microfluidic architecture

Alterations of mitochondrial dynamics allow retrograde propagation of locally initiated axonal insults

International audienceIn chronic neurodegenerative syndromes, neurons progressively die through a generalized retraction pattern triggering retrograde axonal degeneration toward the cell bodies, which molecular mechanisms remain elusive. Recent observations suggest that direct activation of pro-apoptotic signaling in axons triggers local degenerative events associated with early alteration of axonal mitochondrial dynamics. This raises the question of the role of mitochondrial dynamics on both axonal vulnerability stress and their implication in the spreading of damages toward unchallenged parts of the neuron. Here, using microfluidic chambers, we assessed the consequences of interfering with OPA1 and DRP1 proteins on axonal degeneration induced by local application of rotenone. We found that pharmacological inhibition of mitochondrial fission prevented axonal damage induced by rotenone, in low glucose conditions. While alteration of mitochondrial dynamics per se did not lead to spontaneous axonal degeneration, it dramatically enhanced axonal vulnerability to rotenone, which had no effect in normal glucose conditions, and promoted retrograde spreading of axonal degeneration toward the cell body. Altogether, our results suggest a mitochondrial priming effect in axons as a key process of axonal degeneration. In the context of neurodegenerative diseases, like Parkinson’s and Alzheimer’s, mitochondria fragmentation could hasten neuronal death and initiate spatial dispersion of locally induced degenerative events