13 research outputs found
Power to All or Few People? An Exploration of Power Dynamics in Holacracy
Power is key to all organizing. It allows actors to perform actions, make decisions and assign tasks to others. In bureaucratic organizations power is mainly associated with the position that the actor holds. Because actors compete for power, change their position within an organization or leave an organization, power is dynamically changing. We refer to these changes in power as power dynamics. Many New Forms of Organizing, such as Holacracy, claim that individuals have more decision-making capacity, i.e., that power is more equally distributed within the organization. In this paper, we use a unique dataset from a holacratic organization to empirically examine how power dynamics in Holacracy evolve over time. In particular, we use temporal network analysis to reconstruct and contrast two related networks that capture information on how decisions in Holacracy are made. Our findings indicate that also in Holacracy power is not equally distributed, but that few individuals hold most power
Power to All or Few People? An Exploration of Power Dynamics in Holacracy
Power is key to all organizing. It allows actors to perform actions, make decisions and assign tasks to others. In bureaucratic organizations power is mainly associated with the position that the actor holds. Because actors compete for power, change their position within an organization or leave an organization, power is dynamically changing. We refer to these changes in power as power dynamics. Many New Forms of Organizing, such as Holacracy, claim that individuals have more decision-making capacity, i.e., that power is more equally distributed within the organization. In this paper, we use a unique dataset from a holacratic organization to empirically examine how power dynamics in Holacracy evolve over time. In particular, we use temporal network analysis to reconstruct and contrast two related networks that capture information on how decisions in Holacracy are made. Our findings indicate that also in Holacracy power is not equally distributed, but that few individuals hold most power
‘In the end you adapt to anything’: responses to narratives of resilience and entrepreneurship in post-recession Spain
Resilience – the ability to bounce back from hardship – is a concept that has become popular during the years of economic crisis and post-recession. Contemporary citizens are expected to be flexible, have a positive attitude, and take care of themselves in a context of heightened inequality and precarity. The objective of this article is to analyze how citizens in post-recession Spain respond to media representations that prescribe these values. Eight focus groups were held with middle- and working-class men and women (a total of 62 participants) who discussed four short stories written by the researchers which condensed the main concepts found in media narratives studied previously (including TV series, reality TV, advertisements, video games and celebrity culture). The results of our analysis show that participants tended to praise change and adaptability. The ‘complacent citizen’, who seeks security and refuses to adapt to the current precarious and unstable environments, emerges as a ‘bad citizen’, and security and stability are pathologized. There were differences between the middle and workingclass groups: while the former clearly adhered to the neoliberal discourse that sees flexibility and self-improvement as a moral obligation, the latter showed a more ambivalent response to these discourses.The author(s) disclosed receipt of the following financial support for the research, authorship, and/ or publication of this article: This work was supported by the Spanish Ministry of Economy and Competitiveness [grant number CSO2014-56830-P]
AutoSense Model for Word Sense Induction
Word sense induction (WSI), or the task of automatically discovering multiple senses or meanings of a word, has three main challenges: domain adaptability, novel sense detection, and sense granularity flexibility. While current latent variable models are known to solve the first two challenges, they are not flexible to different word sense granularities, which differ very much among words, from aardvark with one sense, to play with over 50 senses. Current models either require hyperparameter tuning or nonparametric induction of the number of senses, which we find both to be ineffective. Thus, we aim to eliminate these requirements and solve the sense granularity problem by proposing AutoSense, a latent variable model based on two observations: (1) senses are represented as a distribution over topics, and (2) senses generate pairings between the target word and its neighboring word. These observations alleviate the problem by (a) throwing garbage senses and (b) additionally inducing fine-grained word senses. Results show great improvements over the stateof-the-art models on popular WSI datasets. We also show that AutoSense is able to learn the appropriate sense granularity of a word. Finally, we apply AutoSense to the unsupervised author name disambiguation task where the sense granularity problem is more evident and show that AutoSense is evidently better than competing models. We share our data and code here: https://github.com/rktamplayo/AutoSense
Competition, competition policy, and the GATT
The authors argue that further moves to liberalize trade and to implement existing GATT rules and principles may have a greater impact on global competition than would the pursuit of harmonization of competition policy. They also suggest that current GATT rules and case law provide scope for disputes to be brought before the GATT that relate to both the application and the nonapplication of existing domestic competition laws of GATT contracting parties. This leads to de facto discrimination between domestic and foreign products. Little use has been made of the GATT in this connection. Perhaps existing indirect avenues for raising competition-related disputes in the GATT should be pursued more actively. This would help identify what specific government policies might be the subject of multilateral negotiations and explicitly incorporated into the GATT framework.Environmental Economics&Policies,TF054105-DONOR FUNDED OPERATION ADMINISTRATION FEE INCOMEAND EXPENSE ACCOUNT,Economic Theory&Research,Access to Markets,Markets and Market Access
Towards validation and standardization of automatic gait event identification algorithms for use in paediatric pathological populations
ISSN:0966-6362ISSN:1879-2219ISSN:1879-221
Outcome of medial hamstring lengthening in children with spastic paresis: A biomechanical and morphological observational study
To improve gait in children with spastic paresis due to cerebral palsy or hereditary spastic paresis, the semitendinosus muscle is frequently lengthened amongst other medial hamstring muscles by orthopaedic surgery. Side effects on gait due to weakening of the hamstring muscles and overcorrections have been reported. How these side effects relate to semitendinosus morphology is unknown. This study assessed the effects of bilateral medial hamstring lengthening as part of single-event multilevel surgery (SEMLS) on (1) knee joint mechanics (2) semitendinosus muscle morphology and (3) gait kinematics. All variables were assessed for the right side only. Six children with spastic paresis selected for surgery to counteract limited knee range of motion were measured before and about a year after surgery. After surgery, in most subjects popliteal angle decreased and knee moment-angle curves were shifted towards a more extended knee joint, semitendinosus muscle belly length was approximately 30% decreased, while at all assessed knee angles tendon length was increased by about 80%. In the majority of children muscle volume of the semitendinosus muscle decreased substantially suggesting a reduction of physiological cross-sectional area. Gait kinematics showed more knee extension during stance (mean change ± standard deviation: 34±13), but also increased pelvic anterior tilt (mean change ± standard deviation: 23±5). In most subjects, surgical lengthening of semitendinosus tendon contributed to more extended knee joint angle during static measurements as well as during gait, whereas extensibility of semitendinosus muscle belly was decreased. Post-surgical treatment to maintain muscle belly length and physiological cross-sectional area may improve treatment outcome of medial hamstring lengthening.Biomechatronics & Human-Machine Contro
Manipulating mtDNA in vivo reprograms metabolism via novel response mechanisms
Author summary Mitochondria, subcellular compartments (organelles) found in virtually all eukaryotes, contain DNA which is believed to be a remnant of an ancestral bacterial genome. They are best known for the synthesis of the universal energy carrier ATP, but also serve as the hub of various metabolic and signalling pathways. We report here that mtDNA integrity is linked to a signaling system that influences metabolic fuel selection between fats and sugars. By disrupting mtDNA in the fruit fly we induced a strong shift towards lipid catabolism. This was caused both by a widespread decrease in post-translational acetylation of proteins, as well as specific inhibition of the machinery that transports glucose into cells across the plasma membrane. This phenomenon is very similar to the pathophysiology of diabetes, where the inability to transport glucose to cells is considered the main hallmark of the disease. Moreover, decreased protein acetylation was associated with lower levels of certain neurotransmitters, causing various effects on feeding and fertility. Our discovery reveals an unexpected role for mtDNA stability in regulating global metabolic balance and suggests that it could be instrumental in pandemic metabolic disorders such as diabetes and obesity.Peer reviewe
Impaired mitochondrial oxidative phosphorylation in the peroxisomal disease X-linked adrenoleukodystrophy
X-linked adrenoleukodystrophy (X-ALD) is an inherited metabolic disorder of the nervous systemcharacterized by axonopathy in spinal cords and/or cerebral demyelination, adrenal insufficiency and accumulation of very long-chain fatty acids (VLCFAs) in plasma and tissues. The disease is caused by malfunction of the ABCD1 gene, which encodes a peroxisomal transporter of VLCFAs or VLCFA-CoA. In the mouse, Abcd1 loss causes late onset axonal degeneration in the spinal cord, associated with locomotor disability resembling the most common phenotype in patients, adrenomyeloneuropathy. We have formerly shown that an excess of the VLCFA C26:0 induces oxidative damage, which underlies the axonal degeneration exhibited by the Abcd1- mice. In the present study, we sought to investigate the noxious effects of C26:0 on mitochondria function. Ourdata indicate that in X-ALDpatients' fibroblasts,excessof C26:0 generatesmt DNA oxidation and specifically impairs oxidative phosphorylation (OXPHOS) triggering mitochondrialROSproduction from electron transport chain complexes. This correlates with impaired complex V phosphorylative activity, as visualized by high-resolution respirometry on spinal cord slices of Abcd1- mice. Further, we identified a marked oxidation of key OXPHOS system subunits in Abcd1- mouse spinal cords at presymptomatic stages. Altogether, our results illustratesomeof themechanistic intricacies bywhichthe excessof a fatty acid targeted to peroxisomesactivates a deleterious process of oxidative damage to mitochondria, leading to amultifaceted dysfunction of this organelle. These findings may be of relevance for patient management while unveiling novel therapeutic targets for X-ALD. © The Author 2013. Published by Oxford University Press. All rights reserved.European Commission (FP7-241622); European Leukodystrophy Association (ELA2009-036C5, ELA2008-040C4, ELA 2010-020F1); Spanish Institute for Health Carlos III (FIS PI080991 and FIS PI11/01043); Autonomous Government of Catalonia (2009SGR85); Spanish Institute for Health Carlos III (Miguel Servet program CP11/00080); CIBER on Rare Diseases (CIBERER); COST action BM0604 ; Department of Education, Universities and Research of the Basque Country Government (BFI07.126); European Leukodystrophy Association ; Spanish Ministry of Science and Innovation (BFU2009-11879/BFI); Spanish Ministry of Health (PI11/1532); the Autonomous Government of Catalonia (2009SGR735); the ‘La Caixa’ Foundation and COST B35 Action of the European Union. D.C. is a fellow from the Spanish Ministry of Health (FI08-00707); SAF2008-01896 and SAF2011-23636 from the Spanish Ministry of Science and InnovationPeer Reviewe
Cortical Spreading Depression Causes Unique Dysregulation of Inflammatory Pathways in a Transgenic Mouse Model of Migraine
Familial hemiplegic migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the α1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (‘FHM1 R192Q mice’) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here, we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 h after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep serial analysis of gene expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine
