How does it feel to act together?

This paper on the phenomenology of joint agency proposes a foray into a little explored territory at the intersection of two very active domains of research: joint action and sense of agency. I explore two ways in which our experience of joint agency may differ from our experience of individual agency. First, the mechanisms of action specification and control involved in joint action are typically more complex than those present in individual actions, since it is crucial for joint action that people coordinate their plans and actions. I discuss the implications that these coordination requirements might have for the strength of the sense of agency an agent may experience for a joint action. Second, engagement in joint action may involve a transformation of agentive identity and a partial or complete shift from a sense of self-agency to a sense of we-agency. I discuss several factors that may contribute to shaping our sense of agentive identity in joint action

Mast cell glycosaminoglycans

Mast cells contain granules packed with a mixture of proteins that are released on degranulation. The proteoglycan serglycin carries an array of glycosaminoglycan (GAG) side chains, sometimes heparin, sometimes chondroitin or dermatan sulphate. Tight packing of granule proteins is dependent on the presence of serglycin carrying these GAGs. The GAGs of mast cells were most intensively studied in the 1970s and 1980s, and though something is known about the fine structure of chondroitin sulphate and dermatan sulphate in mast cells, little is understood about the composition of the heparin/heparan sulphate chains. Recent emphasis on the analysis of mast cell heparin from different species and tissues, arising from the use of this GAG in medicine, lead to the question of whether variations within heparin structures between mast cell populations are as significant as variations in the mix of chondroitins and heparins

The psychology of memory, extended cognition, and socially distributed remembering

This paper introduces a new, expanded range of relevant cognitive psychological research on collaborative recall and social memory to the philosophical debate on extended and distributed cognition. We start by examining the case for extended cognition based on the complementarity of inner and outer resources, by which neural, bodily, social, and environmental resources with disparate but complementary properties are integrated into hybrid cognitive systems, transforming or augmenting the nature of remembering or decision-making. Adams and Aizawa, noting this distinctive complementarity argument, say that they agree with it completely: but they describe it as “a non-revolutionary approach” which leaves “the cognitive psychology of memory as the study of processes that take place, essentially without exception, within nervous systems.” In response, we carve out, on distinct conceptual and empirical grounds, a rich middle ground between internalist forms of cognitivism and radical anti-cognitivism. Drawing both on extended cognition literature and on Sterelny’s account of the “scaffolded mind” (this issue), we develop a multidimensional framework for understanding varying relations between agents and external resources, both technological and social. On this basis we argue that, independent of any more “revolutionary” metaphysical claims about the partial constitution of cognitive processes by external resources, a thesis of scaffolded or distributed cognition can substantially influence or transform explanatory practice in cognitive science. Critics also cite various empirical results as evidence against the idea that remembering can extend beyond skull and skin. We respond with a more principled, representative survey of the scientific psychology of memory, focussing in particular on robust recent empirical traditions for the study of collaborative recall and transactive social memory. We describe our own empirical research on socially distributed remembering, aimed at identifying conditions for mnemonic emergence in collaborative groups. Philosophical debates about extended, embedded, and distributed cognition can thus make richer, mutually beneficial contact with independently motivated research programs in the cognitive psychology of memory.40 page(s

Accelerated atherogenesis and neointima formation in heparin cofactor II-deficient mice

Heparin cofactor II (HCII) is a plasma protein that inhibits thrombin when bound to dermatan sulfate or heparin. HCII-deficient mice are viable and fertile but rapidly develop thrombosis of the carotid artery after endothelial injury. We now report the effects of HCII deficiency on atherogenesis and neointima formation. HCII-null or wild-type mice, both on an apolipoprotein E-null background, were fed an atherogenic diet for 12 weeks. HCII-null mice developed plaque areas in the aortic arch approximately 64% larger than wild-type mice despite having similar plasma lipid and glucose levels. Neointima formation was induced by mechanical dilation of the common carotid artery. Thrombin activity, determined by hirudin binding or chromogenic substrate hydrolysis within 1 hour after injury, was higher in the arterial walls of HCII-null mice than in wild-type mice. After 3 weeks, the median neointimal area was 2- to 3-fold greater in HCII-null than in wild-type mice. Dermatan sulfate administered intravenously within 48 hours after injury inhibited neointima formation in wild-type mice but had no effect in HCII-null mice. Heparin did not inhibit neointima formation. We conclude that HCII deficiency promotes atherogenesis and neointima formation and that treatment with dermatan sulfate reduces neointima formation in an HCII-dependent manner.110134261426

Dermatan sulfate and bone marrow mononuclear cells used as a new therapeutic strategy after arterial injury in mice

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Background aims. Previously, we have demonstrated that administration of dermatan sulfate (DS) suppresses neointima formation in the mouse carotid artery by activating heparin co-factor II. A similar suppressive effect was observed by increasing the number of progenitor cells in circulation. In this study, we investigated the combination of DS and bone marrow mononuclear cells (MNC), which includes potential endothelial progenitors, in neointima formation after arterial injury. Methods. Arterial injury was induced by mechanical dilation of the left common carotid artery. We analyzed the extension of endothelial lesion, thrombus formation, P-selectin expression and CD45(+) cell accumulation 1 and 3 days post-injury, and neointima formation 21 days post-injury. Animals were injected with MNC with or without DS during the first 48 h after injury. Results. The extension of endothelial lesion was similar in all groups 1 day after surgery; however, in injured animals treated with MNC and DS the endothelium recovery seemed to be more efficient 21 days after lesion. Treatment with DS inhibited thrombosis, decreased CD45(+) cell accumulation and P-selectin expression at the site of injury, and reduced the neointimal area by 56%. Treatment with MNC reduced the neointimal area by 54%. The combination of DS and MNC reduced neointima formation by more than 91%. In addition, DS promoted a greater accumulation of MNC at the site of injury. Conclusions. DS inhibits the initial thrombotic and inflammatory processes after arterial injury and promotes migration of MNC to the site of the lesion, where they may assist in the recovery of the injured endothelium.136695704Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)NHLBI [HL55520]Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)FAPESP [2007/01112-6, 2009/00950-3, 2010/01119-3, 2010/11474-5]CNPq [472087/2008-8]NHLBI [HL55520