The Emerald Handbook of Narrative Criminology

Narrative criminology is an approach to studying crime and other harm that puts stories first. It investigates how such stories are composed, when and why they are told and what their effects are. This edited collection explores the methodological challenges of analysing offenders' stories, but pushes the boundaries of the field to consider the narratives of victims, bystanders and criminal justice professionals. This Handbook reflects the diversity of methodological approaches employed in narrative criminology. Chapters discuss the practicalities of listening to and observing narratives through ethnographic and observational research, and offer accessible guides to using diverse methodological approaches for listening to and interpreting narrative data. With contributions from established and emerging scholars from all over the world, and from diverse fields including politics, psychology, sociology and criminology, the Handbook reflects the cutting edge of narrative methodologies for understanding crime, control and victimisation and is an essential resource for academics studying and teaching on narrative criminology

Helping Business Schools Engage with Real Problems: The Contribution of Critical Realism and Systems Thinking

The world faces major problems, not least climate change and the financial crisis, and business schools have been criticised for their failure to help address these issues and, in the case of the financial meltdown, for being causally implicated in it. In this paper we begin by describing the extent of what has been called the rigour/relevance debate. We then diagnose the nature of the problem in terms of historical, structural and contextual mechanisms that initiated and now sustain an inability of business schools to engage with real-world issues. We then propose a combination of measures, which mutually reinforce each other, that are necessary to break into this vicious circle – critical realism as an underpinning philosophy that supports and embodies the next points; holism and transdisciplinarity; multimethodology (mixed-methods research); and a critical and ethical-committed stance. OR and management science have much to contribute in terms of both powerful analytical methods and problem structuring methods

Future therapeutic targets in rheumatoid arthritis?

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent joint inflammation. Without adequate treatment, patients with RA will develop joint deformity and progressive functional impairment. With the implementation of treat-to-target strategies and availability of biologic therapies, the outcomes for patients with RA have significantly improved. However, the unmet need in the treatment of RA remains high as some patients do not respond sufficiently to the currently available agents, remission is not always achieved and refractory disease is not uncommon. With better understanding of the pathophysiology of RA, new therapeutic approaches are emerging. Apart from more selective Janus kinase inhibition, there is a great interest in the granulocyte macrophage-colony stimulating factor pathway, Bruton's tyrosine kinase pathway, phosphoinositide-3-kinase pathway, neural stimulation and dendritic cell-based therapeutics. In this review, we will discuss the therapeutic potential of these novel approaches

The SH3 domain of postsynaptic density 95 mediates inflammatory pain through phosphatidylinositol-3-kinase recruitment

Sensitization to inflammatory pain is a pathological form of neuronal plasticity that is poorly understood and treated. Here we examine the role of the SH3 domain of postsynaptic density 95 (PSD95) by using mice that carry a single amino-acid substitution in the polyproline-binding site. Testing multiple forms of plasticity we found sensitization to inflammation was specifically attenuated. The inflammatory response required recruitment of phosphatidylinositol-3-kinase-C2α to the SH3-binding site of PSD95. In wild-type mice, wortmannin or peptide competition attenuated the sensitization. These results show that different types of behavioural plasticity are mediated by specific domains of PSD95 and suggest novel therapeutic avenues for reducing inflammatory pain

Inductive Praxis and Management Research: Towards a Reflexive Framework

This paper examines how induction legitimately varies according to the impact of different knowledge constituting philosophical assumptions. As a result of its prevalence in qualitative management research, the paper focuses on grounded theory and uses this as a vehicle to explore the key parameters of the philosophical diversity articulated in judgements around neutrality, description and theorization. A reflexive framework of inductive praxis is offered as a heuristic device for interrogating the choices evidently at play in the variable constitution of inductive management research. We indicate how there are multiple modes of engagement, each of which is legitimate within its own philosophical commitments. This implies the need for a more tolerant pluralistic stance in the evaluation of qualitative management research

Functional Crosstalk between Type I and II Interferon through the Regulated Expression of STAT1

Small "priming" quantities of type I interferon enhance cellular responses to type II interferon by maintaining basal levels of STAT1, explaining the observed crosstalk between these two cytokines

Human Integrin α3β1 Regulates TLR2 Recognition of Lipopeptides from Endosomal Compartments

Toll-like receptor (TLR)-2/TLR1 heterodimers recognize bacterial lipopeptides and initiate the production of inflammatory mediators. Adaptors and co-receptors that mediate this process, as well as the mechanisms by which these adaptors and co-receptors function, are still being discovered.Using shRNA, blocking antibodies, and fluorescent microscopy, we show that U937 macrophage responses to the TLR2/1 ligand, Pam(3)CSK(4), are dependent upon an integrin, α(3)β(1). The mechanism for integrin α(3)β(1) involvement in TLR2/1 signaling is through its role in endocytosis of lipopeptides. Using inhibitors of endosomal acidification/maturation and physical tethering of the ligand, we show that the endocytosis of Pam(3)CSK(4) is necessary for the complete TLR2/1-mediated pro-inflammatory cytokine response. We also show that TLR2/1 signaling from the endosome results in the induction of different inflammatory mediators than TLR2/1 signaling from the plasma membrane.Here we identify integrin α(3)β(1) as a novel regulator for the recognition of bacterial lipopeptides. We demonstrate that induction of a specific subset of cytokines is dependent upon integrin α(3)β(1)-mediated endocytosis of the ligand. In addition, we address an ongoing controversy regarding endosomal recognition of bacterial lipopeptides by demonstrating that TLR2/1 signals from within endosomal compartments as well as the plasma membrane, and that downstream responses may differ depending upon receptor localization. We propose that the regulation of endosomal TLR2/1 signaling by integrin α(3)β(1) serves as a mechanism for modulating inflammatory responses

Flexible Working and Performance: A Systematic Review of the Evidence for a Business Case

Interest in the outcomes of flexible working arrangements dates from the mid 1970s, when researchers attempted to assess the impact of flexitime on worker performance. This paper reviews the literature on the link between flexible working arrangements and performance related outcomes. Taken together, the evidence fails to demonstrate a business case for the use of flexible working arrangements. This paper attempts to explain the findings by analysing the theoretical and methodological perspectives adopted, as well as the measurements and designs used. In doing so, gaps in this vast and disparate literature are identified and a research agenda is developed

Restricted growth of Schwann cells lacking Cajal bands slows conduction in myelinated nerves

Nerve impulses are propagated at nodes of Ranvier in the myelinated nerves of vertebrates. Internodal distances have been proposed to affect the velocity of nerve impulse conduction; however, direct evidence is lacking, and the cellular mechanisms that might regulate the length of the myelinated segments are unknown. Ramon y Cajal described longitudinal and transverse bands of cytoplasm or trabeculae in internodal Schwann cells and suggested that they had a nutritive function. Here we show that internodal growth in wild-type nerves is precisely matched to nerve extension, but disruption of the cytoplasmic bands in Periaxin-null mice impairs Schwann cell elongation during nerve growth. By contrast, myelination proceeds normally. The capacity of wild-type and mutant Schwann cells to elongate is cell-autonomous, indicating that passive stretching can account for the lengthening of the internode during limb growth. As predicted on theoretical grounds, decreased internodal distances strikingly decrease conduction velocities and so affect motor function.We propose that microtubule-based transport in the longitudinal bands of Cajal permits internodal Schwann cells to lengthen in response to axonal growth, thus ensuring rapid nerve impulse transmission

IL-4 directly signals tissue-resident macrophages to proliferate beyond homeostatic levels controlled by CSF-1

Macrophages (M Phi s) colonize tissues during inflammation in two distinct ways: recruitment of monocyte precursors and proliferation of resident cells. We recently revealed a major role for IL-4 in the proliferative expansion of resident M Phi s during a Th2-biased tissue nematode infection. We now show that proliferation of M Phi s during intestinal as well as tissue nematode infection is restricted to sites of IL-4 production and requires M Phi-intrinsic IL-4R signaling. However, both IL-4R alpha-dependent and -independent mechanisms contributed to M Phi proliferation during nematode infections. IL-4R-independent proliferation was controlled by a rise in local CSF-1 levels, but IL-4R alpha expression conferred a competitive advantage with higher and more sustained proliferation and increased accumulation of IL-4R alpha(+) compared with IL-4R alpha(-) cells. Mechanistically, this occurred by conversion of IL-4R alpha(+) M Phi s from a CSF-1-dependent to -independent program of proliferation. Thus, IL-4 increases the relative density of tissue M Phi s by overcoming the constraints mediated by the availability of CSF-1. Finally, although both elevated CSF1R and IL-4R alpha signaling triggered proliferation above homeostatic levels, only CSF-1 led to the recruitment of monocytes and neutrophils. Thus, the IL-4 pathway of proliferation may have developed as an alternative to CSF-1 to increase resident M Phi numbers without coincident monocyte recruitment