42 research outputs found
Delocalized single-photon Dicke states and the Leggett- Garg inequality in solid state systems
We show how to realize a single-photon Dicke state in a large one-dimensional
array of two- level systems, and discuss how to test its quantum properties.
Realization of single-photon Dicke states relies on the cooperative nature of
the interaction between a field reservoir and an array of two-level-emitters.
The resulting dynamics of the delocalized state can display Rabi-like
oscillations when the number of two-level emitters exceeds several hundred. In
this case the large array of emitters is essentially behaving like a
mirror-less cavity. We outline how this might be realized using a
multiple-quantum-well structure and discuss how the quantum nature of these
oscillations could be tested with the Leggett-Garg inequality and its
extensions.Comment: 29 pages, 5 figures, journal pape
'Reaching the hard to reach' - lessons learned from the VCS (voluntary and community Sector). A qualitative study.
Background The notion 'hard to reach' is a contested and ambiguous term that is commonly used within the spheres of social care and health, especially in discourse around health and social inequalities. There is a need to address health inequalities and to engage in services the marginalized and socially excluded sectors of society. Methods This paper describes a pilot study involving interviews with representatives from eight Voluntary and Community Sector (VCS) organisations . The purpose of the study was to explore the notion of 'hard to reach' and perceptions of the barriers and facilitators to accessing services for 'hard to reach' groups from a voluntary and community sector perspective. Results The 'hard to reach' may include drug users, people living with HIV, people from sexual minority communities, asylum seekers, refugees, people from black and ethnic minority communities, and homeless people although defining the notion of the 'hard to reach' is not straight forward. It may be that certain groups resist engaging in treatment services and are deemed hard to reach by a particular service or from a societal stance. There are a number of potential barriers for people who may try and access services, including people having bad experiences in the past; location and opening times of services and how services are funded and managed. A number of areas of commonality are found in terms of how access to services for 'hard to reach' individuals and groups could be improved including: respectful treatment of service users, establishing trust with service users, offering service flexibility, partnership working with other organisations and harnessing service user involvement.
Conclusions: If health services are to engage with groups that are deemed 'hard to reach' and marginalised from mainstream health services, the experiences and practices for engagement from within the VCS may serve as useful lessons for service improvement for statutory health services
Reductions in External Divalent Cations Evoke Novel Voltage-Gated Currents in Sensory Neurons
It has long been recognized that divalent cations modulate cell excitability. Sensory nerve excitability is of critical importance to peripheral diseases associated with pain, sensory dysfunction and evoked reflexes. Thus we have studied the role these cations play on dissociated sensory nerve activity. Withdrawal of both Mg2+ and Ca2+ from external solutions activates over 90% of dissociated mouse sensory neurons. Imaging studies demonstrate a Na+ influx that then causes depolarization-mediated activation of voltage-gated Ca2+ channels (CaV), which allows Ca2+ influx upon divalent re-introduction. Inhibition of CaV (ω-conotoxin, nifedipine) or NaV (tetrodotoxin, lidocaine) fails to reduce the Na+ influx. The Ca2+ influx is inhibited by CaV inhibitors but not by TRPM7 inhibition (spermine) or store-operated channel inhibition (SKF96365). Withdrawal of either Mg2+ or Ca2+ alone fails to evoke cation influxes in vagal sensory neurons. In electrophysiological studies of dissociated mouse vagal sensory neurons, withdrawal of both Mg2+ and Ca2+ from external solutions evokes a large slowly-inactivating voltage-gated current (IDF) that cannot be accounted for by an increased negative surface potential. Withdrawal of Ca2+ alone fails to evoke IDF. Evidence suggests IDF is a non-selective cation current. The IDF is not reduced by inhibition of NaV (lidocaine, riluzole), CaV (cilnidipine, nifedipine), KV (tetraethylammonium, 4-aminopyridine) or TRPM7 channels (spermine). In summary, sensory neurons express a novel voltage-gated cation channel that is inhibited by external Ca2+ (IC50∼0.5 µM) or Mg2+ (IC50∼3 µM). Activation of this putative channel evokes substantial cation fluxes in sensory neurons
Emergence and Evolution of Cooperation Under Resource Pressure
We study the influence that resource availability has on cooperation in the context of hunter-gatherer
societies. This paper proposes a model based on archaeological and ethnographic research on resource
stress episodes, which exposes three different cooperative regimes according to the relationship
between resource availability in the environment and population size. The most interesting regime
represents moderate survival stress in which individuals coordinate in an evolutionary way to increase
the probabilities of survival and reduce the risk of failing to meet the minimum needs for survival.
Populations self-organise in an indirect reciprocity system in which the norm that emerges is to share
the part of the resource that is not strictly necessary for survival, thereby collectively lowering the
chances of starving. Our findings shed further light on the emergence and evolution of cooperation in
hunter-gatherer societies.Spanish Ministry of Science and Innovation Project CSD2010-00034
(SimulPast CONSOLIDER-INGENIO 2010) and HAR2009-06996; from the Argentine National Scientific
and Technical Research Council (CONICET): Project PIP-0706; from the Wenner-Gren Foundation for
Anthropological Research: Project GR7846; and from the project H2020 FET OPEN RIA IBSEN/66272
Gene Expression Profile of Neuronal Progenitor Cells Derived from hESCs: Activation of Chromosome 11p15.5 and Comparison to Human Dopaminergic Neurons
BACKGROUND: We initiated differentiation of human embryonic stem cells (hESCs) into dopamine neurons, obtained a purified population of neuronal precursor cells by cell sorting, and determined patterns of gene transcription.
METHODOLOGY: Dopaminergic differentiation of hESCs was initiated by culturing hESCs with a feeder layer of PA6 cells. Differentiating cells were then sorted to obtain a pure population of PSA-NCAM-expressing neuronal precursors, which were then analyzed for gene expression using Massive Parallel Signature Sequencing (MPSS). Individual genes as well as regions of the genome which were activated were determined.
PRINCIPAL FINDINGS: A number of genes known to be involved in the specification of dopaminergic neurons, including MSX1, CDKN1C, Pitx1 and Pitx2, as well as several novel genes not previously associated with dopaminergic differentiation, were expressed. Notably, we found that a specific region of the genome located on chromosome 11p15.5 was highly activated. This region contains several genes which have previously been associated with the function of dopaminergic neurons, including the gene for tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, IGF2, and CDKN1C, which cooperates with Nurr1 in directing the differentiation of dopaminergic neurons. Other genes in this region not previously recognized as being involved in the functions of dopaminergic neurons were also activated, including H19, TSSC4, and HBG2. IGF2 and CDKN1C were also found to be highly expressed in mature human TH-positive dopamine neurons isolated from human brain samples by laser capture.
CONCLUSIONS: The present data suggest that the H19-IGF2 imprinting region on chromosome 11p15.5 is involved in the process through which undifferentiated cells are specified to become neuronal precursors and/or dopaminergic neurons
CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism
In this study, we investigated the role of CD38 in a pristane-induced murine model of lupus. CD38-deficient (Cd38-/-) but not ART2-deficient (Art2-/-) mice developed less severe lupus compared to wild type (WT) mice, and their protective phenotype consisted of (i) decreased IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes/macrophages, (iii) decreased production of anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated glomerulonephritis. Cd38-/- pristane-elicited peritoneal exudate cells had defective CCL2 and TNF-α secretion following TLR7 stimulation. However, Tnf-α and Cxcl12 gene expression in Cd38-/- bone marrow (BM) cells was intact, suggesting a CD38-independent TLR7/TNF-α/CXCL12 axis in the BM. Chemotactic responses of Cd38-/- Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38-/- Ly6Chi monocytes and Ly6Clo monocytes/macrophages had defective apoptosis-mediated cell death. Importantly, mice lacking the cation channel TRPM2 (Trpm2-/-) exhibited very similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and Ly6Clo monocytes/macrophages compared to WT mice. These findings reveal a new role for CD38 in promoting aberrant inflammation and lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given the implications of CD38 in the activation of TRPM2, our data suggest that CD38 modulation of pristane-induced apoptosis is TRPM2-dependent.We would like to thank Dr. Yasuo Mori for providing the
Tr pm 2−/− mice, Clara Sánchez for animal husbandry
at the IPBLN-CSIC Animal Facility, and Thomas S. Simpler and Uma Mudunuru for animal husbandry at the
University of Alabama at Birmingham (UAB). We would also like to thank Laura Montosa from the Centro de
Instrumentación Cientifica (CIC) at the Universidad de Granada (UGR) for technical support with microscopy,
as well as Mohamed Tassi and Ana Santos at CIC, UGR, and Sandra García-Jiménez, Victoria Romero-del-Amo, Gemma Palencia-López, and Samuel Ruiz-Santiago at Campus Formación Granada for tissue preparations,
H&E staining, and other staining procedures. Work performed in the Sancho lab was supported in part by the
European Commission in collaboration with the following Funding Agencies: (i) Junta de Andalucía (J.A.),
Consejería Innovación Ciencia y Empresa y Consejería Educación y Ciencia, Project: PC08-CTS-04046 to J.S. and M.Z., and (ii) Ministerio de Economía y Competitividad (MINECO), Projects: SAF-2011-27261 to J.S. and M.Z. and SAF2014-55088-R to R.M. Work performed in the Lund lab was supported by funds provided by UAB.S
Estilo lingüístico y prosocialidad en un contexto político en Twitter
El comportamiento prosocial ha sido explicado desde diferentes modelos con el propósito de comprender por qué las personas realizan conductas que benefician a otras de manera voluntaria (Barreto, López y Borja, 2015). El comportamiento prosocial contribuye, en algunos casos, a disminuir comportamientos de racismo, indiferencia social, exclusión y agresividad, entre otros fenómenos del comportamiento antisocial. La teoría evolucionista y las teorías sociales son algunos de los modelos explicativos que tienen más evidencia a favor. Desde la perspectiva evolucionista, se explica la aparición del comportamiento prosocial como una forma de garantizar la supervivencia de la especie, mediante comportamientos cooperativos en los que prevalece el interés a favor de la especie, sobre el individual con el fin de que la información genética sea transmitida de generación en generación (Guijo, 2002).1a edició