295 research outputs found
Antiferromagnetism and d-wave superconductivity in cuprates: a uster DMFT study
We present a new approach to investigate the coexistence of
antiferromagnetism and d-wave superconductivity in the two dimensional extended
Hubbard model within a numerically exact cluster dynamical mean-field
approximation. Self-consistent solutions with two non-zero order parameters
exists in the wide range of doping level and temperatures. A linearized
equation for energy spectrum near the Fermi level have been solved. The
resulting d-wave gap has the correct magnitude and k-dependence but some
distortion compare to the pure d_{x^2-y^2} superconducting order parameter due
to the presence of underlying antiferromagnetic ordering.Comment: 4 pages, 3 figure
Involvement of Neuro-Immune Interactions in Pruritus With Special Focus on Receptor Expressions
Pruritus is a common, but very challenging symptom with a wide diversity of underlying causes like dermatological, systemic, neurological and psychiatric diseases. In dermatology, pruritus is the most frequent symptom both in its acute and chronic form (over 6 weeks in duration). Treatment of chronic pruritus often remains challenging. Affected patients who suffer from moderate to severe pruritus have a significantly reduced quality of life. The underlying physiology of pruritus is very complex, involving a diverse network of components in the skin including resident cells such as keratinocytes and sensory neurons as well as transiently infiltrating cells such as certain immune cells. Previous research has established that there is a significant crosstalk among the stratum corneum, nerve fibers and various immune cells, such as keratinocytes, T cells, basophils, eosinophils and mast cells. In this regard, interactions between receptors on cutaneous and spinal neurons or on different immune cells play an important role in the processing of signals which are important for the transmission of pruritus. In this review, we discuss the role of various receptors involved in pruritus and inflammation, such as TRPV1 and TRPA1, IL-31RA and OSMR, TSLPR, PAR-2, NK1R, H1R and H4R, MRGPRs as well as TrkA, with a focus on interaction between nerve fibers and different immune cells. Emerging evidence shows that neuro-immune interactions play a pivotal role in mediating pruritus-associated inflammatory skin diseases such as atopic dermatitis, psoriasis or chronic spontaneous urticaria. Targeting these bidirectional neuro-immune interactions and the involved pruritus-specific receptors is likely to contribute to novel insights into the underlying pathogenesis and targeted treatment options of pruritus
The Electrical-Thermal Switching in Carbon Black-Polymer Composites as a Local Effect
Following the lack of microscopic information about the intriguing well-known
electrical-thermal switching mechanism in Carbon Black-Polymer composites, we
applied atomic force microscopy in order to reveal the local nature of the
process and correlated it with the characteristics of the widely used
commercial switches. We conclude that the switching events take place in
critical interparticle tunneling junctions that carry most of the current. The
macroscopic switched state is then a result of a dynamic-stationary state of
fast switching and slow reconnection of the corresponding junctions.Comment: 14 pages, 5 figures,Typographic correctio
There is no functional small-fibre neuropathy in prurigo nodularis despite neuroanatomical alterations
Prurigo nodularis (PN) is a pruritic condition with altered epidermal neuroanatomy as demonstrated previously. Here we elucidated neuroimmunological mechanisms by combining functional, morphological and gene expression experiments in twelve subjects with PN and eight healthy controls. Subjects with PN showed a reduced intraâepidermal nerve fibre density (IENFD) in lesional skin. Quantitative sensory testing indicated maintenance of somatosensory function compared to controls. None of the tested molecular markers including the neuronâdistracting SEMA3A and neuronâattracting NGF were altered in lesional vs nonâlesional skin in PN subjects. Accordingly, we speculate that scratching may contribute to reduced IENFD rather than an authentic endogenous neuropathy.FSW - Self-regulation models for health behavior and psychopathology - ou
Combination of self-organization mechanisms to enhance service discovery in open systems
Decentralized systems have emerged as an alternative to centralized approaches for
dealing with dynamic requirements in new business models. These systems should provide mechanisms that contribute to flexibility and facilitate adaptation to changes in the environment. In this paper, we present two self-organization mechanisms for a decentralized service discovery system in order to improve its performance. These mechanisms are based on local actions of agents that only consider local information about queries they forward during the discovery process. The self-organization actions are chosen by each agent individually when the agent considers them to be appropriate. The actions are: remaining in the system, leaving the system, cloning, and changing structural relations with other agents. We have evaluated each self-organization mechanism separately but also the combination of the two as the environmental conditions in the service demand change.
The results show that the proposed self-organization mechanisms considerably improve the performance of the service discovery systemDel Val Noguera, E.; Rebollo Pedruelo, M.; Botti Navarro, VJ. (2014). Combination of self-organization mechanisms to enhance service discovery in open systems. Information Sciences. 279:138-162. doi:10.1016/j.ins.2014.03.109S13816227
TIRAP, an Adaptor Protein for TLR2/4, Transduces a Signal from RAGE Phosphorylated upon Ligand Binding
The receptor for advanced glycation end products (RAGE) is thought to be involved in the pathogenesis of a broad range of inflammatory, degenerative and hyperproliferative diseases. It binds to diverse ligands and activates multiple intracellular signaling pathways. Despite these pivotal functions, molecular events just downstream of ligand-activated RAGE have been surprisingly unknown. Here we show that the cytoplasmic domain of RAGE is phosphorylated at Ser391 by PKCÎś upon binding of ligands. TIRAP and MyD88, which are known to be adaptor proteins for Toll-like receptor-2 and -4 (TLR2/4), bound to the phosphorylated RAGE and transduced a signal to downstream molecules. Blocking of the function of TIRAP and MyD88 largely abrogated intracellular signaling from ligand-activated RAGE. Our findings indicate that functional interaction between RAGE and TLRs coordinately regulates inflammation, immune response and other cellular functions
Naphthalene flanked diketopyrrolopyrrole based organic semiconductors for high performance organic field effect transistors
Here, we design and synthesize three new diketopyrrolopyrrole (DPP) derivatives with naphthalene, possessing large-scaled p-delocalized electronic structure, as the flanking groups and both linear (n-decyl and n-dodecyl) and branched (2-hexyldecyl)alkyl chains as substitutions as active layer for high performance organic field-effect transistors (OFETs). The thermal, photophysical properties, energy levels and solid state molecular stacking have been studied in detail. All the materials show excellent thermal stability with a decomposition temperature of 400 °C, high semi-crystallinity feature, suitable HOMO & LUMO energy levels, and varying crystalline domain sizes in thin films. Bottom-contact/top-gate transistor devices are thus fabricated to investigate the mobility. Encouragingly, all compounds function well in OFET devices and show significant potential as p-type semiconducting materials. The monomer with the n-decyl alkyl chain (D-DPPN) shows the highest mobility of 0.019 cm2V-1s-1, with the Ion/Ioffratio reaching 106. We for the first time synthesize naphthalene flanked DPP monomers and achieve high mobility in OFET devices when using these monomers without any further functionalization as semiconductors directly. The primary result that high mobility is observed for monomers only opens a new way for further DPP application and provides more possibilities for constructing high performance polymeric and small molecular semiconductors based on this new DPP dye
The mechanisms by which polyamines accelerate tumor spread
Increased polyamine concentrations in the blood and urine of cancer patients reflect the enhanced levels of polyamine synthesis in cancer tissues arising from increased activity of enzymes responsible for polyamine synthesis. In addition to their de novo polyamine synthesis, cells can take up polyamines from extracellular sources, such as cancer tissues, food, and intestinal microbiota. Because polyamines are indispensable for cell growth, increased polyamine availability enhances cell growth. However, the malignant potential of cancer is determined by its capability to invade to surrounding tissues and metastasize to distant organs. The mechanisms by which increased polyamine levels enhance the malignant potential of cancer cells and decrease anti-tumor immunity are reviewed. Cancer cells with a greater capability to synthesize polyamines are associated with increased production of proteinases, such as serine proteinase, matrix metalloproteinases, cathepsins, and plasminogen activator, which can degrade surrounding tissues. Although cancer tissues produce vascular growth factors, their deregulated growth induces hypoxia, which in turn enhances polyamine uptake by cancer cells to further augment cell migration and suppress CD44 expression. Increased polyamine uptake by immune cells also results in reduced cytokine production needed for anti-tumor activities and decreases expression of adhesion molecules involved in anti-tumor immunity, such as CD11a and CD56. Immune cells in an environment with increased polyamine levels lose anti-tumor immune functions, such as lymphokine activated killer activities. Recent investigations revealed that increased polyamine availability enhances the capability of cancer cells to invade and metastasize to new tissues while diminishing immune cells' anti-tumor immune functions
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