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Presents a study which investigated the effects of interfaces such as metal/polymer interfaces and polymer/polymer interfaces on the space-charge distribution in multiply low-density polyethylene (LDPE) using a pulsed electroacoustic method. Details on the experimental setup; Description of the space-charge profile of LDPE; Overview of the space-charge distribution in a two-layer sample; Modification of electrical field.

Microglia are widely accepted as surveillants in the central nervous system that are continually searching the local environment for signs of injury. Following an inflammatory situation, microglia alter their morphology, extend ramified processes, and undergo cell body hypertrophy. Extracellular nucleotides are recognized as a danger signal by microglia. ADP acting on P2Y12 receptors induce process extension of microglia thereby attracting microglia to the site of adenosine tri-phosphate/ ADP leaking or release. However, the question whether ADP/P2Y12 receptor signaling directly stimulates the production or release of inducible factors such as cytokines remains unclear. In this study, we found that CC chemokine ligand 3 ( CCL3) is induced by ADP-treated primary microglia. Pharmacological characterization using pertussis toxin, a P2Y12 receptor inhibitor, and a calcium chelator revealed that CCL3 induction was caused by P2Y12 receptor-mediated intracellular calcium elevation. Next, nuclear factor of activated T-cell dephosphorylation and nuclear translocalization were observed. Calcineurin, an inhibitor for nuclear factor of activated T cell, suppressed CCL3 induction. These data indicate that microglial P2Y12 receptors are utilized to trigger an acute inflammatory response in microglia via rapid CCL3 induction after ADP stimulation. [ABSTRACT FROM AUTHOR]

Extracellular nucleotides have been implicated as signaling molecules used by microglia to sense adverse physiological conditions, such as neuronal damage. They act through purinoceptors, especially the G-protein-coupled P2Y receptor P2Y12R. Emerging evidence has indicated that activated spinal microglia responding to nerve injury are key cellular intermediaries in the resulting highly debilitating chronic pain state, namely neuropathic pain. However, the role of microglial P2Y12Rs in neuropathic pain remains unknown. Here, we show that the level of P2Y12R mRNA expression was markedly increased in the spinal cord ipsilateral to the nerve injury and that this expression was highly restricted to ionized binding calcium adapter molecule 1-positive microglia. An increase in the immunofluorescence of P2Y12R protein in the ipsilateral spinal cord was also observed after nerve injury, and P2Y12R-positive cells were double labeled with the microglial marker OX-42. Blocking spinal P2Y12R by the intrathecal administration of its antagonist AR-C69931MX prevented the development of tactile allodynia (pain hypersensitivity to innocuous stimuli), a hallmark of neuropathic pain syndrome. Furthermore, mice lacking P2ry12 (P2ry12 -/-) displayed impaired tactile allodynia after nerve injury without any change in basal mechanical sensitivity. Moreover, a single intrathecal administration of AR-C69931MX or oral administration of clopidogrel (a P2Y12R blocker clinically in use) to nerve-injured rats produced a striking alleviation of existing tactile allodynia. Together, our findings indicate that activation of P2Y12Rs in spinal microglia may be a critical event in the pathogenesis of neuropathic pain and suggest that blocking microglial P2Y12R might be a viable therapeutic strategy for treating neuropathic pain. [ABSTRACT FROM AUTHOR]

Abstract: A new fluorescent chemosensor, 1,10-phenanthroline-4,7-dione (1), which is capable of the ratiometric sensing of anions in aqueous MeCN, was developed. Chemosensor 1 recognized an anion via two NH groups in the molecule, and showed a much higher affinity for F− than that of 4-quinolone, which binds to an anion at one NH group of the molecule. Upon binding to F−, the intensity of the emission band ascribed to the complex of 1–F− was drastically enhanced, while the emission intensity of unbound 1 gradually decreased. The changes in these two emission bands enabled the successful ratiometric sensing. [Copyright &y& Elsevier]

Information on space-charge behavior in thick insulated samples aids in understanding the dc characteristics of polymer-insulated dc cables. The pulsed electroacoustic method is used to investigate several space charge formation factors in 2 mm-thick polyethylene (PE). The following results were obtained. For measurement factors: (1) A polymeric semiconducting electrode provides a more accurate measurement than does a metal electrode as a result of better matching of acoustic impedance with PE. (2) Within a dc electrical stress range of several tens kV/mm, the space charge distributions under and after dc voltage application are almost the same; this is due to a comparatively long time of space-charge decay. (3) The space-charge distribution of a plate sample agrees with that of a cable sample having the same insulation thickness. For insulating material factors: (1) The amount of space charge in crosslinked polyethylene (XLPE) is much larger than that in low-density PE (base of XLPE). The space charge of XLPE continues to increase even after dc voltage application (24 h); that of LDPE reaches equilibrium with a few hours. (2) The aforementioned space charge difference between XLPE and LDPE is assumed to be caused by ionic impurities in XLPE, not by the additives themselves (acetophenon and cumylalcohol as byproducts of cross linking and antioxidant). [ABSTRACT FROM AUTHOR]

Investigates light emission in polyethylene with a needle-like microvoid, under a negative impulse voltage at the metal-polymer interface. Examination of the temporal behavior of discharge in the microvoid at the metal-polymer interface; Observation of light emission during voltage rise and fall phases; What the emitted light consisted of; Revelation made from the characteristics of light emission.

Extracellular nucleotides have been implicated as signaling molecules used by microglia to sense adverse physiological conditions, such as neuronal damage. They act through purinoceptors, especially the G-protein-coupled P2Y receptor P2Y(12)R. Emerging evidence has indicated that activated spinal microglia responding to nerve injury are key cellular intermediaries in the resulting highly debilitating chronic pain state, namely neuropathic pain. However, the role of microglial P2Y(12)Rs in neuropathic pain remains unknown. Here, we show that the level of P2Y(12)R mRNA expression was markedly increased in the spinal cord ipsilateral to the nerve injury and that this expression was highly restricted to ionized binding calcium adapter molecule 1-positive microglia. An increase in the immunofluorescence of P2Y(12)R protein in the ipsilateral spinal cord was also observed after nerve injury, and P2Y(12)R-positive cells were double labeled with the microglial marker OX-42. Blocking spinal P2Y(12)R by the intrathecal administration of its antagonist AR-C69931MX prevented the development of tactile allodynia (pain hypersensitivity to innocuous stimuli), a hallmark of neuropathic pain syndrome. Furthermore, mice lacking P2ry(12) (P2ry(12)(-/-)) displayed impaired tactile allodynia after nerve injury without any change in basal mechanical sensitivity. Moreover, a single intrathecal administration of AR-C69931MX or oral administration of clopidogrel (a P2Y(12)R blocker clinically in use) to nerve-injured rats produced a striking alleviation of existing tactile allodynia. Together, our findings indicate that activation of P2Y(12)Rs in spinal microglia may be a critical event in the pathogenesis of neuropathic pain and suggest that blocking microglial P2Y(12)R might be a viable therapeutic strategy for treating neuropathic pain.