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BackgroundThe polypeptide hormone calcitonin is clinically well known for its ability to relieve neuropathic pain such as spinal canal stenosis, diabetic neuropathy and complex regional pain syndrome. Mechanisms for its analgesic effect, however, remain unclear. Here we investigated the mechanism of anti-hyperalgesic action of calcitonin in a neuropathic pain model in rats.ResultsSubcutaneous injection of elcatonin, a synthetic derivative of eel calcitonin, relieved hyperalgesia induced by chronic constriction injury (CCI). Real-time reverse transcriptase-polymerase chain reaction analysis revealed that the CCI provoked the upregulation of tetrodotoxin (TTX)-sensitive Nav.1.3 mRNA and downregulation of TTX-resistant Nav1.8 and Nav1.9 mRNA on the ipsilateral dorsal root ganglion (DRG), which would consequently increase the excitability of peripheral nerves. These changes were reversed by elcatonin. In addition, the gene expression of the calcitonin receptor and binding site of 125I-calcitonin was increased at the constricted peripheral nerve tissue but not at the DRG. The anti-hyperalgesic effect and normalization of sodium channel mRNA by elcatonin was parallel to the change of the calcitonin receptor expression. Elcatonin, however, did not affect the sensitivity of nociception or gene expression of sodium channel, while it suppressed calcitonin receptor mRNA under normal conditions.ConclusionsThese results suggest that the anti-hyperalgesic action of calcitonin on CCI rats could be attributable to the normalization of the sodium channel expression, which might be exerted by an unknown signal produced at the peripheral nerve tissue but not by DRG neurons through the activation of the calcitonin receptor. Calcitonin signals were silent in the normal condition and nerve injury may be one of triggers for conversion of a silent to an active signal.

We test the luxury consumption hypothesis of Ait-Sahalia, Parker, and Yogo (2004), using a unique international art price, import/export flow, and stock market data set. We find that the demand for art by Japanese collectors is positively correlated with art prices and Japanese stock prices. This correlation is magnified during the “bubble period” of the Japanese economy (the mid-1980s to the early 1990s) and gains even further strength for works of art typically favored by Japanese collectors. Our results suggest that Japanese investors (or Japanese asset markets) indeed affect international art prices—especially during the bubble period and its aftermath.

Intramolecular excited-state proton transfer (ESPT) of 3-hydroxychromone (3-HC), 3-hydroxyflavone (3-HF) and 2-(2-naphthyl)-3-hydroxychromone (2-NHC), and of their water clusters, was investigated in a supersonic expansion. The visible tautomer fluorescence excitation spectra of these compounds exhibit considerably well-resolved vibrational structures, while no significant uv fluorescence excitation spectrum due to the normal form was observed. The upper limit of the rate constant of the tautomer formation was estimated to be 1.77×1012 s−1 for 3-HC, 6.5×1011 s−1 for 3-HF, and 1.54×1011 s−1 for 2-NHC in supersonic expansion by simulation of the linewidth of the respective origin bands in the visible fluorescence excitation spectra. The order of rate constants of the tautomer formations in the supersonic free jet are consistent with that of the ESPT of these compounds in nonpolar solution. The fluorescence excitation and dispersed fluorescence spectra demonstrate 1:1 and 1:2 water complex formations of 3-HF and 2-NHC and no ESPT in these water clusters. However, no evidence of water complex formation was obtained in jet-cooled 3-HC.

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