Mid-Holocene Northern Hemisphere warming driven by Arctic amplification.

The Holocene thermal maximum was characterized by strong summer solar heating that substantially increased the summertime temperature relative to preindustrial climate. However, the summer warming was compensated by weaker winter insolation, and the annual mean temperature of the Holocene thermal maximum remains ambiguous. Using multimodel mid-Holocene simulations, we show that the annual mean Northern Hemisphere temperature is strongly correlated with the degree of Arctic amplification and sea ice loss. Additional model experiments show that the summer Arctic sea ice loss persists into winter and increases the mid- and high-latitude temperatures. These results are evaluated against four proxy datasets to verify that the annual mean northern high-latitude temperature during the mid-Holocene was warmer than the preindustrial climate, because of the seasonally rectified temperature increase driven by the Arctic amplification. This study offers a resolution to the "Holocene temperature conundrum", a well-known discrepancy between paleo-proxies and climate model simulations of Holocene thermal maximum

CT Evidence for Subchondral Trabecular Injury of the Femoral Head in Transient Osteoporosis of the Hip: A Case Report

A 28-yr-old woman presented with both hip pain that started sequentially during the peripartum period. Diagnosis of transient osteoporosis of the hip (TOH) was made based on typical findings of plain radiographs and magnetic resonance images. The subchondral trabeculae of the femoral head were evaluated on serially taken coronal multiplanar reformation computerized tomogram images. At 4 weeks after pain onset, marked decrease in the sclerotic density with irregular discontinuation was observed in the primary compression trabeculae. At 12 weeks, a focal area of irregular thickening of trabeculae was observed. At 20 weeks, sclerotic density of trabeculae recovered markedly and the focal area of irregular trabecular thickening disappeared. At 1 yr, subchondral trabeculae recovered almost completely. The evidence of subchondral trabecular injury was observed in the femoral heads of TOH

Detectability of dissipative motion in quantum vacuum via superradiance

We propose an experiment for generating and detecting vacuum-induced dissipative motion. A high frequency mechanical resonator driven in resonance is expected to dissipate energy in quantum vacuum via photon emission. The photons are stored in a high quality electromagnetic cavity and detected through their interaction with ultracold alkali-metal atoms prepared in an inverted population of hyperfine states. Superradiant amplification of the generated photons results in a detectable radio-frequency signal temporally distinguishable from the expected background.Comment: 4 pages, 2 figure

Imiquimod enhances excitability of dorsal root ganglion neurons by inhibiting background (K2P) and voltage-gated (Kv1.1 and Kv1.2) potassium channels

<p>Abstract</p> <p>Background</p> <p>Imiquimod (IQ) is known as an agonist of Toll-like receptor 7 (TLR7) and is widely used to treat various infectious skin diseases. However, it causes severe itching sensation as its side effect. The precise mechanism of how IQ causes itching sensation is unknown. A recent report suggested a molecular target of IQ as TLR7 expressed in dorsal root ganglion (DRG) neurons. However, we recently proposed a TLR7-independent mechanism, in which the activation of TLR7 is not required for the action of IQ in DRG neurons. To resolve this controversy regarding the involvement of TLR7 and to address the exact molecular identity of itching sensation by IQ, we investigated the possible molecular target of IQ in DRG neurons.</p> <p>Findings</p> <p>When IQ was applied to DRG neurons, we observed an increase in action potential (AP) duration and membrane resistance both in wild type and TLR7-deficient mice. Based on these results, we tested whether the treatment of IQ has an effect on the activity of K⁺channels, K_v1.1 and K_v1.2 (voltage-gated K⁺channels) and TREK1 and TRAAK (K_2Pchannels). IQ effectively reduced the currents mediated by both K⁺channels in a dose-dependent manner, acting as an antagonist at TREK1 and TRAAK and as a partial antagonist at K_v1.1 and K_v1.2.</p> <p>Conclusions</p> <p>Our results demonstrate that IQ blocks the voltage-gated K⁺channels to increase AP duration and K_2Pchannels to increase membrane resistance, which are critical for the membrane excitability of DRG neurons. Therefore, we propose that IQ enhances the excitability of DRG neurons by blocking multiple potassium channels and causing pruritus.</p