Experimental high-intensity three-photon entangled source

We experimentally realize a high-intensity three-photon Greenberger-Horne-Zeilinger (GHZ) entanglement source directly following the proposal by Rarity and Tapster [J. G. Rarity and P. R. Tapster, Phys. Rev. A 59, R35 (1999)]. The threefold coincidence rate can be more than 200 Hz with a fidelity of 0.811, and the intensity can be further improved with moderate fidelity degradation. The GHZ entanglement is characterized by testing the Bell-Mermin inequality and using an entanglement witness operator. To optimize the polarization-entangled source, we theoretically analyze the relationship between the mean photon number of the single-photon source and the probability of parametric down-conversion.Comment: 4 pages, 4 figure

A Method against Interrupted-Sampling Repeater Jamming Based on Energy Function Detection and Band-Pass Filtering

Interrupted-sampling repeater jamming (ISRJ) is a new kind of coherent jamming to the large time-bandwidth linear frequency modulation (LFM) signal. Many jamming modes, such as lifelike multiple false targets and dense false targets, can be made through setting up different parameters. According to the “storage-repeater-storage-repeater” characteristics of the ISRJ and the differences in the time-frequency-energy domain between the ISRJ signal and the target echo signal, one new method based on the energy function detection and band-pass filtering is proposed to suppress the ISRJ. The methods mainly consist of two parts: extracting the signal segments without ISRJ and constructing band-pass filtering function with low sidelobe. The simulation results show that the method is effective in the ISRJ with different parameters

Chronic inflammation triggered by the NLRP3 inflammasome in myeloid cells promotes growth plate dysplasia by mesenchymal cells

AbstractSkeletal complications are common features of neonatal-onset multisystem inflammatory disease (NOMID), a disorder caused by NLRP3-activating mutations. NOMID mice in which NLRP3 is activated globally exhibit several characteristics of the human disease, including systemic inflammation and cartilage dysplasia, but the mechanisms of skeletal manifestations remain unknown. In this study, we find that activation of NLRP3 in myeloid cells, but not mesenchymal cells triggers chronic inflammation, which ultimately, causes growth plate and epiphyseal dysplasia in mice. These responses are IL-1 signaling-dependent, but independent of PARP1, which also functions downstream of NLRP3 and regulates skeletal homeostasis. Mechanistically, inflammation causes severe anemia and hypoxia in the bone environment, yet down-regulates the HIF-1α pathway in chondrocytes, thereby promoting the demise of these cells. Thus, activation of NLRP3 in hematopoietic cells initiates IL-1β-driven paracrine cascades, which promote abnormal growth plate development in NOMID mice.</jats:p

IL-17A produced by αβ T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction.

Emerging evidence suggests that the T helper 17 (T(H)17) subset of αβ T cells contributes to the development of allergic asthma. In this study, we found that mice lacking the αvβ8 integrin on dendritic cells did not generate T(H)17 cells in the lung and were protected from airway hyper-responsiveness in response to house dust mite and ovalbumin sensitization and challenge. Because loss of T(H)17 cells inhibited airway narrowing without any obvious effects on airway inflammation or epithelial morphology, we examined the direct effects of T(H)17 cytokines on mouse and human airway smooth muscle function. Interleukin-17A (IL-17A), but not IL-17F or IL-22, enhanced contractile force generation of airway smooth muscle through an IL-17 receptor A (IL-17RA)-IL-17RC, nuclear factor κ light-chain enhancer of activated B cells (NF-κB)-ras homolog gene family, member A (RhoA)-Rho-associated coiled-coil containing protein kinase 2 (ROCK2) signaling cascade. Mice lacking integrin αvβ8 on dendritic cells showed impaired activation of this pathway after ovalbumin sensitization and challenge, and the diminished contraction of the tracheal rings in these mice was reversed by IL-17A. These data indicate that the IL-17A produced by T(H)17 cells contributes to allergen-induced airway hyper-responsiveness through direct effects on airway smooth muscle