Compact Metamaterials Induced Circuits and Functional Devices

In recent years, we have witnessed a rapid expansion of using metamaterials to manipulate light or electromagnetic (EM) wave in a subwavelength scale. Specially, metamaterials have a strict limitation on element dimension from effective medium theory with respect to photonic crystals and other planar structures such as frequency selective surface (FSS). In this chapter, we review our effort in exploring physics and working mechanisms for element miniaturization along with the resulting effects on element EM response. Based on these results, we afford some guidelines on how to design and employ these compact meta-atoms in engineering functional devices with high performances. We found that some specific types of planar fractal or meandered structures are particularly suitable to achieve element miniaturization. In what follows, we review our effort in Section 1 to explore novel theory and hybrid method in designing broadband and dual band planar devices. By using single or double such compact composite right-/left-handed (CRLH) atom, we show that many microwave/RF circuits, i.e., balun, rat-race coupler, power divider and diplexer, can be further reduced while without inducing much transmission loss from two perspectives of lumped and distributed CRLH TLs. In Section 2, we show that a more compact LH atom can be engineered by combining a fractal ring and a meandered thin line. Numerical and experimental results demonstrate that a subwavelength focusing is achieved in terms of smooth outgoing field and higher imaging resolution. Section 3 is devoted to a clocking device from the new concept of superscatterer illusions. To realize the required material parameters, we propose a new mechanism by combining both electric and magnetic particles in a composite meta-atom. Such deep subwavelength particles enable exact manipulation of material parameters and thus facilitate desirable illusion performances of a proof-of-concept sample constructed by 6408 gradually varying meta-atoms. Finally, we summarize our results in the last section

Cell transcriptomic atlas of the non-human primate Macaca fascicularis.

Studying tissue composition and function in non-human primates (NHPs) is crucial to understand the nature of our own species. Here we present a large-scale cell transcriptomic atlas that encompasses over 1 million cells from 45 tissues of the adult NHP Macaca fascicularis. This dataset provides a vast annotated resource to study a species phylogenetically close to humans. To demonstrate the utility of the atlas, we have reconstructed the cell-cell interaction networks that drive Wnt signalling across the body, mapped the distribution of receptors and co-receptors for viruses causing human infectious diseases, and intersected our data with human genetic disease orthologues to establish potential clinical associations. Our M. fascicularis cell atlas constitutes an essential reference for future studies in humans and NHPs.We thank W. Liu and L. Xu from the Huazhen Laboratory Animal Breeding Centre for helping in the collection of monkey tissues, D. Zhu and H. Li from the Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory) for technical help, G. Guo and H. Sun from Zhejiang University for providing HCL and MCA gene expression data matrices, G. Dong and C. Liu from BGI Research, and X. Zhang, P. Li and C. Qi from the Guangzhou Institutes of Biomedicine and Health for experimental advice or providing reagents. This work was supported by the Shenzhen Basic Research Project for Excellent Young Scholars (RCYX20200714114644191), Shenzhen Key Laboratory of Single-Cell Omics (ZDSYS20190902093613831), Shenzhen Bay Laboratory (SZBL2019062801012) and Guangdong Provincial Key Laboratory of Genome Read and Write (2017B030301011). In addition, L.L. was supported by the National Natural Science Foundation of China (31900466), Y. Hou was supported by the Natural Science Foundation of Guangdong Province (2018A030313379) and M.A.E. was supported by a Changbai Mountain Scholar award (419020201252), the Strategic Priority Research Program of the Chinese Academy of Sciences (XDA16030502), a Chinese Academy of Sciences–Japan Society for the Promotion of Science joint research project (GJHZ2093), the National Natural Science Foundation of China (92068106, U20A2015) and the Guangdong Basic and Applied Basic Research Foundation (2021B1515120075). M.L. was supported by the National Key Research and Development Program of China (2021YFC2600200).S

Removal of broken reamer stuck into femoral shaft in implanting PFNA: a case report

Femoral intertrochanteric fracture is very common in elderly population. The usual treatment for these patients is intra-extramedullary fixation. In normal situations, expand medullary cavity is needed, in order to implant various intramedullary implants. On rare occasion, which will in turn lead to the reamer is stuck into the medullary cavity of femoral shaft. Open or closed technique for moving of the broken nails had been reported before. We firstly report a novel technique by using handy tool which included in orthopaedic instrument set to remove the broken reamer stuck into femoral cavity when implanting a PFNA

Design of Automatic Control System of Silica Reactor Based on S7-200 PLC

In view of problems of low production efficiency and bad products quality existed in manual control used by silica production system of one company, the paper proposed a reform scheme of automatic control system of silica reactor based on S7-200 PLC. It analyzed technology process of silica production system and introduced design of hardware and software of the reformed automatic control system in details. The actual application showed that the reformed automatic control system realizes automatic control for flow of acid, alkali and water, automatic control for solution temperature and solution pH value, which improves products quality and production efficiency

Presentation_1_N-Methyl D-aspartate receptor subtype 2B/Ca2+/calmodulin-dependent protein kinase II signaling in the lateral habenula regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia.pdf

Trigeminal neuralgia (TN) is a peripheral nerve disorder often accompanied by abnormalities in mood. The lateral habenula (LHb) plays important roles in the modulation of pain and emotion. In the present study, we investigated the involvement of the LHb in the mechanisms underlying allodynia and anxiety induced by partial transection of the infraorbital nerve (pT-ION) in mice. Our results indicated that pT-ION induced persistent orofacial allodynia and anxiety-like behaviors, which were correlated with increased phosphorylation of N-Methyl D-aspartate receptor (NMDAR) subtype 2B (p-NR2B) and Ca2+/calmodulin-dependent protein kinase II (p-CaMKII) in LHb neurons. Bilateral inhibition of NMDARs and CaMKII in the LHb attenuated the allodynia and anxiety-like behavior induced by pT-ION. Furthermore, bilateral activation of NMDARs in the LHb increased the expression of p-NR2B and p-CaMKII and induced orofacial allodynia and anxiety-like behaviors in naive mice. Adeno-associated virus (AAV)-mediated expression of hM3D(Gq) in CaMKII+ neurons of the bilateral LHb, followed by clozapine-N-oxide (CNO) administration, also triggered orofacial allodynia and anxiety-like behaviors in naïve mice with successful virus infection in LHb neurons (verified based on immunofluorescence). In conclusion, these findings suggest that activation of NMDA/CaMKII signaling in the LHb contributes to the occurrence and development of TN and related anxiety-like behaviors. Therefore, suppressing the activity of CaMKII+ neurons in the bilateral LHb by targeting NMDA/CaMKII may represent a novel strategy for treating pain and anxiety associated with TN.</p

Image_3_N-Methyl D-aspartate receptor subtype 2B/Ca2+/calmodulin-dependent protein kinase II signaling in the lateral habenula regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia.TIF

Trigeminal neuralgia (TN) is a peripheral nerve disorder often accompanied by abnormalities in mood. The lateral habenula (LHb) plays important roles in the modulation of pain and emotion. In the present study, we investigated the involvement of the LHb in the mechanisms underlying allodynia and anxiety induced by partial transection of the infraorbital nerve (pT-ION) in mice. Our results indicated that pT-ION induced persistent orofacial allodynia and anxiety-like behaviors, which were correlated with increased phosphorylation of N-Methyl D-aspartate receptor (NMDAR) subtype 2B (p-NR2B) and Ca2+/calmodulin-dependent protein kinase II (p-CaMKII) in LHb neurons. Bilateral inhibition of NMDARs and CaMKII in the LHb attenuated the allodynia and anxiety-like behavior induced by pT-ION. Furthermore, bilateral activation of NMDARs in the LHb increased the expression of p-NR2B and p-CaMKII and induced orofacial allodynia and anxiety-like behaviors in naive mice. Adeno-associated virus (AAV)-mediated expression of hM3D(Gq) in CaMKII+ neurons of the bilateral LHb, followed by clozapine-N-oxide (CNO) administration, also triggered orofacial allodynia and anxiety-like behaviors in naïve mice with successful virus infection in LHb neurons (verified based on immunofluorescence). In conclusion, these findings suggest that activation of NMDA/CaMKII signaling in the LHb contributes to the occurrence and development of TN and related anxiety-like behaviors. Therefore, suppressing the activity of CaMKII+ neurons in the bilateral LHb by targeting NMDA/CaMKII may represent a novel strategy for treating pain and anxiety associated with TN.</p

ANXA1-derived peptide for targeting PD-L1 degradation inhibits tumor immune evasion in multiple cancers

Background Immune checkpoint inhibitors (ICIs) therapy targeting programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) shows promising clinical benefits. However, the relatively low response rate highlights the need to develop an alternative strategy to target PD-1/PD-L1 immune checkpoint. Our study focuses on the role and mechanism of annexin A1 (ANXA1)-derived peptide A11 degrading PD-L1 and the effect of A11 on tumor immune evasion in multiple cancers.Methods Binding of A11 to PD-L1 was identified by biotin pull-down coupled with mass spectrometry analysis. USP7 as PD-L1’s deubiquitinase was found by screening a human deubiquitinase cDNA library. The role and mechanism of A11 competing with USP7 to degrade PD-L1 were analyzed. The capability to enhance the T cell-mediated tumor cell killing activity and antitumor effect of A11 via suppressing tumor immune evasion were investigated. The synergistic antitumor effect of A11 and PD-L1 mAb (monoclonal antibody) via suppressing tumor immune evasion were also studied in mice. The expression and clinical significance of USP7 and PD-L1 in cancer tissues were evaluated by immunohistochemistry.Results A11 decreases PD-L1 protein stability and levels by ubiquitin proteasome pathway in breast cancer, lung cancer and melanoma cells. Mechanistically, A11 competes with PD-L1’s deubiquitinase USP7 for binding PD-L1, and then degrades PD-L1 by inhibiting USP7-mediated PD-L1 deubiquitination. Functionally, A11 promotes T cell ability of killing cancer cells in vitro, inhibits tumor immune evasion in mice via increasing the population and activation of CD8+ T cells in tumor microenvironment, and A11 and PD-1 mAb possess synergistic antitumor effect in mice. Moreover, expression levels of both USP7 and PD-L1 are significantly higher in breast cancer, non-small cell lung cancer and skin melanoma tissues than those in their corresponding normal tissues and are positively correlated in cancer tissues, and both proteins for predicting efficacy of PD-1 mAb immunotherapy and patient prognosis are superior to individual protein.Conclusion Our results reveal that A11 competes with USP7 to bind and degrade PD-L1 in cancer cells, A11 exhibits obvious antitumor effects and synergistic antitumor activity with PD-1 mAb via inhibiting tumor immune evasion and A11 can serve as an alternative strategy for ICIs therapy in multiple cancers