Efficient 2075-nm Laser Emission From Ho3+-Doped Fluorotellurite Glass in a Compact All-Fiber Structure

In this Letter, we report an Ho3+-doped fluorotellurite glass all-fiber laser at 2075 nm. The gain fiber is pumped in-band with a 1976-nm fiber laser and connected by fusion splicing. A high-quality fusion splicing point with a loss of \u3c 0.1 dB was obtained by finely adjusting the splicing power and offset. In addition, by optimizing the writing parameters, a third-order fiber Bragg grating (FBG) with a reflectivity of 98% was achieved at 2075 nm using the femtosecond laser direct-writing method. Using the FBG as the laser cavity mirror and a relatively short 28-cm-long home-made Ho3+-doped fluorotellurite fiber as the laser medium, a laser with a maximum unsaturated output power of 7.33 W was obtained, and the corresponding slope efficiency was as high as 93.4%. The first, to the best of our knowledge, demonstration of the fluorotellurite glass all-fiber ∼2.1-µm laser presented in this work may pave the way for a high-power 2.1-µm fiber laser with a compact structure

Recent advances in luminescence and lasing research in ZBYA glass

In the last few decades, fluoride glasses have attracted a growing interest due to their unique advantages compared to multi-component oxide glasses. Among them, the most studied and widely used were fluorozirconate glasses, represented by ZrF4–BaF2–LaF3–AlF3–NaF (ZBLAN) glasses. However, compared with ZBLAN glasses, a kind of fluorozirconate glass with the components ZrF4–BaF2–YF3–AlF3 (ZBYA) has higher thermal and chemical stability. In this paper, we first introduce the advantages of ZBYA glasses compared to ZBLAN glasses. Then we review and discuss recent advances in research on luminescence and lasing in ZBYA glass and fiber. These studies suggest that ZBYA glass has strong potential for use as a gain medium material in high power mid-infrared fiber lasers

Direct Femtosecond Laser Inscription of High-Order Bragg Gratings in Fluoroaluminate Glass Fiber

This letter reports the fabrication of fiber Bragg gratings (FBGs) within in-house fabricated fluoroaluminate (AlF3) glass fibers using femtosecond (fs) laser inscription at 800 nm. The grating strength of the FBGs was investigated for different pulse energies and different orders, and a 3rd-order FBG with Bragg wavelength at 1557 nm was found to have the highest reflectivity of 99.5%. In addition, the reflectivity of the mid-IR grating peaks for different orders was also studied, and a 2nd-order FBG with a reflectivity of 98.8% was obtained at 2864 nm. Finally, the temperature characteristics of a mid-IR FBG were studied between 30 °C and 150 °C, showing a linear wavelength dependence and an excellent stability for the refractive index modulation. Such highly reflectivity FBGs in AlF3 fiber have significant potential for applications in the development of compact all-fiber mid-IR fiber lasers

Secured Data Transmission Over Insecure Networks-on-Chip by Modulating Inter-Packet Delays

As the network-on-chip (NoC) integrated into an SoC design can come from an untrusted third party, there is a growing risk that data integrity and security get compromised when supposedly sensitive data flows through such an untrusted NoC. We thus introduce a new method that can ensure secure and secret data transmission over such an untrusted NoC. Essentially, the proposed scheme relies on encoding binary data as delays between packets travelling across the source and destination pair. The maximum data transmission rate of this inter-packet-delay (IPD)-based communication channel can be determined from the analytical model developed in this article. To further improve the undetectability and robustness of the proposed data transmission scheme, a new block coding method and communication protocol are also proposed. Experimental results show that the proposed IPD-based method can achieve a packet error rate (PER) of as low as 0.3% and an effective throughput of $\boldsymbol {2.3\times 10^{5}}$ b/s, outperforming the methods of thermal covert channel, cache covert channel, and circuit-based encryption and, thus, is suitable for secure data transmission in unsecure systems

A miR-155–Peli1–c-Rel pathway controls the generation and function of T follicular helper cells

MicroRNA (miRNA) deficiency impairs the generation of T follicular helper (Tfh) cells, but the contribution of individual miRNAs to this phenotype remains poorly understood. In this study, we performed deep sequencing analysis of miRNAs expressed in Tfh cells and identified a five-miRNA signature. Analyses of mutant mice deficient of these miRNAs revealed that miR-22 and miR-183/96/182 are dispensable, but miR-155 is essential for the generation and function of Tfh cells. miR-155 deficiency led to decreased proliferation specifically at the late stage of Tfh cell differentiation and reduced CD40 ligand (CD40L) expression on antigen-specific CD4+T cells. Mechanistically, miR-155 repressed the expression of Peli1, a ubiquitin ligase that promotes the degradation of the NF-κB family transcription factor c-Rel, which controls cellular proliferation and CD40L expression. Therefore, our study identifies a novel miR-155-Peli1-c-Rel pathway that specifically regulates Tfh cell generation and functionC. Xiao is a Pew Scholar in Biomedical Sciences. This study is supported by the PEW Charitable Trusts, Cancer Research Institute, Lupus Research Institute, National Institutes of Health (grants R01AI087634, R01AI089854, R56AI110403, and R56AI121155 to C. Xiao and grants R01AI103646 and R01AI108651 to L.-F. Lu), National Natural Science Foundation of China (grant 31570882 to W.-H. Liu, grant 31570883 to N. Xiao, and grant 31570911 to G. Fu), 1000 Young Talents Program of China (grant K08008 to N. Xiao), the Fundamental Research Funds for the Central Universities of the People’s Republic of China (grant 20720150065 to N. Xiao and G. Fu), the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, Information and Communications Technology, and Future Planning (grant NRF-2015R1C1A1A01052387 to S.G. Kang), and a 2016 research grant from Kangwon National University (to S.G. Kang

MicroRNA-146 Inhibits Thrombin-Induced NF-jB Activation and Subsequent Inflammatory Responses in Human Retinal Endothelial Cells

PURPOSE. Nuclear factor-jB (NF-jB), a key regulator of immune and inflammatory responses, plays important roles in diabetes-induced microvascular complications including diabetic retinopathy (DR). Thrombin activates NF-jB through protease-activated receptor (PAR)-1, a member of the G-protein-coupled receptor (GPCR) superfamily, and contributes to DR. The current study is to uncover the roles of microRNA (miRNA) in thrombin-induced NF-jB activation and retinal endothelial functions. METHODS. Target prediction was performed using the TargetScan algorithm. Predicted target was experimentally validated by luciferase reporter assays. Human retinal endothelial cells (HRECs) were transfected with miRNA mimics or antimiRs and treated with thrombin. Expression levels of miR-146 and related protein-coding genes were analyzed by quantitative (q)RT-PCR. Functional changes of HRECs were analyzed by leukocyte adhesion assays. RESULTS. We identified that caspase-recruitment domain (CARD)-containing protein 10 (CARD10), an essential scaffold/adaptor protein of GPCR-mediated NF-jB activation pathway, is a direct target of miR-146. Thrombin treatment resulted in NF-jB-dependent upregulation of miR-146 in HRECs; while transfection of miR-146 mimics resulted in significant downregulation of CARD10 and prevented thrombin-induced NF-jB activation, suggest that a negative feedback regulation of miR-146 on thrombin-induced NF-jB through targeting CARD10. Furthermore, overexpression of miR-146 prevented thrombin-induced increased leukocyte adhesion to HRECs. CONCLUSIONS. We uncovered a novel negative feedback regulatory mechanism on thrombininduced GPCR-mediated NF-jB activation by miR-146. In combination with the negative feedback regulation of miR-146 on the IL-1R/toll-like receptor (TLR)-mediated NF-jB activation in RECs that we reported previously, our results underscore a pivotal, negative regulatory role of miR-146 on multiple NF-jB activation pathways and related inflammatory processes in DR. Keywords: microRNA, diabetic retinopathy, retinal endothelial cells, NF-kB activation, thrombin D iabetic retinopathy (DR) is the leading cause of blindness in people between ages of 25 and 74 in the industrialized world. 1 Nearly all individuals who have had type I diabetes for more than 15 years develop DR. Approximately 50% to 80% of type II diabetic patients also develop retinopathy after 20 years of diabetes. 2 Although progress has been made, there is still no preventive treatment. MicroRNAs (miRNAs) are small, noncoding RNAs, and represent a newly recognized, important level of geneexpression regulation. 3,4 However, the roles of miRNAs in DR are still largely unknown. Previously, to identify miRNAs involved in DR, we performed miRNA-expression profiling and established miRNA transcriptomes of the retina and retinal endothelial cells (RECs) of normal control and streptozotocin (STZ)-induced diabetic rats 3 months after the onset of diabetes. 5 Among inflammation-related miRNAs, we showed that miR-146 was upregulated in RECs of diabetic rats

2.9 µm lasing from a Ho³⁺/Pr³⁺ co-doped AlF₃-based glass fiber pumped by a 1150 nm laser

Ho3+/Pr3+ co-doped AlF3-based glass fibers were fabricated by using a rod-in-tube method based on the matrix glass composition of AlF3-BaF2-CaF2-YF3-SrF2-MgF2-LiF-ZrF4-PbF2. Under the pump of a 1150 mW Raman fiber laser, a 2.9 µm laser was observed in a 19 cm long Ho3+/Pr3+ co-doped AlF3-based glass fiber with an output power of 173 mW and a slope efficiency of 10.4%. Ho3+/Pr3+ co-doped AlF3-based glasses were fabricated to investigate the deactivation effects of Pr3+ ions on the Ho3+:5I7 level. Our results showed that the Ho3+/Pr3+ co-doped AlF3-based glass fibers are potential gain media for ~2.9µm lasers