Analysis of Two-Dimensional Feedback Systems over Networks Using Dissipativity

This paper investigates the closed-loop L2 stability of two-dimensional (2-D) feedback systems across a digital communication network by introducing the tool of dissipativity. First, sampling of a continuous 2-D system is considered and an analytical characterization of the QSR-dissipativity of the sampled system is presented. Next, the input-feed forward output-feedback passivity (IF-OFP), a simplified form of QSR-dissipativity, is utilized to study the framework of feedback interconnection of two 2-D systems over networks. Then, the effects of signal quantization in communication links on dissipativity degradation of the 2-D feedback quantized system is analyzed. Additionally,an event-triggered mechanism is developed for 2-D networked control systems while maintaining L2 stability of the closed-loop system. In the end, an illustrative example is provided

miR-homoHSV of Singapore Grouper Iridovirus (SGIV) Inhibits Expression of the SGIV Pro-apoptotic Factor LITAF and Attenuates Cell Death

<div><p>Growing evidence demonstrates that various large DNA viruses could encode microRNAs (miRNAs) that regulate host and viral genes to achieve immune evasion. In this study, we report that miR-homoHSV, an miRNA encoded by Singapore grouper iridovirus (SGIV), can attenuate SGIV-induced cell death. Mechanistically, SGIV miR-homoHSV targets SGIV ORF136R, a viral gene that encodes the pro-apoptotic lipopolysaccharide-induced TNF-α (LITAF)-like factor. miR-homoHSV suppressed exogenous and endogenous SGIV LITAF expression, and thus inhibited SGIV LITAF-induced apoptosis. Meanwhile, miR-homoHSV expression was able to attenuate cell death induced by viral infection, presumably facilitating viral replication through the down-regulation of the pro-apoptotic gene SGIV LITAF. Together, our data suggest miR-homoHSV may serve as a feedback regulator of cell death during viral infection. The findings of this study provide a better understanding of SGIV replication and pathogenesis.</p> </div

Expression profiles of endogenous miR-homoHSV and SGIV LITAF.

<p>The relative expression level of miR-homoHSV rose rapidly reaching its peak 6 h p.i. and then decreased (blue). Relative expression level of miR-homoHSV 6 h p.i. was set to 1 for comparison. The U6 gene was used as an internal control. The amount of SGIV LITAF mRNA accumulated stably from 6 to 48 h p.i. (red). Relative expression level of SGIV LITAF 6 h p.i. was set to 1 for comparison. β-Actin was used as an internal control. Data are means from rapidly at least three independent experiments done in duplicate; error bars indicate SEM.</p

miR-homoHSV inhibits SGIV LITAF-induced apoptosis.

<p>(A) Morphology of FHM cells 48 h after transfection with the empty vector pLL3.7, pLL-homoHSV, pLL3.7 and pEGFP-LITAF, and pLL-homoHSV and pEGFP-LITAF, from left to right. (B) Nuclear morphology of FHM cells 48 h after transfection with the same vectors above. Arrows indicate apoptotic bodies. Many apoptotic bodies were observed in cells co-transfected with pLL3.7 and pEGFP-LITAF. (C) Flow cytometric analysis of dead cells in FHM cells transfected with the vectors above 48 h after transfection. (D) Statistical results for the proportion of PI-stained positive cells 24 h and 48 h after transfection with empty vector pLL3.7, pLL-homoHSV (left panel), pLL3.7 and pEGFP-LITAF, and pLL-homoHSV and pEGFP-LITAF (right panel). Data are means from at least three independent experiments. Error bars indicate SEM. *<i>P</i><0.05.</p

miR-506 expression was down-regulated in human renal cancer.

<p>A. Expression of miR-506 in 4 renal cancer cell lines and human proximal tubule epithelial cell line HK-2; B. Expression of miR-506 in ccRCC tissues and adjacent normal tissues; C. The survival analysis of miR-506. Patients with lower miR-506 expression in tumor tissue were closely correlated with poorer overall survival than patients with higher expression. * P <0.05.</p

Supplementary document for Three-dimensional location system based on an L-shaped array of Rydberg atomic receivers - 6438391.pdf

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si-LITAF specifically blocks SGIV-induced apoptosis.

<p>(A) si-LITAF efficiently suppresses endogenous SGIV LITAF mRNA (left) and protein (right) expression in FHM cells. (B and C) Morphology (B) and nuclear morphology (C) of FHM cells 48 h after infection with SGIV. FHM cells were transfected with si-con (left) or si-LITAF (right), and infected with SGIV 18 h later. Arrows (bottom panels) indicate apoptotic bodies. Many apoptotic bodies were observed in si-con transfected FHM cells. (D) si-LITAF blocks SGIV-induced apoptosis. PI staining and fluorescence-activated cell sorter analysis of FHM cells 48 h after infection (up). Statistical results of the proportion of PI-stained positive cells 48 h after infection with SGIV (bottom). Data are means of at least three independent experiments; error bars indicate SEM. *<i>P</i><0.05. Flow cytometric analysis of apoptotic cells in FHM cells treated as described for panel B. </p

miR-homoHSV inhibits exogenous and endogenous SGIV LITAF expression.

<p>(A) miR-homoHSV located in the antisense strand of ORF136R. (B and C) miR-homoHSV inhibits exogenous (B) and endogenous (C) SGIV LITAF protein expression. (D and E) miR-homoHSV does not affect exogenous SGIV MCP expression at the mRNA (D) or protein (E) level. </p

miR-homoHSV attenuates SGIV-induced apoptosis and promotes SGIV replication.

<p>(A) Morphology of FHM cells 48 h after infection with SGIV. FHM cells was transfected with pLL3.7 (left) or pLL-homoHSV (right), and then infected with SGIV. (B) Nuclear morphology of FHM cells 48 h after infection with SGIV. Cells were treated as described for panel A. Arrows indicate apoptotic bodies. Many apoptotic bodies were observed in pLL3.7 transfected FHM cells (left). (C) Flow cytometric analysis of dead cells in FHM cells treated as described for panel A. Top panels are PI staining and fluorescence-activated cell sorter analysis of FHM cells 48 h after infection. Bottom panel shows the statistical results of the proportion of PI-stained positive cells 24 h and 48 h after SGIV infection. Data are means of at least three independent experiments; error bars indicate SEM. *<i>P</i><0.05. (D and E) miR-homoHSV promotes endogenous SGIV ORF016L (D) and SGIV MCP (E) mRNAs (top) and SGIV MCP protein (bottom) expression in FHM cells. (F) miR-homoHSV promotes SGIV replication. FHM cells overexpressing miR-homoHSV/miR-con were infected with SGIV, and virus was collected 48 h p.i. The viral titer was measured using the TCID50 method. Error bars indicate SEM.</p

Dendrimer-Templated Ultrasmall and Multifunctional Photothermal Agents for Efficient Tumor Ablation

Ultrasmall and multifunctional nanoparticles are highly desirable for photothermal cancer therapy, but the synthesis of these nanoparticles remains a huge challenge. Here, we used a dendrimer as a template to synthesize ultrasmall photothermal agents and further modified them with multifunctional groups. Dendrimer-encapsulated nanoparticles (DENPs) including copper sulfide, platinum, and palladium nanoparticles possessed a sub-5 nm size and exhibited an excellent photothermal effect. DENPs were further modified with TAT or RGD peptides to facilitate their cellular uptake and targeting delivery to tumors. They were also decorated with fluorescent probes for real-time imaging and tracking of the particles’ distribution. The <i>in vivo</i> study revealed RGD-modified DENPs efficiently reduced the tumor growth upon near-infrared irradiation. In all, our study provides a facile and flexible scaffold to prepare ultrasmall and multifunctional photothermal agents