Infrared Optical Response of Metallic Graphene Nanoribbons

We investigate theoretically the infrared optical response characteristics of metallic armchair/zigzag-edge graphene nanoribbons (A/ZGNRs) to an external longitudinally polarized electromagnetic field at low temperatures. Within the framework of linear response theory at the perturbation regime, we examine the optical infrared absorption threshold energy, absorption power, dielectric function, and electron energy loss spectra near the neutrality points of the systems. It is demonstrated that, by some numerical examples, the photon-assisted direct interband absorptions for AGNR exist with different selection rules from those for ZGNR and single-walled carbon nanotube at infrared regime. This infrared optical property dependence of GNRs on field frequency may be used to design graphene-based nanoscale optoelectronic devices for the detection of infrared electromagnetic irradiations

EBV-Encoded LMP1 Upregulates Igκ 3′Enhancer Activity and Igκ Expression in Nasopharyngeal Cancer Cells by Activating the Ets-1 through ERKs Signaling

Accumulating evidence indicates that epithelial cancer cells, including nasopharyngeal carcinoma (NPC) cells, express immunoglobulins (Igs). We previously found that the expression of the kappa light chain protein in NPC cells can be upregulated by the EBV-encoded latent membrane protein 1 (LMP1). In the present study, we used NPC cell lines as models and found that LMP1-augmented kappa production corresponds with elevations in ERKs phosphorylation. PD98059 attenuates LMP1-induced ERKs phosphorylation resulting in decreased expression of the kappa light chain. ERK-specific small interfering RNA blunts LMP1-induced kappa light chain gene expression. Luciferase reporter assays demonstrate that immunoglobulin κ 3′ enhancer (3′Eκ) is active in Igκ-expressing NPC cells and LMP1 upregulates the activity of 3′Eκ in NPC cells. Moreover, mutation analysis of the PU binding site in 3′Eκ and inhibition of the MEK/ERKs pathway by PD98059 indicate that the PU site is functional and LMP1-enhanced 3′Eκ activity is partly regulated by this site. PD98059 treatment also leads to a concentration-dependent inhibition of LMP1-induced Ets-1 expression and phosphorylation, which corresponds with a dose-dependent attenuation of LMP1-induced ERK phosphorylation and kappa light chain expression. Suppression of endogenous Ets-1 by small interfering RNA is accompanied by a decrease of Ig kappa light chain expression. Gel shift assays using nuclear extracts of NPC cells indicate that the transcription factor Ets-1 is recruited by LMP1 to the PU motif within 3′Eκ in vitro. ChIP assays further demonstrate Ets-1 binding to the PU motif of 3′Eκ in cells. These results suggest that LMP1 upregulates 3′Eκ activity and kappa gene expression by activating the Ets-1 transcription factor through the ERKs signaling pathway. Our studies provide evidence for a novel regulatory mechanism of kappa expression, by which virus-encoded proteins activate the kappa 3′ enhancer through activating transcription factors in non-B epithelial cancer cells

Simulation of a 1550-nm InGaAsP-InP transistor laser

A 1550 InGaAsP-InP multiple-quantum-well (MQW) transistor laser is numerically modeled. The proposed structure has a deep-ridge waveguide and asymmetric doping profile in the base (i.e. only the part below QWs of the base is doped) which provides good optical and electrical confinement and effectively reduces the lateral leakage current and optical absorption. The important physical models and parameters are discussed and validated by modeling a conventional ridge-waveguide laser diode and comparing the results with the experiment. The simulation results of the transistor laser demonstrate a low threshold ( 25 % slope efficiency with the current gain of 2 ~ 4. The optical saturation and voltage-controlled operation are also demonstrated. Copyright 2009 Society of Photo-Optical Instrumentation Engineers. One print or electronic copy may be made for personal use only. Systematic reproduction and distribution, duplication of any material in this paper for a fee or for commercial purposes, or modification of the content of the paper are prohibited.Applied Science, Faculty ofElectrical and Computer Engineering, Department ofReviewedFacult

Skin Rash as the First Manifestation of Pediatric Chronic Neutrophilic Leukemia

A 6-year-old girl presented with recurrent skin rash at the initial stage, recent joint pain, and neutrophilia was found during a routine blood test. After a multidisciplinary case discussion, she was diagnosed with chronic neutrophil leukemia, and the symptoms were relieved after hydroxyurea and luxolitinib treatment. She received the allogeneic hematopoietic stem cell transplantation subsequently. At present, she is in stable condition and under follow-up. Chronic neutrophil leukemia is a rare disease, which rarely occurs in children. It is more difficult to diagnose in patients with skin rash as the first manifestation. The diagnosis and treatment of this case reflects the important role of multidisciplinary cooperation in the diagnosis and treatment of difficult and rare diseases

Vortioxetine hydrobromide inhibits the growth of gastric cancer cells in vivo and in vitro by targeting JAK2 and SRC

Abstract Gastric cancer is the fourth leading cause of cancer deaths worldwide. Most patients are diagnosed in the advanced stage. Inadequate therapeutic strategies and the high recurrence rate lead to the poor 5-year survival rate. Therefore, effective chemopreventive drugs for gastric cancer are urgently needed. Repurposing clinical drugs is an effective strategy for discovering cancer chemopreventive drugs. In this study, we find that vortioxetine hydrobromide, an FDA-approved drug, is a dual JAK2/SRC inhibitor, and has inhibitory effects on cell proliferation of gastric cancer. Computational docking analysis, pull-down assay, cellular thermal shift assay (CETSA) and in vitro kinase assays are used to illustrate vortioxetine hydrobromide directly binds to JAK2 and SRC kinases and inhibits their kinase activities. The results of non-reducing SDS-PAGE and Western blotting indicate that vortioxetine hydrobromide suppresses STAT3 dimerization and nuclear translocation activity. Furthermore, vortioxetine hydrobromide inhibits the cell proliferation dependent on JAK2 and SRC and suppresses the growth of gastric cancer PDX model in vivo. These data demonstrate that vortioxetine hydrobromide, as a novel dual JAK2/SRC inhibitor, curbs the growth of gastric cancer in vitro and in vivo by JAK2/SRC-STAT3 signaling pathways. Our results highlight that vortioxetine hydrobromide has the potential application in the chemoprevention of gastric cancer

Additional file 1: Figure S1. of E2 regulates MMP-13 via targeting miR-140 in IL-1β-induced extracellular matrix degradation in human chondrocytes

The expression of MMP-13 mRNA level increased in five OA patients’ articular cartilage tissues. Quantitative reverse transcription-polymerase chain reaction analysis of the matrix metalloproteinase 13 (MMP-13) in articular cartilage tissues from five patients with OA. Figure S2. The gene expressions of cartilage matrix gene for cartilage development show no effect after E2 treatment. (DOCX 25 kb

The MEK inhibitor, PD98059, abolishes the LMP1-increased 3′E_κ enhancer activity.

<p>HNE2 and HNE2-LMP1 cells were co-transfected with <i>pβ-3′E_κwt, pGL3-β,</i> or <i>pGL3-Basic</i> and the internal control <i>pRL-SV40</i> plasmids. Cells were incubated for 24 hr and then treated with PD98059 (50 µM) or DMSO (0.1%) for an additional 12 hr after which activity of firefly and <i>Renilla</i> luciferase was monitored as described in “<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032624#s2" target="_blank">Materials and Methods</a>”. Values for firefly luciferase activity were normalized to those obtained for <i>Renilla</i> luciferase activity. Values obtained for <i>pβ-3′E_κwt-</i> or <i>pGL3-β</i>-transfected cells were divided by the corresponding values obtained for <i>pGL3-Basic-</i>transfected cells. Data are shown as means ± S.D. of three independent experiments performed in triplicate. Statistical significance: *<i>p</i><0.05.</p

Inhibition of the ERKs signaling pathway blunts LMP1-increased kappa light chain expression at both the mRNA and protein levels.

<p>(A) HNE2-LMP1 cells were treated with the indicated concentrations of PD98059 or 0.1% DMSO for 2 hr. Whole cell lysates were prepared and total and phosphorylated ERKs levels were determined by Western blotting. (B) HNE2-LMP1 cells were treated with the indicated concentrations of PD98059 or 0.1% DMSO for 12 hr. Kappa light chain expression in NPC cells was assessed by Western blotting using a specific antibody. (C) HNE2 and HNE2-LMP1 cells were treated with 50 µM PD98059 or 0.1% DMSO for 12 hr and Western blotting was performed to detect kappa light chain expression. (D) HNE2 and HNE2-LMP1 cells were incubated with medium containing the indicated concentration of PD98059 or 0.1% DMSO for 12 hr. Total RNA was isolated from cells and subjected to RT-PCR, using specific primers designed to amplify <i>kappa light chain</i> and <i>actin</i> mRNAs. (E) HNE2-LMP1 cells were transfected with <i>si-ERK</i> or scrambled oligonucleotide. ERK and Ig kappa protein levels were detected by immunoblotting. The results shown are representative of three independent experiments. Phosphorylation or total expression level for each protein as well as mRNA was estimated by densitometry and are presented as a ratio to the respective loading control (right panels). XG7 and XG6 cells are shown as positive and negative controls, respectively, for kappa light chain.</p

Inhibition of ERKs signaling reduces LMP1-induced Ets-1 expression and phosphorylation.

<p>(A) Inhibition of LMP1-upregulated Ets-1 protein expression by the MEK inhibitor, PD98059. HNE2-LMP1 cells were treated with the indicated concentrations of PD98059 or 0.1% DMSO for 12 hr. Ets-1 expression in NPC cells was determined by Western blot. A representive image of three independent experiments with similar results and the Ets-1 expression level quantified by densitometry are shown. α-Tubulin was used to verify equal protein loading. (B) Inhibition of threonine phosphorylation of Ets-1 by the MEK inhibitor, PD98059. NPC cells were treated with the indicated concentrations of PD98059 for 12 hr and whole cell extracts were immunoprecipitated with an anti-Ets-1 antibody. Similar protein levels of Ets-1 were loaded and resolved by SDS-PAGE, and the levels of Ets-1 threonine phosphorylation were determined by Western blot analysis using a pan threonine phosphorylation antibody. The membrane was then stripped and reprobed with anti-Ets-1. The threonine phosphorylation level of Ets-1 was quantified by densitometry. (C) HNE2-LMP1 cells were transfected with <i>si-Ets-1</i> or scrambled oligonucleotide. Ets-1 and Ig kappa protein levels were detected by immunoblotting. The results shown are representative of three independent experiments. Phosphorylation or expression level for each protein was estimated by densitometry and was presented as a ratio to the respective loading control (right panels).</p