Effects of Particle Size and Cement Replacement of LCD Glass Powder in Concrete

The high quality liquid crystal display (LCD) processing waste glass (LPWG) generated from the manufacturing process of Korea’s LCD industries, having the world’s highest technological level and production, was finely ground into particles smaller than cement particles (higher fineness than OPC) to verify their applicability and performance as a replacement for cement. For a concrete mix having a W/B ratio of 0.44, cement was replaced with LPWG glass powder (LGP) at ratios of 5, 10, 15, and 20% (LGP12) and 5 and 10% (LGP5) according to the particle size to prepare test cylinder specimens, which were tested with respect to air contents, slump in fresh concrete, and compressive strength and splitting tensile strength of hardened concrete. The microstructure of the concrete specimens was analyzed through Scanning Electron Microscopy (SEM), Energy Dispersive X-ray (EDX), and a Mercury Intrusion Porosimetry (MIP). Replacement of cement with LGP for cement could effectively decrease the quantity of cement used due to the excellent performance of LGP. It may positively contribute to the sustainable development of the cement industry as well as waste recycling and environment conservation on a national scale

Structural safety inspection of reinforced concrete structures considering failure probabilities of structural members

Regular safety inspections of existing reinforced concrete (RC) structures are required according to the regulations and criteria set by each country. In South Korea, the safety inspection regulations provided by the Korea Infrastructure Safety and Technology Corporation (KISTEC) are followed. These regulations were developed based on fuzzy theory to avoid subjective decisions, and provide standardized deterioration grades for member types, floors, and the entire structure. However, the safety inspection regulation by the KISTEC often provides unconservative evaluation results. In particular, as the importance factors of beam and slab members are set lower than those of other members, there are cases in which deteriorations occurring in beams and slabs are not properly reflected in the floor level evaluation. In this study, to overcome such limitations, case studies were carried out and modified importance factors for structural member types were proposed considering the failure probabilities of each member type based on the reliability theory. The importance modification factor was calculated based on the strength ratio of structural members so that the more dangerous the members are, the more impact they give on the evaluation. Overall, compared to the KISTEC method, the proposed method provided conservative but practical assessment results, and it was found that the proposed importance factors can be very useful to properly reflect the effects of damaged members on the deterioration status evaluation of the floors and the entire structure

NF-κB/STAT3/PI3K signaling crosstalk in iMycEμ B lymphoma

<p>Abstract</p> <p>Background</p> <p>Myc is a well known driver of lymphomagenesis, and Myc-activating chromosomal translocation is the recognized hallmark of Burkitt lymphoma, an aggressive form of non-Hodgkin's lymphoma. We developed a model that mimics this translocation event by inserting a mouse <it>Myc </it>cDNA gene into the immunoglobulin heavy chain locus, just upstream of the intronic Eμ enhancer. These mice, designated iMyc^Eμ, readily develop B-cell lymphoma. To study the mechanism of Myc-induced lymphoma, we analyzed signaling pathways in lymphoblastic B-cell lymphomas (LBLs) from iMyc^Eμmice, and an LBL-derived cell line, iMyc^Eμ-1.</p> <p>Results</p> <p>Nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) were constitutively activated in iMyc^Eμmice, not only in LBLs but also in the splenic B-lymphocytes of young animals months before tumors developed. Moreover, inhibition of either transcription factor in iMyc^Eμ-1 cells suppressed growth and caused apoptosis, and the abrogation of NF-κB activity reduced DNA binding by both STAT3 and Myc, as well as Myc expression. Inhibition of STAT3 signaling eliminated the activity of both NF-κB and Myc, and resulted in a corresponding decrease in the level of Myc. Thus, in iMyc^Eμ-1 cells NF-κB and STAT3 are co-dependent and can both regulate Myc. Consistent with this, NF-κB and phosphorylated STAT3 were physically associated with one another. In addition, LBLs and iMyc^Eμ-1 cells also showed constitutive AKT phosphorylation. Blocking AKT activation by inhibiting PI3K reduced iMyc^Eμ-1 cell proliferation and caused apoptosis, via downregulation of NF-κB and STAT3 activity and a reduction of Myc levels. Co-treatment with NF-κB, STAT3 or/and PI3K inhibitors led to additive inhibition of iMyc^Eμ-1 cell proliferation, suggesting that these signaling pathways converge.</p> <p>Conclusions</p> <p>Our findings support the notion that constitutive activation of NF-κB and STAT3 depends on upstream signaling through PI3K, and that this activation is important for cell survival and proliferation, as well as for maintaining the level of Myc. Together, these data implicate crosstalk among NF-κB, STAT3 and PI3K in the development of iMyc^EμB-cell lymphomas.</p

Inhibitory Effect of Inflexinol on Nitric Oxide Generation and iNOS Expression via Inhibition of NF-κB Activation

Inflexinol, an ent-kaurane diterpenoid, was isolated from the leaves of Isodon excisus. Many diterpenoids isolated from the genus Isodon (Labiatae) have antitumor and antiinflammatory activities. We investigated the antiinflammatory effect of inflexinol in RAW 264.7 cells and astrocytes. As a result, we found that inflexinol (1, 5, 10 μM) suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and astrocytes. Consistent with the inhibitory effect on iNOS and COX-2 expression, inflexinol also inhibited transcriptional and DNA binding activity of NF-κB via inhibition of IκB degradation as well as p50 and p65 translocation into nucleus. These results suggest that inflexinol inhibits iNOS and COX-2 expression through inhibition of NF-κB activation, thereby inhibits generation of inflammatory mediators in RAW 264.7 cells and astrocytes, and may be useful for treatment of inflammatory diseases

Molecular and cytological features of the mouse B-cell lymphoma line iMyc(Eμ)-1

BACKGROUND: Myc-induced lymphoblastic B-cell lymphoma (LBL) in iMyc(Eμ )mice may provide a model system for the study of the mechanism by which human MYC facilitates the initiation and progression of B cell and plasma cell neoplasms in human beings. We have recently shown that gene-targeted iMyc(Eμ )mice that carry a His(6)-tagged mouse Myc cDNA, Myc(His), just 5' of the immunoglobulin heavy-chain enhancer, Eμ, are prone to B cell and plasma cell tumors. The predominant tumor (~50%) that arose in the iMyc(Eμ )mice on the mixed genetic background of segregating C57BL/6 and 129/SvJ alleles was LBL. The purpose of this study was to establish and characterize a cell line, designated iMyc(Eμ)-1, for the in-depth evaluation of LBL in vitro. METHODS: The morphological features and the surface marker expression profile of the iMyc(Eμ)-1 cells were evaluated using cytological methods and FACS, respectively. The cytogenetic make-up of the iMyc(Eμ)-1 cells was assessed by spectral karyotyping (SKY). The expression of the inserted Myc(His )gene was determined using RT-PCR and qPCR. Clonotypic immunoglobulin gene arrangements were detected by Southern blotting. The global gene expression program of the iMyc(Eμ)-1 cells and the expression of 768 "pathway" genes were determined with the help of the Mouse Lymphochip(© )and Superarray(© )cDNA micro- and macroarrays, respectively. Array results were verified, in part, by RT-PCR and qPCR. RESULTS: Consistent with their derivation from LBL, the iMyc(Eμ)-1 cells were found to be neoplastic IgM(high)IgD(low )lymphoblasts that expressed typical B-cell surface markers including CD40, CD54 (ICAM-1), CD80 (B7-1) and CD86 (B7-2). The iMyc(Eμ)-1 cells harbored a reciprocal T(9;11) and three non-reciprocal chromosomal translocations, over-expressed Myc(His )at the expense of normal Myc, and exhibited gene expression changes on Mouse Lymphochip(© )microarrays that were consistent with Myc(His)-driven B-cell neoplasia. Upon comparison to normal B cells using eight different Superarray(© )cDNA macroarrays, the iMyc(Eμ)-1 cells showed the highest number of changes on the NFκB array. CONCLUSION: The iMyc(Eμ)-1 cells may provide a uniquely useful model system to study the growth and survival requirements of Myc-driven mouse LBL in vitro

Intrinsically Stretchable Three Primary Light-Emitting Films Enabled By Elastomer Blend For Polymer Light-Emitting Diodes

Intrinsically stretchable light-emitting materials are crucial for skin-like wearable displays; however, their color range has been limited to green-like yellow lights owing to the restricted stretchable light-emitting materials (super yellow series materials). To develop skin-like full-color displays, three intrinsically stretchable primary light-emitting materials [red, green, and blue (RGB)] are essential. In this study, we report three highly stretchable primary light-emitting films made from a polymer blend of conventional RGB light-emitting polymers and a nonpolar elastomer. The blend films consist of multidimensional nanodomains of light-emitting polymers that are interconnected in an elastomer matrix for efficient light-emitting under strain. The RGB blend films exhibited over 1000 cd/m2 luminance with low turn-on voltage (Von) and the selectively stretched blend films on rigid substrate maintained stable light-emitting performance up to 100% strain even after 1000 multiple stretching cycles

Low-Dose Fluoroscopy Protocol for Diagnostic Cerebral Angiography

Purpose We applied a low-dose fluoroscopic protocol in routine diagnostic cerebral angiography and evaluated the feasibility of the protocol. Materials and Methods We retrospectively reviewed a total of 60 patients who underwent diagnostic cerebral angiography for various neurovascular diseases from September to November 2019. Routine protocols were used for patients in the first phase and low-dose protocols in the second phase. We compared radiation dose, fluoroscopy time, and complications between groups. Results Age, diseases, and operators were not significantly different between the two groups. The mean fluoroscopy dose significantly decreased by 52% in the low-dose group (3.09 vs. 6.38 Gy·cm2); however, the total dose was not significantly different between the two groups (34.07 vs. 33.70 Gy·cm2). The total fluoroscopic time was slightly longer in the low-dose group, but the difference was not statistically significant (12.2. vs. 12.5 minutes). In all patients, angiography was successfully performed without complications. Conclusion The low-dose fluoroscopy protocol is feasible to apply for diagnostic cerebral angiography in that this protocol could significantly reduce the fluoroscopic dose

ATAD5 suppresses centrosome over-duplication by regulating UAF1 and ID1

Centrosomes are the primary microtubule-organizing centers that are important for mitotic spindle assembly. Centrosome amplification is commonly observed in human cancer cells and contributes to genomic instability. However, it is not clear how centrosome duplication is dysregulated in cancer cells. Here, we report that ATAD5, a replisome protein that unloads PCNA from chromatin as a replication factor C-like complex (RLC), plays an important role in regulating centrosome duplication. ATAD5 is present at the centrosome, specifically at the base of the mother and daughter centrioles that undergo duplication. UAF1, which interacts with ATAD5 and regulates PCNA deubiquitination as a complex with ubiquitin-specific protease 1, is also localized at the centrosome. Depletion of ATAD5 or UAF1 increases cells with over-duplicated centrosome whereas ATAD5 overexpression reduces such cells. Consistently, the proportion of cells showing the multipolar mode of chromosome segregation is increased among ATAD5-depleted cells. The localization and function of ATAD5 at the centrosomes do not require other RLC subunits. UAF1 interacts and co-localizes with ID1, a protein that increases centrosome amplification upon overexpression. ATAD5 depletion reduces interactions between UAF1 and ID1 and increases ID1 signal at the centrosome, providing a mechanistic framework for understanding the role of ATAD5 in centrosome duplication