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Abstract We propose a topological coherent perfect absorber that enables almost ideal performance with remarkably compact device footprint and tight incident beams. The proposed structure is based on a topological junction of two guided-mode-resonance gratings. The structure provides robust systematic ways of remarkably tight lateral confinement of the absorbing resonance mode and near-perfect mode-match to arbitrary incident beams, which are unavailable with the conventional approaches. We demonstrate an exemplary amorphous Si thin-film structure that enables near-perfect absorptance modulation between 1.7 and 99% with device footprint width of 30-μm and 10-μm-wide incident Gaussian beams. Therefore, our proposed approach greatly improves practicality of guided-mode-resonance coherent perfect absorbers.

Human coronaviruses (HCoVs) modify host proteins to evade the antiviral defense and sustain viral expansion. Here, we report tonicity-responsive enhancer (TonE) binding protein (TonEBP) as a cellular target of HCoVs. TonEBP was cleaved into N-terminal and C-terminal fragments (TonEBP NT and TonEBP CT, respectively) by NSP5 from all the HCoVs tested. This cleavage resulted in the loss of TonEBP’s ability to stimulate the TonE-driven transcription. On the other hand, TonEBP NT promoted viral expansion in association with the suppression of IFN-β expression. TonEBP NT competed away NF-κB binding to the PRD II domain on the IFN-β promoter. A TonEBP mutant resistant to the cleavage by NSP5 did not promote the viral expansion nor suppress the IFN-β expression. These results demonstrate that HCoVs use a common strategy of targeting TonEBP to suppress the host immune defense.

The underlying mechanisms of how obesity increases asthma prevalence and severity are not well understood. Here, the authors show that antagonizing cholecystokinin and its receptor, CCKAR, in the lung attenuates obesity-associated airway hyperresponsiveness in mice.

This study identifies the types of areas in Seoul where foreigners are concentrated by reflecting the characteristics of their region of origin and residence in Seoul. Lack of cultural understanding and uniform policies for various immigrant communities are causing some social issues. Hence, this study aims to prepare the basic data from which the government can predict changes in ethnic areas and prepare policies suitable for each derived type. The 14 most populous immigrant communities in Seoul were investigated, and cluster analysis and ANOVA test were performed. This examination resulted in four immigrant community types. Each type has specific characteristics, which have influenced the creation and change of the built environment. Types 1 and 4 are collectivistic. These types gradually tend to change urban environments to emulate the environment in their region of origin. In addition, they make little effort to improve their degraded environments, and such areas become increasingly backward. In contrast, types 2 and 3 are individualistic and prefer to assimilate into a migrant region. The formation and change of the urban environment for each type can be predicted on the basis of these characteristics. From this information, the government can prepare an appropriate urban architecture policy for each type.

Abstract Entosis is a non‐apoptotic cell death process that forms characteristic cell‐in‐cell structures in cancers, killing invading cells. Intracellular Ca2+ dynamics are essential for cellular processes, including actomyosin contractility, migration, and autophagy. However, the significance of Ca2+ and Ca2+ channels participating in entosis is unclear. Here, it is shown that intracellular Ca2+ signaling regulates entosis via SEPTIN‐Orai1‐Ca2+/CaM‐MLCK‐actomyosin axis. Intracellular Ca2+ oscillations in entotic cells show spatiotemporal variations during engulfment, mediated by Orai1 Ca2+ channels in plasma membranes. SEPTIN controlled polarized distribution of Orai1 for local MLCK activation, resulting in MLC phosphorylation and actomyosin contraction, leads to internalization of invasive cells. Ca2+ chelators and SEPTIN, Orai1, and MLCK inhibitors suppress entosis. This study identifies potential targets for treating entosis‐associated tumors, showing that Orai1 is an entotic Ca2+ channel that provides essential Ca2+ signaling and sheds light on the molecular mechanism underlying entosis that involves SEPTIN filaments, Orai1, and MLCK.

Abstract The migration of tumorigenic cells is a critical step for metastatic breast cancer progression. Although the role of the extracellular matrix in breast cancer cell migration has been extensively described, the effect of osmotic stress on the migration of tumor breast cohorts remains unclear. Most of our understanding on the effect of osmotic stresses on cell migration comes from studies at the level of the single cell in isolation and does not take cell–cell interactions into account. Here, we study the impact of moderate osmotic stress on the migration of cell clusters composed of either non-tumorigenic or tumorigenic cells. We observe a decrease in migration distance and speed for non-tumorigenic cells but not for tumorigenic ones. To explain these differences, we investigate how osmotic stress impacts the mechanical properties of cell clusters and affects their volumes. Our findings show that tumorigenic mesenchymal cells are less sensitive to osmotic stress than non-tumorigenic cells and suggest that this difference is associated with a lower expression of E-cadherin. Using EGTA treatments, we confirm that the establishment of cell–cell adhesive interactions is a key component of the behavior of cell clusters in response to osmotic stress. This study provides evidence on the low sensitivity of mesenchymal tumorigenic clusters to moderate osmotic stress and highlights the importance of cadherin-based junctions in the response to osmotic stress.

The gap junction complex functions as a transport channel across the membrane. Among gap junction subunits, gap junction protein α1 (GJA1) is the most commonly expressed subunit. A recent study showed that GJA1 is necessary for the maintenance of motile cilia; however, the molecular mechanism and function of GJA1 in ciliogenesis remain unknown. Here, we examined the functions of GJA1 during ciliogenesis in human retinal pigment epithelium-1 and Xenopus laevis embryonic multiciliated-cells. GJA1 localizes to the motile ciliary axonemes or pericentriolar regions beneath the primary cilium. GJA1 depletion caused malformation of both the primary cilium and motile cilia. Further study revealed that GJA1 depletion affected several ciliary proteins such as BBS4, CP110, and Rab11 in the pericentriolar region and basal body. Interestingly, CP110 removal from the mother centriole was significantly reduced by GJA1 depletion. Importantly, Rab11, a key regulator during ciliogenesis, was immunoprecipitated with GJA1 and GJA1 knockdown caused the mislocalization of Rab11. These findings suggest that GJA1 regulates ciliogenesis by interacting with the Rab11-Rab8 ciliary trafficking pathway.

Background : Obesity is a widespread disease and is caused mainly by excessive adipocyte differentiation and fat accumulation. Peroxisome proliferation-activated receptor γ (PPARγ) and CCAAT/enhancer-binding proteins (C/EBP) are major components for regulating adipocyte differentiation. Uncoupling protein 1 (UCP1) is a transmembrane protein that can convert white fat to brown adipose tissue. Artemisia annua L. has long been used in East Asia as an herbal drug for anti-oxidant, anti-bacterial, and anti-obesity purposes. Methods : We investigated the effects of water extracts of A. annua (WEAA) in C3H10T1/2, a mesenchymal stem cell line, by measuring the level of intracellular fat accumulation and the expression of genes associated with adipocyte differentiation. We also evaluated anti-obesity effects of WEAA in Zucker rats, a genetic model for the study of obesity, and in Sprague Dawley rats with high-fat diet (HFD)-induced obesity. Results : In this study, WEAA reduced the expression levels of PPARγ and C/EBPα in C3H10T1/2 cells, as well as the expression of enzymes that regulate fatty acid metabolism. In the Zucker fatty rat model and the HFD-induced obesity rat model, WEAA significantly decreased adipogenic differentiation and white fat accumulation between the scapulae, in contrast to the brown fat that remained unchanged between the groups. A. annua suppressed the expression of the adipocyte differentiation-promoting genes, while increasing the expression of UCP1. Conclusion : These results indicated that WEAA could reduce adipocyte differentiation and fat accumulation in in vitro and in vivo model systems, resulting in suppression of obesity and the occurrence of fatty liver due to a HFD.

Cancer: Protein enhances survival of tumor cells under stress A cytoskeletal protein that helps tumors avoid cell death offers a promising new drug target for fighting cancer. A team led by Jang Hyun Choi and Sun Sil Choi of the Ulsan National Institute of Science and Technology, South Korea, detailed how a protein called Flightless I (FliI) that normally regulates the remodeling of structural filaments in the cell can, in colorectal cancer cells, serve as a tumor promoter through its action on calcium levels. Typically, cells respond to chronic stress by altering calcium signaling to promote their own death. In tumors, however, FliI maintains normal calcium levels to enhance cell survival even in the face of chemotherapy and other stressful stimuli. Suppressing FliI activity could thus help sensitize cancer cells to other stress- and death-inducing drug regimens.

Modularization, which allows for pre-assembly away from a construction site, has been known to be more cost-effective than stick-built; however, contractors have difficulty ascertaining the benefits and adopting it. Calculating the benefits and costs of adopting modularization precedes decision making. However, modular cost estimation is challenging since relevant information in the early stages of a project and historical data about industrial modularization both have limited availability. To solve this problem, this study developed a conceptual cost estimation framework for industrial modular projects by converting stick-built project information. The framework is composed of eight steps based on two approaches. This study conducted a case study to demonstrate the applicability of the framework, which compared the project cost of modularization scenarios 1 and 2 with that of the stick-built version of the ongoing project. In addition, the estimated modular cost was compared with the engineers’ estimation to verify the accuracy of the framework. The contributions of this study are in identifying and quantifying the factors influencing the differences in cost between the modularization and stick-built versions, and developing the conceptual cost estimation framework for an industrial modular project. This framework is expected to support deciding on adopting modularization, budgeting, and project viability.

Abstract Background Pulmonary fibrosis is a progressive disease characterized by structural distortion of the lungs. Transforming growth factor-beta (TGF-beta) is a key cytokine implicated in the pathogenesis of pulmonary fibrosis. TGF-beta-induced myofibroblast differentiation characterized by expression of smooth muscle alpha-actin and extracellular matrix proteins is a key process in pathogenesis of fibrotic disease. Tannic acid is a natural polyphenol with diverse applications. In this study, we investigated the effect of tannic acid on myofibroblast differentiation and pulmonary fibrosis in cultured cells and in bleomycin model of the disease. Methods Primary cultured human lung fibroblasts (HLF) were used. The relative levels of proteins were determined by Western blotting. HLF contraction was measured by traction microscopy. Bleomycin-induced pulmonary fibrosis in mice was used as the disease model. Results Tannic acid inhibited TGF-beta-induced expression of collagen-1 and smooth muscle alpha-actin (SMA) as well as force generation by HLF. Tannic acid did not affect initial phosphorylation of Smad2 in response to TGF-beta, but significantly inhibited sustained Smad2 phosphorylation, which we recently described to be critical for TGF-beta-induced myofibroblast differentiation. Accordingly, tannic acid inhibited Smad-dependent gene transcription in response to TGF-beta, as assessed using luciferase reporter for the activity of Smad-binding elements. Finally, in mouse model of bleomycin-induced pulmonary fibrosis, therapeutic application of tannic acid resulted in a significant reduction of lung fibrosis, decrease in collagen-1 content and of Smad2 phosphorylation in the lungs. Conclusions This study demonstrates the anti-fibrotic effect of tannic acid in vitro and in vivo through a regulation of sustained Smad2 phosphorylation.

Polyacrylamide hydrogels are commonly used in cell biology, notably to cultivate cells on soft surfaces. Polyacrylamide gels are purely elastic and well adapted to cell culture as they are inert and can be conjugated with adhesion proteins. Here, we report a method to make viscoelastic polyacrylamide gels with mechanical properties more closely resembling biological tissues and suitable for cell culture in vitro. We demonstrate that these gels can be used for traction force microscopy experiments. We also show that multiple cell types respond to the viscoelasticity of their substrate and that viscous dissipation has an influence on cell spreading, contractility, and motility. This new material provides new opportunities for investigating how normal or malignant cells sense and respond to viscous dissipation within the extra-cellular matrix.

Numerous events cause delays to entire power projects’ completion timelines, leading to loss. This paper focuses on revealing the critical delay causes in Nigerian power projects and identifying the delay types such as excusable delay, compensable delay, critical delay, and concurrent delay from the different perspectives of owner and contractor. Based on the survey of the 84 industrial experts in power distribution and transmission projects in Nigeria, this study provides the mean score and rank of 39 delay causes. Among the causes, 14 are identified as critical in the Nigerian power project. The top three critical delay causes are corruption and bureaucracy in government, inadequate fund/budget allocation, and price fluctuation/inflation. Owner and contractor do not show the difference in classifying the 14 delay causes into excusable and compensable delays. However, there was a difference between owner and contractor in categorizing whether a cause is critical or not and concurrent or not. A different viewpoint of types of delay cause can lead to a dispute which may lead to other delays and losses, and thus it is meaningful to understand the types of delay perceived from owner and contractor. Even though the delay cause and types are different depending on an individual project, the results of this study serve as a reference and would be beneficial for the practitioners in the construction industry to help identify the delay causes to manage them effectively.

A top emitting organic light-emitting diode (OLED) device with pure aluminum (Al) anode for high-resolution microdisplays was proposed and fabricated. The low work function of the Al anode, even with a native oxide formed on the Al anode surface, increases the energy barrier of the interface between the anode and hole injection layer, and has poor hole-injection properties, which causes the low efficiency of the device. To enhance the hole-injection characteristics of the Al anode, we applied hexaazatriphenylene hexacarbonitrile (HATCN) as the hole-injection layer material. The proposed OLED device with a pure Al anode and native oxide on the anode surface improved efficiency by up to 35 cd/A at 1000 nit, which is 78% of the level of normal OLEDs with indium tin oxide (ITO) anode.

Loss of function of the tumor suppressor p53 is known to increase the rate of migration of cells transiting the narrow pores of the traditional Boyden chamber assay. Here by contrast we investigate how p53 impacts the rate of cellular migration within a 2D confluent cell layer and a 3D collagen-embedded multicellular spheroid. We use two human carcinoma cell lines, the bladder carcinoma EJ and the colorectal carcinoma HCT116. In the confluent 2-D cell layer, for both EJ and HCT cells the migratory speeds and effective diffusion coefficients for the p53 null cells were significantly smaller than in p53-expressing cells. Compared to p53 expressers, p53-null cells exhibited more organized cortical actin rings together with reduced front-rear cell polarity. Furthermore, loss of p53 caused cells to exert smaller traction forces upon their substrates, and reduced formation of cryptic lamellipodia. In the 3D multicellular spheroid, loss of p53 consistently reduced collective cellular migration into surrounding collagen matrix. As regards the role of p53 in cellular migration, extrapolation from the Boyden chamber assay to other cellular microenvironments is seen to be fraught even in terms of the sign of the effect. Together, these paradoxical results show that the effects of p53 on cellular migration are context-dependent.

Inhalation of diesel exhaust particulate (DEP) causes oxidative stress-induced lung inflammation. This study investigated the protective effects of TF-343, an antioxidant and anti-inflammatory agent, in mouse and cellular models of DEP-induced lung inflammation as well as the underlying molecular mechanisms. Mice were intratracheally instilled with DEP or vehicle (0.05% Tween 80 in saline). TF-343 was orally administered for 3 weeks. Cell counts and histological analysis of lung tissue showed that DEP exposure increased the infiltration of neutrophils and macrophages in the peribronchial/perivascular/interstitial regions, with macrophages harboring black pigments observed in alveoli. TF-343 pretreatment reduced lung inflammation caused by DEP exposure. In an in vitro study using alveolar macrophages (AMs), DEP exposure reduced cell viability and increased the levels of intracellular reactive oxygen species and inflammatory genes (IL-1β, inhibitor of nuclear factor- (NF-) κB (IκB), and Toll-like receptor 4), effects that were reduced by TF-343. A western blot analysis showed that the IκB degradation-induced increase in NF-κB nuclear localization caused by DEP was reversed by TF-343. In conclusion, TF-343 reduces DEP-induced lung inflammation by suppressing NF-κB signaling and may protect against adverse respiratory effects caused by DEP exposure.

High refractive index nanoparticle material was applied as a scattering layer on the inner side of a glass substrate of a bottom emission organic light emitting diode (OLED) device to enhance light extraction and to improve angular color shift. TiO2 and YSZ (Yttria Stabilized Zirconia; Y2O3-ZrO2) were examined as the high refractive index nanoparticles. The nanoparticle material was formed as a scattering layer on a glass substrate by a coating method, which is generally used in the commercial display manufacturing process. Additionally, a planarization layer was coated on the scattering layer with the same method. The implemented nanoparticle material and planarization material endured, without deformation, the subsequent thermal annealing process, which was carried out at temperature ranged to 580 °C. We demonstrated a practical and highly efficient OLED device using the conventional display manufacturing process by implementing the YSZ nanoparticle. We obtained a 38% enhanced luminance of the OLED device and a decreased angular color change compared to a conventional OLED device.

In wound healing, tissue growth, and certain cancers, the epithelial or the endothelial monolayer sheet expands. Within the expanding monolayer sheet, migration of the individual cell is strongly guided by physical forces imposed by adjacent cells. This process is called plithotaxis and was discovered using Monolayer Stress Microscopy (MSM). MSM rests upon certain simplifying assumptions, however, concerning boundary conditions, cell material properties and system dimensionality. To assess the validity of these assumptions and to quantify associated errors, here we report new analytical, numerical, and experimental investigations. For several commonly used experimental monolayer systems, the simplifying assumptions used previously lead to errors that are shown to be quite small. Out-of-plane components of displacement and traction fields can be safely neglected, and characteristic features of intercellular stresses that underlie plithotaxis remain largely unaffected. Taken together, these findings validate Monolayer Stress Microscopy within broad but well-defined limits of applicability.

Every adherent eukaryotic cell exerts appreciable traction forces upon its substrate. Moreover, every resident cell within the heart, great vessels, bladder, gut or lung routinely experiences large periodic stretches. As an acute response to such stretches the cytoskeleton can stiffen, increase traction forces and reinforce, as reported by some, or can soften and fluidize, as reported more recently by our laboratory, but in any given circumstance it remains unknown which response might prevail or why. Using a novel nanotechnology, we show here that in loading conditions expected in most physiological circumstances the localized reinforcement response fails to scale up to the level of homogeneous cell stretch; fluidization trumps reinforcement. Whereas the reinforcement response is known to be mediated by upstream mechanosensing and downstream signaling, results presented here show the fluidization response to be altogether novel: it is a direct physical effect of mechanical force acting upon a structural lattice that is soft and fragile. Cytoskeletal softness and fragility, we argue, is consistent with early evolutionary adaptations of the eukaryotic cell to material properties of a soft inert microenvironment.