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Diarylpropionitrile (DPN), a selective agonist for estrogen receptor ß (ERß), has been reported to regulate various hormonal responses through activation of ERß in tissues including the mammary gland and brain. However, the effect of DPN on melanogenesis independent of ERß has not been studied. The aim of this study is to examine the possibility of anti-melanogenic effect of DPN and its underlying mechanism. Melanin contents and cellular tyrosinase activity assay indicated that DPN inhibited melanin biosynthesis in alpha-melanocyte stimulating hormonestimulated B16F10 melanoma cell line. However, DPN had no direct influence on in vitro tyrosinase catalytic activity. On the other hand, 17ß-estradiol had no effect on inhibition of melanogenesis, suggesting that the DPN-mediated suppression of melanin production was not related with estrogen signaling pathway. Immunoblotting analysis showed that DPN down-regulated the expression of microphthalmiaassociated transcription factor (MITF), a central transcription factor of melanogenesis and its down-stream genes including tyrosinase, tyrosinase-related protein (TRP)- 1, and TRP-2. Also, DPN attenuated the phosphorylation of protein kinase A (PKA) and cAMP-response element-binding protein (CREB). Additionally, DPN suppressed the melanin synthesis in UVB-irradiated HaCaT conditioned media culture system suggesting that DPN has potential as an anti-melanogenic activity in physiological conditions. Collectively, our data show that DPN inhibits melanogenesis via downregulation of PKA/CREB/MITF signaling pathway. [ABSTRACT FROM AUTHOR]

First-principles calculations were performed on the electronic structure and x-ray-absorption near-edge structure (XANES) of amorphous Zr-oxide and Hf-oxide thin films. Using the discrete variational X-α method, the authors simulated the films with (Zr4O17)-18 and (Hf4O18)-20 clusters. The O–Zr and O–Hf bonds were found to have different characteristics along the bond orientation. By comparing the experimental and calculated XANES, we analyze the absorption mechanism of amorphous Zr-oxide and Hf-oxide thin films for energies up to 10 eV above the O K edge. [ABSTRACT FROM AUTHOR]

HDAC3, one of the class I histone deacetylase modulates epigenetic landscape through histone modification. HDAC3 also interacts with non-histone proteins including p53 for deacetylation. Moreover, HDAC3 serves as a transcriptional repressor, interacting with NCor1/SMRT complex. Although HDAC3 plays a critical role for cellular homeostasis, regulatory mechanism of HDAC3 have been poorly understood. Here we report a novel regulatory mechanism of HDAC3 about its monoubiquitination and stabilization by Mdm2. HDAC3 levels were increased by ectopic expression of Mdm2 and decreased by Mdm2 ablation in various cell lines. We found that Mdm2 directly interacts with HDAC3 and induces HDAC3 protein levels without alteration of mRNA levels. Ectopic expression of wild type but not RING mutant of Mdm2 increased HDAC3 monoubiquitination. In addition, MdmX is beneficial for mdm2-mediated HDAC3 regulation. Ablation of Mdm2 and Mdm2/MdmX decreased cell migration along with the decrease of HDAC3 levels. These data provide an evidence that Mdm2 positively regulates HDAC3 monoubiquitination and stability. • Ectopic expression of Mdm2 induces HDAC3 expression in various cells by posttranslational modification. • Ablation of Mdm2 reduces HDAC3 expression. • HDAC3 monoubiquitination is increased by Mdm2 wild type but not in RING mutant. • Knockdown of Mdm2/MdmX reduces monoubiquitination and stability of HDAC3. [ABSTRACT FROM AUTHOR]

Purpose The surveillance equipment is one of the most important parts for current air traffic control systems. It provides aircraft position and other relevant information including flight parameters. However, the existing surveillance equipment has certain position errors between true and detected positions. Operators must understand and account for the characteristics on magnitude and frequency of the position errors in the surveillance systems because these errors can influence the safety of aircraft operation. This study aims to develop the simulation model for analysis of these surveillance position errors to improve the safety of aircrafts in airports.Design/methodology/approach This study investigates the characterization of the position errors observed in airport surface detection equipment of an airport ground surveillance system and proposes a practical method to numerically reproduce the characteristics of the errors.Findings The proposed approach represents position errors more accurately than an alternative simple approach. This study also discusses the application of the computational results in a microscopic simulation modeling environment.Practical implications The surveillance error is analyzed from the radar trajectory data, and a random generator is configured to implement these data. These data are used in the air transportation simulation through an application programing interface, which can be applied to the aircraft trajectory data in the simulation. Subsequently, additionally built environment data are used in the actual simulation to obtain the results from the simulation engine.Originality/value The presented surveillance error analysis and simulation with its implementation plan are expected to be useful for air transportation safety simulations. [ABSTRACT FROM AUTHOR]

Dermal papilla (DP) is a pivotal part of hair follicle, and the smaller size of the DP is related with the hair loss. In this study, we investigated the effect of titrated extract ofCentella asiatica(TECA) on hair growth inductive property on 3D spheroid cultured human DP cells (HDP cells). Significantly increased effect of TECA on cell viability was only shown in 3D sphered HPD cells, not in 2D cultured HDP cells. Also, TECA treatment increased the sphere size of HDP cells. The luciferase activity of STAT reporter genes and the expression of STAT-targeted genes, SOCS1 and SOCS3, were significantly decreased. Also, TECA treatment increased the expression of the hair growth-related signature genes in 3D sphered HDP cells. Furthermore, TECA led to downregulation of the level of phosphorylated STAT proteins in 3D sphered HDP cells. Overall, TECA activates the potential of hair inductive capacity in HDP cells. TECA induced the significant enhancement of the 3D sphere formation (A) and the hair growth inductivity of HDP cells by inhibiting the STAT activation (B). [ABSTRACT FROM AUTHOR]

Arctiin, a lignin isolated from Arctium lappa, exhibits a variety of biological effects, including anti-viral, anti-inflammatory, and anti-proliferative actions, in mammalian cells. In a previous study, arctiin was demonstrated to induce procollagen type I synthesis and exhibited protective effects against ultraviolet B (UVB) radiation in normal human dermal fibroblasts (nHDFs). However, the underlying molecular mechanism of arctiin-mediated collagen synthesis remains unknown. In the present study, the mechanism for increased expression of collagen type 1a 1 chain (COL1A1) mRNA in arctiin-induced nHDFs was identified. The expression of microRNA-378b (miR-378b), downregulated by arctiin, was correlated with the expression of sirtuin-6 (SIRT6) mRNA, a regulator of COL1A1 mRNA. Furthermore, it was revealed that arctiin protected the UVB radiation-mediated decrease in COL1A1 mRNA expression, through the miR-378b/SIRT6 signaling pathway. In conclusion, these results suggest that arctiin regulates COL1A1 through the miR-378b-SIRT6 axis. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) light mediates skin aging and induces destruction of the dermis by modulating the expression levels of extracellular matrix-associated genes, including collagen and matrix metalloproteinases. Sirtuin 6 (SIRT6), a member of the sirtuin family of proteins, regulates collagen metabolism and is an established anti-aging protein. However, the exact underlying mechanism by which SIRT6 expression is regulated in dermal fibroblasts during the aging process is unclear. The present study demonstrated that expression of microRNA-378b (miR-378b) is induced in UVB-exposed human dermal fibroblasts (HDFs), and this was inversely associated with the mRNA expression levels of α-1-type 1 collagen (COL1A1). In addition, knockdown of miR-378b enhanced the mRNA expression levels of COL1A1 in HDFs. A target analysis for miR-378b was performed, and the results revealed that SIRT6, a regulator of COL1A1, contains a target sequence for miR-378b in its 3'untranslated region. Notably, the present study demonstrated that an miR-378b mimic and inhibitor may directly regulate SIRT6 expression in HDFs. In conclusion, the present study suggested that miR-378b represses the mRNA expression levels of COL1A1 via interference with SIRT6 in HDFs, and may contribute to the underlying molecular mechanism by which UVB inhibits collagen I in dermal fibroblasts. [ABSTRACT FROM AUTHOR]

Long Term Evolution (LTE) networks that are composed of macrocells and femtocells can provide an efficient solution to not only extend coverage of macrocells but also deal with the growth of traffic within macrocells. LTE is now being considered to be a vital connectivity solution for the success of the Internet of Things (IoT) because it can provide broadband connectivity to the growing number of sensing and monitoring devices and even the wireless sensor networks (WSNs). However, it is still challenging to properly allocate radio frequency resources in the handover procedure between a macrocell and a femtocell. In this paper, we propose a new handover algorithm that increases the efficient utilization of a radio frequency resource and thereby maximizes the capacity of the overall LTE network, including the femtocells within network. The handover decision criteria take into account the strength of the received signal, the radio resource reuse, and the overall capacity of the network throughput. The performance of the proposed algorithm is verified through a simulation, and the simulation results indicate that the proposed handover algorithm improves the reusability of the cell bandwidth and increases the overall capacity of the network. [ABSTRACT FROM AUTHOR]

Dermal papilla (DP) cells function as important regulators of the hair growth cycle. The loss of these cells is a primary cause of diseases characterized by hair loss, including alopecia, and evidence has revealed significantly increased levels of reactive oxygen species (ROS) in hair tissue and DP cells in the balding population. In the present study, troxerutin, a flavonoid derivative of rutin, was demonstrated to have a protective effect against H2O2-mediated cellular damage in human DP (HDP) cells. Biochemical assays revealed that pretreatment with troxerutin exerted a protective effect against H2O2-induced loss of cell viability and H2O2-induced cell death. Further experiments confirmed that troxerutin inhibited the H2O2-induced production of ROS and upregulation of senescence-associated β-galactosidase activity. Using microRNA (miRNA) microarrays, the present study identified 24 miRNAs, which were differentially expressed in the troxerutin-pretreated, H2O2-treated HDP cells. Subsequent prediction using bioinformatics analysis revealed that the altered miRNAs were functionally involved in several cell signaling pathways, including the mitogen-activated protein kinase and WNT pathways. Overall, these results indicated that ROS-mediated cellular damage was inhibited by troxerutin and suggested that the use of troxerutin may be an effective approach in the treatment of alopecia. [ABSTRACT FROM AUTHOR]

The effects of skin pores on skin topographic features can be reduced by decreasing excessive production and accumulation of sebum and elimination of comedones. Therefore, a cosmetic cleanser that regulates sebum homeostasis is required. In the present study, the effects of a cosmetic cleanser that contained Diospyros kaki folium, Polygonum cuspidatum and Castanea crenata var. dulcis (DPC) was examined on the removal of sebum and on skin pore size. Healthy volunteers (n=23) aged 20-50 years were asked to apply the test materials to the face. Skin oil content, pore size, pore number and extracted sebum surface area were measured using various measurement methods. All the measurements were performed at pre- and post-application of the test materials. When the cosmetic cleanser containing DPC was applied to the skin, the oil content decreased by 77.3%, from 6.19 to 1.40. The number of skin pores decreased by 24.83%, from 125.39 to 94.23. Skin pore size decreased from 0.07 to 0.02 µm³ (71.43% decrease). The amount of extracted sebum increased by 335% when the DPC cleanser was used. Compared to the control cleanser, skin oil content was significantly decreased when the cleanser that contained DPC was used. The cleanser containing DPC also decreased pore size and number. Finally, the DPC cleanser easily removed solidified sebum from the skin. [ABSTRACT FROM AUTHOR]

Abstract: This paper presents the design and performance evaluation of a stable pairwise time synchronization protocol (abbreviated SPS) for capillary machine-to-machine (M2M) networks that provides underlying platform independence and operational stability, even under harsh conditions. SPS achieves the first criterion using a novel technique whereby the M2M device captures incoming or outgoing moments of timing messages. The second criterion is achieved by adaptively adjusting the resynchronization interval. Extensive simulations are conducted to demonstrate the validity and effectiveness of SPS. [Copyright &y& Elsevier]

This paper considers the internetwork interference problem in environments with multiple wireless body area networks (WBANs). We propose an asynchronous internetwork interference avoidance scheme (abbreviated as AIIA), which is based on the hybrid multiple access of carrier sense multiple access with collision avoidance (CSMA/CA) and time division multiple access (TDMA). In AIIA, the gateway device of each WBAN maintains a table, called an AIIA table, which includes the timing offset and TDMA transmission schedule information corresponding to the interfering WBANs. By referring to the table, the conflicting TDMA schedule can be checked and updated by itself, in asynchronous and distributed manners. Extensive simulations are conducted to demonstrate the feasibility and effectiveness of AIIA. [ABSTRACT FROM AUTHOR]

This paper presents a selective cooperative transmission scheme (abbreviated SCT) for ad hoc network with directional antennas that leverages the benefits of directional-only antenna approach and cooperative communication. The main feature of SCT is its adaptability to the channel condition in the network. In other words, when the node sends data, SCT determines its transmission strategy on either direct or cooperative transmission via a relay node called a forwarder, depending on the transmission time. Simulation results are provided to validate the effectiveness of the proposed scheme. [ABSTRACT FROM AUTHOR]

This paper presents a numerical analysis of latency and jitter for IEEE 802.11e wireless local area networks (WLANs) in a saturation condition, by using a Markov model. We use this model to explicate how the enhanced distributed coordination function (EDCF) differentiates classes of service and to characterize the probability distribution of the medium access control (MAC) layer packet latency and jitter, on which the quality of the voice over Internet protocol (VoIP) calls is dependent. From the proposed analytic model, we can estimate the available number of nodes determining the system performance, in order to satisfy user demands on the latency and jitter. [ABSTRACT FROM AUTHOR]

Defect inspection is important to ensure consistent quality and efficiency in industrial manufacturing. Recently, machine vision systems integrating artificial intelligence (AI)-based inspection algorithms have exhibited promising performance in various applications, but practically, they often suffer from data imbalance. This paper proposes a defect inspection method using a one-class classification (OCC) model to deal with imbalanced datasets. A two-stream network architecture consisting of global and local feature extractor networks is presented, which can alleviate the representation collapse problem of OCC. By combining an object-oriented invariant feature vector with a training-data-oriented local feature vector, the proposed two-stream network model prevents the decision boundary from collapsing to the training dataset and obtains an appropriate decision boundary. The performance of the proposed model is demonstrated in the practical application of automotive-airbag bracket-welding defect inspection. The effects of the classification layer and two-stream network architecture on the overall inspection accuracy were clarified by using image samples collected in a controlled laboratory environment and from a production site. The results are compared with those of a previous classification model, demonstrating that the proposed model can improve the accuracy, precision, and F1 score by up to 8.19%, 10.74%, and 4.02%, respectively. [ABSTRACT FROM AUTHOR]

The Hsp90-associated protein p23 modulates Hsp90 activity during the final stages of the chaperone pathway to facilitate maturation of client proteins. Previous reports indicate that p23 cleavage induced by caspases during cell death triggers destabilization of client proteins. However, the specific role of truncated p23 (Δp23) in this process and the underlying mechanisms remain to be determined. One such client protein, hTERT, is a telomerase catalytic subunit regulated by several chaperone proteins, including Hsp90 and p23. In the present study, we examined the effects of p23 cleavage on hTERT stability and telomerase activity. Our data showed that overexpression of Δp23 resulted in a decrease in hTERT levels, and a down-regulation in telomerase activity. Serine phosphorylation of Hsp90 was significantly reduced in cells expressing high levels of Δp23 compared with those expressing full-length p23. Mutation analyses revealed that two serme residues (Ser-231 and Ser-263) in Hsp90 are important for activation of telomerase, and down-regulation of telomerase activity by Δp23 was associated with inhibition of cell growth and sensitization of cells to cisplatin. Our data aid in determining the mechanism underlying the regulation of telomerase activity by the chaperone complex during caspasedependent cell death. [ABSTRACT FROM AUTHOR]

Abstract: Redd1, a recently discovered stress-response gene, is regulated by hypoxia via hypoxia-inducible factor 1 (HIF-1) and by DNA damage via p53/p63; however, the signaling pathway by which its expression is induced by hypoxia has not been elucidated. In the present study, we demonstrated that the expression of Redd1 in response to hypoxia (1% O2), hypoxia-mimetic agent, cobalt chloride (CoCl2) and high cell density (HCD) requires coactivation of HIF-1α and Sp1. CoCl2 and HCD induced the activation of HIF-1α and Sp1 in HeLa cells, and siRNAs targeting HIF-1α and Sp1 abrogated Redd1 expression. Inhibition of phosphatidylinositol 3-kinase (PI3K) by LY294002 and by a dominant-negative PI3K mutant reduced the expression of Redd1 and activation of HIF-1α and Sp1 by CoCl2 and HCD. Also, suppression of Akt activation blocked the expression of Redd1 and the activation of HIF-1α and Sp1 by CoCl2 and HCD. Furthermore, we found that the induction of Redd1 expression by CoCl2 can be mediated by activation of Sp1 in HIF-1α-deficient cells but that a higher level of Redd1 expression is achieved when these cells are transfected with HIF-1α. These results demonstrate that hypoxic condition-and HCD-induced expression of Redd1 is mediated by coactivation of Sp1 and HIF-1α downstream of the PI3K/Akt signaling pathway. [Copyright &y& Elsevier]

An automotive 2.1 μm CMOS image sensor has been developed with a full-depth deep trench isolation and an advanced readout circuit technology. To achieve a high dynamic range, we employ a sub-pixel structure featuring a high conversion gain of a large photodiode and a lateral overflow of a small photodiode connected to an in-pixel storage capacitor. With the sensitivity ratio of 10, the expanded dynamic range could reach 120 dB at 85 °C by realizing a low random noise of 0.83 e- and a high overflow capacity of 210 ke-. An over 25 dB signal-to-noise ratio is achieved during HDR image synthesis by increasing the full-well capacity of the small photodiode up to 10,000 e- and suppressing the floating diffusion leakage current at 105 °C. [ABSTRACT FROM AUTHOR]

Electroplating of nanoporous Pt (nPt) induces an extremely strong tensile stress, which results in the exfoliation of nPt on flexible polymer substrate despite plasma treatment to improve adhesion. Here, we overcame this challenge by modifying flexible stainless-steel, and developed wearable, robust, flexible, and non-enzymatic continuous glucose monitoring system. The flexible stainless-steel was highly effective in improving the adhesion between the metal layer and substrate. The developed wireless system included electrochemical analysis circuits, a microcontroller unit, and a wireless communication module. Finally, we evaluated the continuous glucose monitoring system through two animal testing, by implanting into subcutaneous tissue and measuring interstitial fluid (ISF) glucose values at 5–15-min intervals. Comparison of the measured ISF glucose with blood glucose determined by the Clarke error grid analysis showed that 82.76% of the measured glucose was within zone A. Furthermore, the wearable glucose sensor exhibited bio-compatible to implant through various bio-compatibility tests. [ABSTRACT FROM AUTHOR]

Previous studies have shown that hypoxia can reverse DCA/metformin-induced cell death in breast cancer cells. Therefore, targeting hypoxia is necessary for therapies targeting cancer metabolism. In the present study, we found that TRAIL can overcome the effect of hypoxia on the cell death induced by treatment of DCA and metformin in breast cancer cells. Unexpectedly, DR5 is upregulated in the cells treated with DCA/metformin, and sustained under hypoxia. Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death. Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin. These findings support the potential application of combining TRAIL and metabolism-targeting drugs in the treatment of cancers under hypoxia. [ABSTRACT FROM AUTHOR]

Cyclin A1 is an A-type cyclin that directly binds to CDK2 to regulate cell-cycle progression. In the present study, we found that doxorubicin decreased the expression of cyclin A1 at the protein level in A549 lung cancer cells, while markedly downregulating its mRNA levels. Interestingly, doxorubicin upregulated caspase-1 in a concentration-dependent manner, and z-YAVD-fmk, a specific inhibitor of caspase-1, reversed the doxorubicin-induced decrease in cyclin A1 in A549 lung cancer and MCF7 breast cancer cells. Active caspase-1 effectively cleaved cyclin A1 at D165 into two fragments, which in vitro cleavage assays showed were further cleaved by caspase-3. Finally, we found that overexpression of cyclin A1 significantly reduced the cytotoxicity of doxorubicin, and knockdown of cyclin A1 by RNA interference enhanced the sensitivity of cells to ionizing radiation. Our data suggest a new mechanism for the downregulation of cyclin A1 by DNA-damaging stimuli that could be intimately involved in the cell death induced by DNA damage-inducing stimuli, including doxorubicin and ionizing radiation. [ABSTRACT FROM AUTHOR]

To prevent the development of malignancies, mammalian cells activate disposal programs, such as programmed cell death, in response to deregulated oncogene expression. However, the molecular basis for regulation of cellular disposal machinery in response to activated oncogenes is unclear at present. In this study, we show that upregulation of the autophagy-related protein, Atg5, is critically required for the oncogenic H-ras-induced autophagic cell death and that Rac1/mitogen-activated kinase kinase (MKK) 7/c-Jun N-terminal kinase (JNK) signals upregulation of Atg5. Overexpression of H-rasV12 induced marked autophagic vacuole formation and cell death in normal fibroblasts, which remained unaffected by a caspase inhibitor. Pretreatment with Bafilomycin A1, an autophagy inhibitor, completely attenuated H-rasV12-induced cell death as well as autophagic vacuole formation. Selective production of Atg5 was observed in cells overexpressing H-rasV12, and small interfering RNA (siRNA) targeting of Atg5 clearly inhibited autophagic cell death. Interestingly, inhibition of JNK or c-Jun by specific siRNA suppressed Atg5 upregulation and autophagic cell death. Moreover, inhibition of MKK7, but not MKK4, effectively attenuated H-rasV12-induced JNK activation. In addition, ectopic expression of RacN17 or Rac1-siRNA effectively inhibited MKK7–JNK activation, Atg5 upregulation and autophagic cell death. These data support the notion that upregulation of Atg5 is required for the oncogenic H-ras-induced autophagic cell death in normal fibroblasts and that activation of Rac1/MKK7/JNK-signaling pathway leads to upregulation of Atg5 in response to oncogenic H-ras. Our findings suggest that in cells acquiring deregulated oncogene expression, oncogenic stress triggers autophagic cell death, which protects cells against malignant progression. [ABSTRACT FROM PUBLISHER]

Nitric oxide (NO) is a chemical messenger implicated in neuronal damage associated with ischemia neurodegenerative disease and excitotoxicity. In the present study, we examined the biological effects of NO and its mechanisms in human malignant glioblastoma cells. Addition of a NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), induced apoptosis in U87MG human glioblastoma cells, accompanied by opening mitochondrial permeability transition pores, release of cytochrome c and AIF, and subsequently by caspase activation. NO-induced apoptosis occurred concurrently with significantly increased levels of the Bak and Bim. Treatment with SNAP resulted in sustained activation of JNK and its downstream pathway, c-Jun/AP-1. The expression of dominant-negative (DN)-JNK1 and DN-c-Jun suppressed the activation of AP-1, the induction of Bak and Bim, and the SNAP-induced apoptosis. In addition, de novo protein synthesis was required for the initiation of apoptosis in that the protein synthesis inhibitor, cycloheximide (CHX), inhibited NO-induced apoptotic cell death as well as up-regulation of Bak and Bim. These results suggest that NO activates an apoptotic cascade, involving sustained JNK activation, AP-1 DNA binding activity, and subsequent Bak and Bim induction, followed by cytochrome c and AIF releases and caspases cascade activation, resulting in human malignant brain tumor cell death. J. Cell. Physiol. 206: 477–486, 2006. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Electronic structures and chemical bonding were investigated on Bi 4 Ti 3 O 12 substituted with lanthanides, such as La, Ce, Pr, and Nd for Bi, using the discrete variational Xα method. Also, we investigated the effect of substitution atom on net charge and overlap population, which is related to the dielectric constant. We found that the net charge and overlap population were dependent on the substitution atom. We concluded that dielectric constant increases as the atomic number of substitution atom increases. [ABSTRACT FROM AUTHOR]

Electronic structures were investigated on Pb(Zr 1 -x Ti x )O 3 (PZT) using the discrete variational Xαcluster method for obtaining the information of dependence on the amount and position of the substituted Zr atoms. Also, we investigated the effect of them on fatigue. The net charge and the overlap population were discussed together with the energy gap, which is related to fatigue. As a result, the net charge was independent on the amount and position of the substituted Zr atoms, and the overlap population wasn't. Furthermore, from the calculated energy gap, we conclude that Zr-rich PZT is less susceptible to fatigue than Ti-rich PZT. [ABSTRACT FROM AUTHOR]

[Display omitted] Combination of microwave irradiation (MWI) and ionic liquids (IL) is widely used for the synthesis of nanoparticles (NP) via decarbonylation of zero-valent metal carbonyl precursors. However, we carefully raise a question as to whether this combination is always beneficial. Upon MWI, highly-absorbing materials such as ILs would be subject to local intense heating, likely resulting in the occurrence of localized chemical decomposition. The decomposition is expected to influence the growth mechanism of NPs due to changes in the electrostatic and steric effects. If the assumption is valid, it should be possible to decompose IL and destabilize the NPs by modifying the amplitude of the incident microwaves. In other words, it should also be possible to control the particle aggregation by circumventing the decomposition of the IL. A series of comparative studies were conducted using a model system (i.e. [BMIm][BF 4 and Ru 3 (CO) 12). Variables were systematically controlled. After MWI, the decrease in colloidal stability of NPs was identified. In the formation of Ru NPs via decarbonylation, the association between incident microwave intensity, chemical decomposition of IL, and initiation of particle aggregation has been demonstrated. Conditions that can accelerate or alleviate the decomposition and the aggregation are also corroborated. [ABSTRACT FROM AUTHOR]

The hygroscopic property of particulate matter (PM) influencing light scattering and absorption is vital for determining visibility and accurate sensing of PM using a low-cost sensor. In this study, we examined the hygroscopic properties of coarse PM (CPM) and fine PM (FPM; PM2.5) and the effects of their interactions with weather factors on visibility. A censored regression model was built to investigate the relationships between CPM and PM2.5 concentrations and weather observations. Based on the observed and modeled visibility, we computed the optical hygroscopic growth factor, f RH , and the hygroscopic mass growth, G M VIS , which were applied to PM2.5 field measurement using a low-cost PM sensor in two different regions. The results revealed that the CPM and PM2.5 concentrations negatively affect visibility according to the weather type, with substantial modulation of the interaction between the relative humidity (RH) and PM2.5. The modeled f RH agreed well with the observed f RH in the RH range of the haze and mist. Finally, the RH-adjusted PM2.5 concentrations based on the visibility-derived hygroscopic mass growth showed the accuracy of the low-cost PM sensor improved. These findings demonstrate that in addition to visibility prediction, relationships between PMs and meteorological variables influence light scattering PM sensing. [ABSTRACT FROM AUTHOR]

Metformin, a potent AMPK activator is the most commonly used drug for diabetes. According to recent reports, metformin lowers the risk of diabetic complications and inflammatory diseases. We found the expression levels of AMPK subunits including PRKAA1, PRKAA2, PRKAB1 and PRKAB2 are decreased in skin biopsies of dermatitis patients from multiple datasets. Interestingly, metformin treatment ameliorates dermatitis symptom in animal model of dermatitis using O-tetradecanoylphorbol-13-acetate (TPA). Especially, the levels of epidermis and dermis thickness were decreased by metformin. We found NFκB activity as well as of gene expression associated with collagen synthesis are attenuated by metformin treatment. These results suggest that metformin treatment alleviates animal model of dermatitis. [ABSTRACT FROM AUTHOR]

Cellular metabolism is one of the crucial factors to regulate epigenetic landscape in various cells including immune cells, embryonic stem cells and hair follicle stem cells. Dermal papilla cells (DP) interact with epithelial stem cells to orchestrate hair formation. Here we show that active DP exhibit robust aerobic glycolysis. We observed decrease of signature genes associated with hair induction by DP in presence of low glucose (2 mM) and glycolysis inhibitors. Moreover, hair shaft elongation was attenuated by glycolysis inhibitors. Interestingly, excessive glucose is able to increase the expression of hair inductive genes and elongation of hair shaft. We also observed glycolysis-mediated histone acetylation is increased and chemical inhibition of acetyltransferase reduces expression of the signature genes associated with hair induction in active DP. These results suggest that glucose metabolism is required for expression of signature genes associated with hair induction. This finding may be beneficial for establishing and maintaining of active DP to generate hair follicle in vitro. [ABSTRACT FROM AUTHOR]

Nintedanib, a receptor tyrosine kinase (RTK) inhibitor has been developed as therapeutics for idiopathic pulmonary fibrosis and non-small lung cancer. We found that the expression levels of RTK, especially VEGFR1 is increased in skin biopsies of dermatitis patients from multiple independent datasets. Moreover, VEGFR1 is highly expressed by infiltrated cells in dermis from oxazolone (OXA) treated mice. Interestingly, nintedanib alleviates dermatitis symptom in OXA-induced animal model. Especially, levels of epidermis thickness, infiltrated immune cells including mast cells and eosinophils were decreased from mice cotreated with nintedanib and OXA compared with OXA treated mice. Moreover, serum IgE and Th2 cytokines including IL-4 and IL-13 were decreased by nintedanib treatment. These results suggest an evidence that nintedanib alleviates animal model of dermatitis. [ABSTRACT FROM AUTHOR]

HDAC2, one of the class I histone deacetylase regulates epigenetic landscape through histone modification. Because HDAC2 is overexpressed in many cancers, cancer therapeutics against HDAC2 have been developed. Here we show novel mechanism of HDAC2 regulation by E3 ligase RCHY1. We found inverse correlation RCHY1 and HDAC2 levels in tumor tissue from six independent dataset using meta-analysis. Ectopic expression of RCHY1 decreased the level of HDAC2 from cancer cells including p53 wildtype, mutant and null cells. In addition, HDAC2 was increased by RCHY1 knockdown. RCHY1 directly interacts with HDAC2. Ectopic expression of wild type but not RING mutant RCHY1 increased HDAC2 levels. These data provide an evidence that RCHY1 negatively regulates HDAC2. • Inverse correlation of expression levels of RCHY1 and HDAC2 was found in meta-analyses using six different datasets. • Ectopic expression of RCHY1 reduces HDAC2 expression in various cells by posttranslational modification. • Ablation of RCHY1 induces HDAC2 expression. [ABSTRACT FROM AUTHOR]

Digital public displays installed in various locations provide valuable information for the passers-by. However, the static characteristic of the digital public display limits the consumption of the displayed content to a small area. Personal mobile devices such as smartphones are now capable of interacting with digital public displays, which enables the passers-by to “take-away” the content and consume it on-the-go. This process requires device binding, content selection, and transfer between the two devices. In this paper, we propose a device binding method which utilizes the content brightness changing pattern as a unique content ID on the public display and an illuminance sensor on the mobile to bind and transfer between two devices. We conducted performance evaluations for binding algorithm robustness in different conditions. Also comparative studies among other binding interaction methods were conducted. Our results show that our proposed method performed stably across the various conditions and overall performance in interaction completion time and error rate was similar or superior to the existing methods. [ABSTRACT FROM AUTHOR]

Skin photoaging, which is mainly induced by ultraviolet B (UVB) radiation, is prevented by the application of UV‐protective agents. The microalga Nannochloropsis oceanica (N. oceanica) has been primarily reported as a potential biofuel; however, in this study, we investigated whether N. oceanica extracts exerted photoprotective effects against UVB‐irradiated human dermal fibroblasts (HDFs) and which single component was responsible for the protective effect of the extracts. Two extracts—pigment and nonpigment—were prepared from N. oceanica biomass. WST‐1 assay and expression analysis of interleukin genes showed that the pigment extracts were not significantly cytotoxic to HDFs. Further experiments revealed that treatment with the pigment extract upregulated the expression of collagen genes and significantly blocked UVB‐induced damage such as decreased cell viability and increased ROS production. Next, to investigate the pigment composition of the extracts, HPLC analysis was conducted and violaxanthin was identified as the major pigment. The UVB photoprotective effect of the pigment extracts was confirmed in violaxanthin‐treated HDFs. In addition, violaxanthin significantly attenuated UVB‐induced G1 phase arrest, senescence‐associated β‐galactosidase activation, p16 and p21 upregulation, ERK phosphorylation and the downregulation of ECM molecules in HDFs. Therefore, we concluded that violaxanthin was a potential antiphotoaging agent. The photoprotective role of main pigment violaxanthin of Nannochloropsis oceanica against UVB‐mediated skin damages. [ABSTRACT FROM AUTHOR]

Protein phosphatase 2A (PP2A) is a critical tumor suppressor complex responsible for the inactivation of various oncogenes. Recently, PP2A reactivation has emerged as an anticancer strategy. Cancerous inhibitor of protein phosphatase 2A (CIP2A), an endogenous inhibitor of PP2A, is upregulated in many cancer cells, including non-small cell lung cancer (NSCLC) cells. We demonstrated that the antihelminthic drug niclosamide inhibited the expression of CIP2A and reactivated the tumor suppressor PP2A in NSCLC cells. We performed a drug-repurposing screen and identified niclosamide as a CIP2A suppressor in NSCLC cells. Niclosamide inhibited cell proliferation, colony formation, and tumor sphere formation, and induced mitochondrial dysfunction through increased mitochondrial ROS production in NSCLC cells; however, these effects were rescued by CIP2A overexpression, which indicated that the antitumor activity of niclosamide was dependent on CIP2A. We found that niclosamide increased PP2A activity through CIP2A inhibition, which reduced the phosphorylation of several oncogenic proteins. Moreover, we found that a niclosamide analog inhibited CIP2A expression and increased PP2A activity in several types of NSCLC cells. Finally, we showed that other well-known PP2A activators, including forskolin and FTY720, did not inhibit CIP2A and that their activities were not dependent on CIP2A. Collectively, our data suggested that niclosamide effectively suppressed CIP2A expression and subsequently activated PP2A in NSCLC cells. This provided strong evidence for the potential use of niclosamide as a PP2A-activating drug in the clinical treatment of NSCLC. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) light exposure causes skin photoaging, which is known to be preventable and controllable by application of UV-protective agents. In this study, we demonstrated, for the first time, that the extract of microalgae Arthrospira platensis has a reverse effect on UV-induced photodamage such as loss of cell viability, cellular senescence, DNA damage, and collagen destruction in dermal fibroblasts. Forty-eight extracts were prepared from the cell biomass by controlling culture light conditions, extract solvents, and disruption methods. Then, we analyzed their cytotoxicities using WST-1 assay and separated low and high cytotoxic extracts with normal human dermal fibroblasts (nHDFs). Using the low cytotoxic extracts, we performed UVB protection assay and selected the most effective extract demonstrating protective effect against UVB-induced nHDF damage. Flow cytometric analysis and senescence-associated (SA) β-galactosidase assay showed that pretreatment with the extract reversed UVB-induced G2/M phase cell cycle arrest and senescence in nHDFs. Furthermore, UVB-induced DNA damage in nHDFs, such as cyclobutane pyrimidine dimer formation, was significantly suppressed by the extract. Further, quantitative real-time PCR experiments revealed that the extract significantly inhibited UVB-induced upregulation of matrix metalloproteinase 1 ( MMP1 ) and MMP3 expression in nHDFs. Therefore, we concluded that the microalgae extract can be a potential anti-photoaging agent. [ABSTRACT FROM AUTHOR]

An analytical method for the reliable screening and confirmation of 156 illegal drugs (58 erectile dysfunction drugs, 49 synthetic steroids, 26 anabolic steroids, and 23 anti-histamine drugs) in supplementary diets using ultra-high-performance liquid chromatography coupled with quadrupole/time-of-flight mass spectrometry (UHPLC-Q/TOF-MS) was developed. Various types of supplements (liquid, capsule, powder, pill and tablet) with complicated matrices were pretreated by simple liquid–liquid extraction. The wide scope of 156 target compounds was effectively determined within 15 min in the positive ion mode, detecting the compounds at a sub-ppb level. Their MS/MS spectra were preferentially investigated to find diagnostic common ions according to the structural similarity of diverse adulterants. For the rapid screening of multiple classes of the target adulterants, extracted common ion chromatograms (ECICs) based on specific fragments of similar molecular moieties were attempted. A database including the elemental compositions, retention times, and MS/MS spectra was built for the confirmation of adulterants. The established method was validated in terms of the linearity, limits of detection (LOD), precision, and accuracy. The linear correlation coefficient and limit of detection ranged from 0.9880 to 1 and from 0.02 to 16.04 ng/mL, respectively. The precision and accuracy of intra- and inter-day experiments for the spiked samples at the range of 0.2 and 16.0 ng/mL were from 0.16 to 13.50% and 0.19–11.48%, respectively, with relative standard deviation. Mean recoveries ranged from 81.6 to 124.7%, and relative standard deviation was less than 9.20%. The screening and confirmation method demonstrated the usefulness of UHPLC-Q/TOF-MS combined with ECICs as a promising approach for the analysis of multi-class adulterants. Finally, the established method was successfully applied for the monitoring of several types of dietary supplements in routine analysis. [ABSTRACT FROM AUTHOR]

Anti-aging cosmetics are widely used for improving signs of aged skin such as skin wrinkles, decreased elasticity, low dermal density and yellow skin tone. The present study evaluated the effects of cosmetic formulations, eye cream and facial cream, containing palmitoyl peptides, Silybum marianum (S. marianum) seed oil, vitamin E and other functional ingredients on the improvement of facial wrinkles, elasticity, dermal density and skin tone after 4 weeks period of application on aged human skin. Healthy volunteers (n=20) with aged skin were recruited to apply the test materials facially twice per day for 4 weeks. Skin wrinkles, elasticity, dermal density and skin tone were measured instrumentally for assessing the improvement of skin aging. All the measurements were conducted prior to the application of test materials and at 2 and 4 weeks of treatment. Crow's feet wrinkles were decreased 5.97% after 2 weeks of test material application and 14.07% after 4 weeks of application in comparison of pre-application. Skin elasticity was increased 6.81% after 2 weeks and 8.79% after 4 weeks. Dermal density was increased 16.74% after 2 weeks and 27.63% after 4 weeks. With the L* value indicating skin brightness and the a* value indicating erythema (redness), the results showed that brightness was increased 1.70% after 2 weeks and 2.14% after 4 weeks, and erythema was decreased 10.45% after 2 weeks and 22.39% after 4 weeks. Hence, the test materials appear to exert some degree of anti-aging effects on aged human skin. There were no abnormal skin responses from the participants during the trial period. We conclude that the facial and eye cream containing palmitoyl peptides and S. marianum seed oil, vitamin E and other ingredients have effects on the improvement of facial wrinkles, elasticity, dermal density and skin tone. [ABSTRACT FROM AUTHOR]

Despite many studies of the effect of ionizing radiation, biological mechanisms of action might differ greatly depend on dose, dose rate, and cell type. This study was performed to explore the effects of low- and high-dose radiation in human immune cell lines. We examined cell sensitivity after irradiation with 0.05, 0.1, or 2 Gy in two normal cell lines and three tumor cell lines. Low-dose radiation of 0.05 and 0.1 Gy had no effect on cell survival in any tested cell line, with the exception of IM-9 cells, whose viability was transiently increased. However, IM-9 and C1R-sB7 cells were very sensitive to high-dose radiation-induced cell death, whereas Jurkat and JM1 cells showed moderate sensitivity, and THP-1 cells were completely resistant. This radiosensitivity was correlated with basal AKT activation, which is induced by phosphorylation. In radiosensitive IM-9 cells, priming with chronic low-dose irradiation blocked cell death induced by high-dose radiation challenge via inhibition of caspase activation and PARP cleavage. AKT phosphorylation was not altered in IM-9 cells, but ERK phosphorylation was greatly elevated immediately after chronic low-dose irradiation. Taken together, our results suggest that the different responses of normal and tumor cells to low-dose and high-dose radiation depend on AKT activation, which is regulated by protein phosphatase 2 (PP2A). In radiosensitive normal cells lacking basal AKT activity, chronic low-dose radiation increases activation of the ERK pathway, which plays an important role in the adaptive response to radiation, providing a very important insight into understanding the effects of ionizing radiation on health. [ABSTRACT FROM AUTHOR]

Clinical evidence has demonstrated that the accumulation of 5a-dihydrotestosterone (DHT) in dermal papilla cells (DPCs) is implicated in androgenetic alopecia. Whether this accumulation in DHT may have direct cellular effects leading to androgenetic alopecia remains to be elucidated. The present study aimed to determine whether DHT affects cell growth, cell cycle arrest, cell death, senescence and the induction of reactive oxygen species (ROS), and whether these effects are mediated by microRNA (miRNA)-dependent mechanisms. The cell viability and cell cycle were determined, levels of ROS were examined and senescence-associated |3-galactosidase assays were performed in normal human DPCs (nHDPCs). Furthermore, miRNA expression profiling was performed using an miRNA microarray to determine whether changes in the expression levels of miRNA were associated with the cellular effects of DHT. The results revealed that DHT decreased cell growth by inducing cell death and G2 cell cycle arrest, and by increasing the production of ROS and senescence in the nHDPCs. In addition, 55 miRNAs were upregulated and 6 miRNAs were downregulated inthe DHT-treated nHDPCs. Bioinformatic analysis demonstrated that the putative target genes of these upregulated and down-regulated miRNAs were involved in cell growth, cell cycle arrest, cell death, senescence and the production of ROS. Specifically, the target genes of five highly upregulated and downregulated miRNAs were identified and were associated with the aforementioned effects of DHT. These results demonstrated that the expression of miRNA was altered in the DHT-treated nHDPCs and suggest the potential mechanisms of DHT-induced cell growth repression, cell cycle arrest, cell death, senescence and induction of ROS. [ABSTRACT FROM AUTHOR]

Para-phenylenediamine (PPD) is a major component of hair coloring and black henna products. Although it has been largely demonstrated that PPD induces allergic reactions and increases the risk of tumors in the kidney, liver, thyroid gland and urinary bladder, the effect on dermal papilla cells remains to be elucidated. Therefore, the current study evaluated the effects of PPD on growth, cell death and senescence using cell-based assays and microRNA (miRNA) microarray in normal human hair dermal papilla cells (nHHDPCs). Cell viability and cell cycle analyses demonstrated that PPD exhibited a significant cytotoxic effect on nHHDPCs through inducing cell death and G2 phase cell cycle arrest in a dose-dependent manner. It was additionally observed that treatment of nHHDPCs with PPD induced cellular senescence by promoting cellular oxidative stress. In addition, the results of the current study indicated that these PPD-mediated effects were involved in the alteration of miRNA expression profiles. Treatment of nHHDPCs with PPD altered the expression levels of 74 miRNAs by ≥2-fold (16 upregulated and 58 downregulated miRNAs). Further bioinformatics analysis determined that these identified miRNA target genes were likely to be involved in cell growth, cell cycle arrest, cell death, senescence and the induction of oxidative stress. In conclusion, the observations of the current study suggested that PPD was able to induce several cytotoxic effects through alteration of miRNA expression levels in nHHDPCs. [ABSTRACT FROM AUTHOR]

Background: Radiotherapy is widely used to treat cancer alone or in combination with surgery, chemotherapy, and immunotherapy. However, damage to normal tissues and radioresistance of tumor cells are major obstacles to successful radiotherapy. Furthermore, the immune network around tumors appears to be connected to tumor progression and recurrence. Methods: We investigated the cytosolic proteins produced by irradiated tumor cells by using a quantitative proteomic approach based on stable isotope labeling by amino acids in cell culture. MDA-MB-231 breast cancer cells were treated with a single or fractionated 10 Gray dose of 137Cs γ-radiation, which was selected based on cell viability. Results: Radiation-induced proteins were differentially expressed based on the fractionated times of radiation and were involved in multiple biological functions, including energy metabolism and cytoskeleton organization. We identified 46 proteins increased by at least 1.3-fold, and high ranks were determined for cathepsin D, gelsolin, arginino-succinate synthase 1, peroxiredoxin 5, and C-type mannose receptor 2. Conclusion: These results suggest that a number of tumor-derived factors upregulated by γ-radiation are promising targets for modulation of the immune response during radiation treatment. [ABSTRACT FROM AUTHOR]

The article focuses on a study related to elucidation of cellular senescence induced by overdose of methylparaben (MP). Topics discussed include higher epidermis permeation ability of MP as compare to other parabens due to lipophilicity difference, adverse dermatological responses exhibited by MP including allergic reaction, synergistic cytotoxic effect and development of breast cancer and determination of cell cycle arrest due to MP which results in cellular senescence.

Ultraviolet (UV) radiation impairs intracellular functions by directly damaging DNA and by indirectly generating reactive oxygen species (ROS), which induce cell cycle arrest and apoptosis. UV radiation can also alter gene expression profiles, including those of mRNA and microRNA (miRNA). The effects of UV radiation on cellular functions and gene expression have been widely documented in human skin cells such as keratinocytes, melanocytes and dermal fibroblasts, but the effect it has on other types of skin cell such as dermal papilla cells, which are crucial in the induction of hair follicle growth, remains unknown. In the current study, the effect of UV radiation on physiological changes and miRNA-based expression profiles in normal human dermal papilla cells (nHDPs) was investigated. UVB radiation of ⩾50 mJ/cm2 displayed high cytotoxicity and apoptosis in a dose-dependent manner. In addition, ROS generation was exhibited in UVB-irradiated nHDPs. Furthermore, using miRNA microarray analysis, it was demonstrated that the expression profiles of 42 miRNAs in UVB-irradiated nHDPs were significantly altered compared with those in the controls (35 upregulated and 7 downregulated). The biological functions of the differentially expressed miRNAs were studied with gene ontology analysis to identify their putative target mRNAs, and were demonstrated to be involved in cell survival- and death-related functions. Overall, the results of the present study provide evidence that miRNA-based cellular mechanisms may be involved in the UVB-induced cellular response in nHDPs. [ABSTRACT FROM AUTHOR]

Human keratinocytes are located in the outermost skin layer and thus particularly vulnerable to ultraviolet B (UVB) radiation exposure. Previous studies have focused on the cellular and molecular perspectives of UVB-induced keratinocyte damage. In the present study, it was demonstrated that pretreatment with the phytochemical arctiin, one of the lignin compounds, protects human HaCaT keratinocytes from UVB-mediated damage. Biochemical assays revealed that UVB-induced cytotoxicity and cell death were significantly reduced in arctiin-pretreated HaCaT cells. In addition, arctiin promoted the wound healing and DNA repair properties of keratinocytes. The photoprotective effects of arctiin were associated with changes in the expression levels of specific microRNAs (miRNAs) in HaCaT cells. A bioinformatics analysis demonstrated that the miRNAs were functionally involved in cancer, cell cycle, and Wnt and mitogen-activated protein kinase signaling pathways. In the present study, the results from the cellular and molecular assays demonstrated a novel role for arctiin in UVB protection in keratinocytes, which is mediated by miRNA responses and the suppression of UVB-induced cell death. Furthermore, arctiin is implicated as a potential chemopreventive agent through UVB protection of keratinocytes. [ABSTRACT FROM AUTHOR]

Melanogenesis is the process of generating pigmentation via melanin synthesis and delivery. Three key enzymes, tyrosinase, tyrosinase-related protein 1 (TRP1) and TRP2, metabolize melanin from L-tyrosine. Melanin synthesizing enzymes are regulated by microphthalmia-associated transcription factor (MITF). The titrated extract of Centella asiatica (TECA) contains the major components asiatic acid, asiaticoside and madecassic acid. The present study revealed that TECA reduces the melanin content in melanocytes. Moreover, the asiaticoside contained in TECA modulated melanogenesis by inhibiting tyrosinase mRNA expression. The decrease in tyrosinase mRNA levels was mediated through MITF. Uniquely, asiaticoside inhibited MITF by decreasing its DNA binding affinity. In conclusion, the results of the present study indicate that asiaticoside treatment may have beneficial effects in hyperpigmentation diseases or for skin whitening. [ABSTRACT FROM AUTHOR]

microRNAs (miRNAs) are small non-coding RNAs that regulate various biological processes by interfering with the translation of target genes. Several studies have suggested that miRNAs are involved in cellular responses to hydrogen peroxide (H2O2). Reactive oxygen species (ROS) are involved in hair malignancies, however, the H2O2-induced, miRNA-dependent regulatory mechanisms of human dermal papilla (HDP) cells are not fully understood. Our previous study demonstrated that changes in miRNA expression function to regulate growth arrest and apoptosis in UVB-irradiated HDPs. In the present study, miRNA expression was profiled in HDPs treated with H2O2. The transcriptome analysis of H2O2-treated HDPs enabled the identification of 68 differentially expressed miRNAs (62 were upregulated and 6 were downregulated) and 14,316 putative target genes of the miRNAs. Gene ontology (GO) analysis was utilized to verify that the putative target genes of the altered miRNAs were associated with H2O2-induced cell growth arrest and apoptosis. This bioinformatics analysis indicated that H2O2-response pathways involved in growth arrest and apoptosis were significantly affected. The identification of miRNAs and their putative targets may offer new therapeutic strategies for H2O2-induced hair follicle disorders. [ABSTRACT FROM AUTHOR]

In an antenna for a UHF RFID reader of wireless sensor networks (WSN), receiver sensitivity in sensing multitags from remote distances is an important performance index. This study designed a dual structured Z-slot antenna with optimized receiver sensitivity to enhance the sensitivity to a circularly polarized antenna with an isotropic pattern for a UHF RFID. Through analysis of performance in the designed antenna, the following was verified: return loss (S11) was about -62.21 dB at 925.25MHz, antenna gain was 7.36 dBi, and ΔPr, isotropic gain deviation, was 1.3 dB. Impedance matching was about 50.069 Ω at 925.25MHz and VSWR was from 1.001 to 1.028. Through this research it was discovered that this can be applied to the design of all RFID readers of WSN. Based on the above results, it is suggested that a circularly polarized Z-slot antenna which can enhance receiver sensitivity over a wide range can be widely applied to UHF RFID readers of WSN. [ABSTRACT FROM AUTHOR]

The role of the initial defects of graphene characterized by Raman spectroscopy is correlated with the physical mechanisms causing the hysteretic device characteristics of graphene field effect transistors (FETs). Fast charging related to the tunneling-induced charge exchange is found to be closely correlated with the initial defect density, while slow charging related to environmental influences such as the water redox reaction showed a weak correlation. It can be concluded that the intrinsic quality of graphene should be improved to minimize the hysteresis of graphene FETs even in an air-tight environment. [ABSTRACT FROM AUTHOR]

Highlights: [•] The stable expression of Redd1 triggers Akt phosphorylation. [•] Redd1-induced Akt activation is at least partly mediated by mTORC1. [•] Dual inhibition of mTORC1/2 enhances cisplatin sensitivity, in cells in which Akt is activated by mTORC1 inhibition. [Copyright &y& Elsevier]

Dermal fibroblasts are differentiated mesenchymal cells that regulate the extracellular matrix through the production of dermis components. Dermal fibroblasts can be damaged by reactive oxygen species induced by ultraviolet rays and chemicals. In addition to its effects on the dermis, oxidative stress poses a major threat to organisms and is believed to play an essential role in many disease processes. In this study, we show that human dermal fibroblasts (HDFs) express sphingosine-1-phosphate (S1P) receptors S1P, S1P, and S1P. In addition, cell viability of HDFs is increased by phytosphingosine-1-phosphate (PhS1P) via regulation of the Jun N-terminal kinase (JNK)/Akt pathway. Interestingly, regulation of the JNK/Akt pathway by PhS1P attenuated HO-induced cell growth arrest. Together, our data indicate that PhS1P attenuates HO-induced growth arrest through regulation of the signal molecules Akt and JNK, and suggest that PhS1P may have value as an anti-aging material in cosmetics and medicine. [ABSTRACT FROM AUTHOR]