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- ArticleCao T, Zou Y, Adawi AM, Cryan MJ.Opt Express. 2014 Sep 22;22(19):22699-706.We numerically demonstrate an impedance-matched multilayer stacked fishnet metamaterial that has zero index with flat high transmittance from 600 nm to 620 nm. The effective refractive index(n(eff)) is calculated to be -0.045 + 0.466 i and the normalize effective impedance(Z(eff)/Z(0)) is 0.956-0.368 i at 610 nm. The light emitted by a red conjugated polymer layer embedded in such a zero index metamaterial (ZIM) is concentrated in a narrow cone in the surrounding media, where the half-power beam width (HPBW) of the center lobe of the radiation pattern is around 25° in the wavelength range between 600 nm and 620 nm, giving directive emission in the visible region. This proposed light focusing system can be applied to sensing, beam collimating and filtering functionalities.
- ArticleRamu AG, Choi D.Sci Rep. 2021 11 22;11(1):22699.Azo dyes and nitrophenols have been widely used in the various industry which are highly toxic and affecting the photosynthetic cycle of aquatic organism. The industry disposals increase the accumulation of azo compounds in the environment. In the present study, we synthesized the low cost, PdO-doped NiO hetero-mixture via simple hydrothermal combined calcination process. The morphology results proved that, the spherical PdO nanoparticles are evenly doped with NiO nanoparticles. The band gap values of metal oxides NiO, PdO and PdO-NiO composite were found to be 4.05 eV, 3.84 eV and 4.24 eV, respectively. The high optical bandgap (Eg) value for composite suggests that the PdO interface and NiO interface are closely combined in the composite. The catalytic activity of the PdO-NiO was analyzed for the reduction of different toxic azo compounds namely, 4-nitrophenol (NP), 2,4-dinitrophenol (DNP), 2,4,6-trinitrophenol (TNP), methylene blue (MB), rhodamine B (RhB) and methyl orange (MO) separately and their mixture with the presence of a NaBH4. For the first time, the large volume of the toxic azo compounds was reduced into non-toxic compounds with high reduction rate. The proposed PdO-NiO catalyst exhibit excellent rate constant 0.1667, 0.0997, 0.0686 min-1 for NP, DNP and TNT and 0.099, 0.0416 and 0.0896 min-1 for MB, RhB and MO dyes respectively which is higher rate constant than the previously reported catalysts. Mainly, PdO-NiO completes the reduction of mixture of azo compounds within 8 min. Further, PdO-NiO exhibit stable reduction rate of azo compounds over five cycles with no significant loss. Hence, the proposed low cost and high efficient PdO-NiO catalyst could be the promising catalyst for degradation of azo compounds.
- ArticleZhang X, Zhang S, Wang C, Li L, Zhao J, Cui J.Opt Express. 2013 Sep 23;21(19):22699-704.We first report a diode-pumped continuous wave orthogonally polarized dual-wavelength single-longitudinal-mode laser with a single c-cut Tm,Ho:LuLiF₄ laser crystal. The simultaneous dual-wavelength single-longitudinal-mode laser near 2 μm is realized by using two uncoated intracavity Fabry-Perot etalons. The output wavelengths are 2064 nm in π-polarization and 2066 nm in σ-polarization respectively, which are orthogonal to each other. At the absorbed pump power of 1 W, the maximum single-longitudinal-mode output powers at 2064 and 2066 nm are 76 and 32 mW respectively. The orthogonally polarized dual-wavelength single-longitudinal-mode laser is possible to be applied to the 2 μm differential absorption lidar and the generation of THz radiation.
- Articlede Araujo ED, Alvarez CP, López-Alonso JP, Sooklal CR, Stagljar M, Kanelis V.J Biol Chem. 2015 Sep 11;290(37):22699-714.The sulfonylurea receptor 2B (SUR2B) forms the regulatory subunit of ATP-sensitive potassium (KATP) channels in vascular smooth muscle. Phosphorylation of the SUR2B nucleotide binding domains (NBD1 and NBD2) by protein kinase A results in increased channel open probability. Here, we investigate the effects of phosphorylation on the structure and nucleotide binding properties of NBD1. Phosphorylation sites in SUR2B NBD1 are located in an N-terminal tail that is disordered. Nuclear magnetic resonance (NMR) data indicate that phosphorylation of the N-terminal tail affects multiple residues in NBD1, including residues in the NBD2-binding site, and results in altered conformation and dynamics of NBD1. NMR spectra of NBD1 lacking the N-terminal tail, NBD1-ΔN, suggest that phosphorylation disrupts interactions of the N-terminal tail with the core of NBD1, a model supported by dynamic light scattering. Increased nucleotide binding of phosphorylated NBD1 and NBD1-ΔN, compared with non-phosphorylated NBD1, suggests that by disrupting the interaction of the NBD core with the N-terminal tail, phosphorylation also exposes the MgATP-binding site on NBD1. These data provide insights into the molecular basis by which phosphorylation of SUR2B NBD1 activates KATP channels.
- ArticlePan Y, Chen W, Yan H, Wang M, Xiang X.Aging (Albany NY). 2020 11 16;12(22):22688-22699.Previous observational studies have reported an association between impaired glucose metabolism and Alzheimer's disease. This study aimed to examine the causal association of glycemic traits with Alzheimer's disease. We used a two-sample Mendelian randomization approach to evaluate the causal effect of six glycemic traits (type 2 diabetes, fasting glucose, fasting insulin, hemoglobin A1c, homeostasis model assessment- insulin resistance and HOMA-β-cell function) on Alzheimer's disease. Summary data on the association of single nucleotide polymorphisms with these glycemic traits were obtained from genome-wide association studies of the DIAbetes Genetics Replication And Meta-analysis and Meta-Analyses of Glucose and Insulin-related traits Consortium. Summary data on the association of single nucleotide polymorphisms with Alzheimer's disease were obtained from the International Genomics of Alzheimer's Project. The Mendelian randomization analysis showed that 1-standard deviation higher fasting glucose and lower HOMA-β-cell function (indicating pancreatic β-cell dysfunction) were causally associated with a substantial increase in risk of Alzheimer's disease (odds ratio=1.33, 95% confidence interval: 1.04-1.68, p=0.02; odds ratio=1.92, 95% confidence interval: 1.15-3.21, p=0.01). However, no significant association was observed for other glycemic traits. This Mendelian randomization analysis provides evidence of causal associations between glycemic traits, especially high fasting glucose and pancreatic β-cell dysfunction, and high risk of Alzheimer's disease.
- ArticleJin Y, Wu J, Song X, Song Q, Cully BL, Messmer-Blust A, Xu M, Foo SY, Rosenzweig A, Li J.J Biol Chem. 2011 Jun 24;286(25):22699-705.The amount of available hypoxia-inducible factor (HIF)-1α has been considered to be largely a consequence of post-translational modification by multiple ubiquitin-proteasome pathways. However, the role of transcriptional regulation of HIF-1α is less certain, and the mechanisms of transcriptional regulation of HIF-1α require further investigation. Here we report that related transcriptional enhancer factor-1 (RTEF-1), a member of the TEF transcriptional factor family, transcriptionally regulates the HIF-1α gene under normoxic and hypoxic conditions. The expression of HIF-1α mRNA was decreased in endothelial cells in which RTEF-1 was knocked down with siRNA. Sequential deletional analysis of the HIF-1α promoter revealed that the MCAT-like element in the HIF-1α promoter was essential for HIF-1α transcription. Binding of RTEF-1 to the MCAT-like element was confirmed by ChIP. Treatment of endothelial cells with a HIF-1 inhibitor resulted in retardation of RTEF-1-induced proliferation and tube formation. Moreover, increased HIF-1α expression was observed in transgenic mice expressing RTEF-1 under the VE-cadherin promoter (VE-Cad/RTEF-1). VE-Cad/RTEF-1 mice subjected to hindlimb ischemia demonstrated increased levels of HIF-1α, accelerated recovery of blood flow, and increased capillary density compared with littermate controls. These results identify RTEF-1 as a regulator of HIF-1α transcription, which results in up-regulation of HIF-1α and acceleration of recovery from ischemia.
- ArticleKhalid S, Cao C, Wang L, Zhu Y.Sci Rep. 2016 Mar 03;6:22699.Large areal capacitance is essentially required to integrate the energy storage devices at the microscale electronic appliances. Energy storage devices based on metal oxides are mostly fabricated with low mass loading per unit area which demonstrated low areal capacitance. It is still a challenge to fabricate supercapacitor devices of porous metal oxides with large areal capacitance. Herein we report microwave method followed by a pyrolysis of the as-prepared precursor is used to synthesize porous nickel cobaltite microspheres. Porous NiCo2O4 microspheres are capable to deliver large areal capacitance due to their high specific surface area and small crystallite size. The facile strategy is successfully demonstrated to fabricate aqueous-based asymmetric &symmetric supercapacitor devices of porous NiCo2O4 microspheres with high mass loading of electroactive materials. The asymmetric &symmetric devices exhibit maximum areal capacitance and energy density of 380 mF cm(-2) &19.1 Wh Kg(-1) and 194 mF cm(-2) &4.5 Wh Kg(-1) (based on total mass loading of 6.25 &6.0 mg) respectively at current density of 1 mA cm(-2). The successful fabrication of symmetric device also indicates that NiCo2O4 can also be used as the negative electrode material for futuristic asymmetric devices.
- ArticleGrigorian M, Andresen S, Tulchinsky E, Kriajevska M, Carlberg C, Kruse C, Cohn M, Ambartsumian N, Christensen A, Selivanova G, Lukanidin E.J Biol Chem. 2001 Jun 22;276(25):22699-708.A physical and functional interaction between the Ca(2+)-binding protein Mts1 (S100A4) and the tumor suppressor p53 protein is shown here for the first time. We demonstrate that Mts1 binds to the extreme end of the C-terminal regulatory domain of p53 by several in vitro and in vivo approaches: co-immunoprecipitation, affinity chromatography, and far Western blot analysis. The Mts1 protein in vitro inhibits phosphorylation of the full-length p53 and its C-terminal peptide by protein kinase C but not by casein kinase II. The Mts1 binding to p53 interferes with the DNA binding activity of p53 in vitro and reporter gene transactivation in vivo, and this has a regulatory function. A differential modulation of the p53 target gene (p21/WAF, bax, thrombospondin-1, and mdm-2) transcription was observed upon Mts1 induction in tet-inducible cell lines expressing wild type p53. Mts1 cooperates with wild type p53 in apoptosis induction. Our data imply that the ability of Mts1 to enhance p53-dependent apoptosis might accelerate the loss of wild type p53 function in tumors. In this way, Mts1 can contribute to the development of a more aggressive phenotype during tumor progression.
- ArticleKang JH, Asai D, Tsuchiya A, Mori T, Niidome T, Katayama Y.PLoS One. 2011;6(7):e22699.Peptide substrates sensitive for a certain protein kinase could be important for new-drug development and to understand the mechanism of diseases. Rho-associated kinase (Rho-kinase/ROCK) is a serine/threonine kinase, and plays an important part in cardiovascular disease, migration and invasion of tumor cells, and in neurological disorders. The purpose of this study was to find substrates with high affinity and sensitivity for ROCK2. We synthesized 136 peptide substrates from protein substrates for ROCK2 with different lengths and charged peptides. Incorporation of (32)P [counts per minute (CPM)] for each peptide substrate was determined by the radiolabel assay using [γ-(32)P]ATP. When the top five peptide substrates showing high CPMs (R4, R22, R133, R134, and R135) were phosphorylated by other enzymes (PKA, PKCα, and ERK1), R22, R133, and R135 displayed the highest CPM level for ROCK2 compared with other enzymes, whereas R4 and R134 showed similar CPM levels for ROCK2 and PKCα. We hypothesize that R22, R133, and R135 can be useful peptide substrates for ROCK2.
- ArticleTang C, Hou YX, Shi PX, Zhu CH, Lu X, Wang XL, Que LL, Zhu GQ, Liu L, Chen Q, Li CF, Xu Y, Li JT, Li YH.FASEB J. 2023 01;37(1):e22699.Cardiac fibrosis is an essential pathological process in pressure overload (PO)-induced heart failure. Recently, myocyte-fibroblast communication is proven to be critical in heart failure, in which, pathological growth of cardiomyocytes (CMs) may promote fibrosis via miRNAs-containing exosomes (Exos). Peli1 regulates the activation of NF-κB and AP-1, which has been demonstrated to engage in miRNA transcription in cardiomyocytes. Therefore, we hypothesized that Peli1 in CMs regulates the activation of cardiac fibroblasts (CFs) through an exosomal miRNA-mediated paracrine mechanism, thereby promoting cardiac fibrosis. We found that CM-conditional deletion of Peli1 improved PO-induced cardiac fibrosis. Moreover, Exos from mechanical stretch (MS)-induced WT CMs (WT MS-Exos) promote activation of CFs, Peli1-/- MS-Exos reversed it. Furthermore, miRNA microarray and qPCR analysis showed that miR-494-3p was increased in WT MS-Exos while being down regulated in Peli1-/- MS-Exos. Mechanistically, Peli1 promoted miR-494-3p expression via NF-κB/AP-1 in CMs, and then miR-494-3p induced CFs activation by inhibiting PTEN and amplifying the phosphorylation of AKT, SMAD2/3, and ERK. Collectively, our study suggests that CMs Peli1 contributes to myocardial fibrosis via CMs-derived miR-494-3p-enriched exosomes under PO, and provides a potential exosomal miRNA-based therapy for cardiac fibrosis.
- ArticleVezzani A, Lang B, Aronica E.Cold Spring Harb Perspect Med. 2015 Dec 18;6(2):a022699.This review reports the available evidence on the activation of the innate and adaptive branches of the immune system and the related inflammatory processes in epileptic disorders and the putative pathogenic role of inflammatory processes developing in the brain, as indicated by evidence from experimental and clinical research. Indeed, there is increasing knowledge supporting a role of specific inflammatory mediators and immune cells in the generation and recurrence of epileptic seizures, as well as in the associated neuropathology and comorbidities. Major challenges in this field remain: a better understanding of the key inflammatory pathogenic pathways activated in chronic epilepsy and during epileptogenesis, and how to counteract them efficiently without altering the homeostatic tissue repair function of inflammation. The relevance of this information for developing novel therapies will be highlighted.
- ArticleFu Y, Huang ZJ.Proc Natl Acad Sci U S A. 2010 Dec 28;107(52):22699-704.Neurexins (NRXs) and neuroligins are key synaptic adhesion molecules that also recruit synaptic signaling machineries. Neurexins consist of α- and β-isoforms, but how they couple synaptic transmission and adhesion to regulate activity-dependent synapse development remains unclear, in part because of poor understanding of their cell biology and regulation in the relevant neurons. Here, we examined the subaxonal localization, dynamics, and regulation of NRX1α and NRX1β in cortical perisomatic inhibitory synapses. Both isoforms are delivered to presynaptic terminals but show significant and different turnover rate at the membrane. Although NRX1α is highly diffuse along developing axons and filopodia, NRX1β is strictly anchored at terminals through binding to postsynaptic ligands. The turnover rate of NRX1β is attenuated by neural activity and presynaptic GABA(B) receptors. NRXs, thus, are intrinsically dynamic but are stabilized by local transmitter release. Such an activity-adjusted adhesion system seems ideally suited to rapidly explore and validate synaptic partners guided by synaptic transmission.
- ArticlePerrone S, Vilaseca R, Masoller C.Opt Express. 2012 Sep 24;20(20):22692-9.We study numerically the dynamics of a vertical-cavity surface-emitting laser (VCSEL) with optical injection and show that the interplay of polarization bistability and noise yields a reliable logic output to two logic inputs. Specifically, by encoding the logic inputs in the strength of the light injected into the suppressed polarization mode of the VCSEL (the so-called 'orthogonal' injection), and by decoding the output logic response from the polarization state of the emitted light, we demonstrate an all-optical stochastic logic gate that exploits the ubiquitous presence of noise. It gives the correct logic output response for as short as 5 ns bit times when the dimensionless spontaneous emission coefficient, β(sp), is within the range 10(-4)-10(-1). Considering that typical values of β(sp) in semiconductor lasers are in the range 10(-5)-10(-4), the VCSEL-based logic gate can be implemented with nowadays commercially available VCSELs, exploiting either their intrinsic noise, or external and background noise sources.
- ArticleWei SC, Anang NAS, Sharma R, Andrews MC, Reuben A, Levine JH, Cogdill AP, Mancuso JJ, Wargo JA, Pe'er D, Allison JP.Proc Natl Acad Sci U S A. 2019 11 05;116(45):22699-22709.Immune checkpoint blockade therapy targets T cell-negative costimulatory molecules such as cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed cell death-1 (PD-1). Combination anti-CTLA-4 and anti-PD-1 blockade therapy has enhanced efficacy, but it remains unclear through what mechanisms such effects are mediated. A critical question is whether combination therapy targets and modulates the same T cell populations as monotherapies. Using a mass cytometry-based systems approach, we comprehensively profiled the response of T cell populations to monotherapy and combination anti-CTLA-4 plus anti-PD-1 therapy in syngeneic murine tumors and clinical samples. Most effects of monotherapies were additive in the context of combination therapy; however, multiple combination therapy-specific effects were observed. Highly phenotypically exhausted cluster of differentiation 8 (CD8) T cells expand in frequency following anti-PD-1 monotherapy but not combination therapy, while activated terminally differentiated effector CD8 T cells expand only following combination therapy. Combination therapy also led to further increased frequency of T helper type 1 (Th1)-like CD4 effector T cells even though anti-PD-1 monotherapy is not sufficient to do so. Mass cytometry analyses of peripheral blood from melanoma patients treated with immune checkpoint blockade therapies similarly revealed mostly additive effects on the frequencies of T cell subsets along with unique modulation of terminally differentiated effector CD8 T cells by combination ipilimumab plus nivolumab therapy. Together, these findings indicate that dual blockade of CTLA-4 and PD-1 therapy is sufficient to induce unique cellular responses compared with either monotherapy.