Study of Interference Detection of Rail Transit Wireless Communication System Based on Fourth-Order Cyclic Cumulant.

The wireless communication system is used to provide dispatching, control, communication and other services for rail transit operations. In practice, interference from other wireless communication systems will affect the normal operation of trains, so it is an urgent problem to study the interference detection algorithms for rail transit applications. In this paper, the fourth-order cyclic cumulant (FOCC) of signals with different modulation modes is analyzed for the narrow-band wireless communications system of rail transit. Based on the analysis results, an adjacent-frequency interference detection algorithm is proposed according to the FOCC of the received signal within the predetermined cyclic frequency range. To detect interference with the same carrier frequency, a same-frequency interference detection algorithm using the relationship between the FOCC and the received power is proposed. The performance of the proposed detection algorithms in terms of correct rate and computational complexity is analyzed and compared with the traditional second-order statistical methods. Simulation results show that when an interference signal coexists with the expected signal, the correct rates of the adjacent-frequency and the same-frequency interference detection algorithms are greater than 90% when the signal-to-noise ratio (SNR) is higher than 2 dB and -4 dB, respectively. Under the practical rail transit wireless channel with multipath propagation and the Doppler effect, the correct rates of the adjacent-frequency and the same-frequency interference detection algorithms are greater than 90% when the SNR is higher than 3 dB and 7 dB, respectively. Compared with the existing second-order statistical methods, the proposed method can detect both the adjacent-frequency and the same-frequency interference when the interference signals coexist with the expected signal. Although the computational complexity of the proposed method is increased, it is acceptable in the application of rail transit wireless communication interference detection.

By blocking hexokinase-2 phosphorylation, limonin suppresses tumor glycolysis and induces cell apoptosis in hepatocellular carcinoma.

INTRODUCTION: The purpose of present study was to investigate the effect of limonin on tumor glycolysis and the underlying mechanisms in hepatocellular carcinoma (HCC). METHODS: Cell proliferation and colony formation assays were performed to evaluate the potency of limonin against HCC cells in vitro. The glucose consumption and lactate production after limonin treatment was determined. The effect of limonin on hexokinase-2 (HK-2) activity was assessed and the mitochondrial location of HK-2 was studied by immunoprecipitation. Cell apoptosis and protein expression were detected by flow cytometry and western blotting respectively. Protein overexpression by plasmid transfection was adopted to investigate the molecular mechanisms. RESULTS: HCC proliferation and colony formation were inhibited by limonin in vitro. With the suppression of HK-2 activity, the glycolytic level in HCC cells was substantially reduced, which was evidenced by the decrease of glucose consumption and lactate production. The phosphorylation of HK-2 was substantially inhibited by limonin, which resulted in the disassociation of HK-2 from mitochondria. Due to the reduction of HK-2 in mitochondria, increasing Bax were shifted to the mitochondria and gave rise to the release of cytochrome C, which induced HCC cells to subject to mitochondria-mediated apoptosis. Mechanism investigations revealed that the decrease of HK-2 phosphorylation was mainly due to the inhibition of Akt activity. In Akt exogenously overexpressed HCC cells, limonin-mediated cell proliferation inhibition, glycolysis suppression and apoptosis induction were significantly impaired. CONCLUSION: Limonin inhibited the tumor glycolysis in hepatocellular carcinoma by suppressing HK-2 activity, and the suppression of HK-2 was closely related to the decrease of Akt activity.

Dynamin 3 suppresses growth and induces apoptosis of hepatocellular carcinoma cells by activating inducible nitric oxide synthase production.

Dynamin 3 (DNM3) is candidate tumor suppressor against hepatocellular carcinoma (HCC). Downregulation of DNM3 is more frequently identified in HCC tissues than in normal liver tissues. However, the mechanism underlying DNM3-mediated inhibition of HCC remains unclear. The present study demonstrated that DNM3 expression was decreased in human HCC tissues and cell lines. The downregulation of DNM3 promoted cell proliferation by increasing cell cycle-associated proteins, including cyclin D1, cyclin-dependent kinase (CDK) 2 and CDK4. The upregulation of DNM3 induced HCC cell apoptosis and inhibited tumor growth. The present study also revealed that overexpression of DNM3 induced nitric oxide (NO) production and intracellular reactive oxygen species (ROS) accumulation. DNM3 overexpression also increased the protein expression level of inducible nitric oxide synthase (iNOS) in HCC cells and subcutaneous HCC tumor xenografts. The inhibition of iNOS by L-canavanine attenuated the DNM3-induced ROS accumulation and apoptotic cell death. In conclusion, the results indicate that DNM3 overexpression may induce apoptosis and inhibit tumor growth of HCC by activating iNOS production and the subsequent NO-ROS signaling pathways.

Chaos-based wireless communication resisting multipath effects.

In additive white Gaussian noise channel, chaos has been shown to be the optimal coherent communication waveform in the sense of using a very simple matched filter to maximize the signal-to-noise ratio. Recently, Lyapunov exponent spectrum of the chaotic signals after being transmitted through a wireless channel has been shown to be unaltered, paving the way for wireless communication using chaos. In wireless communication systems, inter-symbol interference caused by multipath propagation is one of the main obstacles to achieve high bit transmission rate and low bit-error rate (BER). How to resist the multipath effect is a fundamental problem in a chaos-based wireless communication system (CWCS). In this paper, a CWCS is built to transmit chaotic signals generated by a hybrid dynamical system and then to filter the received signals by using the corresponding matched filter to decrease the noise effect and to detect the binary information. We find that the multipath effect can be effectively resisted by regrouping the return map of the received signal and by setting the corresponding threshold based on the available information. We show that the optimal threshold is a function of the channel parameters and of the information symbols. Practically, the channel parameters are time-variant, and the future information symbols are unavailable. In this case, a suboptimal threshold is proposed, and the BER using the suboptimal threshold is derived analytically. Simulation results show that the CWCS achieves a remarkable competitive performance even under inaccurate channel parameters.

Molecular design and validation of halogen bonding orthogonal to hydrogen bonding in breast cancer MDM2-peptide complex.

Peptide therapeutics has been raised as an attractive approach for the treatment of breast cancer by targeting the oncogenic protein MDM2 that inactivates p53 tumor suppressor. Here, we performed molecular design of halogen bonding orthogonal to hydrogen bonding at the complex interface of MDM2 protein with its cognate peptide ligand to improve the peptide binding affinity and specificity. Crystal structure analysis, high-level quantum chemistry (QC) calculations and combined quantum mechanics/molecular mechanics (QM/MM) modeling revealed that halogen substitution at position 3 of the benzene moiety of peptide Phe3 residue can constitute a putative halogen bonding, which is shown to be geometrically perpendicular to and energetically independent of a native hydrogen bonding that share a common carbonyl oxygen acceptor. The designed halogen bonding was then validated by surface plasmon resonance (SPR) assays, that is, substitution with bromine at position 3 can considerably improve peptide affinity by ∼4-fold, but the peptide binding does not change substantially upon the bromine substitution at other positions of the Phe3 benzene moiety (the negative controls that are theoretically unable to form the halogen bonding), indicating that the orthogonal molecular interaction (OMI) system between the designed halogen bonding and native hydrogen bonding can co-work well at the complex interface of MDM2 protein with its halogenated peptide ligands.

Impacts of terminal modification of [Ru(phen)2dppz](2+) on the luminescence properties: a theoretical study.

[Ru(phen)2dppz](2+) and other closely related ruthenium(II) complexes containing π-extended ligands were found to be non or weakly emissive in water, while exhibiting significant luminescence intensity growth when bound to DNA, however, a satisfactory interpretation has not been provided on this "light switch" mechanism. In the present study, we investigated the vertical transitions and triplet excited states of [Ru(phen)2dppz](2+) (1), [Ru(phen)2dppzi](2+) (2) and [Ru(phen)2dppz-idzo](2+) (3) in the gas phase and aqueous solution, through time dependent-density functional theory (TDDFT). Based on the optimized (3)MLCT and (3)LLCT structures and energies, we found that the (3)MLCT state might be responsible for the emissions of the complexes. Interesting connections between the singlet vertical transitions and the luminescence properties were noticed. Through ZORA-TDDFT calculation with perturbative SOC, we evaluated the intersystem crossing between the lowest singlet excited state, and both (3)MLCT state and (3)LLCT state, which gave a reasonable explanation for the luminescence properties of these complexes.

Molecular "light switch" [Ru(phen)2dppzidzo](2+) monitoring the aggregation of tau.

Monitoring the aggregation of the tau protein is a key protocol for elucidating the pathogenic mechanism of Alzheimer's disease. In the present article, [Ru(phen)2dppzidzo](2+), a "light switch" ruthenium(ii) complex, was presented as a new monitoring probe for the aggregation of a tau R3 peptide, the third repeat unit of the tau microtubule-binding domain. Having little impact on the aggregation process, large fixed Stokes shift and small background luminescence made the complex a better probe for monitoring the aggregation process and quantitatively detecting tau filaments compared to thioflavin S, a commonly used fluorescent dye for staining neurofibrillary tangles and monitoring tau aggregation. Furthermore, a long luminescence lifetime of this complex could also expand its potential usage in the detection of tau filaments in the presence of short-lived fluorescent backgrounds.

Genetic variability of glutathione S-transferases influences treatment outcome of breast cancer.

We investigated the relationship between the clinical outcome and the GSTM1 null/present, GSTT1 null/present, and GSTP1 IIe105Val polymorphisms in breast cancer patients with chemotherapy. A total of 420 consecutive breast cancer patients diagnosed between January 2010 and December 2011 were eligible for inclusion in our retrospective study. The designs of the assay and SNP genotyping of GSTM1 null/present, GSTT1 null/present, and GSTP1 IIe105Val were performed using the Sequenom MassARRAY platform. In the univariate analysis, patients who carried TT genotype and CT + TT genotype of GSTP1 IIe105Val showed a significant poorer tumor response to chemotherapy when compared with CC genotype (for TT genotype, adjusted OR = 0.44, 95 % CI = 0.22-0.89; for CT + TT genotype, adjusted OR = 0.59, 95 % CI = 0.39-0.92). By Cox multivariate analysis, TT genotype and CT + TT genotype were associated with increased risk of death from breast cancer, and the relationship was more obvious after being adjusted by potential confounding factors (for TT genotype, adjusted OR = 4.23, 95 % CI = 2.33-8.76; for CT + TT genotype, adjusted OR = 2.53, 95% CI = 1.60-4.03). Polymorphism of GSTP1 IIe105Val might affect the clinical outcome in breast cancer patients.

Two structurally analogous ruthenium complexes as naked-eye and reversible molecular "light switch" for G-quadruplex DNA.

A pair of symmetrical furyl based ruthenium(II) complexes ([Ru(phen)2dpq-df](2+) (1) and [Ru(bpy)2dpq-df](2+) (2) (phen=1,10-phenanthroline, bpy=2,2'-bipyridine, dpq-df=dipyrido (3,2-a:2',3'-c) quinoxaline-difuran) have been prepared and characterized. The binding properties of both complexes toward G-quadruplex DNA have been investigated by fluorescence spectroscopy, UV-Vis spectroscopy, circular dichroism (CD), fluorescence resonance energy transfer (FRET) melting assays and molecular docking studies. The experimental results indicated that both Ru-complexes exhibited a remarkable "light switch" effect in the presence of hybrid G-quadruplex DNA. Interestingly, the "light switch" can be repeated off and on through the successive addition of Cu(2+) ions and EDTA, and all these behaviors can be observed even by the naked eyes. Moreover, FRET melting assay revealed that both complexes could be potential stabilizers for G-quadruplex architectures. The computational studies not only confirmed that the two complex molecules bound to one G-quadruplex DNA molecule, but also explained the "light switch" effect.

Ultrasensitive fluorescence detection of heparin based on quantum dots and a functional ruthenium polypyridyl complex.

A new strategy for the detection of heparin is developed by utilizing quantum dots (QDs) and a functional ruthenium polypyridyl complex [Ru(phen)2(dppz-idzo)](2+) (phen=1,10-phenanthroline, dppz-idzo=dipyrido-[3,2-a:2',3'-c] phenazine-imidazolone). The emission of CdTe QDs is found to be quenched by Ru complex due to electron transfer. Upon addition of the polyanionic heparin, it could remove the quencher (Ru complex) from the surface of QDs owing to the electrostatic and/or hydrogen bonding interactions between heparin and Ru complex, which led to significant fluorescence recovery of CdTe QDs. The fluorescence intensity enhanced with the increase of heparin and a linear relationship was observed in the range of 21-77 nM for heparin detection in buffer solution and the limit of detection (LOD) is 0.38 nM. Moreover, the strategy was successfully applied to detect heparin as low as 0.68 nM with a linear range of 35-98 nM in fetal bovine serum samples. The selectivity results of the fluorescence assay revealed that our system displayed excellent fluorescence selectivity towards heparin over its analogues, such as chondroitin 4-sulfate (Chs) or hyaluronic acid (Hya). This fluorescence "switch on" assay for heparin is label-free, convenient, sensitive and selective, which can be used to detect heparin in biological systems even with the naked eyes.

A new fluorescence "switch on" assay for heparin detection by using a functional ruthenium polypyridyl complex.

In the present study, a new strategy for heparin detection and quantification in biological media, such as fetal bovine serum (FBS), is developed by monitoring the emission change of a functional ruthenium polypyridyl complex ([Ru(phen)(2)dppz-idzo](2+), complex 1) in buffer solution. Polyanionic heparin is found to interact with a positively charged Ru-complex through electrostatic effects and/or hydrogen bonding interactions, which leads to a significant fluorescence enhancement of the Ru-complex. To get insight into this fluorescence "switch on" behavior, the binding model of the Ru-complex to heparin is established by employing molecular docking simulations based on the fluorescence and UV absorption results. The selectivity results of the fluorescence assay reveal that our complex displayed good fluorescence selectivity towards heparin over its analogues, such as chondroitin 4-sulfate (Chs) or hyaluronic acid (Hya), which have lower charge density and/or structural compatibility as compared to that of heparin. Quantification of heparin is also performed and a linear calibration curve is observed in the range of 0.01-4.87 U mL(-1) (the limit of detection is 0.01 U mL(-1)) for heparin detection in diluted FBS solution. This "one-step" fluorescence "switch on" assay for heparin detection is label-free, convenient, sensitive and selective, and has a long emission wavelength and large Stokes shift.

Molecular hairpin: a possible model for inhibition of tau aggregation by tannic acid.

Inhibition of anomalous aggregation of tau protein would be an attractive therapeutic target for Alzheimer's disease (AD). In this study, tannic acid (TA), a polymeric plant polyphenol, and its monomer, gallic acid (GA), were introduced as the references to afford a molecular framework that integrates tau binding properties and inhibitory effects. Using a thioflavin S fluorescence assay and electron microscopy, we demonstrated that TA could competently inhibit the in vitro aggregation of tau peptide R3, corresponding to the third repeat unit of the microtubule-binding domain, with an IC50 of 3.5 µM, while GA's inhibition was comparatively piddling (with an IC50 of 92 µM). In the isothermal titration calorimetry experiment, we found that TA could strongly bind to R3 with a large amount of heat released. Circular dichroism spectra showed TA dose-dependently suppressed the conformational transition of R3 from a random coil structure to a ß-sheet structure during the aggregation process. Finally, a structural model was built using molecular docking simulation to elucidate the possible binding sites for TA on the tau peptide surface. Our results suggest that TA recognizably interacts with tau peptide by forming a hairpin binding motif, a key framework required for inhibiting tau polymerization, in addition to hydrogen bonding, hydrophilic-hydrophobic interactions, and static electrical interactions, as reported previously. The inhibitory effect of TA on human full-length tau protein (tau441) was also verified by electron microscopy. This finding hints at the possibility of TA as a leading compound of anti-AD drugs and offers a new stratagem for the rational molecular design of a tau aggregation inhibitor.

[Ru(bpy)2dppz-idzo]2+: a colorimetric molecular "light switch" and powerful stabilizer for G-quadruplex DNA.

A new ruthenium complex, [Ru(bpy)2dppz-idzo](2+) (bpy = 2,2'-bipyridine, dppz-idzo = dipyrido-[3,2-a:2',3'-c] phenazine-imidazolone), was synthesized and characterized. The luminescent titrations showed that the Ru-complex exhibited an outstanding "light switch" effect with an emission enhancement factor of about 300 in the presence of G-quadruplex DNA in a K(+) solution. This remarkable "light switch" behavior can even be observed by the naked eye under irradiation with UV light. To get an insight into the "light switch" mechanism, quantum-chemical calculations were performed based on the DFT/TDDFT/PCM method at the B3LYP/6-31G* level. Furthermore, the CD titrations and thermal melting experiments indicated that [Ru(bpy)2dppz-idzo](2+) could not only induce the formation of an antiparallel G-quadruplex structure in the absence of monocations, but also has the ability to stabilize the G-quadruplex architecture, implying potential applications in anticancer therapeutics. Both the "light switch" effect and the structure stabilization ability of [Ru(bpy)2dppz-idzo](2+) were found to be superior to the well-known DNA molecular "light switch" [Ru(bpy)2dppz](2+). Finally, a "sandwich-like" binding model was proposed on the basis of molecular docking simulations.

A comparative study of the interaction of two structurally analogous ruthenium complexes with human telomeric G-quadruplex DNA.

Two new polypyridine ligands and their corresponding ruthenium(II) complexes have been prepared and characterized. The interactions of both complexes with human telomere quadruplex DNA (both the antiparallel basket and the mixed-hybrid G-quadruplex) have been studied by circular dichroism (CD), CD melting, UV-visible (UV-Vis), fluorescent intercalator displacement (FID) assays and molecular docking studies. The results show that both complexes can stabilize G-quadruplexes DNA and two complexes show different binding affinity for different G-quadruplexes DNA. The 1:1 stoichiometry was confirmed in the buffered solutions by the UV-Vis spectrophotometer using Job's plot method and molecular docking studies. We have also investigated the interaction between the complexes and duplex DNA to gain some insight into the selectivity of the complexes for G-quadruplex structures. FID studies have shown that the complexes have a modest selectivity for G-quadruplex versus duplex DNA.

Label-free fluorescent DNA sensor for the detection of silver ions based on molecular light switch Ru complex and unmodified quantum dots.

Using molecular light switch Ru complex Ru(bpy)(2)(dppz)(2+) and CdTe quantum dots (QDs), we have designed a label-free DNA fluorescent sensor for the detection of Ag(+) in aqueous solution.

A naked-eye on-off-on molecular "light switch" based on a reversible "conformational switch" of G-quadruplex DNA.

Herein, we report a new strategy for developing an on-off-on molecular "light switch" by utilizing the pH value to control the "conformational switch" of G-quadruplex DNA. A novel ruthenium(II) complex with an emission enhancement factor of 150 was synthesized and introduced to detect the switch by the naked eye. The "light switch" can be repeatedly cycled off and on through the addition of H(+) and OH(-), respectively. The conformational transitions of G-quadruplex DNA in K(+) solution at different pH values in the acidic region were evidenced by circular dichroism and fluorescence titrations. Computational calculations by applying density functional theory (DFT)/time-dependent DFT and molecular docking were also carried out to gain insight into the "light-switch" mechanism.

Molecular "light switch" for G-quadruplex DNA: cycling the switch on and off.

We report a new G-quadruplex DNA "light switch", where the light switch can be cycled on and off through the successive introduction of G-quadruplex DNA and [Fe(CN)(6)](4-) ions.