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Tao Yang

Publications and source records attributed to Tao Yang.

At least 37 records · Page 2Linked to original sources
PubMed2006

Experimental quantum communication without a shared reference frame.

We present an experimental realization of a robust quantum communication scheme [Phys. Rev. Lett. 93, 220501 (2004)] using pairs of photons entangled in polarization and time. Our method overcomes errors due to collective rotation of the polarization modes (e.g., birefringence in optical fiber or misalignment), is insensitive to the phase's fluctuation of the interferometer, and does not require any shared reference frame including time reference, except the need to label different photons. The practical robustness of the scheme is further shown by implementing a variation of the Bennett-Brassard 1984 quantum key distribution protocol over 1 km optical fiber.

Journal Article↗
PubMed2006

Protein-tyrosine phosphatase (PTP) wedge domain peptides: a novel approach for inhibition of PTP function and augmentation of protein-tyrosine kinase function.

Inhibition of protein-tyrosine phosphatases (PTPs) counterbalancing protein-tyrosine kinases (PTKs) offers a strategy for augmenting PTK actions. Conservation of PTP catalytic sites limits development of specific PTP inhibitors. A number of receptor PTPs, including the leukocyte common antigen-related (LAR) receptor and PTPmu, contain a wedge-shaped helix-loop-helix located near the first catalytic domain. Helix-loop-helix domains in other proteins demonstrate homophilic binding and inhibit function; therefore, we tested the hypothesis that LAR wedge domain peptides would exhibit homophilic binding, bind to LAR, and inhibit LAR function. Fluorescent beads coated with LAR or PTPmu wedge peptides demonstrated PTP-specific homophilic binding, and LAR wedge peptide-coated beads precipitated LAR protein. Administration of LAR wedge Tat peptide to PC12 cells resulted in increased proliferation, decreased cell death, increased neurite outgrowth, and augmented Trk PTK-mediated responses to nerve growth factor (NGF), a phenotype matching that found in PC12 cells with reduced LAR levels. PTPmu wedge Tat peptide had no effect on PC12 cells but blocked the PTPmu-dependent phenotype of neurite outgrowth of retinal ganglion neurons on a PTPmu substrate, whereas LAR wedge peptide had no effect. The survival- and neurite-promoting effect of the LAR wedge peptide was blocked by the Trk inhibitor K252a, and reciprocal co-immunoprecipitation demonstrated LAR/TrkA association. The addition of LAR wedge peptide inhibited LAR co-immunoprecipitation with TrkA, augmented NGF-induced activation of TrkA, ERK, and AKT, and in the absence of exogenous NGF, induced activation of TrkA, ERK, and AKT. PTP wedge domain peptides provide a unique PTP inhibition strategy and offer a novel approach for augmenting PTK function.

Amino Acid Sequence↗
PubMed2006

Experimental synchronization of independent entangled photon sources.

We report the generation of independent entangled photon pairs from two synchronized but mutually incoherent laser sources. The quality of synchronization is confirmed by observing a violation of Bell's inequality with 3.2 standard deviations in an entanglement swapping experiment. The techniques developed in our experiment are not only important for realistic linear optical quantum-information processing, but also enable new tests of local realism.

Journal Article↗
PubMed2006

VKORC1 haplotypes are associated with arterial vascular diseases (stroke, coronary heart disease, and aortic dissection).

BACKGROUND: The haplotypes in the gene vitamin K epoxide reductase complex subunit 1 (VKORC1) have been found to affect warfarin dose response through effects on the formation of reduced-form vitamin K, a cofactor for gamma-carboxylation of vitamin K-dependent proteins, which is involved in the coagulation cascade and has a potential impact on atherosclerosis. We hypothesized that VKORC1-dependent effects on the coagulation cascade and atherosclerosis would contribute to susceptibility for vascular diseases. METHODS AND RESULTS: To test the hypothesis, we studied the association of polymorphisms of VKORC1 with stroke (1811 patients), coronary heart disease (740 patients), and aortic dissection (253 patients) compared with matched controls (n=1811, 740, and 416, respectively). Five common noncoding single-nucleotide polymorphisms of VKORC1 were identified in a natural haplotype block with strong linkage disequilibrium (D'>0.9, r2>0.9), then single-nucleotide polymorphism (SNP) +2255 in the block was selected for the association study. We found that the presence of the C allele of the +2255 locus conferred almost twice the risk of vascular disease (odds ratio [OR] 1.95, 95% confidence interval [CI] .58 to 2.41, P<0.001 for stroke; OR 1.72, 95% CI 1.24 to 2.38, P<0.01 for coronary heart disease; and OR 1.90, 95% CI 1.04 to 3.48, P<0.05 for aortic dissection). We also observed that subjects with the CC and CT genotypes had lower levels of undercarboxylated osteocalcin (a regulator for the bone), probably vascular calcification, and lower levels of protein induced in vitamin K absence or antagonism II (PIVKA-II, a des-gamma-carboxy prothrombin) than those with TT genotypes. CONCLUSIONS: The haplotype of VKORC1 may serve as a novel genetic marker for the risk of stroke, coronary heart disease, and aortic dissection.

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PubMed2006

Electrocatalytic hydrogenation of 4-chlorophenol on the glassy carbon electrode modified by composite polypyrrole/palladium film.

A polypyrrole/palladium composite film was prepared on a glassy carbon electrode by the electrochemical deposition method. The palladium particles were uniformly dispersed on a polypyrrole film that was previously electrodeposited on a glassy carbon electrode. By controlling the polymerization process of pyrrole, a highly porous polypyrrole film was obtained; this kind of structure provided more surface areas for depositing palladium particles. The sizes of Pd particles deposited on the porous polypyrrole film are about 15-30 nm. The X-ray photoelectron spectroscopy results showed there was strong interaction between polypyrrole film and palladium particles. This modified electrode showed excellent current efficiency (49.5%) for electrochemical hydrogenation of 4-chlorophenol and the phenol was the sole product. The potential effect on the dechlorination process was also investigated.

Journal Article↗
PubMed2006

Downregulation of the LAR protein tyrosine phosphatase receptor is associated with increased dentate gyrus neurogenesis and an increased number of granule cell layer neurons.

Growth factors stimulating neurogenesis act through protein tyrosine kinases which are counterbalanced by protein tyrosine phosphatases (PTPs); thus, downregulation of progenitor PTP function might provide a novel strategy for promoting neurogenesis. We tested the hypotheses that the leukocyte common antigen-related (LAR) PTP is present in adult dentate gyrus progenitors, and that its downregulation would promote neurogenesis. In adult mice, LAR immunostaining was present in Ki-67- and PCNA-positive subgranular zone cells. At 1 h post-BrdU administration, LAR-/- mice demonstrated an approximately 3-fold increase in BrdU- and PCNA-positive cells, indicating increased progenitor proliferation. At 1 day and 4 weeks following 6 days of BrdU administration, LAR-/- mice exhibited a significant increase in BrdU and NeuN colabeled cells consistent with increased neurogenesis. In association with increased neurogenesis in LAR-/- mice, stereological analysis revealed a significant 37% increase in the number of neurons present in the granule cell layer. In cultured progenitor clones derived from LAR+/+ mice, LAR immunostaining was present in PCNA- and BrdU-positive cells. Progenitor clones derived from adult LAR-/- hippocampus or LAR+/+ clones made LAR-deficient with LAR siRNA demonstrated increased proliferation and, under differentiation conditions, increased proportions of Tuj1- and MAP2-positive cells. These studies introduce LAR as the first PTP found to be expressed in dentate progenitors and point to inhibition of LAR as a potential strategy for promoting neurogenesis. These findings also provide a rare in vivo demonstration of an association between increased dentate neurogenesis and an expanded population of granule cell layer neurons.

Animals↗
PubMed2006

Ferromagnetic ordering in a new nickel polyborate NiB12O14(OH)10.

A new nickel polyborate, NiB12O14(OH)10 was synthesized using boric acid as a flux. This material has two-dimensional borate layers with a quasi-square lattice of Ni2+. The Ni2+ ions locate in the plane of the two-dimensional layer, bridged through BnO(n+1) chains in the plane and connected with the three-membered ring borate groups out of the plane. The dc and ac magnetic susceptibility, magnetization and specific heat measurements show that this material undergoes a weak ferromagnetic phase transition at Tc = 5.8 K. At T < Tc, a metamagnetic phase transition is observed at about 5 T, associated by a spin-flop, suggesting the ferromagnetic ordering is induced by an antiferromagnetic interaction. A broad maximum in the ac susceptibility at TM = 23-24 K indicates an intermediate short-range ordering.

Journal Article↗
PubMed2006

Recombinase-mediated cassette exchange to rapidly and efficiently generate mice with human cardiac sodium channels.

SCN5A encodes the predominant voltage-gated sodium channel isoform in human heart and nearly 100 variants have now been described and studied in vitro. However, development of animal models to analyze function of such large numbers of human gene variants represents a continuing challenge in translational medicine. Here, we describe the implementation of a two stage procedure, recombinase-mediated cassette exchange (RMCE), to efficiently and rapidly generate mice in which a full-length human cDNA replaces expression of the murine ortholog. In the first step of RMCE, conventional homologous recombination in mouse ES cells was used to replace scn5a exon 2 (that contains the translation start site) with a cassette acceptor that includes the thymidine kinase gene, flanked by loxP/inverted loxP sites. In the second step, the cassette acceptor site was replaced by the full-length wild-type human SCN5A cDNA by Cre/loxP-mediated recombination. The exchange event occurred in 7/29 (24%) colonies, and the time from electroporation to first homozygotes was only 8 months. PCR-restriction fragment length polymorphism (RFLP) showed that the murine isoform was replaced by the human one, and functional studies indicated that mice with human cardiac sodium channels have wild-type sodium current density, action potential durations, heart rates, and QRS durations. These data demonstrate that RMCE can be used to generate mice in which a targeted allele can be rapidly and efficiently replaced by variants of choice, and thereby can serve as an enabling approach for the functional characterization of ion channel and other DNA variants.

Animals↗
PubMed2006

LAR protein tyrosine phosphatase receptor associates with TrkB and modulates neurotrophic signaling pathways.

The identities of receptor protein tyrosine phosphatases (PTPs) that associate with Trk protein tyrosine kinase (PTK) receptors and modulate neurotrophic signaling are unknown. The leukocyte common antigen-related (LAR) receptor PTP is present in neurons expressing TrkB, and like TrkB is associated with caveolae and regulates survival and neurite outgrowth. We tested the hypothesis that LAR associates with TrkB and regulates neurotrophic signaling in embryonic hippocampal neurons. Coimmunoprecipitation and coimmunostaining demonstrated LAR interaction with TrkB that is increased by BDNF exposure. BDNF neurotrophic activity was reduced in LAR-/- and LAR siRNA-treated LAR+/+ neurons and was augmented in LAR-transfected neurons. In LAR-/- neurons, BDNF-induced activation of TrkB, Shc, AKT, ERK, and CREB was significantly decreased; while in LAR-transfected neurons, BDNF-induced CREB activation was augmented. Similarly, LAR+/+ neurons treated with LAR siRNA demonstrated decreased activation of Trk and AKT. LAR is known to activate the Src PTK by dephosphorylation of its negative regulatory domain and Src transactivates Trk. In LAR-/- neurons, or neurons treated with LAR siRNA, phosphorylation of the Src regulatory domain was increased (indicating Src inactivation), consistent with a role for Src in mediating LAR's ability to up-regulate neurotrophic signaling. Interactions between LAR, TrkB, and Src were further confirmed by the findings that Src coimmunoprecipitated with LAR, that the Src inhibitor PP2 blocked the ability of LAR to augment TrkB signaling, and that siRNA-induced depletion of Src decreased LAR interaction with TrkB. These studies demonstrate that receptor PTPs can associate with Trk complexes and promote neurotrophic signaling and point to receptor PTP-based strategies as a novel approach for modulating neurotrophin function.

Animals↗
PubMed2006

Loop shaping design for tracking performance in machine axes.

A modern interpretation of classical loop shaping control design methods is presented in the context of tracking control for linear motor stages. Target applications include noncontacting machines such as laser cutters and markers, water jet cutters, and adhesive applicators. The methods are directly applicable to the common PID controller and are pertinent to many electromechanical servo actuators other than linear motors. In addition to explicit design techniques a PID tuning algorithm stressing the importance of tracking is described. While the theory behind these techniques is not new, the analysis of their application to modern systems is unique in the research literature. The techniques and results should be important to control practitioners optimizing PID controller designs for tracking and in comparing results from classical designs to modern techniques. The methods stress high-gain controller design and interpret what this means for PID. Nothing in the methods presented precludes the addition of feedforward control methods for added improvements in tracking. Laboratory results from a linear motor stage demonstrate that with large open-loop gain very good tracking performance can be achieved. The resultant tracking errors compare very favorably to results from similar motions on similar systems that utilize much more complicated controllers.

Journal Article↗
PubMed2006

[Generation high yield vaccine strain wholly derived from avian influenza viruses by reverse genetics].

Highly pathogenic avian influenza A (HPAI) viruses of the H5N1 subtypes caused enormous economical loss to poultry farms in China and Southeastern Asian countries. The vaccination program is a reliable strategy in controlling the prevalence of these disastrous diseases. The six internal genes of the high-yield influenza virus A/Goose/Dalian/3/01 (H9N2), the hemagglutinin (HA) gene of A/Goose/HLJ/QFY/04 (H5N1) strain, and the neuraminidase gene from A/Duck/Germany/1215/73 (H2N3) reference strain were amplified by RT-PCR technique. The HA gene was modified by the deletion of four basic amino acids of the connecting peptide between HA1 and HA2. Eight gene expressing plasmids were constructed, and the recombinant virus rH5N3 was generated by cells transfection. The infection of chicken embryos and the challenge tests involving chickens demonstrated that the recombinant H5N3 (rH5N3) influenza virus is avirulent. The allantoic fluids of rH5N3-infected eggs contain high-titer influenza viruses with hemagglutination unit of 1:2048, which are eight times those of the parental H5N1 virus. The rH5N3 oil-emulsified vaccine could induce hemagglutination inhibition (HI) antibodies in chickens in 2 weeks post-vaccination, and maximum geometric mean HI-titer were observed 4 approximately 5 weeks post-vaccination and were kept under observation for 18 weeks. The rH5N3-vaccinated chickens were fully protected against morbidity and mortality of the lethal challenge of the H5N1 HPAI viruses, A/Goose/Guangdong/1/96 and A/Goose/HLJ/QFY/04, which had 8 years expansion and differences among multiple amino acids in HA protein. The N3 neuraminidase protein marker makes it possible to distinguish between H5N1 infected- and H5N3 vaccinated animals.

Animals↗
PubMed2006

Chaetocochins A-C, epipolythiodioxopiperazines from Chaetomium cochliodes.

Three new epipolythiodioxopiperazines, chaetocochins A (1), B (2), and C (3), along with dethio-tetra (methylthio) chetomin (4) and chetomin (5), were isolated from the ethyl acetate extract of the solid-state fermented rice culture of the fungus Chaetomium cochliodes. Their structures were elucidated on the basis of spectroscopic analysis. Compounds 1, 3, and 4 exhibited significant cytotoxicity in vitro against cancer cell lines Bre-04, Lu-04, and N-04.

Antineoplastic Agents↗
PubMed2006

A Cdc2-related protein kinase hPFTAIRE1 from human brain interacting with 14-3-3 proteins.

hPFTAIRE1 (PFTK1), a Cdc2-related protein kinase, is highly expressed in human brain. It exhibits cytoplasmic distribution in Hela cells, although it contains two nuclear localization signals (NLSs) in its N-terminus. To search for its substrates and regulatory components, we screened a two-hybrid library by using the full-length hPFTAIRE1 as a bait. Four 14-3-3 isoforms (beta, epsilon, eta, tau) were identified interacting with the hPFTAIRE1. We found a putative 14-3-3 binding consensus motif (RHSSPSS) in the hPFTAIRE1, which overlapped with its second NLS. Deletion of the RHSSPSS motif or substitution of Ser119 with Ala in the conserved binding motif abolished the specific interaction between the hPFTAIRE1 and the 14-3-3 proteins. The mutant S120A hPFTAIRE1 also showed a weak interaction to the 14-3-3 proteins. The results suggested that the Ser119 is crucial for the interaction between hPFTAIRE1 and the 14-3-3 proteins. All the hPFTAIRE1 mutants distributed in cytoplasm of Hela cells and human neuroblastoma cells (SH-SY5Y) when fused to the C-terminus of a green fluorescent protein (GFP), indicating that binding with the 14-3-3 proteins does not contribute to the subcellular localization of the hPFTAIRE1, although the binding may be involved in its signaling regulation.

14-3-3 Proteins↗
PubMed2006

Conversion of taxane glycosides to 10-deacetylbaccatin III.

10-Deacetylbaccatin III (10-DAB III) (2) was obtained by a series of treatment of a mixture of taxane glycosides (3, 4, and 5) without isolation before treatment. Since the taxane glycosides are isolated with paclitaxel from yew trees and can be found during the process of the production of paclitaxel, their conversion to 10-DAB III improves the total yield of paclitaxel (1) and docetaxel.

Chromatography, High Pressure Liquid↗
PubMed2006

Analysis of the interaction between hPFTAIRE1 and PLZF in a yeast two-hybrid system.

hPFTAIRE1 is a Cdc2-related kinase family member. To search its substrates and regulatory proteins, hPFTAIRE1 was fused to LexA and used as a bait to screen a human brain LexA two-hybrid library. In this screening, seven hPFTAIRE1 interacting proteins, including promyelocytic leukemia zinc finger (PLZF), were obtained. The interaction between PLZF and hPFTAIRE1 was confirmed by beta-galactosidase assay and Leu growth activity. PLZF encodes a transcription factor belonging to the POZ/BTB domain and Krüpel zinc finger (POK) family. The highly conserved POZ/BTB domain plays a critical role in protein-protein interaction. We deleted the POZ/BTB and Krüpel zinc finger domains, respectively, and observed the interaction between hPFTAIRE1 and truncated PLZFs by liquid beta-galactosidase activity assay. A weak interaction was detected between hPFTAIRE1 and PLZF. We also observed the interaction between PLZF and another Cdc2-related kinase, PCTAIRE1. A similar result was observed. The interaction between PLZF and hPFTAIRE1 or PCTAIRE1 was confirmed by co-immunoprecipitation assay in a yeast system. PLZF is a phosphoprotein and plays multiple roles during cell growth. Our results suggest that hPFTAIRE1 and PCTAIRE1 may play important roles in the functional regulation of PLZF.

Animals↗
PubMed2006

Small molecule approaches for promoting neurogenesis.

The discovery of small molecules capable of promoting neurogenesis will contribute to the elucidation of the physiological roles of neurogenesis and to novel therapeutic approaches. Small molecule development can be targeted to the promotion of precursor proliferation, survival, migration or maturation and might be applied to augmenting physiological neurogenesis already present in the dentate gyrus or subventricular zone/olfactory bulb or to normally non-neurogenic regions relevant to neuropathological states. Current small molecule discovery can be assessed from the perspective of the following categories: compounds modulating physiological signaling pathways regulating neurogenesis including the sonic hedgehog, bone morphogenic protein Wnt/,-catenin, Notch and chemokine systems; growth factor mimetics; protein tyrosine phosphatase inhibitors; existing drugs including antidepressants, lithium, valproate, sildenafil and statins; hormones, steroids and peptides; and neurotransmitter receptor agonists and antagonists. Unbiased, high throughput screening will likely lead to the discovery of additional active compounds and the recognition of novel mechanisms regulating neurogenesis. A major therapeutic challenge will consist of the identification of molecular targets and mechanisms relatively specific for precursor cells of interest.

Drug Delivery Systems↗
PubMed2006

[Intervention of xuefu zhuyu oral liquid on expression of adhesion molecule CDllb/CD18 in neutrophils in patients with ateriosclerosis obliterans].

OBJECTIVE: To observe the expression of adhesion molecular CD11b/CD18 in peripheral neutrophils and its relation with arteriosclerotic obliterans (ASO), and to study the effect of Xuefu Zhuyu Oral Liquid (XZOL) on it. METHODS: Flow cytometery analysis was used to detect the expression of CD11b/CD18 in peripheral neutrophils of 30 patients with ASO and 30 healthy subjects by direct immunofluroscent technique. Neutrophils were separated from whole blood of ASO patients and cultured, CD11b/CD18 were detected after the cultured cells were interfered with XZOL dilution at different time points (1h,6h,12h). RESULTS: The expression of CD11b/CD18 in neutrophils in ASO patients was significantly higher than that in the healthy subjects (P < 0.05) and stepped in keeping with the severity of the disease. It was significantly lowered in the treated group 6 and 12 h after XZOL intervention, showing significant difference as compared with that in the control group and the level 1 h after medication (P < 0.05). CONCLUSION: CD11b/CD18 may involve in the pathogenesis of ASO and be related to the severity of arteriosclerosis. The possible mechanism of XZOL in treating and preventing ASO might be through reducing the expression of CD11b/CD18 in peripheral neutrophils to interfere the adhesive function of them.

Aged↗