Regional difference of the start time of the recent warming in Eastern China: prompted by a 165-year temperature record deduced from tree rings in the Dabie Mountains

Tree-ring studies from tropical to subtropical regions are rarer than that from extratropical regions, which greatly limit our understanding of some critical climate change issues. Based on the tree-ring-width chronology of samples collected from the Dabie Mountains, we reconstructed the April-June mean temperature for this region with an explained variance of 46.8%. Five cold (1861-1869, 1889-1899, 1913-1920, 1936-1942 and 1952-1990) and three warm (1870-1888, 1922-1934 and 2000-2005) periods were identified in the reconstruction. The reconstruction not only agreed well with the instrumental records in and around the study area, but also showed good resemblance to previous temperature reconstructions from nearby regions, indicating its spatial and temporal representativeness of the temperature variation in the central part of eastern China. Although no secular warming trend was found, the warming trend since 1970 was unambiguous in the Dabie Mountains (0.064 A degrees C/year). Further temperature comparison indicated that the start time of the recent warming in eastern China was regional different. It delayed gradually from north to south, starting at least around 1940 AD in the north part, around 1970 AD in the central part and around 1980s in the south part. This work enriches the high-resolution temperature reconstructions in eastern China. We expect that climate warming in the future would promote the radial growth of alpine Pinus taiwanensis in the subtropical areas of China, therefore promote the carbon capture and carbon storage in the Pinus taiwanensis forest. It also helps to clarify the regional characteristic of recent warming in eastern China.</p

Alisertib, an Aurora kinase A inhibitor, induces apoptosis and autophagy but inhibits epithelial to mesenchymal transition in human epithelial ovarian cancer cells.

Ovarian cancer is a leading killer of women, and no cure for advanced ovarian cancer is available. Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, has shown potent anticancer effects, and is under clinical investigation for the treatment of advanced solid tumor and hematologic malignancies. However, the role of ALS in the treatment of ovarian cancer remains unclear. This study investigated the effects of ALS on cell growth, apoptosis, autophagy, and epithelial to mesenchymal transition (EMT), and the underlying mechanisms in human epithelial ovarian cancer SKOV3 and OVCAR4 cells. Our docking study showed that ALS, MLN8054, and VX-680 preferentially bound to AURKA over AURKB via hydrogen bond formation, charge interaction, and &pi;-&pi; stacking. ALS had potent growth-inhibitory, proapoptotic, proautophagic, and EMT-inhibitory effects on SKOV3 and OVCAR4 cells. ALS arrested SKOV3 and OVCAR4 cells in G2/M phase and induced mitochondria-mediated apoptosis and autophagy in both SKOV3 and OVCAR4 cell lines in a concentration-dependent manner. ALS suppressed phosphatidylinositol 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) and p38 mitogen-activated protein kinase pathways but activated 5\u27-AMP-dependent kinase, as indicated by their altered phosphorylation, contributing to the proautophagic activity of ALS. Modulation of autophagy altered basal and ALS-induced apoptosis in SKOV3 and OVCAR4 cells. Further, ALS suppressed the EMT-like phenotype in both cell lines by restoring the balance between E-cadherin and N-cadherin. ALS downregulated sirtuin 1 and pre-B cell colony enhancing factor (PBEF/visfatin) expression levels and inhibited phosphorylation of AURKA in both cell lines. These findings indicate that ALS blocks the cell cycle by G2/M phase arrest and promotes cellular apoptosis and autophagy, but inhibits EMT via phosphatidylinositol 3-kinase/Akt/mTOR-mediated and sirtuin 1-mediated pathways in human epithelial ovarian cancer cells. Further studies are warranted to validate the efficacy and safety of ALS in the treatment of ovarian cancer

Entanglement of single-atom quantum bits at a distance

Quantum information science involves the storage, manipulation and communication of information encoded in quantum systems, where the phenomena of superposition and entanglement can provide enhancements over what is possible classically(1,2). Large-scale quantum information processors require stable and addressable quantum memories, usually in the form of fixed quantum bits ( qubits), and a means of transferring and entangling the quantum information between memories that may be separated by macroscopic or even geographic distances. Atomic systems are excellent quantum memories, because appropriate internal electronic states can coherently store qubits over very long timescales. Photons, on the other hand, are the natural platform for the distribution of quantum information between remote qubits, given their ability to traverse large distances with little perturbation. Recently, there has been considerable progress in coupling small samples of atomic gases through photonic channels(2,3), including the entanglement between light and atoms(4,5) and the observation of entanglement signatures between remotely located atomic ensembles(6) (-8). In contrast to atomic ensembles, single-atom quantum memories allow the implementation of conditional quantum gates through photonic channels2,9, a key requirement for quantum computing. Along these lines, individual atoms have been coupled to photons in cavities(2,10-12), and trapped atoms have been linked to emitted photons in free space(13-17). Here we demonstrate the entanglement of two fixed single-atom quantum memories separated by one metre. Two remotely located trapped atomic ions each emit a single photon, and the interference and detection of these photons signals the entanglement of the atomic qubits. We characterize the entangled pair by directly measuring qubit correlations with near-perfect detection efficiency. Although this entanglement method is probabilistic, it is still in principle useful for subsequent quantum operations and scalable quantum information applications(18-20).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62780/1/nature06118.pd

Realisation of a programmable two-qubit quantum processor

The universal quantum computer is a device capable of simulating any physical system and represents a major goal for the field of quantum information science. Algorithms performed on such a device are predicted to offer significant gains for some important computational tasks. In the context of quantum information, "universal" refers to the ability to perform arbitrary unitary transformations in the system's computational space. The combination of arbitrary single-quantum-bit (qubit) gates with an entangling two-qubit gate is a gate set capable of achieving universal control of any number of qubits, provided that these gates can be performed repeatedly and between arbitrary pairs of qubits. Although gate sets have been demonstrated in several technologies, they have as yet been tailored toward specific tasks, forming a small subset of all unitary operators. Here we demonstrate a programmable quantum processor that realises arbitrary unitary transformations on two qubits, which are stored in trapped atomic ions. Using quantum state and process tomography, we characterise the fidelity of our implementation for 160 randomly chosen operations. This universal control is equivalent to simulating any pairwise interaction between spin-1/2 systems. A programmable multi-qubit register could form a core component of a large-scale quantum processor, and the methods used here are suitable for such a device.Comment: 7 pages, 4 figure

NSC23925, Identified in a High-Throughput Cell-Based Screen, Reverses Multidrug Resistance

Multidrug resistance (MDR) is a major factor which contributes to the failure of cancer chemotherapy, and numerous efforts have been attempted to overcome MDR. To date, none of these attempts have yielded a tolerable and effective therapy to reverse MDR; thus, identification of new agents would be useful both clinically and scientifically.To identify small molecule compounds that can reverse chemoresistance, we developed a 96-well plate high-throughput cell-based screening assay in a paclitaxel resistant ovarian cancer cell line. Coincubating cells with a sublethal concentration of paclitaxel in combination with each of 2,000 small molecule compounds from the National Cancer Institute Diversity Set Library, we identified a previously uncharacterized molecule, NSC23925, that inhibits Pgp1 and reverses MDR1 (Pgp1) but does not inhibit MRP or BCRP-mediated MDR. The cytotoxic activity of NSC23925 was further evaluated using a panel of cancer cell lines expressing Pgp1, MRP, and BCRP. We found that at a concentration of >10 microM NSC23925 moderately inhibits the proliferation of both sensitive and resistant cell lines with almost equal activity, but its inhibitory effect was not altered by co-incubation with the Pgp1 inhibitor, verapamil, suggesting that NSC23925 itself is not a substrate of Pgp1. Additionally, NSC23925 increases the intracellular accumulation of Pgp1 substrates: calcein AM, Rhodamine-123, paclitaxel, mitoxantrone, and doxorubicin. Interestingly, we further observed that, although NSC23925 directly inhibits the function of Pgp1 in a dose-dependent manner without altering the total expression level of Pgp1, NSC23925 actually stimulates ATPase activity of Pgp, a phenomenon seen in other Pgp inhibitors.The ability of NSC23925 to restore sensitivity to the cytotoxic effects of chemotherapy or to prevent resistance could significantly benefit cancer patients

Quantum Computing

Quantum mechanics---the theory describing the fundamental workings of nature---is famously counterintuitive: it predicts that a particle can be in two places at the same time, and that two remote particles can be inextricably and instantaneously linked. These predictions have been the topic of intense metaphysical debate ever since the theory's inception early last century. However, supreme predictive power combined with direct experimental observation of some of these unusual phenomena leave little doubt as to its fundamental correctness. In fact, without quantum mechanics we could not explain the workings of a laser, nor indeed how a fridge magnet operates. Over the last several decades quantum information science has emerged to seek answers to the question: can we gain some advantage by storing, transmitting and processing information encoded in systems that exhibit these unique quantum properties? Today it is understood that the answer is yes. Many research groups around the world are working towards one of the most ambitious goals humankind has ever embarked upon: a quantum computer that promises to exponentially improve computational power for particular tasks. A number of physical systems, spanning much of modern physics, are being developed for this task---ranging from single particles of light to superconducting circuits---and it is not yet clear which, if any, will ultimately prove successful. Here we describe the latest developments for each of the leading approaches and explain what the major challenges are for the future.Comment: 26 pages, 7 figures, 291 references. Early draft of Nature 464, 45-53 (4 March 2010). Published version is more up-to-date and has several corrections, but is half the length with far fewer reference

Assessment of intrahepatic blood flow by Doppler ultrasonography: Relationship between the hepatic vein, portal vein, hepatic artery and portal pressure measured intraoperatively in patients with portal hypertension

<p>Abstract</p> <p>Background</p> <p>Abnormality of hepatic vein (HV) waveforms evaluated by Doppler ultrasonography has been widely studied in patients with chronic liver disease. We investigated the correlation between changes in HV waveforms and portal vein velocity (PVVel), the hepatic artery pulsatility index (HAPI), and also the extent of abnormal Doppler HV waveforms expressed as damping index (DI), severity of portal hypertension expressed as Child-Pugh scores and portal pressure (PP) measured directly from patients with portal hypertension (PHT) to evaluate the indicative value of abnormal HV waveforms and discuss the cause of abnormal HV waveform.</p> <p>Methods</p> <p>Sixty patients who had been diagnosed with PHT and accepted surgical therapy of portosystemic shunts were investigated. PP was measured intraoperatively. Thirty healthy volunteers with no history of chronic liver disease were enrolled as the control group. HV waveforms were categorized as triphasic, biphasic or monophasic. DI was compared as the quantitative indicator of abnormal HV waveforms. Another two Doppler parameters, PVVel and HAPI were also measured. These Doppler features were compared with PP, Child-Pugh scores and histological changes assessed by liver biopsy.</p> <p>Results</p> <p>In the patient group, the Doppler flow waveforms in the middle HV were triphasic in 31.6%, biphasic in 46.7%, and monophasic in 21.6% of subjects. These figures were 86.7%, 10.0%, and 3.3%, respectively, in healthy subjects. With the flattening of HV waveforms, the HAPI increased significantly (<it>r </it>= 00.438, <it>p </it>< 0.0001), whereas PVVel decreased significantly (<it>r </it>= -0.44, <it>p <</it>0.0001). Blood flow parameters, HAPI, PVVel and HV-waveform changes showed no significant correlations with Child-Pugh scores. The latter showed a significant correlation with PP (<it>r </it>= 0.589, <it>p </it>= 0.044). Changes of HV waveform and DI significantly correlated with PP (<it>r </it>= 0.579, <it>r </it>= 0.473, <it>p <</it>0.0001), and significant correlation between DI and Child-Pugh scores was observed (<it>r </it>= 0.411, <it>p = </it>0.001). PP was significantly different with respect to nodule size (<it>p </it>< 0.05), but HV-waveform changes were not significantly correlated with pathological changes.</p> <p>Conclusion</p> <p>In patients with PHT, a monophasic HV waveform indicates higher portal pressure. Furthermore, quantitative indicator DI can reflect both higher portal pressure and more severe liver dysfunction. Flattening of HV waveforms accompanied by an increase in the HAPI and decrease in PVVel support the hypothesis that histological changes reducing HV compliance be the cause of abnormality of Doppler HV waveforms from the hemodynamic angle.</p

Nuclear Factor-Kappa B Inhibition Can Enhance Apoptosis of Differentiated Thyroid Cancer Cells Induced by 131I

Objective: To evaluate changes of nuclear factor-kappa B (NF-kB) during radioiodine 131 ( 131 I) therapy and whether NF-kB inhibition could enhance 131 I-induced apoptosis in differentiated thyroid cancer (DTC) cells in a synergistic manner. Methods: Three human DTC cell lines were used. NF-kB inhibition was achieved by using a NF-kB inhibitor (Bay 11-7082) or by p65 siRNA transfection. Methyl-thiazolyl-tetrazolium assay was performed for cell viability assessment. DNA-binding assay, luciferase reporter assay, and Western blot were adopted to determine function and expression changes of NF-kB. Then NF-kB regulated anti-apoptotic factors XIAP, cIAP1, and Bcl-xL were measured. Apoptosis was analyzed by Western blot for caspase 3 and PARP, and by flow cytometry as well. An iodide uptake assay was performed to determine whether NF-kB inhibition could influence radioactive iodide uptake. Results: The methyl-thiazolyl-tetrazolium assay showed significant decrease of viable cells by combination therapy than by mono-therapies. The DNA-binding assay and luciferase reporter assay showed enhanced NF-kB function and reporter gene activities due to 131 I, yet significant suppression was achieved by NF-kB inhibition. Western blot proved 131 I could increase nuclear NF-kB concentration, while NF-kB inhibition reduced NF-kB concentration. Western blot also demonstrated significant up-regulation of XIAP, cIAP1, and Bcl-xL after 131 I therapy. And inhibition of NF-kB could significantly downregulate these factors. Finally, synergism induced by combined therapy was displayed by significant enhancements o

Wheat TaRab7 GTPase Is Part of the Signaling Pathway in Responses to Stripe Rust and Abiotic Stimuli

Small GTP-binding proteins function as regulators of specific intercellular fundamental biological processes. In this study, a small GTP-binding protein Rab7 gene, designated as TaRab7, was identified and characterized from a cDNA library of wheat leaves infected with Puccinia striiformis f. sp. tritici (Pst) the wheat stripe rust pathogen. The gene was predicted to encode a protein of 206 amino acids, with a molecular mass of 23.13 KDa and an isoeletric point (pI) of 5.13. Further analysis revealed the presence of a conserved signature that is characteristic of Rab7, and phylogenetic analysis demonstrated that TaRab7 has the highest similarity to a small GTP binding protein gene (BdRab7-like) from Brachypodium distachyon. Quantitative real-time PCR assays revealed that the expression of TaRab7 was higher in the early stage of the incompatible interactions between wheat and Pst than in the compatible interaction, and the transcription level of TaRab7 was also highly induced by environmental stress stimuli. Furthermore, knocking down TaRab7 expression by virus induced gene silencing enhanced the susceptibility of wheat cv. Suwon 11 to an avirulent race CYR23. These results imply that TaRab7 plays an important role in the early stage of wheat-stripe rust fungus interaction and in stress tolerance