A candidate redshift z ≈ 10 galaxy and rapid changes in that population at an age of 500 Myr

Searches for very-high-redshift galaxies over the past decade have yielded a large sample of more than 6,000 galaxies existing just 900-2,000?million years (Myr) after the Big Bang (redshifts 6?>?z?>?3; ref. 1). The Hubble Ultra Deep Field (HUDF09) data have yielded the first reliable detections of z?≈?8 galaxies that, together with reports of a γ-ray burst at z?≈?8.2 (refs 10, 11), constitute the earliest objects reliably reported to date. Observations of z?≈?7-8 galaxies suggest substantial star formation at z?>?9-10 (refs 12, 13). Here we use the full two-year HUDF09 data to conduct an ultra-deep search for z?≈?10 galaxies in the heart of the reionization epoch, only 500?Myr after the Big Bang. Not only do we find one possible z?≈?10 galaxy candidate, but we show that, regardless of source detections, the star formation rate density is much smaller (～10%) at this time than it is just ～200?Myr later at z?≈?8. This demonstrates how rapid galaxy build-up was at z?≈?10, as galaxies increased in both luminosity density and volume density from z?≈?10 to z?≈?8. The 100-200?Myr before z?≈?10 is clearly a crucial phase in the assembly of the earliest galaxies.     

The signature of orbital motion from the dayside of the planet τ Boötis b

The giant planet orbiting τ Bo?tis (named τ Bo?tis b) was amongst the first extrasolar planets to be discovered. It is one of the brightest exoplanets and one of the nearest to us, with an orbital period of just a few days. Over the course of more than a decade, measurements of its orbital inclination have been announced and refuted, and have hitherto remained elusive. Here we report the detection of carbon monoxide absorption in the thermal dayside spectrum of τ Bo?tis b. At a spectral resolution of ～100,000, we trace the change in the radial velocity of the planet over a large range in phase, determining an orbital inclination of 44.5°?±?1.5° and a mass 5.95?±?0.28 times that of Jupiter, demonstrating that atmospheric characterization is possible for non-transiting planets. The strong absorption signal points to an atmosphere with a temperature that is decreasing towards higher altitudes, in contrast to the temperature inversion inferred for other highly irradiated planets. This supports the hypothesis that the absorbing compounds believed to cause such atmospheric inversions are destroyed in τ Bo?tis b by the ultraviolet emission from the active host star.     

Sequence- and target-independent angiogenesis suppression by siRNA via TLR3

Clinical trials of small interfering RNA (siRNA) targeting vascular endothelial growth factor-A (VEGFA) or its receptor VEGFR1 (also called FLT1), in patients with blinding choroidal neovascularization (CNV) from age-related macular degeneration, are premised on gene silencing by means of intracellular RNA interference (RNAi). We show instead that CNV inhibition is a siRNA-class effect: 21-nucleotide or longer siRNAs targeting non-mammalian genes, non-expressed genes, non-genomic sequences, pro- and anti-angiogenic genes, and RNAi-incompetent siRNAs all suppressed CNV in mice comparably to siRNAs targeting Vegfa or Vegfr1 without off-target RNAi or interferon-alpha/beta activation. Non-targeted (against non-mammalian genes) and targeted (against Vegfa or Vegfr1) siRNA suppressed CNV via cell-surface toll-like receptor 3 (TLR3), its adaptor TRIF, and induction of interferon-gamma and interleukin-12. Non-targeted siRNA suppressed dermal neovascularization in mice as effectively as Vegfa siRNA. siRNA-induced inhibition of neovascularization required a minimum length of 21 nucleotides, a bridging necessity in a modelled 2:1 TLR3-RNA complex. Choroidal endothelial cells from people expressing the TLR3 coding variant 412FF were refractory to extracellular siRNA-induced cytotoxicity, facilitating individualized pharmacogenetic therapy. Multiple human endothelial cell types expressed surface TLR3, indicating that generic siRNAs might treat angiogenic disorders that affect 8% of the world's population, and that siRNAs might induce unanticipated vascular or immune effects.     

1／r,pj=1／Lmax在应交工时间可控时有效点集的求解

对应交工时间可控时的排序时间１／ｒ,ｐｊ＝１／Ｌｍａｘ,以Ｆ１Ｌ表示Ｌｍａｘ,Ｆ２表示应交工时间带后和,Ｆ１、Ｆ２同时极小化,文中给出一寻找有效点集的伪多项式时间算法。     

From endoplasmic-reticulum stress to the inflammatory response

The endoplasmic reticulum is responsible for much of a cell's protein synthesis and folding, but it also has an important role in sensing cellular stress. Recently, it has been shown that the endoplasmic reticulum mediates a specific set of intracellular signalling pathways in response to the accumulation of unfolded or misfolded proteins, and these pathways are collectively known as the unfolded-protein response. New observations suggest that the unfolded-protein response can initiate inflammation, and the coupling of these responses in specialized cells and tissues is now thought to be fundamental in the pathogenesis of inflammatory diseases. The knowledge gained from this emerging field will aid in the development of therapies for modulating cellular stress and inflammation.     

Systematic identification of genomic markers of drug sensitivity in cancer cells

Clinical responses to anticancer therapies are often restricted to a subset of patients. In some cases, mutated cancer genes are potent biomarkers for responses to targeted agents. Here, to uncover new biomarkers of sensitivity and resistance to cancer therapeutics, we screened a panel of several hundred cancer cell lines--which represent much of the tissue-type and genetic diversity of human cancers--with 130 drugs under clinical and preclinical investigation. In aggregate, we found that mutated cancer genes were associated with cellular response to most currently available cancer drugs. Classic oncogene addiction paradigms were modified by additional tissue-specific or expression biomarkers, and some frequently mutated genes were associated with sensitivity to a broad range of therapeutic agents. Unexpected relationships were revealed, including the marked sensitivity of Ewing's sarcoma cells harbouring the EWS (also known as EWSR1)-FLI1 gene translocation to poly(ADP-ribose) polymerase (PARP) inhibitors. By linking drug activity to the functional complexity of cancer genomes, systematic pharmacogenomic profiling in cancer cell lines provides a powerful biomarker discovery platform to guide rational cancer therapeutic strategies.     

Realization of three-qubit quantum error correction with superconducting circuits

Quantum computers could be used to solve certain problems exponentially faster than classical computers, but are challenging to build because of their increased susceptibility to errors. However, it is possible to detect and correct errors without destroying coherence, by using quantum error correcting codes. The simplest of these are three-quantum-bit (three-qubit) codes, which map a one-qubit state to an entangled three-qubit state; they can correct any single phase-flip or bit-flip error on one of the three qubits, depending on the code used. Here we demonstrate such phase- and bit-flip error correcting codes in a superconducting circuit. We encode a quantum state, induce errors on the qubits and decode the error syndrome--a quantum state indicating which error has occurred--by reversing the encoding process. This syndrome is then used as the input to a three-qubit gate that corrects the primary qubit if it was flipped. As the code can recover from a single error on any qubit, the fidelity of this process should decrease only quadratically with error probability. We implement the correcting three-qubit gate (known as a conditional-conditional NOT, or Toffoli, gate) in 63 nanoseconds, using an interaction with the third excited state of a single qubit. We find 85?±?1 per cent fidelity to the expected classical action of this gate, and 78?±?1 per cent fidelity to the ideal quantum process matrix. Using this gate, we perform a single pass of both quantum bit- and phase-flip error correction and demonstrate the predicted first-order insensitivity to errors. Concatenation of these two codes in a nine-qubit device would correct arbitrary single-qubit errors. In combination with recent advances in superconducting qubit coherence times, this could lead to scalable quantum technology.