Measurement of the Λ(b)(0), Ξ (b)(-), and Ω(b((-) Baryon masses.

Bottom baryons decaying to a J/ψ meson and a hyperon are reconstructed using 1.0 fb(-1) of data collected in 2011 with the LHCb detector. Significant Λ(b)(0) → J/ψΛ, Ξ(b((-) → J/ψΞ(-) and Ω(b)(-) → J/ψΩ(-) signals are observed and the corresponding masses are measured to be M(Λ(b)(0))=5619.

First observation of the decay Bs2*(5840)(0)→B*+ K- and studies of excited Bs(0) mesons.

The properties of the orbitally excited (L=1) Bs(0) states are studied by using 1.0  fb(-1) of pp collisions at sqrt[s]=7  TeV collected with the LHCb detector. The first observation of the Bs2*(5840)(0) meson decaying to B*+ K- is reported, and the corresponding branching fraction measured relative to the B+ K- decay mode.

MicroRNA-93 controls perfusion recovery after hindlimb ischemia by modulating expression of multiple genes in the cell cycle pathway.

Background: MicroRNAs are key regulators of gene expression in response to injury, but there is limited knowledge of their role in ischemia-induced angiogenesis, such as in peripheral arterial disease. Here, we used an unbiased strategy and took advantage of different phenotypic outcomes that follow surgically induced hindlimb ischemia between inbred mouse strains to identify key microRNAs involved in perfusion recovery from hindlimb ischemia.

Methods And Results: From comparative microRNA profiling between inbred mouse strains that display profound differences in their extent of perfusion recovery after hindlimb ischemia, we found that the mouse strain with higher levels of microRNA-93 (miR-93) in hindlimb muscle before ischemia and the greater ability to upregulate miR-93 in response to ischemia had better perfusion recovery.

Observation of D0-D0 oscillations.

We report a measurement of the time-dependent ratio of D(0) → K(+) π- to D(0) → K(-) π(+) decay rates in D(*+)-tagged events using 1.0 fb(-1) of integrated luminosity recorded by the LHCb experiment. We measure the mixing parameters x('2) = (-0.

Quantitative trait loci for bone mineral density and femoral morphology in an advanced intercross population of mice.

Osteoporosis, characterized by low levels of bone mineral density (BMD), is a prevalent medical condition in humans. We investigated its genetic and environmental basis by searching for quantitative trait loci (QTLs) affecting six skeletal (including three BMD) traits in a G10 advanced intercross population produced from crosses of mice from the inbred strain C57BL/6J with mice from a strain selected for high voluntary wheel running. The mice in this population were fed either a high-fat or a matched control diet throughout the study, allowing us to test for QTL by diet interactions for the skeletal traits.

First evidence for the decay B(s)(0)→μ+ μ-.

A search for the rare decays B(s)(0)→μ+ μ- and B(0)→μ+ μ- is performed with data collected in 2011 and 2012 with the LHCb experiment at the Large Hadron Collider. The data samples comprise 1.1  fb(-1) of proton-proton collisions at sqrt[s]=8  TeV and 1.

Measurement of the CP asymmetry in B(0)→K(*0)μ(+)μ(-) decays.

A measurement of the CP asymmetry in B(0)→K(*0)μ(+)μ(-) decays is presented, based on 1.0 fb(-1) of pp collision data recorded by the LHCb experiment during 2011. The measurement is performed in six bins of invariant mass squared of the μ(+)μ(-) pair, excluding the J/ψ and ψ(2S) resonance regions.

Measurements of B(c)+ production and mass with the B(c)+ → J/ψπ+ decay.

Measurements of B(c)(+) production and mass are performed with the decay mode B(c)(+)→J/ψπ(+) using 0.37 fb(-1) of data collected in pp collisions at √[s]=7 TeV by the LHCb experiment. The ratio of the production cross section times branching fraction between the B(c)(+)→J/ψπ(+) and the B(+)→J/ψK(+) decays is measured to be (0.

Systems-level analysis of genome-wide association data.

Genome-wide association studies (GWAS) have emerged as the method of choice for identifying common variants affecting complex disease. In a GWAS, particular attention is placed, for obvious reasons, on single-nucleotide polymorphisms (SNPs) that exceed stringent genome-wide significance thresholds. However, it is expected that many SNPs with only nominal evidence of association (e.

Systems genetic analysis of osteoblast-lineage cells.

The osteoblast-lineage consists of cells at various stages of maturation that are essential for skeletal development, growth, and maintenance. Over the past decade, many of the signaling cascades that regulate this lineage have been elucidated; however, little is known of the networks that coordinate, modulate, and transmit these signals. Here, we identify a gene network specific to the osteoblast-lineage through the reconstruction of a bone co-expression network using microarray profiles collected on 96 Hybrid Mouse Diversity Panel (HMDP) inbred strains.

Contemporary Approaches for Identifying Rare Bone Disease Causing Genes.

Recent improvements in the speed and accuracy of DNA sequencing, together with increasingly sophisticated mathematical approaches for annotating gene networks, have revolutionized the field of human genetics and made these once time consuming approaches assessable to most investigators. In the field of bone research, a particularly active area of gene discovery has occurred in patients with rare bone disorders such as osteogenesis imperfecta (OI) that are caused by mutations in single genes. In this perspective, we highlight some of these technological advances and describe how they have been used to identify the genetic determinants underlying two previously unexplained cases of OI.

Measurements of the branching fractions of [Formula: see text] decays.

The branching fractions of the decay [Formula: see text] for different intermediate states are measured using data, corresponding to an integrated luminosity of 1.0 fb, collected by the LHCb experiment. The total branching fraction, its charmless component [Formula: see text] and the branching fractions via the resonant [Formula: see text] states (1) and (2) relative to the decay via a / intermediate state are [Formula: see text] Upper limits on the branching fractions into the (2) meson and into the charmonium-like states (3872) and (3915) are also obtained.

Measurement of the forward energy flow in collisions at [Formula: see text].

The energy flow created in collisions at [Formula: see text] is studied within the pseudorapidity range 1.9<<4.9 with data collected by the LHCb experiment.

Measurement of / polarization in collisions at [Formula: see text].

An angular analysis of the decay /→ is performed to measure the polarization of prompt / mesons produced in collisions at [Formula: see text]. The dataset corresponds to an integrated luminosity of 0.37 fb collected with the LHCb detector.

Observation of excited Λ(b)(0) baryons.

Using pp collision data corresponding to 1.0 fb(-1) integrated luminosity collected by the LHCb detector, two narrow states are observed in the Λ(b)(0)π(+)π(-) spectrum with masses 5911.97±0.

Measurement of the B¯(s)(0) effective lifetime in the J/ψf0(980) final state.

The effective lifetime of the B ¯(s)(0) meson in the decay mode B¯(s)(0)→J/ψf(0)(980) is measured using 1.0 fb(-1) of data collected in pp collisions at √s=7 TeV with the LHCb detector. The result is 1.

Unraveling inflammatory responses using systems genetics and gene-environment interactions in macrophages.

Many common diseases have an important inflammatory component mediated in part by macrophages. Here we used a systems genetics strategy to examine the role of common genetic variation in macrophage responses to inflammatory stimuli. We examined genome-wide transcript levels in macrophages from 92 strains of the Hybrid Mouse Diversity Panel.

Peer review versus editorial review and their role in innovative science.

Peer review is a widely accepted instrument for raising the quality of science. Peer review limits the enormous unstructured influx of information and the sheer amount of dubious data, which in its absence would plunge science into chaos. In particular, peer review offers the benefit of eliminating papers that suffer from poor craftsmanship or methodological shortcomings, especially in the experimental sciences.

Observation of B0→D¯(0)K(+)K(-) and evidence for B(s)(0)→D¯(0)K(+)K(-).

The first observation of the decay B0→D¯(0)K(+)K(-) is reported from an analysis of 0.62 fb(-1) of pp collision data collected with the LHCb detector. Its branching fraction is measured relative to that of the topologically similar decay B(0)→D ¯(0)π(+)π(-) to be (B(B(0)→D¯(0)K(+)K(-))/B(B(0)→D¯(0)π(+)π(-))=0.

First observation of the decay B(c)+ → J/ψπ(+) π- π+.

The decay B(c)(+) → J/ψπ(+) π(-) π(+) is observed for the first time, using 0.8 fb(-1) of pp collisions at sqrt[s] = 7 TeV collected by the LHCb experiment. The ratio of branching fractions B(B(c)(+) → J/ψπ(+) π(-) π(+))/B(B(c)(+)→J/ψπ^{+}) is measured to be 2.

Determination of the sign of the decay width difference in the B(s)(0) system.

The interference between the K+ K- S-wave and P-wave amplitudes in B(s)(0) → J/ψK+ K- decays with the K+ K- pairs in the region around the ϕ(1020) resonance is used to determine the variation of the difference of the strong phase between these amplitudes as a function of K+ K- invariant mass. Combined with the results from our CP asymmetry measurement in B(s)(0) → J/ψϕ decays, we conclude that the B(s)(0) mass eigenstate that is almost CP = +1 is lighter and decays faster than the mass eigenstate that is almost CP = -1. This determines the sign of the decay width difference ΔΓ(s) ≡ Γ(L) - Γ(H) to be positive.

Strong constraints on the rare decays B(s)(0) → μ+ μ- and B0 → μ+ μ-.

A search for B(s)(0) → μ+ μ- and B0 → μ+ μ decays is performed using 1.0  fb(-1) of pp collision data collected at sqrt[s] = 7  TeV with the LHCb experiment at the Large Hadron Collider. For both decays, the number of observed events is consistent with expectation from background and standard model signal predictions.

Hybrid mouse diversity panel: a panel of inbred mouse strains suitable for analysis of complex genetic traits.

We have developed an association-based approach using classical inbred strains of mice in which we correct for population structure, which is very extensive in mice, using an efficient mixed-model algorithm. Our approach includes inbred parental strains as well as recombinant inbred strains in order to capture loci with effect sizes typical of complex traits in mice (in the range of 5% of total trait variance). Over the last few years, we have typed the hybrid mouse diversity panel (HMDP) strains for a variety of clinical traits as well as intermediate phenotypes and have shown that the HMDP has sufficient power to map genes for highly complex traits with resolution that is in most cases less than a megabase.

Unexpected thermal decomposition of the "Alder carbene" (iPr2N)2C.

The "Alder carbene" (iPr(2)N)(2)C undergoes a β-fragmentation in solution already at room temperature, affording propene and N,N,N'-triisopropylformamidine. This stands in sharp contrast to the indefinite stability previously claimed for this iconic compound.