We have designed a threshold Cherenkov detector at the Rutherford-Appleton Laboratory to identify muons with momenta between 230 and 350 MeV/c. We investigated the properties of three aerogels for ...the design. The nominal indices of refraction were n = 1.03, 1.07, 1.12, respectively. Two of the samples are of high density aerogel not commonly used for Cherenkov light detection. We present results of an examination of some optical properties of the aerogel samples and present basic test beam results.
We present a measurement of the asymmetry A_{CP} between same-sign inclusive dilepton samples ℓ^{+}ℓ^{+} and ℓ^{-}ℓ^{-} (ℓ=e, μ) from semileptonic B decays in ϒ(4S)→BBover ¯ events, using the ...complete data set recorded by the BABAR experiment near the ϒ(4S) resonance, corresponding to 471×10^{6} BBover ¯ pairs. The asymmetry A_{CP} allows comparison between the mixing probabilities P(Bover ¯^{0}→B^{0}) and P(B^{0}→Bover ¯^{0}), and therefore probes CP and T violation. The result, A_{CP}=-3.9±3.5(stat)±1.9(syst)×10^{-3}, is consistent with the standard model expectation.
The photon spectrum in the inclusive electromagnetic radiative decays of the B meson, B → X(s)γ plus B → X(d)γ, is studied using a data sample of (382.8 ± 4.2) × 10(6)Υ(4S) → BB decays collected by ...the BABAR experiment at SLAC. The spectrum is used to extract the branching fraction B(B → X(s)γ) = (3.21 ± 0.33) × 10(-4) for E(γ) >1.8 GeV and the direct CP asymmetry A(CP) (B → X(s+d)γ) = 0.057 ± 0.063. The effects of detector resolution and Doppler smearing are unfolded to measure the photon energy spectrum in the B meson rest frame.
Phys. Rev. D 89, 051101 (2014) We describe searches for B meson decays to the charmless vector-vector final
states omega omega and omega phi with 471 x 10^6 B Bbar pairs produced in e+ e-
...annihilation at sqrt(s) = 10.58 GeV using the BABAR detector at the PEP-II
collider at the SLAC National Accelerator Laboratory. We measure the branching
fraction B(B0 --> omega omega) = (1.2 +- 0.3 +0.3-0.2) x 10^-6, where the first
uncertainty is statistical and the second is systematic, corresponding to a
significance of 4.4 standard deviations. We also determine the upper limit B(B0
--> omega phi) < 0.7 x 10^-6 at 90% confidence level. These measurements
provide the first evidence for the decay B0 --> omega omega, and an improvement
of the upper limit for the decay B0 --> omega phi.
We study the decay
$\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}$, reconstructing
the \Lambda_{c}^{+} baryon in the $p K^{-}\pi^{+}$ mode, using a data sample of
$467\times 10^{6}$ ...$B\bar{B}$ pairs collected with the BaBar detector at the
PEP-2 storage rings at SLAC. We measure branching fractions for decays with
intermediate $\Sigma_{c}$ baryons to be ${\cal
B}\bar{B}^{0}\rightarrow\Sigma_{c}(2455)^{++}\bar{p}\pi^{-}=(21.3 \pm 1.0 \pm
1.0 \pm 5.5) \times 10^{-5}$, ${\cal
B}\bar{B}^{0}\rightarrow\Sigma_{c}(2520)^{++}\bar{p}\pi^{-}=(11.5\pm 1.0 \pm
0.5 \pm 3.0)\times 10^{-5}$, ${\cal
B}\bar{B}^{0}\rightarrow\Sigma_{c}(2455)^{0}\bar{p}\pi^{+}=(9.1 \pm 0.7 \pm
0.4 \pm 2.4)\times10^{-5}$, and ${\cal
B}\bar{B}^{0}\rightarrow\Sigma_{c}(2520)^{0}\bar{p}\pi^{+}= (2.2 \pm 0.7 \pm
0.1\pm 0.6) \times 10^{-5}$, where the uncertainties are statistical,
systematic, and due to the uncertainty on the
$\Lambda_{c}^{+}\rightarrow\proton\Km\pi^{+}$ branching fraction, respectively.
For decays without $\Sigma_{c}(2455)$ or $\Sigma_{c}(2520)$ resonances, we
measure ${\cal
B}\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}_{\mathrm{non-\Sigma_{c}}}=(79
\pm 4 \pm 4 \pm 20)\times10^{-5}$. The total branching fraction is determined
to be ${\cal
B}\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}_{\mathrm{total}}=(123
\pm 5 \pm 7 \pm 32)\times10^{-5}$. We examine multibody mass combinations in
the resonant three-particle $\Sigma_{c}\bar{p}\pi$ final states and in the
four-particle $\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}$ final state, and observe
different characteristics for the $\bar{p}\pi$ combination in neutral versus
doubly-charged $\Sigma_{c}$ decays.
Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA are frequently observed in COVID-19 patients. However, it is unclear whether SARS-CoV-2 replicates in the human intestine and ...contributes to possible fecal-oral transmission. Here, we report productive infection of SARS-CoV-2 in ACE2
mature enterocytes in human small intestinal enteroids. Expression of two mucosa-specific serine proteases, TMPRSS2 and TMPRSS4, facilitated SARS-CoV-2 spike fusogenic activity and promoted virus entry into host cells. We also demonstrate that viruses released into the intestinal lumen were inactivated by simulated human colonic fluid, and infectious virus was not recovered from the stool specimens of COVID-19 patients. Our results highlight the intestine as a potential site of SARS-CoV-2 replication, which may contribute to local and systemic illness and overall disease progression.
We study the decay \(\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}\), reconstructing the \Lambda_{c}^{+} baryon in the \(p K^{-}\pi^{+}\) mode, using a data sample of \(467\times ...10^{6}\) \(B\bar{B}\) pairs collected with the BaBar detector at the PEP-2 storage rings at SLAC. We measure branching fractions for decays with intermediate \(\Sigma_{c}\) baryons to be \({\cal B}\bar{B}^{0}\rightarrow\Sigma_{c}(2455)^{++}\bar{p}\pi^{-}=(21.3 \pm 1.0 \pm 1.0 \pm 5.5) \times 10^{-5}\), \({\cal B}\bar{B}^{0}\rightarrow\Sigma_{c}(2520)^{++}\bar{p}\pi^{-}=(11.5\pm 1.0 \pm 0.5 \pm 3.0)\times 10^{-5}\), \({\cal B}\bar{B}^{0}\rightarrow\Sigma_{c}(2455)^{0}\bar{p}\pi^{+}=(9.1 \pm 0.7 \pm 0.4 \pm 2.4)\times10^{-5}\), and \({\cal B}\bar{B}^{0}\rightarrow\Sigma_{c}(2520)^{0}\bar{p}\pi^{+}= (2.2 \pm 0.7 \pm 0.1\pm 0.6) \times 10^{-5}\), where the uncertainties are statistical, systematic, and due to the uncertainty on the \(\Lambda_{c}^{+}\rightarrow\proton\Km\pi^{+}\) branching fraction, respectively. For decays without \(\Sigma_{c}(2455)\) or \(\Sigma_{c}(2520)\) resonances, we measure \({\cal B}\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}_{\mathrm{non-\Sigma_{c}}}=(79 \pm 4 \pm 4 \pm 20)\times10^{-5}\). The total branching fraction is determined to be \({\cal B}\bar{B}^{0}\rightarrow\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}_{\mathrm{total}}=(123 \pm 5 \pm 7 \pm 32)\times10^{-5}\). We examine multibody mass combinations in the resonant three-particle \(\Sigma_{c}\bar{p}\pi\) final states and in the four-particle \(\Lambda_{c}^{+}\bar{p}\pi^{+}\pi^{-}\) final state, and observe different characteristics for the \(\bar{p}\pi\) combination in neutral versus doubly-charged \(\Sigma_{c}\) decays.
Adaptive cellular responses are often required during wound repair. Following disruption of the intestinal epithelium, wound‐associated epithelial (WAE) cells form the initial barrier over the wound. ...Our goal was to determine the critical factor that promotes WAE cell differentiation. Using an adaptation of our in vitro primary epithelial cell culture system, we found that prostaglandin E2 (PGE2) signaling through one of its receptors, Ptger4, was sufficient to drive a differentiation state morphologically and transcriptionally similar to in vivo WAE cells. WAE cell differentiation was a permanent state and dominant over enterocyte differentiation in plasticity experiments. WAE cell differentiation was triggered by nuclear β‐catenin signaling independent of canonical Wnt signaling. Creation of WAE cells via the PGE2‐Ptger4 pathway was required in vivo, as mice with loss of Ptger4 in the intestinal epithelium did not produce WAE cells and exhibited impaired wound repair. Our results demonstrate a mechanism by which WAE cells are formed by PGE2 and suggest a process of adaptive cellular reprogramming of the intestinal epithelium that occurs to ensure proper repair to injury.
Synopsis
Intestinal wound‐associated epithelial (WAE) cells are a transient class of repair cells critical for repair initiation. Prostaglandin PGE2 triggers WAE cell generation in response to injury, acting through its epithelial receptor EP4.
The prostaglandin PGE2 stimulates wound‐associated epithelial cell formation in mouse and human cells.
PGE2 acts through the receptor Ptger4 (EP4) on intestinal epithelial cells.
WAE cell differentiation suppresses enterocyte differentiation of epithelial progenitors.
Intestinal wound‐associated epithelial (WAE) cells are a transient class of repair cells critical for repair initiation. Prostaglandin PGE2 triggers WAE cell generation in response to injury, acting through its epithelial receptor EP4.
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