119,494 research outputs found
Search for violation in decays and observation of the Cabibbo-suppressed decay
We search for violation by measuring a -odd asymmetry in the
Cabibbo-suppressed decay, and
in the Cabibbo-favored and
decays. We use 980 of data collected by the Belle detector running at the KEKB
asymmetric-energy collider. The -violating -odd parameter
is measured to be
and
where the first
uncertainty is statistical and the second is systematic. We also report the
first observation of the Cabibbo-suppressed decay . The branching fraction is measured relative to
that of the analogous Cabibbo-favored decay :
Branching fraction and CP asymmetry of the decays B+→K0Sπ+ and B+→K0SK+
An analysis of B+ → K0
Sπ+ and B+ → K0
S K+ decays is performed with the LHCb experiment. The pp
collision data used correspond to integrated luminosities of 1 fb−1 and 2 fb−1 collected at centre-ofmass
energies of
√
s = 7 TeV and
√
s = 8 TeV, respectively. The ratio of branching fractions and the
direct CP asymmetries are measured to be B(B+ → K0
S K+
)/B(B+ → K0
Sπ+
) = 0.064 ± 0.009 (stat.) ±
0.004 (syst.), ACP(B+ → K0
Sπ+
) = −0.022 ± 0.025 (stat.) ± 0.010 (syst.) and ACP(B+ → K0
S K+
) =
−0.21 ± 0.14 (stat.) ± 0.01 (syst.). The data sample taken at
√
s = 7 TeV is used to search for
B+
c
→ K0
S K+ decays and results in the upper limit ( fc · B(B+
c
→ K0
S K+
))/( fu · B(B+ → K0
Sπ+
)) <
5.8 × 10−2 at 90% confidence level, where fc and fu denote the hadronisation fractions of a ¯b
quark
into a B+
c or a B+ meson, respectively
Search for CP violation in D s + → K S 0 K − π + π + decays using triple and quadruple products
Abstract We perform the first search for CP violation in D s + → K S 0 K − π + π + decays. We use a combined data set from the Belle and Belle II experiments, which study e + e − collisions at center-of-mass energies at or near the Υ(4S) resonance. We use 980 fb −1 of data from Belle and 428 fb −1 of data from Belle II. We measure six CP-violating asymmetries that are based on triple products and quadruple products of the momenta of final-state particles, and also the particles’ helicity angles. We obtain a precision at the level of 0.5% for D + → K S 0 K − π + π + decays, and better than 0.3% for D s + → K S 0 K − π + π + decays. No evidence of CP violation is found. Our results for the triple-product asymmetries are the most precise to date for singly-Cabibbo-suppressed D + decays. Our results for the other asymmetries are the first such measurements performed for charm decays
Measurements of K S 0 - K L 0 asymmetries in the decays Λ c + → p K L , S 0 , p K L , S 0 π + π − and p K L , S 0 π 0
Abstract Using e + e − annihilation data sets corresponding to an integrated luminosity of 4.5 fb −1, collected with the BESIII detector at center-of-mass energies between 4.600 and 4.699 GeV, we report the first measurements of the absolute branching fractions B Λ c + → p K L 0 = (1.67 ± 0.06 ± 0.04)%, B Λ c + → p K L 0 π + π − = (1.69 ± 0.10 ± 0.05)%, and B Λ c + → p K L 0 π 0 = (2.02 ± 0.13 ± 0.05)%, where the first uncertainties are statistical and the second systematic. Combining with the known branching fractions of Λ c + → p K S 0 , Λ c + → p K S 0 π + π − , and Λ c + → p K S 0 π 0 , we present the first measurements of the K S 0 - K L 0 asymmetries R Λ c + K S , L 0 X = B Λ c + → K S 0 X − B Λ c + → K L 0 X B Λ c + → K S 0 X + B Λ c + → K L 0 X in charmed baryon decays: R Λ c + p K S , L 0 = − 0.025 ± 0.031 , R Λ c + p K S , L 0 π + π − = − 0.027 ± 0.048 and R Λ c + p K S , L 0 π 0 = − 0.015 ± 0.046 . No significant asymmetries with statistical significance are observed
lin-31, a Caenorhabditis elegans HNF-3/fork head transcription factor homolog, specifies three alternative cell fates in vulva development
Late events in the cell-cell signalling pathway that controls the specification of vulva cell fates in C. elegans are characterized. The lin-31 gene acts downstream of the ras homolog let-60 and encodes a member of the HNF-3/fork head family of DNA-binding transcription factors. lin-31 regulates how vulval precursor cells choose their fate and in lin-31 mutants, these cells do not properly choose which fate to express and therefore adopt any of the 3 possible vulval cell fates in a deregulated manner..RE: 68 ref.; SC: CA; PE; 0TSource type: Electronic(1) http://upei-resolver.asin-risa.ca?sid=SP:CABI&id=pmid:&id=&issn=0890-9369&isbn=&volume=7&issue=6&spage=933&pages=933-947&date=1993&title=Genes%20and%20Development&atitle=lin-31%2c%20a%20Caenorhabditis%20elegans%20HNF-3%2ffork%20head%20transcription%20factor%20homolog%2c%20specifies%20three%20alternative%20cell%20fates%20in%20vulva%20development.&aulast=Miller&pid=%3Cauthor%3EMiller%2c%20L%20M%3bGallegos%2c%20M%20E%3bMorisseau%2c%20B%20A%3bKim%2c%20S%20K%3C%2Fauthor%3E%3CAN%3E19932337278%3C%2FAN%3E%3CDT%3EJournal%20article%3C%2FDT%3
Spatial Chow-Lin Methods for Data Completion in Econometric Flow Models
Flow data across regions can be modeled by spatial econometric models, see LeSage and Pace (2009). Recently, regional studies became interested in the aggregation and disaggregation of flow models, because trade data cannot be obtained at a disaggregated level but data are published on an aggregate level. Furthermore, missing data in disaggregated flow models occur quite often since detailed measurements are often not possible at all observation points in time and space. In this paper we develop classical and Bayesian methods to complete flow data. The Chow and Lin (1971) method was developed for completing disaggregated incomplete time series data. We will extend this method in a general framework to spatially correlated flow data using the cross-sectional Chow-Lin method of Polasek et al. (2009). The missing disaggregated data can be obtained either by feasible GLS prediction or by a Bayesian (posterior) predictive density.Missing values in spatial econometrics, MCMC, non-spatial Chow-Lin (CL) and spatial Chow-Lin (SCL) methods, spatial internal flow (SIF) models, origin and destination (OD) data
Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution
Non-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (Em) and altered surface expression of K+ channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100μM), phenylbutazone (100μM) and NS-398 (100μM) but not by SC-560 (1μM). NSAID-inhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of Em, whereas treatment with SC-560 had no effect on Em. The Em of IEC-Cdx2 cells was: −38.5±1.8mV under control conditions; −35.9±1.6mV after treatment with SC-560; −18.8±1.2mV after treatment with indomethacin; and −23.7±1.4mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of Kv1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of Kv1.4, but also the cell surface expression of both Kv1.4 and Kv1.6 channel subunits in IEC-Cdx2. Both Kv1.4 and Kv1.6 channel proteins were immunoprecipitated by Kv1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric Kv channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of Em and decreased surface expression of heteromeric Kv1 channels.ID: S0006295207001931; M3: Article; Accession Number: S0006295207001931; Author: L.C. Freeman (b); Author: D.F. Narvaez (a); Author: A. McCoy (a); Author: F.B. von Stein (c); Author: S. Young (b); Author: K. Silver (a); Author: S. Ganta (b); Author: D. Koch (b); Author: R. Hunter (b); Author: R.F. Gilmour (c); Author: J.D. Lillich (a, ⁎); Affiliation: Department of Clinical Sciences, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, United States; Keyword: Non-steroidal anti-inflammatory drugs; Keyword: Intestinal epithelial cells; Keyword: Membrane potential; Keyword: Potassium channels; Number of Pages: 12; Language: English;Source type: Electronic(1)http://search.ebscohost.com/login.aspx?direct=true&db=edselp&AN=S0006295207001931&site=eds-live&scope=sit
Inverse systems of spectra and generalizations of a theorem of W.H. Lin
In this thesis we generalize a theorem of W. H. Lin.
Lin's results are concerned with the homotopy and cohomotopy
of an inverse system of spectra {P-k }. Using the quadratic
construction we construct an inverse system of spectra {P-k(E)}
We generalize Lin's results by studying the homotopy and cohomotopy
of {P-k(E)}
Yi-Fang Lin Piano Recital Program Notes
This report is Yi-Fang Lin Piano Recital Program Notes on April., 23, 2019. The two pieces on the program include Piano Sonata in C minor, K.457 by W.A. Mozart, and Piano Concerto No.1 in F-Sharp minor, Op.1 by S. Rachmaninoff. The note will introduce the life of two composers, the compositional background of individual work, and the analysis of the structure, including tonal design and thematic material in each work
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