446 research outputs found
Conformal Symmetry of a Black Hole as a Scaling Limit: A Black Hole in an Asymptotically Conical Box
We show that the previously obtained subtracted geometry of four-dimensional
asymptotically flat multi-charged rotating black holes, whose massless wave
equation exhibit symmetry may be
obtained by a suitable scaling limit of certain asymptotically flat
multi-charged rotating black holes, which is reminiscent of near-extreme black
holes in the dilute gas approximation. The co-homogeneity-two geometry is
supported by a dilation field and two (electric) gauge-field strengths. We also
point out that these subtracted geometries can be obtained as a particular
Harrison transformation of the original black holes. Furthermore the subtracted
metrics are asymptotically conical (AC), like global monopoles, thus describing
"a black hole in an AC box". Finally we account for the the emergence of the
symmetry as a consequence of the
subtracted metrics being Kaluza-Klein type quotients of .
We demonstrate that similar properties hold for five-dimensional black holes.Comment: Sections 3 and 4 significantly augmente
Higher-order multipole amplitudes in charmonium radiative transitions
Using 24 million decays in CLEO-c, we have searched
for higher multipole admixtures in electric-dipole-dominated radiative
transitions in charmonia. We find good agreement between our data and
theoretical predictions for magnetic quadrupole (M2) amplitudes in the
transitions and ,
in striking contrast to some previous measurements. Let and
denote the normalized M2 amplitudes in the respective aforementioned decays,
where the superscript refers to the angular momentum of the . By
performing unbinned maximum likelihood fits to full five-parameter angular
distributions, we determine the ratios and , where
the theoretical predictions are independent of the charmed quark magnetic
moment and are and .Comment: 32 pages, 7 figures, acceptance updat
Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26
<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p
Dalitz Plot Analysis of Ds to K+K-pi+
We perform a Dalitz plot analysis of the decay Ds to K+K-pi+ with the CLEO-c
data set of 586/pb of e+e- collisions accumulated at sqrt(s) = 4.17 GeV. This
corresponds to about 0.57 million D_s+D_s(*)- pairs from which we select 14400
candidates with a background of roughly 15%. In contrast to previous
measurements we find good agreement with our data only by including an
additional f_0(1370)pi+ contribution. We measure the magnitude, phase, and fit
fraction of K*(892) K+, phi(1020)pi+, K0*(1430)K+, f_0(980)pi+, f_0(1710)pi+,
and f_0(1370)pi+ contributions and limit the possible contributions of other KK
and Kpi resonances that could appear in this decay.Comment: 21 Pages,available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PR
Characterization of novel isoforms and evaluation of SNF2L/SMARCA1 as a candidate gene for X-linked mental retardation in 12 families linked to Xq25-26
<p>Abstract</p> <p>Background</p> <p>Mutations in genes whose products modify chromatin structure have been recognized as a cause of X-linked mental retardation (XLMR). These genes encode proteins that regulate DNA methylation (<it>MeCP2</it>), modify histones (<it>RSK2 </it>and <it>JARID1C</it>), and remodel nucleosomes through ATP hydrolysis (<it>ATRX</it>). Thus, genes encoding other chromatin modifying proteins should also be considered as disease candidate genes. In this work, we have characterized the <it>SNF2L </it>gene, encoding an ATP-dependent chromatin remodeling protein of the ISWI family, and sequenced the gene in patients from 12 XLMR families linked to Xq25-26.</p> <p>Methods</p> <p>We used an <it>in silico </it>and RT-PCR approach to fully characterize specific SNF2L isoforms. Mutation screening was performed in 12 patients from individual families with syndromic or non-syndromic XLMR. We sequenced each of the 25 exons encompassing the entire coding region, complete 5' and 3' untranslated regions, and consensus splice-sites.</p> <p>Results</p> <p>The <it>SNF2L </it>gene spans 77 kb and is encoded by 25 exons that undergo alternate splicing to generate several distinct transcripts. Specific isoforms are generated through the alternate use of exons 1 and 13, and by the use of alternate donor splice sites within exon 24. Alternate splicing within exon 24 removes a NLS sequence and alters the subcellular distribution of the SNF2L protein. We identified 3 single nucleotide polymorphisms but no mutations in our 12 patients.</p> <p>Conclusion</p> <p>Our results demonstrate that there are numerous splice variants of SNF2L that are expressed in multiple cell types and which alter subcellular localization and function. <it>SNF2L </it>mutations are not a cause of XLMR in our cohort of patients, although we cannot exclude the possibility that regulatory mutations might exist. Nonetheless, <it>SNF2L </it>remains a candidate for XLMR localized to Xq25-26, including the Shashi XLMR syndrome.</p
Search for D0 to p e- and D0 to pbar e+
Using data recorded by CLEO-c detector at CESR, we search for simultaneous
baryon and lepton number violating decays of the D^0 meson, specifically, D^0
--> p-bar e^+, D^0-bar --> p-bar e^+, D^0 --> p e^- and D^0-bar --> p e^-. We
set the following branching fraction upper limits: D^0 --> p-bar e^+ (D^0-bar
--> p-bar e^+) p e^- (D^0-bar --> p e^-) < 1.2 *
10^{-5}, both at 90% confidence level.Comment: 10 pages, available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PRD. Comments: changed abstract, added reference for section 1,
vertical axis in Fig.5 changed (starts from 1.5 rather than 2.0), fixed typo
Charmonium decays to gamma pi0, gamma eta, and gamma eta'
Using data acquired with the CLEO-c detector at the CESR e+e- collider, we
measure branching fractions for J/psi, psi(2S), and psi(3770) decays to gamma
pi0, gamma eta, and gamma eta'. Defining R_n = B[ psi(nS)-->gamma eta ]/B[
psi(nS)-->gamma eta' ], we obtain R_1 = (21.1 +- 0.9)% and, unexpectedly, an
order of magnitude smaller limit, R_2 < 1.8% at 90% C.L. We also use
J/psi-->gamma eta' events to determine branching fractions of improved
precision for the five most copious eta' decay modes.Comment: 14 pages, available through http://www.lns.cornell.edu/public/CLNS/,
published in Physical Review
Precision Measurement of the Mass of the h_c(1P1) State of Charmonium
A precision measurement of the mass of the h_c(1P1) state of charmonium has
been made using a sample of 24.5 million psi(2S) events produced in e+e-
annihilation at CESR. The reaction used was psi(2S) -> pi0 h_c, pi0 -> gamma
gamma, h_c -> gamma eta_c, and the reaction products were detected in the
CLEO-c detector.
Data have been analyzed both for the inclusive reaction and for the exclusive
reactions in which eta_c decays are reconstructed in fifteen hadronic decay
channels. Consistent results are obtained in the two analyses. The averaged
results of the present measurements are M(h_c)=3525.28+-0.19 (stat)+-0.12(syst)
MeV, and B(psi(2S) -> pi0 h_c)xB(h_c -> gamma eta_c)= (4.19+-0.32+-0.45)x10^-4.
Using the 3PJ centroid mass, Delta M_hf(1P)= - M(h_c) =
+0.02+-0.19+-0.13 MeV.Comment: 9 pages, available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PR
Precision Measurement of B(D+ -> mu+ nu) and the Pseudoscalar Decay Constant fD+
We measure the branching ratio of the purely leptonic decay of the D+ meson
with unprecedented precision as B(D+ -> mu+ nu) = (3.82 +/- 0.32 +/-
0.09)x10^(-4), using 818/pb of data taken on the psi(3770) resonance with the
CLEO-c detector at the CESR collider. We use this determination to derive a
value for the pseudoscalar decay constant fD+, combining with measurements of
the D+ lifetime and assuming |Vcd| = |Vus|. We find fD+ = (205.8 +/- 8.5 +/-
2.5) MeV. The decay rate asymmetry [B(D+ -> mu+ nu)-B(D- -> mu- nu)]/[B(D+ ->
mu+ nu)+B(D- -> mu- nu)] = 0.08 +/- 0.08, consistent with no CP violation. We
also set 90% confidence level upper limits on B(D+ -> tau+ nu) < 1.2x10^(-3)
and B(D+ -> e+ nu) < 8.8x10^(-6).Comment: 24 pages, 11 figures and 6 tables, v2 replaced some figure vertical
axis scales, v3 corrections from PRD revie
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