116 research outputs found
New limits on "odderon" amplitudes from analyticity constraints
In studies of high energy and scattering, the odd (under
crossing) forward scattering amplitude accounts for the difference between the
and cross sections. Typically, it is taken as
(),
which has as , where is the
ratio of the real to the imaginary portion of the forward scattering amplitude.
However, the odd-signatured amplitude can have in principle a strikingly
different behavior, ranging from having non-zero constant to
having as , the maximal behavior
allowed by analyticity and the Froissart bound. We reanalyze high energy
and scattering data, using new analyticity constraints, in order to
put new and precise limits on the magnitude of ``odderon'' amplitudes.Comment: 13 pages LaTex, 6 figure
Odderon in the Color Glass Condensate
We discuss the definition and the energy evolution of scattering amplitudes
with -odd ("odderon") quantum numbers within the effective theory for the
Color Glass Condensate (CGC) endowed with the functional, JIMWLK, evolution
equation. We explicitly construct gauge-invariant amplitudes describing
multiple odderon exchanges in the scattering between the CGC and two types of
projectiles: a color--singlet quark--antiquark pair (or `color dipole') and a
system of three quarks in a colorless state. We deduce the energy evolution of
these amplitudes from the general JIMWLK equation, which for this purpose is
recast in a more synthetic form, which is manifestly infrared finite. For the
dipole odderon, we confirm and extend the non--linear evolution equations
recently proposed by Kovchegov, Szymanowski and Wallon, which couple the
evolution of the odderon to that of the pomeron, and predict the rapid
suppression of the odderon exchanges in the saturation regime at high energy.
For the 3--quark system, we focus on the linear regime at relatively low
energy, where our general equations are shown to reduce to the
Bartels--Kwiecinski--Praszalowicz equation. Our gauge--invariant amplitudes,
and the associated evolution equations, stay explicitly outside the M\"obius
representation, which is the Hilbert space where the BFKL Hamiltonian exhibits
holomorphic separability.Comment: 43 pages, 1 figur
The spin dependence of high energy proton scattering
Motivated by the need for an absolute polarimeter to determine the beam
polarization for the forthcoming RHIC spin program, we study the spin
dependence of the proton-proton elastic scattering amplitudes at high energy
and small momentum transfer.We examine experimental evidence for the existence
of an asymptotic part of the helicity-flip amplitude phi_5 which is not
negligible relative to the largely imaginary average non-flip amplitude phi_+.
We discuss theoretical estimates of r_5, essentially the ratio of phi_5 to
phi_+, based upon extrapolation of low and medium energy Regge phenomenological
results to high energies, models based on a hybrid of perturbative QCD and
non-relativistic quark models, and models based on eikonalization techniques.
We also apply the model-independent methods of analyticity and unitarity.The
preponderence of evidence at available energy indicates that r_5 is small,
probably less than 10%. The best available experimental limit comes from
Fermilab E704:those data indicate that |r_5|<15%. These bounds are important
because rigorous methods allow much larger values. In contradiction to a
widely-held prejudice that r_5 decreases with energy, general principles allow
it to grow as fast as ln(s) asymptotically, and some models show an even faster
growth in the RHIC range. One needs a more precise measurement of r_5 or to
bound it to be smaller than 5% in order to use the classical Coulomb-nuclear
interference technique for RHIC polarimetry. As part of this study, we
demonstrate the surprising result that proton-proton elastic scattering is
self-analysing, in the sense that all the helicity amplitudes can, in
principle, be determined experimentally at small momentum transfer without a
knowledge of the magnitude of the beam and target polarization
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Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.
[This corrects the article DOI: 10.1038/s42003-018-0226-0.]
A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction
The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function
Identification of genes required for eye development by high-throughput screening of mouse knockouts.
Despite advances in next generation sequencing technologies, determining the genetic basis of ocular disease remains a major challenge due to the limited access and prohibitive cost of human forward genetics. Thus, less than 4,000 genes currently have available phenotype information for any organ system. Here we report the ophthalmic findings from the International Mouse Phenotyping Consortium, a large-scale functional genetic screen with the goal of generating and phenotyping a null mutant for every mouse gene. Of 4364 genes evaluated, 347 were identified to influence ocular phenotypes, 75% of which are entirely novel in ocular pathology. This discovery greatly increases the current number of genes known to contribute to ophthalmic disease, and it is likely that many of the genes will subsequently prove to be important in human ocular development and disease
Identification of genes required for eye development by high-throughput screening of mouse knockouts
International audienc
The Regulatory Factor ZFHX3 Modifies Circadian Function in SCN via an AT Motif-Driven Axis
SummaryWe identified a dominant missense mutation in the SCN transcription factor Zfhx3, termed short circuit (Zfhx3Sci), which accelerates circadian locomotor rhythms in mice. ZFHX3 regulates transcription via direct interaction with predicted AT motifs in target genes. The mutant protein has a decreased ability to activate consensus AT motifs in vitro. Using RNA sequencing, we found minimal effects on core clock genes in Zfhx3Sci/+ SCN, whereas the expression of neuropeptides critical for SCN intercellular signaling was significantly disturbed. Moreover, mutant ZFHX3 had a decreased ability to activate AT motifs in the promoters of these neuropeptide genes. Lentiviral transduction of SCN slices showed that the ZFHX3-mediated activation of AT motifs is circadian, with decreased amplitude and robustness of these oscillations in Zfhx3Sci/+ SCN slices. In conclusion, by cloning Zfhx3Sci, we have uncovered a circadian transcriptional axis that determines the period and robustness of behavioral and SCN molecular rhythms
The Regulatory Factor ZFHX3 Modifies Circadian Function in SCN via an at Motif-Driven Axis
We identified a dominant missense mutation in the SCN transcription factor Zfhx3, termed short circuit (Zfhx3Sci), which accelerates circadian locomotor rhythms in mice. ZFHX3 regulates transcription via direct interaction with predicted AT motifs in target genes. The mutant protein has a decreased ability to activate consensus AT motifs in vitro. Using RNA sequencing, we found minimal effects on core clock genes in Zfhx3Sci/+ SCN, whereas the expression of neuropeptides critical for SCN intercellular signaling was significantly disturbed. Moreover, mutant ZFHX3 had a decreased ability to activate AT motifs in the promoters of these neuropeptide genes. Lentiviral transduction of SCN slices showed that the ZFHX3-mediated activation of AT motifs is circadian, with decreased amplitude and robustness of these oscillations in Zfhx3Sci/+ SCN slices. In conclusion, by cloning Zfhx3Sci, we have uncovered a circadian transcriptional axis that determines the period and robustness of behavioral and SCN molecular rhythms
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