The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
π
0
and
η
photoproduction off quasi-free protons and, for the first time, ...off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
γ
p
→
π
0
p
and
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
η
n
system at
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
S
11
(
1535
)
and
S
11
(
1650
)
resonances within the
S
11
-partial wave.
Abstract
The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
$$\pi ^0$$
π
0
and
$$\eta $$
η
photoproduction off quasi-free ...protons and, for the first time, off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
$$\gamma p \rightarrow \pi ^0 p$$
γ
p
→
π
0
p
and
$$\gamma p \rightarrow \eta p$$
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
$$\eta n$$
η
n
system at
$$W = 1.68\ \textrm{GeV}$$
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
$$S_{11}(1535)$$
S
11
(
1535
)
and
$$S_{11}(1650)$$
S
11
(
1650
)
resonances within the
$$S_{11}$$
S
11
-partial wave.
The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
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\begin{document}$$\pi ^0$$\end{document}
π
0
and
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η
photoproduction off quasi-free protons and, for the first time, off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
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\usepackage{amssymb}
\usepackage{amsbsy}
\usepackage{mathrsfs}
\usepackage{upgreek}
\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\gamma p \rightarrow \pi ^0 p$$\end{document}
γ
p
→
π
0
p
and
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\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\gamma p \rightarrow \eta p$$\end{document}
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
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\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\eta n$$\end{document}
η
n
system at
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\setlength{\oddsidemargin}{-69pt}
\begin{document}$$W = 1.68\ \textrm{GeV}$$\end{document}
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
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\begin{document}$$S_{11}(1535)$$\end{document}
S
11
(
1535
)
and
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\begin{document}$$S_{11}(1650)$$\end{document}
S
11
(
1650
)
resonances within the
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\begin{document}$$S_{11}$$\end{document}
S
11
-partial wave.
The Crystal Barrel is an electromagnetic calorimeter consisting of 1380 CsI(Tl) scintillators, and is currently installed at the CBELSA/TAPS experiment where it is used to detect decay products from ...photoproduction of mesons. The readout of the Crystal Barrel has been upgraded in order to integrate the detector into the first level of the trigger and to increase its sensitivity for neutral final states. The new readout uses avalanche photodiodes in the front-end and a dual back-end with branches optimized for energy and time measurement, respectively. An FPGA-based cluster finder processes the whole hit pattern within less than 100 ns. The important downside of APDs -- the temperature dependence of their gain -- is handled with a temperature stabilization and a compensating bias voltage supply. Additionally, a light pulser system allows the APDs' gains to be measured during beamtimes.
Heart failure is often preceded by cardiac hypertrophy, which is characterized by increased cell size, altered protein abundance, and actin cytoskeletal reorganization. Profilin is a well-conserved, ...ubiquitously expressed, multifunctional actin-binding protein, and its role in cardiomyocytes is largely unknown. Given its involvement in vascular hypertrophy, we aimed to test the hypothesis that profilin-1 is a key mediator of cardiomyocyte-specific hypertrophic remodelling.
Profilin-1 was elevated in multiple mouse models of hypertrophy, and a cardiomyocyte-specific increase of profilin in Drosophila resulted in significantly larger heart tube dimensions. Moreover, adenovirus-mediated overexpression of profilin-1 in neonatal rat ventricular myocytes (NRVMs) induced a hypertrophic response, measured by increased myocyte size and gene expression. Profilin-1 silencing suppressed the response in NRVMs stimulated with phenylephrine or endothelin-1. Mechanistically, we found that profilin-1 regulates hypertrophy, in part, through activation of the ERK1/2 signalling cascade. Confocal microscopy showed that profilin localized to the Z-line of Drosophila myofibrils under normal conditions and accumulated near the M-line when overexpressed. Elevated profilin levels resulted in elongated sarcomeres, myofibrillar disorganization, and sarcomeric disarray, which correlated with impaired muscle function.
Our results identify novel roles for profilin as an important mediator of cardiomyocyte hypertrophy. We show that overexpression of profilin is sufficient to induce cardiomyocyte hypertrophy and sarcomeric remodelling, and silencing of profilin attenuates the hypertrophic response.
Aims: To use random mutagenesis for the characterization of Legionella pneumophila lipopolysaccharide (LPS) components and serotypes.
Methods and Results: Five strains belonging to different ...serogroups and/or monoclonal subgroups were mutagenized using a mini‐Tn10 transposon. Exactly 11 819 mutants were checked for alterations in LPS using at least 11 monoclonal antibodies (mAbs) that define L. pneumophila serotypes. Among the mutants, five different mini‐Tn10 insertions were identified. Four mutants originating from serogroup‐1 did not lose their serogroup‐specific epitope, but did sustain subtler changes that resulted in switches to different mAb subgroups. In contrast, a mutant from serogroup‐6 lost its serogroup‐specific epitope, while retaining a serogroup‐cross‐reacting epitope.
Conclusions: Random mutagenesis is a valuable tool for LPS epitope mapping. While some characteristics of L. pneumophila LPS can be altered, others appear resistant to mutagenesis. This underscores both the flexibility and rigidity of LPS architecture in L. pneumophila.
Significance and Impact of the Study: Losses of L. pneumophila LPS epitopes can result in new serotypes, changes that might escape detection by current DNA‐based typing schemes. But, as the frequency of these changes is rare, based upon our observations, serotyping should remain an important tool for identifying L. pneumophila in water systems that are implicated in human infection.
We have determined the molecular and ultrastructural defects associated with three homozygous-viable myosin heavy chain mutations of Drosophila melanogaster. These mutations cause a dominant ...flightless phenotype but allow relatively normal assembly of indirect flight muscle myofibrils. As adults age, the contents of the indirect flight muscle myofibers are pulled to one end of the thorax. This apparently results from myofibril "hyper-contraction", and leads to sarcomere rupture and random myofilament orientation. All three mutations cause single amino acid changes in the light meromyosin region of the myosin rod. Two change the same glutamic acid to a lysine residue and the third affects an amino acid five residues away, substituting histidine for arginine. Both affected residues are conserved in muscle myosins, cytoplasmic myosins and paramyosins. The mutations are associated with age-dependent, site-specific degradation of myosin heavy chain and failure to accumulate phosphorylated forms of flightin, an indirect flight muscle-specific protein previously localized to the thick filament. Given the repeating nature of the hydrophobic and charged amino acid residues of the myosin rod and the near-normal assembly of myofibrils in the indirect flight muscle of these mutants, it is remarkable that single amino acid changes in the rod cause such severe defects. It is also interesting that these severe defects are not apparent in other muscles. These phenomena likely arise from the highly organized nature and rigorous performance requirements of indirect flight muscle, and perhaps from the interaction of myosin with flightin, a protein specific to this muscle type.
By comparing the structure of wild-type and mutant muscle myosin heavy chain (MHC) genes of Drosophila melanogaster, we have identified the defect in the homozygous-viable, flightless mutant Mhc10. ...The mutation is within the 3' splice acceptor of an alternative exon (exon 15a) that encodes the central region of the MHC hinge. The splice acceptor defect prevents the accumulation of mRNAs containing exon 15a, whereas transcripts with a divergent copy of this exon (exon 15b) are unaffected by the mutation. In situ hybridization and Northern blot analysis of wild-type organisms reveals that exon 15b is used in larval MHCs, whereas exons 15a and/or 15b are used in adult tissues. Because Mhc10 mutants fail to accumulate transcripts encoding MHC protein with hinge region a, analysis of their muscle-specific reduction in thick filament number serves as a sensitive assay system for determining the pattern of accumulation of MHCs with alternative hinge regions. Electron microscopic comparisons of various muscles from wild-type and Mhc10 adults reveals that those that contract rapidly or develop high levels of tension utilize only hinge region a, those that contract at moderate rates accumulate MHCs of both types, and those that are slowly contracting have MHCs with hinge region b. The presence of alternative hinge-coding exons and their highly tissue-specific usage suggests that this portion of the MHC molecule is important to the isoform-specific properties of MHC that lead to the different physiological and ultrastructural characteristics of various Drosophila muscle types. The absence of other alternative exons in the rod-coding region, aside from those shown previously to encode alternative carboxyl termini, demonstrates that the bulk of the myosin rod is not involved in the generation of isoform-specific properties of the MHC molecule.
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