66 research outputs found
A Coherent Interpretation of the Form Factors of the Nucleon in Terms of a Pion Cloud and Constituent Quarks
The recent unbiased measurements of the electric form factor of the neutron
suggest that its shape may be interpreted as a smooth broad distribution with a
bump at Q^2 \approx 0.3(GeV/c)^2 superimposed. As a consequence the
corresponding charge distribution in the Breit frame shows a negative charge
extending as far out as 2fm. It is natural to identify this charge with the
pion cloud. This realisation is then used to reanalyse all old and new data of
the electric and magnetic from factors of the proton and the neutron by a
phenomenological fit and by a fit based on the constituent quark model. It is
shown that it is possible to fit all form factors coherently with both
ansaetzen and that they all show the signal of the pion cloud.Comment: 17 pages, 17 figure
Polarization transfer in the HeH reaction
Polarization transfer in the 4He(e,e'p)3H reaction at a Q^2 of 0.4 (GeV/c)^2
was measured at the Mainz Microtron MAMI. The ratio of the transverse to the
longitudinal polarization components of the ejected protons was compared with
the same ratio for elastic ep scattering. The results are consistent with a
recent fully relativistic calculation which includes a predicted medium
modification of the proton form factor based on a quark-meson coupling model.Comment: 5 pages, Latex, 2 postscript figures, submitted to Physics Letters
A Histone Map of Human Chromosome 20q13.12
We present a systematic search for regulatory elements in a 3.5 Mb region on human chromosome 20q13.12, a region associated with a number of medical conditions such as type II diabetes and obesity.We profiled six histone modifications alongside RNA polymerase II (PolII) and CTCF in two cell lines, HeLa S3 and NTERA-2 clone D1 (NT2/D1), by chromatin immunoprecipitation using an in-house spotted DNA array, constructed with 1.8 kb overlapping plasmid clones. In both cells, more than 90% of transcription start sites (TSSs) of expressed genes showed enrichments with PolII, di-methylated lysine 4 of histone H3 (H3K4me2), tri-methylated lysine 4 of histone H3 (H3K4me3) or acetylated H3 (H3Ac), whereas mono-methylated lysine 4 of histone H3 (H3K4me1) signals did not correlate with expression. No TSSs were enriched with tri-methylated lysine 27 of histone H3 (H3K27me3) in HeLa S3, while eight TSSs (4 expressed) showed enrichments in NT2/D1. We have also located several CTCF binding sites that are potential insulator elements.In summary, we annotated a number of putative regulatory elements in 20q13.12 and went on to verify experimentally a subset of them using dual luciferase reporter assays. Correlating this data to sequence variation can aid identification of disease causing variants
Behavioral Defects in Chaperone-Deficient Alzheimer's Disease Model Mice
Molecular chaperones protect cells from the deleterious effects of protein misfolding and aggregation. Neurotoxicity of amyloid-beta (Aβ) aggregates and their deposition in senile plaques are hallmarks of Alzheimer's disease (AD). We observed that the overall content of αB-crystallin, a small heat shock protein molecular chaperone, decreased in AD model mice in an age-dependent manner. We hypothesized that αB-crystallin protects cells against Aβ toxicity. To test this, we crossed αB-crystallin/HspB2 deficient (CRYAB-/-HSPB2-/-) mice with AD model transgenic mice expressing mutant human amyloid precursor protein. Transgenic and non-transgenic mice in chaperone-sufficient or deficient backgrounds were examined for representative behavioral paradigms for locomotion and memory network functions: (i) spatial orientation and locomotion was monitored by open field test; (ii) sequential organization and associative learning was monitored by fear conditioning; and (iii) evoked behavioral response was tested by hot plate method. Interestingly, αB-crystallin/HspB2 deficient transgenic mice were severely impaired in locomotion compared to each genetic model separately. Our results highlight a synergistic effect of combining chaperone deficiency in a transgenic mouse model for AD underscoring an important role for chaperones in protein misfolding diseases
αA-crystallin R49Cneo mutation influences the architecture of lens fiber cell membranes and causes posterior and nuclear cataracts in mice
<p>Abstract</p> <p>Background</p> <p>αA-crystallin (CRYAA/HSPB4), a major component of all vertebrate eye lenses, is a small heat shock protein responsible for maintaining lens transparency. The R49C mutation in the αA-crystallin protein is linked with non-syndromic, hereditary human cataracts in a four-generation Caucasian family.</p> <p>Methods</p> <p>This study describes a mouse cataract model generated by insertion of a neomycin-resistant (neo<sup>r</sup>) gene into an intron of the gene encoding mutant R49C αA-crystallin. Mice carrying the neo<sup>r </sup>gene and wild-type <it>Cryaa </it>were also generated as controls. Heterozygous knock-in mice containing one wild type gene and one mutated gene for αA-crystallin (WT/R49C<sup>neo</sup>) and homozygous knock-in mice containing two mutated genes (R49C<sup>neo</sup>/R49C<sup>neo</sup>) were compared.</p> <p>Results</p> <p>By 3 weeks, WT/R49C<sup>neo </sup>mice exhibited large vacuoles in the cortical region 100 μm from the lens surface, and by 3 months posterior and nuclear cataracts had developed. WT/R49C<sup>neo </sup>mice demonstrated severe posterior cataracts at 9 months of age, with considerable posterior nuclear migration evident in histological sections. R49C<sup>neo</sup>/R49C<sup>neo </sup>mice demonstrated nearly complete lens opacities by 5 months of age. In contrast, R49C mice in which the neo<sup>r </sup>gene was deleted by breeding with CreEIIa mice developed lens abnormalities at birth, suggesting that the neo<sup>r </sup>gene may suppress expression of mutant R49C αA-crystallin protein.</p> <p>Conclusion</p> <p>It is apparent that modification of membrane and cell-cell interactions occurs in the presence of the αA-crystallin mutation and rapidly leads to lens cell pathology <it>in vivo</it>.</p
Relapse prevention for addictive behaviors
The Relapse Prevention (RP) model has been a mainstay of addictions theory and treatment since its introduction three decades ago. This paper provides an overview and update of RP for addictive behaviors with a focus on developments over the last decade (2000-2010). Major treatment outcome studies and meta-analyses are summarized, as are selected empirical findings relevant to the tenets of the RP model. Notable advances in RP in the last decade include the introduction of a reformulated cognitive-behavioral model of relapse, the application of advanced statistical methods to model relapse in large randomized trials, and the development of mindfulness-based relapse prevention. We also review the emergent literature on genetic correlates of relapse following pharmacological and behavioral treatments. The continued influence of RP is evidenced by its integration in most cognitive-behavioral substance use interventions. However, the tendency to subsume RP within other treatment modalities has posed a barrier to systematic evaluation of the RP model. Overall, RP remains an influential cognitive-behavioral framework that can inform both theoretical and clinical approaches to understanding and facilitating behavior change
Real-time regional automatic mapping of nocturnal winter road temperatures. Application of a methodology of analogous situations. The case of the Walloon Region (Belgium). American Meteorological Society
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