Meson-induced correlations of nucleons in nuclear Compton scattering

The non-resonant (seagull) contribution to the nuclear Compton amplitude at low energies is strongly influenced by nucleon correlations arising from meson exchange. We study this problem in a modified Fermi gas model, where nuclear correlation functions are obtained with the help of perturbation theory. The dependence of the mesonic seagull amplitude on the nuclear radius is investigated and the influence of a realistic nuclear density on this amplitude is dicussed. We found that different form factors appear for the static part (proportional to the enhancement constant $\kappa$) of the mesonic seagull amplitude and for the parts, which contain the contribution from electromagnetic polarizabilities.Comment: 15 pages, Latex, epsf.sty, 9 eps figures

Compton Scattering from the Deuteron and Extracted Neutron Polarizabilities

Differential cross sections for Compton scattering from the deuteron were measured at MAX-lab for incident photon energies of 55 MeV and 66 MeV at nominal laboratory angles of $45^\circ$, $125^\circ$, and $135^\circ$. Tagged photons were scattered from liquid deuterium and detected in three NaI spectrometers. By comparing the data with theoretical calculations in the framework of a one-boson-exchange potential model, the sum and difference of the isospin-averaged nucleon polarizabilities, $\alpha_N + \beta_N = 17.4 \pm 3.7$ and $\alpha_N - \beta_N = 6.4 \pm 2.4$ (in units of $10^{-4}$ fm$^3$), have been determined. By combining the latter with the global-averaged value for $\alpha_p - \beta_p$ and using the predictions of the Baldin sum rule for the sum of the nucleon polarizabilities, we have obtained values for the neutron electric and magnetic polarizabilities of $\alpha_n= 8.8 \pm 2.4$(total) $\pm 3.0$(model) and $\beta_n = 6.5 \mp 2.4$(total) $\mp 3.0$(model), respectively.Comment: 4 pages, 2 figures, revtex. The text is substantially revised. The cross sections are slightly different due to improvements in the analysi

Regulation of monocyte cell fate by blood vessels mediated by Notch signalling

A population of monocytes, known as Ly6Clo monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6Chi monocytes into Ly6Clo monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation

Regulation of monocyte cell fate by blood vessels mediated by Notch signalling

A population of monocytes, known as Ly6C(lo) monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6C(hi) monocytes into Ly6C(lo) monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation

Phylogenetic Distribution of Intron Positions in Alpha-Amylase Genes of Bilateria Suggests Numerous Gains and Losses

Most eukaryotes have at least some genes interrupted by introns. While it is well accepted that introns were already present at moderate density in the last eukaryote common ancestor, the conspicuous diversity of intron density among genomes suggests a complex evolutionary history, with marked differences between phyla. The question of the rates of intron gains and loss in the course of evolution and factors influencing them remains controversial. We have investigated a single gene family, alpha-amylase, in 55 species covering a variety of animal phyla. Comparison of intron positions across phyla suggests a complex history, with a likely ancestral intronless gene undergoing frequent intron loss and gain, leading to extant intron/exon structures that are highly variable, even among species from the same phylum. Because introns are known to play no regulatory role in this gene and there is no alternative splicing, the structural differences may be interpreted more easily: intron positions, sizes, losses or gains may be more likely related to factors linked to splicing mechanisms and requirements, and to recognition of introns and exons, or to more extrinsic factors, such as life cycle and population size. We have shown that intron losses outnumbered gains in recent periods, but that “resets” of intron positions occurred at the origin of several phyla, including vertebrates. Rates of gain and loss appear to be positively correlated. No phase preference was found. We also found evidence for parallel gains and for intron sliding. Presence of introns at given positions was correlated to a strong protosplice consensus sequence AG/G, which was much weaker in the absence of intron. In contrast, recent intron insertions were not associated with a specific sequence. In animal Amy genes, population size and generation time seem to have played only minor roles in shaping gene structures

The cinnamyl alcohol dehydrogenase gene structure in <em class="EmphasisTypeItalic">Picea abies</em> (L.) Karst.: genomic sequences, Southern hybridization, genetic analysis and phylogenetic relationships.

Based on PCR technologies, we have isolated three genomic cinnamyl alcohol dehydrogenase (CAD) clones from Norway spruce, Picea abies (L.) Karst., revealing about 99% identity within their protein coding regions. All clones contain five introns with an identity of 97&ndash;100% for intervening sequences II, III and IV, whereas intron V sequences revealed only 87&ndash;89% identity. Intron I sequences share an identity of 85&ndash;98% among all three clones. Intron IV is only present in Norway spruce and not found in published genomic CAD sequences of angiosperms. Tandem repeats between 24 and 49&nbsp;bp were discovered within intervening sequences I and V. Southern hybridization of seedling DNA and PCR-based intron analyses using diploid leaf buds and haploid megagametophytes indicate the existence of a small CAD gene family within the spruce genome, consisting of at least two loci. Evolutionary analyses of CAD encoding sequences using distance matrix- and parsimony-based methods revealed that CADs from angiosperms form a clade distinct from those of gymnosperms. Confirmed by maximal bootstrap values of 100%, a gene duplication gave rise to two different groups of angiospermous CADs and this duplication may have occurred in an early stage of angiosperm radiation, certainly before the separation of the Dilleniidae and Rosidae lineages. Phylogenetic investigations suggest angiosperm CAD II sequences to have evolved more rapidly than angiosperm CAD I genes. On the other hand, CAD gene evolution appears to be significantly slower in conifers than in angiosperms