B∗Bπ(γ)B^*B\pi(\gamma) couplings and D^*\rar D\pi(\gamma) -decays within a 1/M1/M-expansion in fullfull QCD

To leading order in $\alpha_s$, we evaluate the leading and non-leading $1/M_b$ corrections to the $B^*B\pi$ and $B^*B\gamma$ couplings using QCD spectral moment sum rules in the full theory. We find that, for large $M_b$ and contrary to the heavy-to-light B\rar \pi(\rho) l\bar \nu form factors, which are dominated by the $soft$ light quark vacuum condensate, these couplings are governed by the $hard$ perturbative graph, like other heavy-to-heavy transitions. We also find that for the B^{*}\rar B\gamma, the $1/M_b$ correction is mainly due to the perturbative and light quark condensate contributions originating from the graphs involving the heavy quark part of the electromagnetic current, which are essential for explaining the large charge dependence in the observed D^{*-}\rar D^-\gamma and D^{*0}\rar D^0\gamma decays. Our $best$ numerical predictions {\it without any free parameters} for the $B^*$-meson are: $g_{B^{*-}B^0\pi^-}\simeq 14\pm 4$, \Gamma_{B^{*-}\rar B^-\gamma}\simeq (0.10\pm 0.03) keV and the large charge dependence of the ratio: {\Gamma_{B^{*-}\rar B^- \gamma}}/ {\Gamma_{B^{*0}\rar B^0 \gamma}}\simeq 2.5~. For the $D^*$-meson, we find: \Gamma_{D^{*-}\rar D^0\pi^-}\simeq 1.54\Gamma_{D^{*0}\rar D^0\pi^0} \simeq (8\pm 5) keV, \Gamma_{D^{*-}\rar D^-\gamma}\simeq (0.09^{+0.40}_{-0.07} ) keV and \Gamma_{D^{*0}\rar D^0\gamma}\simeq (3.7\pm 1.2) keV, where the branching ratios agree within the errors with the present data, while the total widths \Gamma_{D^{*0}\rar all} \simeq (11\pm 4) keV and \Gamma_{D^{*-}\rar all}\simeq (12\pm 7) keV are much smaller than the present experimental upper limits.Comment: published version to appear in Phys. Lett. B (minor modifications compared with the previous version

Observation of the decay \psip\rar\kstark

Using 14 million $\psi(2S)$ events collected with the BESII detector, branching fractions of \psip\rar\kstarkpm and \kstarknn are determined to be: \calB(\psip\rar\kstarkpm)=(2.9^{+1.3}_{-1.7}\pm0.4)\times 10^{-5} and \calB(\psip\rar\kstarknn)=(13.3^{+2.4}_{-2.7}\pm1.9)\times 10^{-5}. The results confirm the violation of the "12%" rule for these two decay channels with higher precision. A large isospin violation between the charged and neutral modes is observed.Comment: 5 pages, 3 figure

A coordinated phosphorylation cascade initiated by MSK1 directs RAR alpha recruitment to target gene promoters

The nuclear retinoic acid (RA) receptor alpha (RARα) is a transcriptional transregulator that controls the expression of specific gene subsets through binding at response elements and dynamic interactions with coregulators, which are coordinated by the ligand. Here, we highlighted a novel paradigm in which the transcription of RARα-target genes is controlled by phosphorylation cascades initiated by the rapid RA activation of the p38MAPK/MSK1 pathway. We demonstrate that MSK1 phosphorylates RARα at S369 located in the Ligand Binding Domain, allowing the binding of TFIIH and thereby phosphorylation of the N-terminal domain at S77 by cdk7/cyclin H. MSK1 also phosphorylates Histone H3 at S10. Finally, the phosphorylation cascade initiated by MSK1 is required for the recruitment of RARα/TFIIH complexes to response elements and subsequently for RARα target genes activation. Cancer cells characterized by a deregulated p38MAPK/MSK1 pathway, do not respond to RA, outlining the essential contribution of the RA-triggered phosphorylation cascade in RA signaling

A hydrogenic molecular atmosphere of a neutron star

A model of a hydrogenic content of atmosphere of the isolated neutron star 1E1207.4-5209 is proposed. It is based on the assumption that the main component in the atmosphere is the exotic molecular ion $H_3^{2+}$ and that there exists a magnetic field in the range of $(4 \pm 2) \times 10^{14}$ G. Photoionization H_3^{2+} \rar e + 3p and photodissociation H_3^{2+} \rar H + 2p correspond to two absorption features at 0.7 KeV and 1.4 KeV, respectively, discovered by {\it Chandra} observatory (Sanwal et al, 2002). The model predicts one more absorption feature at 80-150 eV corresponding to photodissociation H_3^{2+} \rar H_2^+ + p.Comment: 8 pages, 1 figur

The radial acceleration relation is a natural consequence of the baryonic Tully-Fisher relation

Galaxies covering several orders of magnitude in stellar mass and a variety of Hubble types have been shown to follow the "Radial Acceleration Relation" (RAR), a relationship between $g_{\rm obs}$, the observed circular acceleration of the galaxy, and $g_{\rm bar}$, the acceleration due to the total baryonic mass of the galaxy. For accelerations above $10^{10}~{\rm m \, s}^{-2}$, $g_{\rm obs}$ traces $g_{\rm bar}$, asymptoting to the 1:1 line. Below this scale, there is a break in the relation such that $\rm g_{\rm obs} \sim g_{\rm bar}^{1/2}$. We show that the RAR slope, scatter and the acceleration scale are all natural consequences of the well-known baryonic Tully-Fisher relation (BTFR). We further demonstrate that galaxies with a variety of baryonic and dark matter (DM) profiles and a wide range of dark halo and galaxy properties (well beyond those expected in CDM) lie on the RAR if we simply require that their rotation curves satisfy the BTFR. We explore conditions needed to break this degeneracy: sub-kpc resolved rotation curves inside of "cored" DM-dominated profiles and/or outside $\gg 100\,$kpc could lie on BTFR but deviate in the RAR, providing new constraints on DM.Comment: 5 pages, submitted to MNRA

Dominance of the light-quark condensate in the heavy-to-light exclusive decays

Using the QCD {\it hybrid} (moments-Laplace) sum rule, we show $semi$-$analytically$ that, in the limit M_b \rar \infty, the $q^2$ and $M_b$ behaviours of the heavy-to-light exclusive (\bar B\rar \rho~(\pi) semileptonic as well as the B\rar \rho\gamma rare) decay--form factors are $universally$ dominated by the contribution of the soft light-quark condensate rather than that of the hard perturbative diagram. The QCD-analytic $q^2$ behaviour of the form factors is a polynomial in $q^2/M^2_b$, which mimics quite well the usual pole parametrization, except in the case of the $A_1^B$ form factor, where there is a significant deviation from this polar form. The $M_b$-dependence of the form factors expected from HQET and lattice results is recovered. We extract with a good accuracy the ratios: $V^B(0)/A^B_1(0) \simeq A^B_2(0)/A^B_1(0) \simeq 1.11\pm 0.01$, and $A^B_1(0)/F^B_1(0) \simeq 1.18 \pm 0.06$; combined with the ``world average" value of $f^B_+(0)$ or/and $F^B_1(0)$, these ratios lead to the decay rates: $\Gamma_{\bar B\rar \pi e\bar \nu} \simeq (4.3 \pm 0.7)Comment: 10 pages, CERN-TH 7237/94 (the previous version contains numerical errors). Latex file (run twice) 3 ps.figures available by mai

Retinoic Acid Receptor Overexpression in Human Umbilical Cord-derived Mesenchymal Stem Cells

Introduction: Retinoic acid (RA) involves in vertebrate morphogenesis, growth and apoptosis through two classes of receptors encoded by six genes; RAR, and RXR, . The former utilizes either all-trans RA or 9-cis-RA as ligands, whereas the RXRs utilize only 9-cis-RA. Using the human umbilical cord derived stem cells (HUCSCs) as an in vitro model of human fetal cells we aimed to evaluate RAR overexpression following to RA treatment. Methods: HUCSCs were cultured in DMEM + 10% FBS at a density of 1 × 103/ well. Upon adhering, the medium was changed to DMEM containing RA for 4-6 days during which RA refreshed every 2 days. The untreated cells were considered as a control group. Using a combination of flowcytometry, MTT colorimetric assay and conventional RT-PCR techniques, CD markers, cell viability and RAR expression profile of HUCSCs were measured, respectively. Results: Flowcytometry analysis clearly indicated 5.4% of HUCSCs co-expressed CD34 and CD45, while 63.7% of cells expressed both CD44 and CD73. 36.5% of cells expressed CD90 compared to 0.05% for CD105.MTT assay also showed that about 60% of HUCSCsˈ viability decreased at higher doses (10-7 – 10-5M) of RA compared to control group. RT-PCR analysis also revealed that RAR and were upregulated in the RA–treated cells. Conclusions: This study clearly shows that the HUCSCs express CD44, CD73 and CD90 and RA in a dose-dependent manner has a cytotoxicity effect on HUCSCs that is mediated by RAR an