Effective Lagrangian Approach to Weak Radiative Decays of Heavy Hadrons

Motivated by the observation of the decay $\bar{B}\to \bar{K}^*\gamma$ by CLEO, we have systematically analyzed the two-body weak radiative decays of bottom and charmed hadrons. There exist two types of weak radiative decays: One proceeds through the short-distance $b\to s\gamma$ transition and the other occurs through $W$-exchange accompanied by a photon emission. Effective Lagrangians are derived for the $W$-exchange bremsstrahlung processes at the quark level and then applied to various weak electromagnetic decays of heavy hadrons. Predictions for the branching ratios of $\bar{B}^0\to D^{*0} \gamma,~\Lambda_b^0\to\Sigma_c^0\gamma,~\Xi_b^0\to \Xi_c^0\gamma$ and \Xi_b^0\to\xip_c^0\gamma are given. In particular, we found ${\cal B}(\bar{B}^0 \to D^{*0}\gamma)\approx 0.9\times 10^{-6}$. Order of magnitude estimates for the weak radiative decays of charmed hadrons: $~D^0\to \bar{K}^{*0}\gamma,~\Lambda_c^+\to\Sigma^+\gamma$ and $\Xi_c^0\to\Xi^0\gamma$ are also presented. Within this approach, the decay asymmetry for antitriplet to antitriplet heavy baryon weak radiative transitions is uniquely predicted by heavy quark symmetry. The electromagnetic penguin contribution to $\Lambda_b^0\to\Lambda\gamma$ is estimated by two different methods and its branching ratio is found to be of order $1\times 10^{-5}$. We conclude that weak radiative decays of bottom hadrons are dominated by the short-distance $b\to s\gamma$ mechanism.Comment: 28 pages + 3 figures (not included), CLNS 94/1278, IP-ASTP-04-94. [Main changes in this revised version: (i) Sect 2 and subsection 4.1 are revised, (ii) A MIT bag method for calculating the decay rate of $Lambda_b \to\Lambda+gamma$ is presented, (iii) All predictions are updated using the newly available 1994 Particle Data Group, and (iv) Appendix and subsections 3.3 and 4.4 are deleted.

Chiral Lagrangians for Radiative Decays of Heavy Hadrons

The radiative decays of heavy mesons and heavy baryons are studied in a formalism which incorporates both the heavy quark symmetry and the chiral symmetry. The chiral Lagrangians for the electromagnetic interactions of heavy hadrons consist of two pieces: one from gauging electromagnetically the strong-interaction chiral Lagrangian, and the other from the anomalous magnetic moment interactions of the heavy baryons and mesons. Due to the heavy quark spin symmetry, the latter contains only one independent coupling constant in the meson sector and two in the baryon sector. These coupling constants only depend on the light quarks and can be calculated in the nonrelativistic quark model. However, the charm quark is not heavy enough and the contribution from its magnetic moment must be included. Applications to the radiative decays $D^\ast \rightarrow D \gamma~,~B^\ast \rightarrow B \gamma~,~ \Xi^\prime_c \rightarrow \Xi_c \gamma~, \Sigma_c \rightarrow \Lambda_c \gamma$ and $\Sigma_c \rightarrow \Lambda_c \pi \gamma$ are given. Together with our previous results on the strong decay rates of $D^\ast \rightarrow D \pi$ and $\Sigma_c \rightarrow \Lambda_c \pi$, predictions are obtained for the total widths and branching ratios of $D^\ast$ and $\Sigma_c$. The decays $\Sigma^+_c \rightarrow \Lambda^+_c \pi^0 \gamma$ and $\Sigma^0_c \rightarrow \Lambda^+_c \pi^- \gamma$ are discussed to illustrate the important roles played by both the heavy quark symmetry and the chiral symmetry.Comment: 30 pages (one figure, available on request), CLNS 92/1158 and IP-ASTP-13-9

Corrections to Chiral Dynamics of Heavy Hadrons: (I) 1/M Correction

In earlier publications we have analyzed the strong and radiative decays of heavy hadrons in a formalism which incorporates both heavy-quark and chiral symmetries. In particular, we have derived a heavy-hadron chiral Lagrangian whose coupling constants are related by the heavy-quark flavor-spin symmetry arising from the QCD Lagrangian with infinitely massive quarks. In this paper, we re-examine the structure of the above chiral Lagrangian by including the effects of $1/m_Q$ corrections in the heavy quark effective theory. The relations among the coupling constants, originally derived in the heavy-quark limit, are modified by heavy quark symmetry breaking interactions in QCD. Some of the implications are discussed.Comment: PHYZZX, 45 pages, 1 figure (not included), CLNS 93/1192, IP-ASTP-02-93, ITP-SB-93-0

An animal-specific FSI model of the abdominal aorta in anesthetized mice

Recent research has revealed that angiotensin II-induced abdominal aortic aneurysm in mice can be related to medial ruptures occurring in the vicinity of abdominal side branches. Nevertheless a thorough understanding of the biomechanics near abdominal side branches in mice is lacking. In the current work we present a mouse-specific fluid-structure interaction (FSI) model of the abdominal aorta in ApoE(-/-) mice that incorporates in vivo stresses. The aortic geometry was based on contrast-enhanced in vivo micro-CT images, while aortic flow boundary conditions and material model parameters were based on in vivo high-frequency ultrasound. Flow waveforms predicted by FSI simulations corresponded better to in vivo measurements than those from CFD simulations. Peak-systolic principal stresses at the inner and outer aortic wall were locally increased caudal to the celiac and left lateral to the celiac and mesenteric arteries. Interestingly, these were also the locations at which a tear in the tunica media had been observed in previous work on angiotensin II-infused mice. Our preliminary results therefore suggest that local biomechanics play an important role in the pathophysiology of branch-related ruptures in angiotensin-II infused mice. More elaborate follow-up research is needed to demonstrate the role of biomechanics and mechanobiology in a longitudinal setting

A human PrM antibody that recognizes a novel cryptic epitope on dengue E glycoprotein

10.1371/journal.pone.0033451PLoS ONE74

Differential Inhibitory Effects of CysLT1 Receptor Antagonists on P2Y6 Receptor-Mediated Signaling and Ion Transport in Human Bronchial Epithelia

BACKGROUND: Cysteinyl leukotriene (CysLT) is one of the proinflammatory mediators released by the bronchi during inflammation. CysLTs exert their biological effects via specific G-protein-coupled receptors. CysLT(1) receptor antagonists are available for clinical use for the treatment of asthma. Recently, crosstalk between CysLT(1) and P2Y(6) receptors has been delineated. P2Y receptors are expressed in apical and/or basolateral membranes of virtually all polarized epithelia to control the transport of fluid and electrolytes. Previous research suggests that CysLT(1) receptor antagonists inhibit the effects of nucleotides acting at P2Y receptors. However, the detailed molecular mechanism underlying the inhibition remains unresolved. METHODOLOGY/PRINCIPAL FINDINGS: In this study, western blot analysis confirmed that both CysLT(1) and P2Y(6) receptors were expressed in the human bronchial epithelial cell line 16HBE14o-. All three CysLT(1) antagonists inhibited the uridine diphosphate (UDP)-evoked I(SC), but only montelukast inhibited the UDP-evoked [Ca(2+)](i) increase. In the presence of forskolin or 8-bromoadenosine 3'5' cyclic monophosphate (8-Br-cAMP), the UDP-induced I(SC) was potentiated but was reduced by pranlukast and zafirlukast but not montelukast. Pranlukast inhibited the UDP-evoked I(SC) potentiated by an Epac activator, 8-(4-Chlorophenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate (8-CPT-2'-O-Me-cAMP), while montelukast and zafirlukast had no such effect. Pranlukast inhibited the real-time increase in cAMP changes activated by 8-CPT-2'-O-Me-cAMP as monitored by fluorescence resonance energy transfer imaging. Zafirlukast inhibited the UDP-induced I(SC) potentiated by N(6)-Phenyladenosine-3',5'-cyclic monophosphorothioate, Sp-isomer (Sp-6-Phe-cAMP; a PKA activator) and UDP-activated PKA activity. CONCLUSIONS/SIGNIFICANCE: In summary, our data strongly suggest for the first time that in human airway epithelia, the three specific CysLT(1) receptor antagonists exert differential inhibitory effects on P2Y(6) receptor-coupled Ca(2+) signaling pathways and the potentiating effect on I(SC) mediated by cAMP and Epac, leading to the modulation of ion transport activities across the epithelia

MicroRNA-145 Regulates Human Corneal Epithelial Differentiation

Epigenetic factors, such as microRNAs, are important regulators in the self-renewal and differentiation of stem cells and progenies. Here we investigated the microRNAs expressed in human limbal-peripheral corneal (LPC) epithelia containing corneal epithelial progenitor cells (CEPCs) and early transit amplifying cells, and their role in corneal epithelium.Human LPC epithelia was extracted for small RNAs or dissociated for CEPC culture. By Agilent Human microRNA Microarray V2 platform and GeneSpring GX11.0 analysis, we found differential expression of 18 microRNAs against central corneal (CC) epithelia, which were devoid of CEPCs. Among them, miR-184 was up-regulated in CC epithelia, similar to reported finding. Cluster miR-143/145 was expressed strongly in LPC but weakly in CC epithelia (P = 0.0004, Mann-Whitney U-test). This was validated by quantitative polymerase chain reaction (qPCR). Locked nucleic acid-based in situ hybridization on corneal rim cryosections showed miR-143/145 presence localized to the parabasal cells of limbal epithelium but negligible in basal and superficial epithelia. With holoclone forming ability, CEPCs transfected with lentiviral plasmid containing mature miR-145 sequence gave rise to defective epithelium in organotypic culture and had increased cytokeratin-3/12 and connexin-43 expressions and decreased ABCG2 and p63 compared with cells transfected with scrambled sequences. Global gene expression was analyzed using Agilent Whole Human Genome Oligo Microarray and GeneSpring GX11.0. With a 5-fold difference compared to cells with scrambled sequences, miR-145 up-regulated 324 genes (containing genes for immune response) and down-regulated 277 genes (containing genes for epithelial development and stem cell maintenance). As validated by qPCR and luciferase reporter assay, our results showed miR-145 suppressed integrin β8 (ITGB8) expression in both human corneal epithelial cells and primary CEPCs.We found expression of miR-143/145 cluster in human corneal epithelium. Our results also showed that miR-145 regulated the corneal epithelium formation and maintenance of epithelial integrity, via ITGB8 targeting