Non-factorizable contributions in hadronic weak decays of charm mesons

Two body decays of charm mesons are studied by describing their amplitude in terms of a sum of factorizable and non-factorizable ones. The former is estimated by using a naive factorization while the latter is calculated by using a hard pseudo-scalar-meson approximation. The hard pseudo-scalar-meson amplitude is given by a sum of the so-called equal-time commutator term and surface term which contains all possible pole contributions of various mesons, not only the ordinary $\{q\bar q\}$ but also four-quark $\{qq\bar q\bar q\}$, hybrid $\{q\bar qg\}$ and glue-balls. Naively factorized amplitudes for the spectator decays which lead to too big rates can interfere destructively with exotic meson pole amplitudes and the total amplitudes can reproduce their observed rates. The non-factorizable contributions can supply sufficiently large contributions to the color suppressed decays which are strongly suppressed in the naive factorization. A possible solution to the long standing puzzle that the ratio of decay rates for $D^0\to K^+K^-$ to $D^0\to \pi^+\pi^-$ is around 2.5 is given by different contributions of exotic meson poles.Comment: 22 pages, RevTe

Radiative Kaon Decays K±→π±π0γK^\pm\to\pi^\pm\pi^0\gamma and Direct CP Violation

It is stressed that a measurement of the electric dipole amplitude for direct photon emission in \kpm decays through its interference with inner bremsstrahlung is important for differentiating among various models. Effects of amplitude CP violation in the radiative decays of the charged kaon are analyzed in the Standard Model in conjunction with the large $N_c$ approach. We point out that gluon and electromagnetic penguin contributions to the CP-violating asymmetry between the Dalitz plots of \kpm are of equal weight. The magnitude of CP asymmetry ranges from $2\times 10^{-6}$ to $1\times 10^{-5}$ when the photon energy in the kaon rest frame varies from 50 MeV to 170 MeV.Comment: Latex, 11 pages, ITP-SB-93-36, IP-ASTP-22-9

Towards resolution of the scalar meson nonet enigma

By the application of a linear mass spectrum to a composite system of both the pseudoscalar and scalar meson nonets, we find three mass relations for the masses of the scalar states which suggest the $q\bar{q}$ assignment for the scalar meson nonet: $a_0(1320),$ $K_0^\ast (1430),$ $f_0(1500),$ $f_0'(980).$Comment: 16 pages, LaTe

Newly observed two-body decays of B mesons in a hybrid perspective

In consistency with the b --> c type of (quasi) two body decays, recently observed two body decays of B mesons are studied in a hybrid perspective in which their amplitude is given by a sum of factorizable and non-factorizable ones, and a role of the latter in these decays are discussed.Comment: 7 page

The genetic landscape and clinical implication of pediatric Moyamoya angiopathy in an international cohort

Pediatric Moyamoya Angiopathy (MMA) is a progressive intracranial occlusive arteriopathy that represents a leading cause of transient ischemic attacks and strokes in childhood. Despite this, up to now no large, exclusively pediatric MMA cohort has been subjected to systematic genetic investigation. In this study, we performed molecular karyotyping, exome sequencing and automated structural assessment of missense variants on a series of 88 pediatric MMA patients and correlated genetic, angiographic and clinical (stroke burden) findings. The two largest subgroups in our cohort consisted of RNF213 and neurofibromatosis type 1 (NF1) patients. While deleterious RNF213 variants were associated with a severe MMA clinical course with early symptom onset, frequent posterior cerebral artery involvement and higher stroke rates in multiple territories, NF1 patients had a similar infarct burden compared to non-NF1 individuals and were often diagnosed incidentally during routine MRIs. Additionally, we found that MMA-associated RNF213 variants have lower predicted functional impact compared to those associated with aortic disease. We also raise the question of MMA as a feature of recurrent as well as rare chromosomal imbalances and further support the possible association of MMA with STAT3 deficiency. In conclusion, we provide a comprehensive characterization at the genetic and clinical level of a large exclusively pediatric MMA population. Due to the clinical differences found across genetic subgroups, we propose genetic testing for risk stratification as part of the routine assessment of pediatric MMA patients

Vascular adaptation to exercise in humans: Role of hemodynamic stimuli

On the 400th anniversary of Harvey’s Lumleian lectures, this review focuses on “hemodynamic” forces associated with the movement of blood through arteries in humans and the functional and structural adaptations that result from repeated episodic exposure to such stimuli. The late 20th century discovery that endothelial cells modify arterial tone via paracrine transduction provoked studies exploring the direct mechanical effects of blood flow and pressure on vascular function and adaptation in vivo. In this review, we address the impact of distinct hemodynamic signals that occur in response to exercise, the interrelationships between these signals, the nature of the adaptive responses that manifest under different physiological conditions, and the implications for human health. Exercise modifies blood flow, luminal shear stress, arterial pressure, and tangential wall stress, all of which can transduce changes in arterial function, diameter, and wall thickness. There are important clinical implications of the adaptation that occurs as a consequence of repeated hemodynamic stimulation associated with exercise training in humans, including impacts on atherosclerotic risk in conduit arteries, the control of blood pressure in resistance vessels, oxygen delivery and diffusion, and microvascular health. Exercise training studies have demonstrated that direct hemodynamic impacts on the health of the artery wall contribute to the well-established decrease in cardiovascular risk attributed to physical activity. © 2017 the American Physiological Society

η→π0γγ\eta \to \pi^0 \gamma \gamma decay within unitarized chiral perturbation theory

We improve the calculations of the $\eta \to \pi^0 \gamma \gamma$ decay within the context of meson chiral lagrangians. We use a chiral unitary approach for the meson-meson interaction, thus generating the $a_0(980)$ resonance and fixing the longstanding sign ambiguity on its contribution. This also allows us to calculate the loops with one vector meson exchange, thus removing a former source of uncertainty. In addition we ensure the consistency of the approach with other processes. First, by using vector meson dominance couplings normalized to agree with radiative vector meson decays. And, second, by checking the consistency of the calculations with the related $\gamma \gamma \to \pi^0 \eta$ reaction. We find an $\eta \to \pi^0 \gamma \gamma$ decay width of $0.47\pm 0.10$ eV, in clear disagreement with published data but in remarkable agreement with the most recent measurement.Comment: 15 pages, 10 figures, published versio

Assessing clinical utility of preconception expanded carrier screening regarding residual risk for neurodevelopmental disorders

The magnitude of clinical utility of preconception expanded carrier screening (ECS) concerning its potential to reduce the risk of affected offspring is unknown. Since neurodevelopmental disorders (NDDs) in their offspring is a major concern of parents-to-be, we addressed the question of residual risk by assessing the risk-reduction potential for NDDs in a retrospective study investigating ECS with different criteria for gene selection and definition of pathogenicity. We used exome sequencing data from 700 parents of children with NDDs and blindly screened for carrier-alleles in up to 3046 recessive/X-linked genes. Depending on variant pathogenicity thresholds and gene content, NDD-risk-reduction potential was up to 43.5% in consanguineous, and 5.1% in nonconsanguineous couples. The risk-reduction-potential was compromised by underestimation of pathogenicity of missense variants (false-negative-rate 4.6%), inherited copy-number variants and compound heterozygosity of one inherited and one de novo variant (0.9% each). Adherence to the ACMG recommendations of restricting ECS to high-frequency genes in nonconsanguineous couples would more than halve the detectable inherited NDD-risk. Thus, for optimized clinical utility of ECS, screening in recessive/X-linked genes regardless of their frequency (ACMG Tier-4) and sensible pathogenicity thresholds should be considered for all couples seeking ECS

The Mixed Vector Current Correlator <0|T(V^3_\mu V^8_\nu )|0> To Two Loops in Chiral Perturbation Theory

The isospin-breaking correlator of the product of flavor octet vector currents, $V^3_\mu$ and $V^8_\nu$, $\Pi^{38}_{\mu\nu}(q^2)$ is computed to next-to-next- to-leading (two-loop) order in Chiral Perturbation Theory. Large corrections to both the magnitude and $q^2$-dependence of the one-loop result are found, and the reasons for the slow convergence of the chiral series for the correlator given. The two-loop expression involves a single ${\cal O}(q^6)$ counterterm, present also in the two-loop expressions for $\Pi^{33}_{\mu\nu}(q^2)$ and $\Pi^{88}_{\mu\nu}(q^2)$, which counterterm contributes a constant to the scalar correlator $\Pi^{38}(q^2)$. The feasibility of extracting the value of this counterterm from other sources is discussed. Analysis of the slope of the correlator with respect to $q^2$ using QCD sum rules is shown to suggest that, even to two-loop order, the chiral series for the correlator may not yet be well-converged.Comment: 32 pages, uses REVTEX and epsfig.sty with 7 uuencoded figures. Entire manuscript available as a ps file at http://www.physics.adelaide.edu.au/theory/home.html Also available via anonymous ftp at ftp://adelphi.adelaide.edu.au/pub/theory/ADP-95-27.T181.p

Study of 3-prong Hadronic τ\tau Decays with Charged Kaons

Using a sample of 4.7/fb integrated luminosity accumulated with the CLEO-II detector at the Cornell Electron Storage Ring (CESR), we have measured the branching fractions of the tau lepton into $K^- h^+ \pi^- \nu_\tau$ and $K^- K^+ \pi^- \nu_\tau$ relative to $h^- h^+ h^- \nu_\tau; K^- h^+ \pi^- \pi^0\nu_\tau$ and $K^- K^+ \pi^- \pi^0\nu_\tau$ relative to $h^- h^+ h^- \pi^0 \nu_\tau$. The relative branching fractions are: (5.16+-0.20+-0.50)*$10^{-2}$, (1.52+-0.14+-0.29)*$10^{-2}$, (2.54+-0.44+-0.39)*$10^{-2}$ and $<0.0154$ at 95% C.L., respectively. Coupled with additional experimental information, we use our results to extract information on the structure of three-prong tau decays to charged kaons.Comment: 16 pages postscript file also available through http://w4.lns.cornell.edu/public/CLN