Isospin Mixing and Model Dependence

We show that recent calculations of \Delta I=3/2 effects in nonleptonic hyperon decay induced by m_d-m_u\neq 0 are subject to significant model dependence.Comment: 8 page standard Latex fil

Superpartner Solutions of a BPS Monopole in Noncommutative Space

We construct U(2) BPS monopole superpartner solutions in N=2 non-commutative super Yang-Mills theory. Calculation to the second order in the noncommutative parameter $\theta$ shows that there is no electric quadrupole moment that is expected from the magnetic dipole structure of noncommtative U(2) monopole. This might give an example of the nature of how supersymmetry works not changing between the commutative and noncommutative theories.Comment: 8 page

Electric Dipole Moment of a BPS Monopole

Monopole ``superpartner'' solutions are constructed by acting with finite, broken supersymmetry transformations on a bosonic N=2 BPS monopole. The terms beyond first order in this construction represent the backreaction of the the fermionic zero-mode state on the other fields. Because of the quantum nature of the fermionic zero-modes, the superpartner solution is necessarily operator valued. We extract the electric dipole moment operator and show that it is proportional to the fermion zero-mode angular momentum operator with a gyroelectric ratio g=2. The magnetic quadrupole operator is shown to vanish identically on all states. We comment on the usefulness of the monopole superpartner solution for a study of the long-range spin dependent dynamics of BPS monopoles.Comment: 8 pages, references and note adde

Asymptotic Limits and Structure of the Pion Form Factor

We use dispersive techniques to address the behavior of the pion form factor as $Q^2 \to \infty$ and $Q^2 \to 0$. We perform the matching with the constraints of perturbative QCD and chiral perturbation theory in the high energy and low energy limits, leading to four sum rules. We present a version of the dispersive input which is consistent with the data and with all theoretical constraints. The results indicate that the asymptotic perturbative QCD limit is approached relatively slowly, and give a model independent determination of low energy chiral parameters.Comment: 8 pages, Latex, 2 figure

Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males

The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA₂) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA₂ in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.PLA2G7 V279F genotypes were initially compared in 2890 male cases diagnosed with CAD before age 60 with 3128 male controls without CAD at age 50 and above and subsequently in a second independent male dataset of 877 CAD cases and 1230 controls. In the first dataset, the prevalence of the 279F null allele was 11.5% in cases and 12.8% in controls. After adjustment for age, body mass index, diabetes, smoking, glucose and lipid levels, the OR (95% CI) for CAD for this allele was 0.80 (0.66-0.97, p = 0.02). The results were very similar in the second dataset, despite lower power, with an allele frequency of 11.2% in cases and 12.5% in controls, leading to a combined OR of 0.80 (0.69-0.92), p = 0.002. The magnitude and direction of this genetic effect were fully consistent with large epidemiological studies on plasma Lp-PLA₂ activity and CAD risk.Natural deficiency in Lp-PLA₂ activity due to carriage of PLA2G7 279F allele protects from CAD in Korean men. These results provide evidence for a causal relationship between Lp-PLA₂ and CAD, and support pharmacological inhibition of this enzyme as an innovative way to prevent CAD

Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males

The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA₂) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA₂ in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.PLA2G7 V279F genotypes were initially compared in 2890 male cases diagnosed with CAD before age 60 with 3128 male controls without CAD at age 50 and above and subsequently in a second independent male dataset of 877 CAD cases and 1230 controls. In the first dataset, the prevalence of the 279F null allele was 11.5% in cases and 12.8% in controls. After adjustment for age, body mass index, diabetes, smoking, glucose and lipid levels, the OR (95% CI) for CAD for this allele was 0.80 (0.66-0.97, p = 0.02). The results were very similar in the second dataset, despite lower power, with an allele frequency of 11.2% in cases and 12.5% in controls, leading to a combined OR of 0.80 (0.69-0.92), p = 0.002. The magnitude and direction of this genetic effect were fully consistent with large epidemiological studies on plasma Lp-PLA₂ activity and CAD risk.Natural deficiency in Lp-PLA₂ activity due to carriage of PLA2G7 279F allele protects from CAD in Korean men. These results provide evidence for a causal relationship between Lp-PLA₂ and CAD, and support pharmacological inhibition of this enzyme as an innovative way to prevent CAD

Asymptotic Limits and Structure of the Pion Form-Factor

We use dispersive techniques to address the behavior of the pion form factor as Q2→∞ and Q2→0. We perform the matching with the constraints of perturbative QCD and chiral perturbation theory in the high-energy and low-energy limits, leading to four sum rules. We present a version of the dispersive input which is consistent with the data and with all theoretical constraints. The results indicate that the asymptotic perturbative QCD limit is approached relatively slowly, and give a model-independent determination of low-energy chiral parameters