A lattice study of the exclusive B→K∗γB \to K^* \gamma decay amplitude, using the Clover action at β=6.0\beta=6.0

We present the results of a numerical calculation of the $B\to K^* \gamma$ form factors. The results have been obtained by studying the relevant correlation functions at $\beta=6.0$, on an $18^3 \times 64$ lattice, using the ${\rm O(a)}$-improved fermion action, in the quenched approximation. From the study of the matrix element $$ we have obtained the form factor $T_1(0)$ which controls the exclusive decay rate. The results are compared with the recent results from CLEO. We also discuss the compatibility between the scaling laws predicted by the Heavy Quark Effective Theory (HQET) and pole dominance, by studying the mass- and $q^2$-dependence of the form factors. From our analysis, it appears that the form factors follow a mass behaviour compatible with the predictions of the HQET and that the $q^2$-dependence of $T_2$ is weaker than would be predicted by pole dominance.Comment: 17 pages, LaTeX + epsf.sty. Uuencoded, compressed, tar archive including the text and one postscript figur

Translating evidence into policy for cardiovascular disease control in India

Cardiovascular diseases (CVD) are leading causes of premature mortality in India. Evidence from developed countries shows that mortality from these can be substantially prevented using population-wide and individual-based strategies. Policy initiatives for control of CVD in India have been suggested but evidence of efficacy has emerged only recently. These initiatives can have immediate impact in reducing morbidity and mortality. Of the prevention strategies, primordial involve improvement in socioeconomic status and literacy, adequate healthcare financing and public health insurance, effective national CVD control programme, smoking control policies, legislative control of saturated fats, trans fats, salt and alcohol, and development of facilities for increasing physical activity through better urban planning and school-based and worksite interventions. Primary prevention entails change in medical educational curriculum and improved healthcare delivery for control of CVD risk factors-smoking, hypertension, dyslipidemia and diabetes. Secondary prevention involves creation of facilities and human resources for optimum acute CVD care and secondary prevention. There is need to integrate various policy makers, develop effective policies and modify healthcare systems for effective delivery of CVD preventive care

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

Lattice calculation of the penguin diagram decay B→K*γ

We calculate the leading-order matrix element for the decay B --> K gamma in the quenched approximation of lattice QCD on a 24(3) x 48 lattice at beta = 6.2, using an O(a)-improved fermion action. Extrapolating to physical quark masses gives an on-shell form factor of T1(q2=0) = 0.15(-14)+12 (stat). We find T1 is approximately independent of the spectator quark mass and extract T1(q2=0) = 0.15(-4)+5 if this independence is assumed. We find the results to be consistent (in the standard model) with the CLEO experimental branching ratio of B(B --> K*-gamma) = (4.5 +/- 1.5 +/-0.9) x 10(-5)