Mercosure, The Free Trade Area of the Americas, and the Future of U.S. Hegemony in Latin America

The purpose of this Article is to examine U.S. hegemony in Latin America by looking at the impact of the Free Trade Area of the Americas ( FTAA ) negotiations on U.S.-Latin American relations. Does the FTAA process confirm the claim that since World War II ... the general trend has always been for the United States to exert a great degree of influence over Latin American countries... ? Does it mark the beginning of a new, more balanced relationship between the United States and Latin America, a mature partnership based on reciprocity, mutuality of interests and mutual respect? Alternatively, are the United States and Latin America growing apart? Can Latin America say good-bye to the United States and establish a presence of its own on the world stage

Search for the rare decay D-0 -> mu(+) mu(-)

A search for the rare decay D-0 -> mu(+) mu(-) is performed using a data sample, corresponding to an integrated luminosity of 0.9 fb(-1), of pp collisions collected at a centre-of-mass energy of 7 TeV by the LHCb experiment. The observed number of events is consistent with the background expectations and corresponds to an upper limit of B(D-0 -> mu(+) mu(-)) < 6.2 (7.6) x 10(-9) at 90% (95%) confidence level. This result represents an improvement of more than a factor twenty with respect to previous measurements

Model-independent search for CP violation in D-0 > K-K+pi(-)pi(+) and D-0 -> pi(-)pi(+)pi(+)pi(-) decays

A search for CP violation in the phase-space structures of 130 and 15 decays to the final states K-K+pi(-)pi(+) and pi(-)pi(+)pi(+)pi(-) is presented. The search is carried out with a data set corresponding to an integrated luminosity of 1.0 fb(-1) collected in 2011 by the LHCb experiment in pp collisions at a centre-of-mass energy of 7 TeV. For the K-K+pi(-)pi(+) final state, the four-body phase space is divided into 32 bins, each bin with approximately 1800 decays. The p-value under the hypothesis of no CP violation is 9.1%, and in no bin is a CP asymmetry greater than 6.5% observed. The phase space of the pi(-)pi(+)pi(+)pi(-). final state is partitioned into 128 bins, each bin with approximately 2500 decays. The p-value under the hypothesis of no CP violation is 41%, and in no bin is a CP asymmetry greater than 5.5% observed. All results are consistent with the hypothesis of no CP violation at the current sensitivity

Observation of the decay B-s(0) -> (D)over-bar(0)phi

First observation of the decay B-s(0) -> (D) over bar (0)phi is reported using pp collision data, corresponding to an integrated luminosity of 1.0 fb(-1), collected by the LHCb experiment at a centre-of-mass energy of 7 TeV. The significance of the signal is 6.5 standard deviations. The branching fraction is measured relative to that of the decay B-S(0) -> (D) over bar (0)phi to be beta B-S(0) -> (D) over bar (0)phi/beta B-S(0) -> (D) over bar (0)(K) over bar*(0) = 0.069 +/- 0.013 (stat) +/- 0.007 (syst). The first measurement of the ratio of branching fractions for the decays beta B-S(0) -> (D) over bar (0)(K) over bar*(0) and beta B-S(0) -> (D) over bar (0)(K) over bar*(0) is found to be beta B-S(0) -> (D) over bar (0)(K) over bar*(0/)beta B-S(0) -> (D) over bar (0)(K) over bar*(0=7.8) +/- 0.7(stat) +/- 0.3 (syst) +/- 0.6 (f(s)/f(d)) where the last uncertainty is due to the ratio of the B(s)(0)and B-0 fragmentation fractions

Measurement of the flavour-specific CP-violating asymmetry a(sl)(s) in B-s(0) decays

The CP-violating asymmetry a(sl)(s), is studied using semileptonic decays of B-s(0) and (B) over bar (0)(s) mesons produced in pp collisions at a centre-of-mass energy of 7 TeV at the LHC, exploiting a data sample corresponding to an integrated luminosity of 1.0 fb(-1). The reconstructed final states are D-s(+/-)mu(+/-)(s), with the D-s(+/-) particle decaying in the phi pi(+/-) mode. The D-s(+/-)mu(+/-)(s) yields are summed over B-s(0) and (B) over bar (0)(s) initial states, and integrated with respect to decay time. Data-driven methods are used to measure efficiency ratios. We obtain a(sl)(s) = (-0.06 +/- 0.50 +/- 0.36)%, where the first uncertainty is statistical and the second systematic

First measurement of time-dependent CP violation in Bs0→K+K− B_s^0\to K^+K^- decays

Direct and mixing-induced CP-violating asymmetries in B-s(0) -> K+K- decays are measured for the first time using a data sample of p p collisions, corresponding to an integrated luminosity of 1.0 fb(-1), collected with the LHCb detector at a centre-of-mass energy of 7 TeV. The results are C-KK = 0.14 +/- 0.11 +/- 0.03 and S-KK = 0.30 +/- 0.12 +/- 0.04, where the first uncertainties are statistical and the second systematic. The corresponding quantities are also determined for B-0 -> pi(+)pi(-) decays to be C-pi pi = -0.38 +/- 0.15 +/- 0.02 and S-pi pi = -0.71 +/- 0.13 +/- 0.02, in good agreement with existing measurements

Observation of B-s(0) -> chi(c1)phi decay and study of B-0 -> chi K-c1,K-2*(0) decays

The first observation of the decay B-s(0) -> chi(c1)phi and a study of B-0 -> chi K-c1,K-2*(0) decays are presented. The analysis is performed using a dataset, corresponding to an integrated luminosity of 1.0 fb(-1), collected by the LHCb experiment in pp collisions at a centre-of-mass energy of 7 TeV. The following ratios of branching fractions are measured: B(B-s(0) -> chi(c1)phi)/B(B-s(0) -> J/psi phi) = (18.9 +/- 1.8 (stat) +/- 1.3 (syst) +/- 0.8(B)) x 10(-2), B(B-0 -> chi K-c1*(0))//B(B-0 -> J/psi K*(0)) = (19.8 +/- 1.1 (stat) +/- 1.2 (syst) +/- 0.9(B)) x 10(-2), B(B-0 -> chi K-c2*(0))//B(B-0 -> chi K-c1*(0)) = (17.1 +/- 5.0 (stat) +/- 1.7 (syst) +/- 1.1(B)) x 10(-2), where the third uncertainty is due to the limited knowledge of the branching fractions of chi(c) -> J/psi gamma modes

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab.

Background: Apolipoprotein B (apoB) provides an integrated measure of atherogenic risk. Whether apoB levels and apoB lowering hold incremental predictive information on residual risk after acute coronary syndrome beyond that provided by low-density lipoprotein cholesterol is uncertain. Methods: The ODYSSEY OUTCOMES trial (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) compared the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome and elevated atherogenic lipoproteins despite optimized statin therapy. Primary outcome was major adverse cardiovascular events (MACE; coronary heart disease death, nonfatal myocardial infarction, fatal/nonfatal ischemic stroke, hospitalization for unstable angina). Associations between baseline apoB or apoB at 4 months and MACE were assessed in adjusted Cox proportional hazards and propensity score–matched models. Results: Median follow-up was 2.8 years. In proportional hazards analysis in the placebo group, MACE incidence increased across increasing baseline apoB strata (3.2 [95% CI, 2.9–3.6], 4.0 [95% CI, 3.6–4.5], and 5.5 [95% CI, 5.0–6.1] events per 100 patient-years in strata 35–<50, and ≤35 mg/dL, respectively). Compared with propensity score–matched patients from the placebo group, treatment hazard ratios for alirocumab also decreased monotonically across achieved apoB strata. Achieved apoB was predictive of MACE after adjustment for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol but not vice versa. Conclusions: In patients with recent acute coronary syndrome and elevated atherogenic lipoproteins, MACE increased across baseline apoB strata. Alirocumab reduced MACE across all strata of baseline apoB, with larger absolute reductions in patients with higher baseline levels. Lower achieved apoB was associated with lower risk of MACE, even after accounting for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol, indicating that apoB provides incremental information. Achievement of apoB levels as low as ≤35 mg/dL may reduce lipoprotein-attributable residual risk after acute coronary syndrome. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01663402.gov; Unique identifier: NCT01663402.URL: https://www