Rapidity dependence of antiproton to proton ratios in Au+Au collisions at sqrt{s_{NN}}=130 GeV

Measurements, with the BRAHMS detector, of the antiproton to proton ratio at central and forward rapidities are presented for Au+Au reactions at sqrt{s_{NN}}=130 GeV, and for three different collision centralities. For collisions in the 0-40% centrality range we find $N(\bar{{\rm p}})/N({\rm p}) = 0.64 +- 0.04 (stat.) +- 0.06 (syst.) at y ~0, 0.66 +- 0.03 +- 0.06 at y ~ 0.7, and 0.41 +- 0.04 +- 0.06 at y ~ 2. The ratios are found to be nearly independent of collision centrality and transverse momentum. The measurements demonstrate that the antiproton and proton rapidity densities vary differently with rapidity, and indicate that a net-baryon free midrapidity plateau (Bjorken limit) is not reached at this RHIC energy.Comment: 8 pages, 3 figure

MYOCARDIAL PERFUSION ASSESSMENT IN FORECASTING EFFECT OF CORONARY ANGIOPLASTY IN PATIENTS WITH ISCHEMIC CHRONIC HEART FAILURE

Aim. To define influence of the left ventricle (LV) perfusion defects on the clinical status dynamics after coronary angioplasty in patients with the expressed myocardium dysfunction of ischemic etiology. Materials and methods. Examined 86 patients (81 men and 5 women aged from 46 to 73 years) before and in 2–3 days after percutaneous coronary intervention with diagnosis: CAD, CHF with NYHA class III–IV, echocardiography parameters of LV: ejection fraction less than 40%, end-diastolic volume is more than 200 ml. Perfusion defects of myocardium estimated with use of ECG-gated single photon emission computed tomography. Predictors were defined: perfusion defects on LV apex (in score), perfusion defects in the area of LAD, LCx and RCA (%), the LV global perfusion defects (in score and %). Results. In 42% of cases 6-minute walk test increased to 3 times; The NYHA class decreased by 2 classes (group 1). In 28 cases 6-minute walk test increased to 2 times and the NYHA class decreased on 1 class. In 22 patients 6-minute walk test increased less than 50% of reference values and there was no dynamics NYHA class (50 patients of the group 2). Initial extent of LV global perfusion defects in group 1 – 41,2 ± 4,0%, in group 2 – 58,3 ± 2,4% (р = 0,0004). Similar values are received for perfusion indicators in the area of LAD and the LV apex. Prevalence of myocardial perfusion defects at rest reflects prevalence of a cardiosclerosis in a cardiac muscle. Conclusion. Degree of LV myocardial perfusion defects in patients with the expressed heart failure of ischemic etiology is the key indicator influencing clinical efficiency of coronary angioplasty. Critical size for definition of the favorable forecast of revascularization are 60% and more perfusion defects testifying that in a cardiac muscle the focal cardiosclerosis prevails over the functioning myocardium