Measurement of Direct-Photon Cross Section and Double-Helicity Asymmetry at sqrt[s]=510 GeV in p[over →]+p[over →] Collisions.

We present measurements of the cross section and double-helicity asymmetry A_{LL} of direct-photon production in p[over →]+p[over →] collisions at sqrt[s]=510 GeV. The measurements have been performed at midrapidity (|η|<0.25) with the PHENIX detector at the Relativistic Heavy Ion Collider. At relativistic energies, direct photons are dominantly produced from the initial quark-gluon hard scattering and do not interact via the strong force at leading order. Therefore, at sqrt[s]=510 GeV, where leading-order-effects dominate, these measurements provide clean and direct access to the gluon helicity in the polarized proton in the gluon-momentum-fraction range 0.02

Probing Gluon Spin-Momentum Correlations in Transversely Polarized Protons through Midrapidity Isolated Direct Photons in p

Studying spin-momentum correlations in hadronic collisions offers a glimpse into a three-dimensional picture of proton structure. The transverse single-spin asymmetry for midrapidity isolated direct photons in p^{↑}+p collisions at sqrt[s]=200 GeV is measured with the PHENIX detector at the Relativistic Heavy Ion Collider (RHIC). Because direct photons in particular are produced from the hard scattering and do not interact via the strong force, this measurement is a clean probe of initial-state spin-momentum correlations inside the proton and is in particular sensitive to gluon interference effects within the proton. This is the first time direct photons have been used as a probe of spin-momentum correlations at RHIC. The uncertainties on the results are a 50-fold improvement with respect to those of the one prior measurement for the same observable, from the Fermilab E704 experiment. These results constrain gluon spin-momentum correlations in transversely polarized protons.

Hemodynamic effects after conversion of arrhythmias.

Systemic and coronary hemodynamic parameters were determined during an arrhythmia and immediately after a direct current transthoracic shock given in an attempt to convert the arrhythmia to a sinus mechanism. No anesthesia or drugs were administered between the two studies. 16 patients with atrial fibrillation converted to sinus rhythm and five did not. In two patients with atrial flutter and one with supraventricular tachycardia, the arrhythmia was corrected. The arrhythmia persisted in a single patient with ventricular tachycardia. Utilizing each patient as his own control, we compared statistically various hemodynamic parameters before and after the shock. In addition, the group of patients whose atrial fibrillation terminated was compared to the group treated in the same manner but in which the atrial fibrillation persisted. Pressures in the right side of the heart decreased in both groups so that the changes appeared to be caused by factors associated with the transthoracic direct current shock or the catheterization procedure. The differences between those with atrial fibrillation who converted to sinus rhythm as compared to those who did not were a decrease in heart rate, an increase in stroke volume, and an increase in cardiac efficiency. There was no immediate effect on the cardiac output or coronary blood flow.

Clinical guidelines for exercise training.

Exercise training may be useful for a variety of patients with and without established cardiovascular disease. The degree to which a patient participates in a prescribed exercise program depends strongly on initial motivation. The primary care physician can provide appropriate reinforcement with careful explanation of the effects of exercise on cardiovascular and metabolic function. Exercise programs may be combined effectively with other life-style adjustments, including weight loss, blood pressure control, and discontinuation of smoking. As a single intervention factor, exercise cannot prevent the evolution of cardiovascular disease in multiple-risk patients. Exercise is best used in combination with a program of comprehensive cardiovascular risk factor modification.

Pulmonary hypertension with coexisting portal hypertension.

A 10-year-old boy who had portal hypertension secondary to portal fibrosis/intrahepatic biliary atresia developed syncopal episodes related to strenuous activity. A work-up excluded a metabolic or neurologic etiology and cardiac catheterization demonstrated significant pulmonary hypertension. Six months later he died and an autopsy revealed pulmonary plexogenic arteriopathy without microemboli. Previous reported cases of this symptom complex are reviewed. In addition, he had a history of nonspecific colitis, ulcerative stomatitis, and conjunctivitis responsive to steroid therapy. The possible relationship of these manifestations to the portal pulmonary pathology is discussed.