Measurement of the B0 anti-B0 oscillation frequency using l- D*+ pairs and lepton flavor tags

The oscillation frequency Delta-md of B0 anti-B0 mixing is measured using the partially reconstructed semileptonic decay anti-B0 -> l- nubar D*+ X. The data sample was collected with the CDF detector at the Fermilab Tevatron collider during 1992 - 1995 by triggering on the existence of two lepton candidates in an event, and corresponds to about 110 pb-1 of pbar p collisions at sqrt(s) = 1.8 TeV. We estimate the proper decay time of the anti-B0 meson from the measured decay length and reconstructed momentum of the l- D*+ system. The charge of the lepton in the final state identifies the flavor of the anti-B0 meson at its decay. The second lepton in the event is used to infer the flavor of the anti-B0 meson at production. We measure the oscillation frequency to be Delta-md = 0.516 +/- 0.099 +0.029 -0.035 ps-1, where the first uncertainty is statistical and the second is systematic.Comment: 30 pages, 7 figures. Submitted to Physical Review

Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury

Delayed vasospasm that develops 3–7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies

No apparent role for neutrophils and neutrophil-derived myeloperoxidase in experimental subarachnoid haemorrhage and vasospasm: A preliminary study

Objective. The literature contains investigations and discussion of the role of neutrophils and neutrophil-derived myeloperoxidase (MPO) in inflammatory processes, local ischaemia, and ischaemia-reperfusion injury models. Our aim was to determine whether the same roles existed for neutrophils and the system involving neutrophil-derived MPO in experimental subarachnoid haemorrhage (SAH) and associated ischaemia

Effect of mexiletine on lipid peroxidation and early ultrastructural findings in experimental spinal cord injury

Object. The purpose of this study was to investigate the effect of mexiletine on lipid peroxidation and on ultrastructural findings after induced spinal cord injury (SCI). The authors also compared the activity of mexiletine to that of the well-known antioxidant, methylprednisolone sodium succinate (MPSS)

The Effect of Phosphodiesterase Inhibitor Tadalafil on Vasospasm Following Subarachnoid Hemorrhage in an Experimental Rabbit Model

Background: Despite the years of study on it, cerebral vasospasm following subarachnoid hemorrhage is still an important cause of mortality and morbidity. The presented study was undertaken to show whether phosphodiesterase inhibitor tadalafil can attenuate the vasospasm process following subarachnoid bleeding

A Multicentered Study on Epidemiologic and Clinical Characteristics of 37 Neonates With Community-acquired COVID-19

PMID = 3293232