No abstract

After completion of the data taking for the v(mu) -> v(tau) oscillation search, the CHORUS lead-scintillator calorimeter was used in the 1998 run as an active target. High-statistics samples of charged-current interactions were collected in the CERN SPS west area neutrino beam. This beam contained predominantly muon (anti-)neutrinos from sign-selected pious and kaons. We measure the flux and energy spectrum of the incident neutrinos and compare them with beam simulations. The neutrino-nucleon and anti-neutrino-nucleon differential cross-sections are measured in the range 0.01 < x < 0.7, 0.05 < y < 0.95, 10 < E-v < 200 GeV. We extract the neutrino-nucleon structure functions F-2(x, Q(2)), xF(3) (x, Q(2)), and R(x, Q2) and compare these with results from other experiments. (c) 2005 Elsevier B.V. All rights reserved

The nuclear emulsion target of the CHORUS detector was exposed to the wide-band neutrino beam of the CERN SPS of 27 GeV average neutrino energy from 1994 to 1997. In total about 100000 charged-current neutrino interactions with at least one identified muon were located in the emulsion target and fully reconstructed, using newly developed automated scanning systems. Charmed particles were searched for by a program recognizing particle decays. The observation of the decay in nuclear emulsion makes it possible to select a sample with very low background and minimal kinematical bias. 2013 charged-current interactions with a charmed hadron candidate in the final state were selected and confirmed through visual inspection. The charm production rate induced by neutrinos relative to the charged-current cross-section is measured to be σ(ν µ N → µ − CX)/σ(CC) = (5.75 ± 0.32(stat) ± 0.30(syst))%. The charm production cross-section as a function of the neutrino energy is also obtained. The results are in good agreement with previous measurements. The charm-quark hadronization produces the following charmed hadrons with relative fractions (in %): f D 0 = 43.7 ± 4.5, f Λ + c = 19.2 ± 4.2, f D + = 25.3 ± 4.2, and f D + s = 11.8 ± 4.7.

No abstract

Ischemia and reperfusion (IR) injury of the liver consists of two distinct phases. The first phase is caused by acute cellular injury at 3 to 6 h postreperfusion, which may be mainly induced by the increased production of oxygen radical species. The secondary, subacute, phase results from inflammatory responses at 18 to 24 h, leading to the progression of liver damage. The inflammatory response observed here is caused by proinflammatory cytokines and accumulating neutrophils which secrete oxidants, proteases, and so on. The production of proinflammatory cytokines, including chemokines and adhesion molecules, is regulated by transcriptional factors nuclear factor kappa B (NFKappaB), and AP-1. The progression of the injury is generated by the recruiting leucocytes which release oxidants and proteases. Recruitment and adhesion of neutrophils to the liver are accomplished by multiple steps in which many chemoattractants and adhesion molecules participate. Recent investigations suggest that calcium-dependent proteases, among various kinds of proteases, also play important roles in the aggravation of IR injury. Based on the mechanisms stated above, numerous strategies have been proposed as for prophylaxis and treatment. Most of these therapeutic strategies are derived from the inhibition of the production of oxygen radicals, inflammatory cytokines, and adhesion molecules; inhibition of leucocyte infiltration and elastase production; and inhibition of microcirculatory impairment, apoptosis-related molecules, and the breakdown of membrane phospholipids; and so on. Moreover, recent studies clarified that short periods of ischemia and subsequent reperfusion, termed ischemic preconditioning, exert a preventive effect against IR injuries in various organs, including the liver. Based on clarification of the candidates responsible for this phenomenon, pharmacological ischemic preconditioning has been proposed. In this review article, the authors outline the current progress in the understanding of and therapeutic strategies for hepatic IR injury.