Hydroxyl radicals were generated radiolytically in N2O-saturated aqueous solutions of thiourea and tetramethylthiourea. The rate constant of the reaction of OH radicals with thiourea (tetramethylthiourea) has been determined using 2-propanol as well as NaN3 as competitors to be 1.2 × 1010 dm3 mol-1 s-1 (8.0 × 109 dm3 mol-1 s-1). A transient appears after a short induction period and shows a well-defined absorption spectrum with λmax = 400 nm (ε = 7400 dm3 mol-1 cm-1); that of tetramethylthiourea has λmax = 450 nm (ε = 6560 dm3 mol-1 cm-1). Using conductometric detection, it has been shown that, in both cases, OH- and a positively charged species are produced. These results indicate that a radical cation is formed. These intermediates with λmax = 400 nm (450 nm) are not the primary radical cations, since the intensity of the absorbance depends on the substrate concentration. The absorbance build-up follows a complex kinetics best described by the reversible formation of a dimeric radical cation by addition of a primary radical cation to a molecule of thiourea. The equilibrium constant for this addition has been determined by competition kinetics to be 5.5 × 105 dm3 mol-1 for thiourea (7.6 × 104 dm3 mol-1 for tetramethylthiourea). In the bimolecular decay of the dimeric radical cation (thiourea, 2k = 9.0 × 108 dm3 mol-1 s-1; tetramethylthiourea, 1.3 × 109 dm3 mol-1 s-1), formamidine (tetramethylformamidine) disulfide is formed. In basic solutions of thiourea, the absorbance at 400 nm of the dimeric radical cation decays rapidly, giving rise (5.9 × 107 dm3 mol-1 s-1) to a new intermediate with a broad maximum at 510 nm (ε = 750 dm3 mol-1 cm-1). This reaction is not observed in tetramethylthiourea. The absorption at 510 nm is attributed to the formation of a dimeric radical anion, via neutralization of the dimeric radical cation and subsequent deprotonation of the neutral dimeric radical. The primary radical cation of thiourea is deprotonated by OH- (2.8 × 109 dm3 mol-1 s-1) to give a neutral thiyl radical. The latter reacts rapidly with thiourea, yielding a dimeric radical, which is identical to the species from the reaction of OH- with the dimeric radical cation. The dimeric radical cations of thiourea and tetramethylthiourea are strong oxidants and readily oxidize the superoxide radical (4.5 × 109 dm3 mol-1 s-1 for thiourea and 3.8 × 109 dm3 mol-1 s-1 for tetramethylthiourea), phenolate ion (3 × 108 dm3 mol-1 s-1 for tetramethylthiourea), and even azide ion (4 × 106 dm3 mol-1 s-1 for thiourea and ∼106 dm3 mol-1 s-1 for tetramethylthiourea). With O2, the dimeric radical cation of thiourea reacts relatively slowly (1.2 × 107 dm3 mol-1 s-1) and reversibly (2 × 103 s-1).
An enhancement near threshold is observed in the omega(phi) invariant mass spectrum from the doubly Okubo-Zweig-Iizuka-suppressed decays of J/psi-->gamma(omega)phi, based on a sample of 5.8 x 10(7) J/psi events collected with the BESII detector. A partial wave analysis shows that this enhancement favors JP=0+, and its mass and width are M=1812(+19)(-26)(stat)+/-18(syst) MeV/c2 and Gamma=105+/-20(stat)+/-28(syst) MeV/c2. The product branching fraction is determined to be B(J/psi-->gammaX)B(X-->omega(phi))=[2.61+/-0.27(stat)+/-0.65(syst)]x10(-4).
We present measurements of the branching fraction and time-dependent CP asymmetries in B0-->J/psipi0 decays based on 466 x 10(6) Upsilon(4S)-->BB over events collected with the BABAR detector at the SLAC PEP-II asymmetric-energy B factory. We measure the CP asymmetry parameters S= -1.23+/-0.21(stat)+/-0.04(syst) and C= -0.20+/-0.19(stat)+/-0.03(syst), where the measured value of (S, C) is 4.0 standard deviations from (0, 0) including systematic uncertainties. The branching fraction is determined to be B(B0-->J/psipi0)=[1.69+/-0.14(stat)+/-0.07(syst)]x10(-5).
Guillain-Barre syndrome (GBS) is an autoimmune disease of the nervous system and is the most common acute polyneuropathy. Both cellular and humoral immunity are believed to be involved in the pathogenesis of GBS, and various types of activated CD4+ T cells are thought to orchestrate the onset and progression of GBS. Lymphoplasma exchange (LPE) filtering out activated lymphocytes while exchanging plasma has been used for GBS treatment for years. However the treatment is still not yet optimal. In order to assess the efficacy of this treatment, we evaluate the effect of LPE and determine the appropriate frequency of LPE treatments for GBS patients through comparing the neurological deficit scores and the changes in related immunology indicators of GBS patients before and after LPE treatment. Twenty-four patients with GBS who received LPE were evaluated for immunologic indicants before treatment, on the second day, and the fourth day after the treatment. The immunoglobulin complement and CD4+ T lymphocyte subsets were tested by flow cytometry. The patients' Medical Research Council sum scores were increased from 25.7±10.4 up to. 36.7±10.4 (P=0.019) and their Hughes scores decreased from 3.7±0.76 to 3.1±0.73 (P=0.027) at 7 days after LPE. In the peripheral blood from patients received LPE treatment, the levels of immunoglobulin, complement, monocytes and fibrinogen were significantly reduced. The percentages of Th1 and Th17 cells in the CD4+ T lymphocyte subsets were significantly decreased, whereas the Th2 and Treg cells were increased in patients after treatment. The changes in CD4+T lymphocyte subsets were correlated with patient MRC score changes. Our data indicate that LPE is effective in treating GBS patients by directly removing immunoglobulin, complement, monocytes, and fibrinogen as well as regulating lymphocyte subsets in the peripheral blood.
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