The oxidation reaction of the thallium(I) ion to the thallium(III) ion by the peroxodisulfate ion has been studied in an aqueous acidic solution. The reaction constituted a chain reaction initiated by the thermal decomposition of the peroxodisulfate ion, the reaction involving no direct reactions between the thallium(I) and peroxodisulfate ions. At thallium(I) ion concentrations larger than 0.004 mol dm−3, the reaction mechanism was assumed to be: S2O82−\oversetk1→2SO4\ewdot; S2O82−+H+\oversetk2→HSO4−+1/2O2+SO3; Tl(I)+SO4\ewdot\oversetk3→Tl(II)+SO42−; S2O82−+Tl(II)\oversetk4→Tl(III)+SO4\ewdot+SO42−; 2Tl(II)\oversetk5\undersetk−5\ightleftharpoonsTl(I)+Tl(III). The rate of the reaction was described as −d[S2O82−]/dt=(k1+k2[H+])[S2O82−]+k4(k1⁄k5)1⁄2[S2O82−]3⁄2. The rate constants at an ionic strength of 0.16 mol dm−3 were determined to be k1=1.99×1019exp[−157 kJ mol−1/RT]s−1, k2=2.75×1012exp[−103 kJ mol−1/RT] dm3 mol−1 s−1, and k4(k1⁄k5)1⁄2=2.81×1013exp[−108 kJ mol−1/RT] dm3⁄2 mol−1⁄2 s−1 in 0.01 mol dm−3 perchloric acid, the k4 value being increased with a decrease in the hydrogen-ion concentration. The ionic strength (μ) dependence was described as logk4(k1⁄k5)1⁄2=−4.17–1.05 μ1⁄2 in 0.01 mol dm−3 perchloric acid at 40 °C. The reaction rate was completely retarded by the addition of 1% acrlyronitrile, 5×10−6 mol dm−3 cerium(III) sulfate, 1×10−3 mol dm−3 cerium(IV) sulfate, or 0.1 mol dm−3 sodium acetate, and it was also remarkably retarded by the addition of 1×10−3 mol dm−3 tetranitromethane. The copper(II) ion and molecular oxygen did not appreciably affect the reaction rate, but the iron (III) ion accelerated it greatly.

We demonstrated that acylation of TG made it resistant to intestinal proteases and caused it to enhance absorption of drugs, including itself, across Caco-2 monolayers. Further, bacitracin acted as both a protease inhibitor and an absorption enhancer.

Systemic sclerosis (SSc) is a multi‐system autoimmune disease. Anti‐neutrophil cytoplasmic antibodies (ANCA) are autoantibodies directed against enzymes found within primary granules of neutrophils and lysosomes in monocytes. Although up to 12% of SSc patients have ANCA, only a minority of these patients develop an overlap syndrome with ANCA‐associated vasculitis. We summarize previous reports on SSc patients with ANCA‐associated neuropathy. In all the reported cases, the SSc diagnosis preceded the ANCA‐associated neuropathy diagnosis. Seven of the eight patients with limited cutaneous SSc had interstitial lung disease (ILD). Thus, patients with ANCA‐associated neuropathy in lSSc may be prone to complication with ILD.