A detailed analysis is presented of the diffractive deep-inelastic scattering process ep → eXY , where Y is a proton or a low mass proton excitation carrying a fraction 1−x I P > 0.95 of the incident proton longitudinal momentum and the squared four-momentum transfer at the proton vertex satisfies |t| < 1 GeV 2 . Using data taken by the H1 experiment, the cross section is measured for photon virtualities in the range 3.5 ≤ Q 2 ≤ 1600 GeV 2 , triple differentially in x I P , Q 2 and β = x/x I P , where x is the Bjorken scaling variable. At low x I P , the data are consistent with a factorisable x I P dependence, which can be described by the exchange of an effective pomeron trajectory with intercept α IP (0) = 1.118 ± 0.008 (exp.) +0.029 −0.010 (model). Diffractive parton distribution functions and their uncertainties are determined from a next-to-leading order DGLAP QCD analysis of the Q 2 and β dependences of the cross section. The resulting gluon distribution carries an integrated fraction of around 70% of the exchanged momentum in the Q 2 range studied. Total and differential cross sections are also measured for the diffractive charged current process e + p →ν e XY and are found to be well described by predictions based on the diffractive parton distributions. The ratio of the diffractive to the inclusive neutral current ep cross sections is studied. Over most of the kinematic range, this ratio shows no significant dependence on Q 2 at fixed x I P and x or on x at fixed Q 2 and β.
A major limitation associated with systemic administration of cationic lipid:plasmid DNA (pDNA) complexes is the vector toxicity at the doses necessary to produce therapeutically relevant levels of transgene expression. Systematic evaluation of these toxicities has revealed that mice injected intravenously with cationic lipid:pDNA complexes develop significant, dose-dependent hematologic and serologic changes typified by profound leukopenia, thrombocytopenia, and elevated levels of serum transaminases indicative of hepatocellular necrosis. Vector administration also induced a potent inflammatory response characterized by complement activation and the induction of the cytokines IFN-gamma, TNF-alpha, IL-6, and IL-12. These toxicities were found to be transient, resolving with different kinetics to pretreatment levels by 14 days posttreatment. The toxic syndrome observed was independent of the cationic lipid:pDNA ratio, the cationic lipid species, and the level of transgene expression attained. Mechanistic studies determined that neither the complement cascade nor TNF-alpha were key mediators in the development of these characteristic toxicities. Administration of equivalent doses of the individual vector components revealed that cationic liposomes or pDNA alone did not generate the toxic responses observed with cationic lipid:pDNA complexes. Only moderate leukopenia was associated with administration of cationic liposomes or pDNA alone, while only mild thrombocytopenia was noted in pDNA-treated animals. These results establish a panel of objective parameters that can be used to quantify the acute toxicities resulting from systemic administration of cationic lipid:pDNA complexes, which in turn provides a means to compare the therapeutic indices of these vectors.
The cross section for the diffractive deep-inelastic scattering process ep → eXp is measured, with the leading final state proton detected in the H1 Forward Proton Spectrometer. The data analysed cover the range x IP < 0.1 in fractional proton longitudinal momentum loss, 0.08 < |t| < 0.5 GeV −2 in squared four-momentum transfer at the proton vertex, 2 < Q 2 < 50 GeV 2 in photon virtuality and 0.004 < β = x/x IP < 1, where x is the Bjorken scaling variable. For x IP < ∼ 10 −2 , the differential cross section has a dependence of approximately dσ/dt ∝ e 6t , independently of x IP , β and Q 2 within uncertainties. The cross section is also measured triple differentially in x IP , β and Q 2 . The x IP dependence is interpreted in terms of an effective pomeron trajectory with intercept α IP (0) = 1.114±0.018 (stat.)±0.012 (syst.) +0.040 −0.020 (model) and a sub-leading exchange. The data are in good agreement with an H1 measurement for which the event selection is based on a large gap in the rapidity distribution of the final state hadrons, after accounting for proton dissociation contributions in the latter. Within uncertainties, the dependence of the cross section on x and Q 2 can thus be factorised from the dependences on all studied variables which characterise the proton vertex, for both the pomeron and the sub-leading exchange.
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