Design of a secure e-business application

The present economical situation in China asks the enterprises to change the traditional transaction style and implement e-business. The most important problems the e-business is facing are: the information confidentiality, the data availability, the data integrity, the user's identity, the non-repudiation of the data's original sender and the legal user, etc. The subject of this thesis analyzes the basic concepts, the security infrastructure and payment system of electronic commerce, makes a thorough and comprehensive research on the security technology, authentication and transaction process, points out some deficiencies in Secure Electronic Transaction (SET) protocol. Then an improved method is given out with the data flow and data structure, finally a secure electronic commerce payment system and its software based on the improved SET model are designed. This thesis brings forward the improved method for improving the speed of transaction, and strengthening the security of protocol and adapting it to any circumstance easily

Goodness of fit of PTX and DEX synergy model for separate newborn and adult cohorts.

<p>Goodness of fit of PTX and DEX synergy model for separate newborn and adult cohorts.</p

Higher levels of synergistic inhibition of TLR-mediated TNF and IL-1β production in newborn cord blood with combined (PTX+DEX).

<p>Higher levels of synergistic inhibition of TLR-mediated TNF and IL-1β production in newborn cord blood with combined (PTX+DEX).</p

Summary of statistically significant synergistic anti-inflammatory combinations.

<p>Summary of statistically significant synergistic anti-inflammatory combinations.</p

Parameter estimate for PTX and DEX synergy model for separate newborn and adult cohorts.

<p>Parameter estimate for PTX and DEX synergy model for separate newborn and adult cohorts.</p

Timing of anti-inflammatory treatment effects extent of inhibition of LPS-induced inflammatory cytokine production.

<p>Newborn cord and adult peripheral blood were stimulated with 10 ng/ml LPS. Samples were treated with PTX (50 or 200 μM), DEX (10⁻⁸ or 10⁻⁷ M), AZI (2.5 or 20 μM) or vehicle control, which were added either 2 hours before, simultaneously, or 2 hours after TLR stimulation. Following LPS stimulation, samples were cultured for further 6 hours. Supernatant cytokines were expressed as a percentage compared to TLRAs alone, defined as 100%. For delayed treatment samples, cytokine concentrations measured at the start of anti-inflammatory treatment were subtracted from the corresponding delayed treatment samples, in order not to underestimate the delayed treatment effects. Effects of timing and concentration of (a) PTX [Fig 2a adapted from 20, <i>Speer EM</i>, <i>et al</i>. <i>Pediatr Res</i>. <i>2017;81</i>: <i>806–816</i>], (b) DEX, and (c) AZI on LPS-induced cytokine production (mean ± SEM) in newborn and adult blood combined. To determine significant differences between time points (*p<0.05, **p<0.01, and ***p<0.001), linear mixed models were employed to analyze each cytokine and stimulation independently. The covariance structure between anti-inflammatory concentrations within a subject was modeled as unstructured variance, and the covariance structure among time points within the same concentration was modeled as compound symmetry. Significant changes in cytokine production of samples treated with high (light gray columns) or low (dark gray columns) concentrations of anti-inflammatory agents vs. untreated samples (black columns), calculated from log transformed raw pg/ml values, were indicated as #. Linear mixed models were developed to analyze each cytokine and time point independently as described above, with p<0.05 considered significant. N = 5 per age group.</p

PTX, DEX and AZI inhibit LPS-, R848-, and LPS/ATP-induced cytokine production in newborn cord blood.

<p>Human cord blood (n = 10) was pretreated with (a) PTX (50–200 μM), (b) DEX (10⁻¹⁰–10⁻⁷ M), (c) AZI (2.5–20 μM) or vehicle control for 2 hours. Samples were stimulated with 10 ng/ml LPS, 1 μg/ml R848, or LPS followed by 5 mM ATP for inflammasome induction, and cultured for 6 hours at 37°C in 5% CO₂. Supernatant cytokine concentrations were measured, and results expressed as a percentage (mean ± SEM) compared to TLRAs alone, which were defined as 100%. The corresponding mean cytokine concentrations in pg/ml induced by TLRAs alone were represented in brackets next to each cytokine as part of the graph legends.</p

PTX, DEX and AZI demonstrate distinct inhibition of TLR-mediated cytokine mRNA and intracellular protein expression.

<p>Whole blood was pretreated for 2 hours with PTX (200 μM), DEX (10⁻⁷ M), AZI (20 μM) or vehicle control (V), either alone or in combination. Samples were stimulated with 10 ng/ml LPS or 1 μM R848, and cultured for 2 hours (mRNA expression) or 6 hours (flow cytometry) at 37°C in 5% CO₂, in the presence (TNF, IL-6 and IL-10) or absence (IL-1β) of Brefeldin A for flow cytometric assays. MFI of monocytes, gated with forward and side scatter as CD45⁺CD14⁺ cells, was measured as described in <i>Methods</i>. (a) LPS-induced relative mRNA expression (mean ± SEM) in cord and adult blood (n = 5 each, analyzed combined) in response to anti-inflammatory agents compared to LPS-stimulation alone, defined as 100%. Effects of anti-inflammatory treatment on (b) LPS- and (c) R848-induced intracellular cytokines in newborn monocytes (n = 8), plotted as MFI fold changes (± SEM) compared to TLRA stimulation alone (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0196352#pone.0196352.s019" target="_blank">S6 Data file</a> for raw MFI data). Significant differences based on linear mixed models were indicated: *p<0.05, **p<0.01, ***p<0.001.</p

Stimulus-dependent inhibition of cytokine production in newborn blood by PTX, DEX, and AZI.

<p>Stimulus-dependent inhibition of cytokine production in newborn blood by PTX, DEX, and AZI.</p

(PTX+DEX) and (PTX+AZI) synergistically inhibit TLR-mediated pro-inflammatory cytokine production in whole blood assays.

<p>Newborn cord and adult peripheral blood (n = 8 per cohort for (PTX+DEX) and n = 5 per cohort for (PTX+AZI), analyzed combined) was pretreated with vehicle control, PTX (50–100 μM), DEX (10⁻⁸–10⁻⁷ M), AZI (5–20 μM) or combined (PTX+DEX) or (PTX+AZI) for 2 hours. Samples were stimulated with 10 ng/ml LPS or 1 μg/ml R848, and cultured for 6 hours at 37°C in 5% CO₂. Supernatant cytokine concentrations were measured, and results expressed as a percentage (mean ± SEM) compared to TLRAs alone, which were defined as 100% (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0196352#pone.0196352.s021" target="_blank">S8 Data file</a> for absolute cytokine concentrations). Synergistic inhibition of LPS- and R848-induced (a) TNF and (b) IL-1β production employing selected concentrations of (PTX+DEX) and (c) IL-1β production with (PTX+AZI). Significant differences based on paired t-tests between single anti-inflammatory agents and their corresponding combinations of agents at the same concentrations as the individual compounds were indicated: *p<0.05, **p<0.01, ***p<0.001.).</p