Nodes immunization effects on the prevention and control of rumors-spread.

<p>A) Changes in the density of R1 stiflers over time (<i>t</i>) as a function of the immunization rate <i>p</i>. B) Changes in the density of R2 stiflers over time (<i>t</i>) as a function of the immunization rate <i>p</i>. C) Changes in the final value of the R1 and R2 stiflers, and the final size of the rumor (<i>R</i>) as a function of the proportion of the population that is immunized <i>p</i>. The values of the model parameters are <i>λ</i> = 0.45, <i>β</i> = 0.02, <i>γ</i> = 0.53, <i>α</i> = 0.45, <i>θ</i> = 0.50, <i>δ</i> = 0.35, and <math><mrow><mi>k</mi><mo>¯</mo><mo>=</mo><mn>10</mn></mrow></math>.</p

Densities of the four groups in the rumor model over time(<i>t</i>).

<p>The parameters are <i>λ</i> = 0.85, <i>β</i> = 0.03, <i>γ</i> = 0.12, <i>α</i> = <i>θ</i> = 0.25, <i>δ</i> = 0.35, and <math><mrow><mi>k</mi><mo>¯</mo><mo>=</mo><mn>10</mn></mrow></math>.</p

The role of miR-1 in the regulation of phagocytosis in mammalian macrophages.

<p>(A) Expression levels of miR-1 and phagocytic activities in the isolated murine macrophage, the immortalized macrophage ANA-1 and the cancerous macrophage RAW264.7. The expression of miR-1 was quantified with real-time PCR (left). The phagocytic activity was evaluated using FITC-labeled <i>E. coli</i> (right). The data referred to the means ± standard deviations of triplicate assays. (B) Overexpression of miR-1 in RAW264.7 and ANA-1 cells. Cells were transfected with miR-1 precursor or control miRNA. At 24 h after transfection, the total RNAs were isolated from transfected cells and subjected to Northern blot. The expression level of miR-1 was normalized with U6. (C) Evaluation of phagocytic activities in RAW264.7 and ANA-1 cells against FITC-labeled <i>E. coli</i> by flow cytometry. Cells transfected with miR-1 precursor or control miRNA were challenged with FITC-labeled <i>E. coli</i>, followed by phagocytosis assays. (D) Knockdown of miR-1 in RAW264.7 and ANA-1 cells. The cells were transfected with AMO-miR-1 or AMO-miR-1-scrambled. Twenty four hours later, the total RNAs were isolated from transfected cells. The expression of miR-1 was determined by quantitative real-time PCR. (E) Phagocytosis percentages of RAW264.7 and ANA-1 cells treated with AMO-miR-1 or AMO-miR-1 -scrambled. At 24 h after transfection of AMOs, the phagocytosis was evaluated using FITC-labeled <i>E. coli</i>. In all panels, plotted data points referred to the means ± standard deviations of triplicate assays and asterisks represented statistically significant differences (**, <i>p</i><0.01; *, <i>p</i><0.05).</p

Immunization against the Spread of Rumors in Homogenous Networks

<div><p>Since most rumors are harmful, how to control the spread of such rumors is important. In this paper, we studied the process of "immunization" against rumors by modeling the process of rumor spreading and changing the termination mechanism for the spread of rumors to make the model more realistic. We derived mean-field equations to describe the dynamics of the rumor spread. By carrying out steady-state analysis, we derived the spreading threshold value that must be exceeded for the rumor to spread. We further discuss a possible strategy for immunization against rumors and obtain an immunization threshold value that represents the minimum level required to stop the rumor from spreading. Numerical simulations revealed that the average degree of the network and parameters of transformation probability significantly influence the spread of rumors. More importantly, the simulations revealed that immunizing a higher proportion of individuals is not necessarily better because of the waste of resources and the generation of unnecessary information. So the optimal immunization rate should be the immunization threshold.</p></div

The mechanism of phagocytosis regulation mediated by miR-1.

<p>(A) miR-1 targets analysis. Clathrin heavy chain 1 gene (<i>CLTC1</i>) was a predicted target gene of miR-1. (B) The interaction between miR-1 and <i>CLTC1</i> gene. RAW264.7 cells were simultaneously transfected with miR-1 or control (plasmid only) and the <i>CLTC1</i> gene 3′ UTR, followed by a dual luciferase reporter assay. The <i>CLTC1</i> gene 3′ UTR mutant was included in the assays. (C) Downregulation of endogenous <i>CLTC1</i> gene by miR-1 in RAW264.7 cells. The miR-1 precursor and the negative control were transfected into RAW264.7 cells, respectively. Subsequently the <i>CLTC1</i> mRNA was detected using real-time quantitative PCR (left) and the <i>CLTC1</i> protein was examined with Western blot (right). In real-time PCR, the expression level of <i>CLTC1</i> gene was normalized to that of glyceraldehyde-3-phosphate dehydrogenase gene. In Western blot, the antibodies used were indicated on the right. (D) The role of <i>CLTC1</i> in phagocytosis of macrophages. RAW264.7. Cells were transfected with <i>CLTC1</i>-siRNA to silence the expression of <i>CLTC1</i>. <i>CLTC1</i>-siRNA-scrambled was used as a control. At 48 h after transfection, the expression of <i>CLTC1</i> was detected with quantitative real-time PCR (left). At the same time, the phagocytosis percentages of RAW264.7 cells were evaluated using flow cytometry (right). (E) Model for miR-1-mediated pathway in phagocytosis. In all panels, the data referred to the means ± standard deviation of triplicate assays. Statistically significant differences between treatments were indicated with asterisk (*, <i>p</i><0.05).</p

The relationship between the spread threshold (<i>λ</i>_<i>c</i>) and the immunization threshold (<i>p</i>_<i>c</i>).

<p>The parameters are <i>λ</i> = 0.85, <i>θ</i> = 0.45, <i>α</i> = 0.25.</p

Shape of the function <i>g</i>(<i>R</i>).

<p>The parameters are <math><mrow><mi>β</mi><mo>=</mo><mn>0</mn><mo>.</mo><mn>03</mn><mo>,</mo><mi>γ</mi><mo>=</mo><mn>0</mn><mo>.</mo><mn>15</mn><mo>,</mo><mi>θ</mi><mo>=</mo><mn>0</mn><mo>.</mo><mn>45</mn><mo>,</mo><mi>α</mi><mo>=</mo><mn>0</mn><mo>.</mo><mn>25</mn><mo>,</mo><mi>δ</mi><mo>=</mo><mn>0</mn><mo>.</mo><mn>35</mn><mo>,</mo><mi>k</mi><mo>¯</mo><mo>=</mo><mn>10</mn><mo>,</mo></mrow></math> and <i>p</i> = 0.2.</p

Shape of the function <i>f</i>(<i>R</i>).

<p>The parameters are <i>β</i> = 0.03, <i>γ</i> = 0.15, <i>θ</i> = 0.45, <i>α</i> = 0.25, <i>δ</i> = 0.35, and <math><mrow><mi>k</mi><mo>¯</mo><mo>=</mo><mn>10</mn></mrow></math>.</p

The regulation of phagocytosis mediated by miR-1 in shrimp.

<p>(A) Nucleotide sequences and modifications of the anti-miRNA-1 oligonucleotide (AMO-miR-1) and AMO-miR-1-scrambled. (B) Silencing of miR-1 expression in shrimp hemocytes <i>in vivo</i>. The miR-1-specific AMO (AMO-miR-1) and the negative control AMO-miR-1-scrambled were injected into shrimp, respectively. The shrimp hemocytes were subjected to Northern blot using miR-1 or U6 probe. (C) The effect of miR-1 expression silencing on phagocytic activity of shrimp hemocytes. The phagocytic activity of FITC-labeled WSSV was evaluated with flow cytometry. The plotted data points referred to the means ± standard deviations of triplicate assays and the asterisk represented statistically significant differences (*, <i>p</i><0.05). (D) The interaction between miR-1 and <i>CLTC1</i> gene. The miR-1 precursor and the plasmid EGFP-<i>CLTC1</i> or EGFP-<i>CLTC1</i>-mutant or EGFP were cotransfected into insect High Five cells. Then the fluorescence intensity of cells was monitored with a fluorescence microscope. The columns represented the means ± standard deviations of triplicate assays. The significant differences between treatments were indicated with asterisks (**, <i>p</i><0.01). (E) The effect of <i>CLTC1</i> on phagocytosis of shrimp hemocytes. The shrimp were injected with <i>CLTC1</i>-siRNA or <i>CLTC1</i>-siRNA- scrambled as a control. Then the shrimp were subjected to Northern blots (left) and phagocytosis assays (right). In Northern blots, the shrimp β-actin was used as a control. The significant differences between treatments were indicated with asterisk (*, <i>p</i><0.05). (F) Sequence alignment of miR-1 from six typical species. * indicated the identical nucleotides.</p