21 research outputs found

    Case Study of Selected Network Vulnerabilities

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    The main goal of this thesis is to deal with databases of vulnerable code bases and vulnerable applications, and to implement a tool for autonomous search and saving data from those databases to a local one. The thesis is divided into theoretical and practical parts. The theoretical part deals with my current knowledge of the main topic and creates a foundation for the implementation. Various kinds of vulnerabilities and network attacks are described in detail in this part. The practical part describes implementation of the tool and its real use

    Diabetes alters release of vascular reparative cells into circulation.

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    <p>(A) CACs as a percentage of total bone marrow cells, *** p<0.001 (B) CACs as a percentage of total splenocytes. (C) CACs as a percentage of total blood cells. CACs are gated as Lin<sup>-</sup> CD34<sup>+</sup> CD309<sup>+</sup> cells. Representative flow charts of GFP<sup>+</sup> CACs in control and diabetic BM, spleen and blood are shown below. * p<0.05, N = 4–8.</p

    Diabetes reduces number of BM-derived endothelial cells in retina.

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    <p>GFP<sup>+</sup> endothelial cells (gated as CD45<sup>-</sup> Tie-2<sup>+</sup> CD31<sup>+</sup> cells) are expressed as a percentage of total GFP<sup>+</sup> retinal cells, and indicate a significant decrease in BM-derived endothelial cells in diabetic mice. Representative flow charts of GFP<sup>+</sup> endothelial cells in the retina are shown. N = 4–5.</p

    Diabetes alters BM-derived microglia in retina.

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    <p>(A) Percentage of BM-derived microglia per mm<sup>2</sup> area of control or diabetic retina. N = 7–8. (B) GFP<sup>+</sup> microglia (gated as GFP<sup>+</sup> cells that are Thy1<sup>-</sup>, Ly6G<sup>-</sup>, Ly6C<sup>-</sup>, CD45<sup>dim</sup> CD11b<sup>+</sup> cells) are expressed as a percentage of total GFP<sup>+</sup> retinal cells in control and diabetic retina of chimeric mice, and indicate increase in BM-derived microglia in diabetic mice. Representative flow charts of GFP<sup>+</sup> microglia in the retina are shown. N = 3–5, ** p< 0.01. (C) Confocal images of retina isolated from control or diabetic GFP<sup>+</sup> BM-transplanted mice. Microglial marker Iba-1<sup>+</sup> staining (red) with GFP<sup>+</sup> (green) cells, showing colocalization (yellow) in retina. Increased retraction of processes observed in BM-derived microglia in diabetic GFP<sup>+</sup> chimeric mouse retina compared to ramified, resting phenotype of microglia in control retinas (white arrowheads). Scale bars are 50 μm. (D) Quantification of dendrite length of microglia in diabetic and control chimeric mouse retinas is shown. N = 4–5, *** p< 0.001.</p

    Diabetes alters response of BM-derived cells and splenocytes to LPS stimulation.

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    <p>Increased secretion of cytokines IL-1β and TNF-α in (A) BM-derived dendritic cell-enriched population (B) splenocytes stimulated with LPS. N = 4–5, * p< 0.05.</p

    Diabetes alters homing efficiency of CACs.

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    <p>(A) Scheme for testing homing efficiency of diabetic CACs to the BM. Male C57BL/6-Tg(CAG-EGFP) mice were made diabetic by STZ injections. After 8 months of diabetes, 10,000 CACs were isolated from BM of diabetic and control GFP<sup>+</sup> mice, and injected into the vitreous of healthy mice. Seven days post injection the BM and retinas were collected and analyzed by flow cytometry and confocal microscopy for presence of GFP<sup>+</sup> CACs. (B) Control or diabetic GFP<sup>+</sup> CACs (green) injected into the vitreous of mice with healthy retinal vasculature stained red using anti-collagen IV antibody. Quantitation of area of green CACs observed in confocal retinal images is shown. Scale bars are 50 μm, N = 10–12. (C) Quantification of GFP<sup>+</sup> cells from bone marrow of tibia and femurs of recipient mice shows homing of diabetic GFP<sup>+</sup> CACs to the recipient bone marrow was significantly lower compared to control GFP<sup>+</sup> CACs. N = 4–6. (D) Diabetes significantly alters expression of integrins β2 and β3 on diabetic CACs in blood. N = 3, * p< 0.05, ** p<0.01.</p

    BM-derived cells in the retina of chimeric mice.

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    <p>(A) Number of BM-derived cells per mm<sup>2</sup> area of control or diabetic retina. Representative flow charts of GFP<sup>+</sup> cells in the retina shown below. (B) ~ 93% of GFP<sup>+</sup> cells detected in the retina are CD45<sup>-</sup> cells. Diabetes does not change the number of CD45<sup>-</sup> cells in the retina. Representative flow charts gated on GFP<sup>+</sup> cells of CD45<sup>-</sup> and CD45<sup>+</sup> cells shown below. N = 4.</p

    Activation of STAT1 in NK cells requires the direct action of type I IFNs during influenza infection.

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    <p>NK cells from infected (open histograms) and uninfected (shaded histograms) mice were analyzed for intracellular pSTAT1 following adoptive transfer (A) or co-culture (B). Adoptive transfer was as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0051858#pone-0051858-g002" target="_blank">Figure 2</a>. For in vitro infection, CD45.2<b><sup>+</sup></b> splenocytes from IFNAR<b><sup>+/−</sup></b> or IFNAR<b><sup>−/−</sup></b> mice were combined with CD45.1<b><sup>+</sup></b> B6 splenocytes at 1∶1 ratio, then infected with flu. NK cells (NK1.1<b><sup>+</sup></b>CD3<b><sup>−</sup></b>) from infected (open histograms) and uninfected (shaded histograms) samples were analyzed for intracellular pSTAT1. Values represent the percentages of pSTAT1<b><sup>+</sup></b> NK cells. Data are representative of three independent experiments with 2–4 (A) or 1–3 (B) mice per group.</p

    Type I IFNs are required for NK cell activation in response to flu infection.

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    <p>Following i.v. infection with flu, splenic NK cells (NK1.1<b><sup>+</sup></b>CD3<b><sup>−</sup></b>CD19<b><sup>−</sup></b>) from B6 WT, IFNAR<b><sup>−/−</sup></b>, IL-12R<b><sup>−/−</sup></b> and IL-18R<b><sup>−/−</sup></b> mice were analyzed at 9h post-infection. (A) IFN-γ and granzyme B expression are shown. Mouse genotypes are indicated above the dot plots or histograms. Inset values represent the percentages of IFN-γ<b><sup>+</sup></b> (upper panels) or granzyme B<b><sup>+</sup></b> (lower panels) NK cells. (B) CD69 expression levels on NK cells from uninfected and infected mice are shown. Percentages of NK cells located within the CD69<b><sup>+</sup></b>gate are indicated. (C) CD107a expression and IFN-γ production were analyzed in NK cells after incubation with YAC-1 cells. Percentages of NK cells within each quadrant are indicated. Data are representative of at least three mice per group.</p

    Activation of STAT4 is partially dependent on the direct action of type I IFNs during influenza infection.

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    <p>NK cells from infected (open histograms) and uninfected (shaded histograms) mice were analyzed for intracellular pSTAT4 following adoptive transfer (A) or co-culture (B). Adoptive transfer was as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0051858#pone-0051858-g002" target="_blank">Figure 2</a>. For in vitro infection, CD45.2<b><sup>+</sup></b> splenocytes from IFNAR<b><sup>+/−</sup></b> or IFNAR<b><sup>−/−</sup></b> mice were combined with CD45.1<b><sup>+</sup></b> B6 splenocytes at 1∶1 ratio, then infected with flu. NK cells (NK1.1<b><sup>+</sup></b>CD3<b><sup>−</sup></b>) from infected (open histograms) and uninfected (shaded histograms) samples were analyzed for intracellular pSTAT4. Values represent the percentages of pSTAT4<b><sup>+</sup></b> NK cells. Data are representative of three independent experiments with 2–4 (A) or 1–3 (B) mice per group.</p
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