Možnosti využití technického automobilu TA-4 v podmínkách HZS okresu Sokolov

Import 20/04/2006Prezenční výpůjčkaVŠB - Technická univerzita Ostrava. Fakulta hornicko-geologická. Institut bezpečnostního inženýrství (547

Additional file 4: of Intrabodies against the Polysialyltransferases ST8SiaII and ST8SiaIV inhibit Polysialylation of NCAM in rhabdomyosarcoma tumor cells

Luminescence picture after injection of tumor cells expressing anti-ST8SiaII-IB and anti-ST8SiaIV-IB in mice (week 4). Luminescence was determined at week 4 using in vivo imaging system. On the ride side are seen the luminescence signals (p/Sec/cm2/sr). (TIF 286 kb

Influenza A virus infection predisposes for invasive disease through <i>Streptococcus pneumoniae</i>.

<p>(A) C57Bl/6 mice were intranasally inoculated with medium, 0.04 MLD₅₀ Influenza A virus (IAV) PR8/A/34 or 1×10⁵ CFU <i>Streptococcus pneumoniae</i> TIGR4 (T4) and weighed daily. Body weight is shown as % relative to the starting weight. (B) <i>S. pneumoniae</i> CFU counts in tracheal lavage of survivors seven days after i.n. infection. (C) Survival rates of C57Bl/6 mice after i.n. infection with IAV PR8/A/34 alone (day 0), <i>S. pneumoniae</i> T4 alone (day 7) or <i>S. pneumoniae</i> T4 (day 7) following IAV (day 0). (D) CFU counts in lung homogenates of <i>S. pneumoniae</i> only infected and Influenza A virus pre-infected C57Bl/6 mice in which infection was lethal. All data shown are compiled from at least two independent experiments with groups of 5 or more mice. No bacteria could be detected in the lungs of mice surviving the infections (not shown).</p

Systemic TLR7 triggering leads to transient peripheral blood lymphopenia but does not cause increased susceptibility for lethal <i>Streptococcus pneumoniae</i> infection in C57Bl/6 mice.

<p>(A) Mice were injected with PBS or R-848 intraperitoneally and bled from the tail vein immediately before, 1, 24 and 48 h after treatment. Samples were analysed for B220-, CD4- and CD8-positive cells by flow cytometry. Cell numbers are expressed as relative % compared to pre-treatment levels. Data show means±s.e.m. compiled from three independent experiments. (B) Likewise, lung tissue of R-848- or PBS-treated animals was analysed for the content of CD4⁺, CD8⁺ and CD19⁺ cells 1 h after treatment. Data show means±s.e.m. compiled from five individual animals. Additionally, different groups of mice were intranasally inoculated with 1×10⁵ CFU <i>Streptococcus pneumoniae</i> TIGR4 (T4) together with (C) or 12 hours before (D) intraperitoneal R-848 injection and survival was assessed. The lymphopenia in these mice was also verified (not shown). Data show compiled results of two independent experiments performed with five mice per group (*** p<0.001, * p<0.05).</p

Influenza A virus infection renders mice unable to control <i>Streptococcus pneumoniae</i> growth in the upper and lower respiratory tract.

<p>C57Bl/6 mice were inoculated with medium (•) or 0.04 MLD₅₀ Influenza A virus (IAV) PR8/A/34 (○) seven days before infection with 1×10⁵ CFU <i>Streptococcus pneumoniae</i> TIGR4 (T4). Mice were sacrificed 4 and 24 hours after bacterial infection and <i>S. pneumoniae</i> CFU counts in nasopharyngeal lavage (A), bronchoalveolar lavage (B) and lung homogenates (C) were assessed. Data show values of individual mice together with group means (horizontal lines) and are compiled from two independent experiments.</p

Forced lymphopenia does not interfere with bacterial clearance in <i>S. pneumoniae</i> infected hosts.

<p>C57Bl/6 mice were intranasally infected with 1×10⁵ CFU <i>Streptococcus pneumoniae</i> TIGR4 and at the same time intraperitoneally injected with PBS (•) or R-848 (○). Mice were sacrificed 4 and 24 hours later and <i>S. pneumoniae</i> CFU counts in nasopharyngeal lavage (A), bronchoalveolar lavage (B) and lung homogenates (C) were assessed. Data show values of individual mice together with group means (horizontal lines) and are compiled from two independent experiments.</p

Antibody mediated depletion of PMN does not interfere with bacterial clearance in <i>S. pneumoniae</i> infected hosts.

<p>C57Bl/6 mice were intraperitoneally injected with rat IgG (•) as control or RB6-8C5 antibody (○) to deplete PMN. To confirm depletion of PMN, mouse peripheral blood samples were FACS analysed for Gr-1 positive cells on days 1, 2, 5, 6 and 7 post RB6-8C5 antibody treatment. Data show the percentage of Gr-1_high cells out of the respective total granulocyte population for one representative out of two analysed animals per group (A). Likewise, numbers of Gr-1_high/CD11b⁺ cells (neutrophils) in lung tissue or BAL fluid were analysed by flow cytometry 24 h post antibody treatment (B). On the day following antibody treatment, mice were intranasally infected with 1×10⁵ CFU <i>Streptococcus pneumoniae</i> TIGR4 and sacrificed 24 hours after infection to assess <i>S. pneumoniae</i> CFU counts in nasopharyngeal lavage, bronchoalveolar lavage and lung homogenates (C). Additional groups of mice were treated equally to assess CFU counts in nasopharyngeal lavage seven days following infection (C) and survival rates (D). CFU counts show values of individual mice together with group means (horizontal lines). Data are compiled from two independent experiments with groups of at least 5 mice. For lung and BAL fluid neutrophil numbers, data from 5 mice/group are shown (+/−s.e.m.).</p

Additional file 1: Figure S1. of Type I Interferon response in olfactory bulb, the site of tick-borne flavivirus accumulation, is primarily regulated by IPS-1

IPS-1 −/− mice have lower IFN-α levels in serum after LGTV infection compared to WT mice. WT and IPS-1 −/− mice were infected intraperitoneally with 104 FFU of LGTV, and serum samples were collected at indicated time points (n = 5–10). The amount of IFN-α in the mouse serum was determined by enzyme linked immunosorbent assay (ELISA) according to the manufacturer’s instructions (PBL). Significance was calculated with student’s T test, *p < 0.05. (PDF 53.6 KB

Additional file 2: Figure S2. of Type I Interferon response in olfactory bulb, the site of tick-borne flavivirus accumulation, is primarily regulated by IPS-1

Effect of IPS-1 signaling on BBB permeability upon LGTV infection. WT and IPS-1 −/− mice were mock or intraperitoneally infected with 104 FFU of LGTV (n = 3). Mice were intravenously injected with 100 μl 2 % Evans blue (Sigma) in PBS 4 and 7 dpi. After 1 h, animals were transcardially perfused with 20 ml PBS and the brains were removed. The brains were weighted and homogenized in 50 % TCA, and absorbance was measured at 610 nm. The absorbance was divided by the weight of the sample and normalized to mock infected samples. (PDF 42.5 KB

Additional file 5: Figure S4. of Type I Interferon response in olfactory bulb, the site of tick-borne flavivirus accumulation, is primarily regulated by IPS-1

Enhanced viral replication in olfactory bulb of IPS-1 −/− mice 4 dpi. WT and IPS-1 deficient mice were infected intraperitoneal with LGTV and olfactory bulb, cerebrum, cerebellum and brain stem was collected 4 dpi. LGTV RNA levels were quantified with the NS3 real-time qPCR assay (detection limit 10 copies). Asterisks indicates statistical significance between IPS-1 −/− olfactory bulb compared to other brain regions and calculated by Mann-Whitney test. Number sign indicates not detectable. (PDF 45.6 KB