20 research outputs found

    Data_Sheet_1_Herd Immunity to Ebolaviruses Is Not a Realistic Target for Current Vaccination Strategies.xlsx

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    <p>The recent West African Ebola virus pandemic, which affected >28,000 individuals increased interest in anti-Ebolavirus vaccination programs. Here, we systematically analyzed the requirements for a prophylactic vaccination program based on the basic reproductive number (R<sub>0</sub>, i.e., the number of secondary cases that result from an individual infection). Published R<sub>0</sub> values were determined by systematic literature research and ranged from 0.37 to 20. R<sub>0</sub>s β‰₯ 4 realistically reflected the critical early outbreak phases and superspreading events. Based on the R<sub>0</sub>, the herd immunity threshold (I<sub>c</sub>) was calculated using the equation I<sub>c</sub> = 1β€‰βˆ’β€‰(1/R<sub>0</sub>). The critical vaccination coverage (V<sub>c</sub>) needed to provide herd immunity was determined by including the vaccine effectiveness (E) using the equation V<sub>c</sub> = I<sub>c</sub>/E. At an R<sub>0</sub> of 4, the I<sub>c</sub> is 75% and at an E of 90%, more than 80% of a population need to be vaccinated to establish herd immunity. Such vaccination rates are currently unrealistic because of resistance against vaccinations, financial/logistical challenges, and a lack of vaccines that provide long-term protection against all human-pathogenic Ebolaviruses. Hence, outbreak management will for the foreseeable future depend on surveillance and case isolation. Clinical vaccine candidates are only available for Ebola viruses. Their use will need to be focused on health-care workers, potentially in combination with ring vaccination approaches.</p

    Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment-2

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    <p><b>Copyright information:</b></p><p>Taken from "Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment"</p><p>http://www.biomedcentral.com/1472-6750/8/3</p><p>BMC Biotechnology 2008;8():3-3.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2254390.</p><p></p>in NPD and the other in DI medium and both were kept in standard culture conditions. After a week of growth the supernatants were collected, and the antibody concentrations were measured by a standard sandwich ELISA. Each column represents the mean antibody concentration that was measured in NPD and DI cultures. The error bars denote the standard error of the means. We have observed increased secretion of monoclonal antibody with a series of stable hybridoma clones and presented a detailed analysis with one of them in this manuscript. Panel A: Total antibody concentration measured in the culture supernatants; Panel B: Antibody concentration normalized per cell

    Data_Sheet_2_Herd Immunity to Ebolaviruses Is Not a Realistic Target for Current Vaccination Strategies.PDF

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    <p>The recent West African Ebola virus pandemic, which affected >28,000 individuals increased interest in anti-Ebolavirus vaccination programs. Here, we systematically analyzed the requirements for a prophylactic vaccination program based on the basic reproductive number (R<sub>0</sub>, i.e., the number of secondary cases that result from an individual infection). Published R<sub>0</sub> values were determined by systematic literature research and ranged from 0.37 to 20. R<sub>0</sub>s β‰₯ 4 realistically reflected the critical early outbreak phases and superspreading events. Based on the R<sub>0</sub>, the herd immunity threshold (I<sub>c</sub>) was calculated using the equation I<sub>c</sub> = 1β€‰βˆ’β€‰(1/R<sub>0</sub>). The critical vaccination coverage (V<sub>c</sub>) needed to provide herd immunity was determined by including the vaccine effectiveness (E) using the equation V<sub>c</sub> = I<sub>c</sub>/E. At an R<sub>0</sub> of 4, the I<sub>c</sub> is 75% and at an E of 90%, more than 80% of a population need to be vaccinated to establish herd immunity. Such vaccination rates are currently unrealistic because of resistance against vaccinations, financial/logistical challenges, and a lack of vaccines that provide long-term protection against all human-pathogenic Ebolaviruses. Hence, outbreak management will for the foreseeable future depend on surveillance and case isolation. Clinical vaccine candidates are only available for Ebola viruses. Their use will need to be focused on health-care workers, potentially in combination with ring vaccination approaches.</p

    Data_Sheet_4_Herd Immunity to Ebolaviruses Is Not a Realistic Target for Current Vaccination Strategies.PDF

    No full text
    <p>The recent West African Ebola virus pandemic, which affected >28,000 individuals increased interest in anti-Ebolavirus vaccination programs. Here, we systematically analyzed the requirements for a prophylactic vaccination program based on the basic reproductive number (R<sub>0</sub>, i.e., the number of secondary cases that result from an individual infection). Published R<sub>0</sub> values were determined by systematic literature research and ranged from 0.37 to 20. R<sub>0</sub>s β‰₯ 4 realistically reflected the critical early outbreak phases and superspreading events. Based on the R<sub>0</sub>, the herd immunity threshold (I<sub>c</sub>) was calculated using the equation I<sub>c</sub> = 1β€‰βˆ’β€‰(1/R<sub>0</sub>). The critical vaccination coverage (V<sub>c</sub>) needed to provide herd immunity was determined by including the vaccine effectiveness (E) using the equation V<sub>c</sub> = I<sub>c</sub>/E. At an R<sub>0</sub> of 4, the I<sub>c</sub> is 75% and at an E of 90%, more than 80% of a population need to be vaccinated to establish herd immunity. Such vaccination rates are currently unrealistic because of resistance against vaccinations, financial/logistical challenges, and a lack of vaccines that provide long-term protection against all human-pathogenic Ebolaviruses. Hence, outbreak management will for the foreseeable future depend on surveillance and case isolation. Clinical vaccine candidates are only available for Ebola viruses. Their use will need to be focused on health-care workers, potentially in combination with ring vaccination approaches.</p

    Data_Sheet_3_Herd Immunity to Ebolaviruses Is Not a Realistic Target for Current Vaccination Strategies.PDF

    No full text
    <p>The recent West African Ebola virus pandemic, which affected >28,000 individuals increased interest in anti-Ebolavirus vaccination programs. Here, we systematically analyzed the requirements for a prophylactic vaccination program based on the basic reproductive number (R<sub>0</sub>, i.e., the number of secondary cases that result from an individual infection). Published R<sub>0</sub> values were determined by systematic literature research and ranged from 0.37 to 20. R<sub>0</sub>s β‰₯ 4 realistically reflected the critical early outbreak phases and superspreading events. Based on the R<sub>0</sub>, the herd immunity threshold (I<sub>c</sub>) was calculated using the equation I<sub>c</sub> = 1β€‰βˆ’β€‰(1/R<sub>0</sub>). The critical vaccination coverage (V<sub>c</sub>) needed to provide herd immunity was determined by including the vaccine effectiveness (E) using the equation V<sub>c</sub> = I<sub>c</sub>/E. At an R<sub>0</sub> of 4, the I<sub>c</sub> is 75% and at an E of 90%, more than 80% of a population need to be vaccinated to establish herd immunity. Such vaccination rates are currently unrealistic because of resistance against vaccinations, financial/logistical challenges, and a lack of vaccines that provide long-term protection against all human-pathogenic Ebolaviruses. Hence, outbreak management will for the foreseeable future depend on surveillance and case isolation. Clinical vaccine candidates are only available for Ebola viruses. Their use will need to be focused on health-care workers, potentially in combination with ring vaccination approaches.</p

    Data_Sheet_5_Herd Immunity to Ebolaviruses Is Not a Realistic Target for Current Vaccination Strategies.PDF

    No full text
    <p>The recent West African Ebola virus pandemic, which affected >28,000 individuals increased interest in anti-Ebolavirus vaccination programs. Here, we systematically analyzed the requirements for a prophylactic vaccination program based on the basic reproductive number (R<sub>0</sub>, i.e., the number of secondary cases that result from an individual infection). Published R<sub>0</sub> values were determined by systematic literature research and ranged from 0.37 to 20. R<sub>0</sub>s β‰₯ 4 realistically reflected the critical early outbreak phases and superspreading events. Based on the R<sub>0</sub>, the herd immunity threshold (I<sub>c</sub>) was calculated using the equation I<sub>c</sub> = 1β€‰βˆ’β€‰(1/R<sub>0</sub>). The critical vaccination coverage (V<sub>c</sub>) needed to provide herd immunity was determined by including the vaccine effectiveness (E) using the equation V<sub>c</sub> = I<sub>c</sub>/E. At an R<sub>0</sub> of 4, the I<sub>c</sub> is 75% and at an E of 90%, more than 80% of a population need to be vaccinated to establish herd immunity. Such vaccination rates are currently unrealistic because of resistance against vaccinations, financial/logistical challenges, and a lack of vaccines that provide long-term protection against all human-pathogenic Ebolaviruses. Hence, outbreak management will for the foreseeable future depend on surveillance and case isolation. Clinical vaccine candidates are only available for Ebola viruses. Their use will need to be focused on health-care workers, potentially in combination with ring vaccination approaches.</p

    Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment-4

    No full text
    <p><b>Copyright information:</b></p><p>Taken from "Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment"</p><p>http://www.biomedcentral.com/1472-6750/8/3</p><p>BMC Biotechnology 2008;8():3-3.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2254390.</p><p></p>m powder forms with either NPD or DI water. For each fusion, PBMC from a single batch were divided into two equal fractures and used to prepare two parallel experiments, in NPD or DI based reagents. The figure presents percent of hybridoma-positive wells in each fusion experiment. The percent was calculated as the number of hybridoma-positive wells from 96-well plates where the cells were seeded and grown after the fusion process. The difference between the NPD- and DI-fusion results was found to be statistically significant by Chi-square analysis (

    Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment-3

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    <p><b>Copyright information:</b></p><p>Taken from "Enhancement of hybridoma formation, clonability and cell proliferation in a nanoparticle-doped aqueous environment"</p><p>http://www.biomedcentral.com/1472-6750/8/3</p><p>BMC Biotechnology 2008;8():3-3.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2254390.</p><p></p>ased medium supplemented with 3% FCS. Before seeding the cells were washed in serum-free media to verify the removal of any residual serum. During a period of two weeks the supernatants were collected as indicated and the cells were counted on the same day. The cultures were fed on the 4and 10day and medium was placed in the cultures on day 6. Although the cells in DI culture proliferated normally under these conditions, they failed to produce measurable quantities of antibody. Panel A: IgM production per hybridoma cell in 3% FCS; Panel B: Number of live cells at each antibody titration

    A human monoclonal autoantibody to breast cancer identifies the PDZ domain containing protein GIPC1 as a novel breast cancer-associated antigen-3

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    St epithelium cell line HBL100 and breast cancer cell lines MCF-7, T47D, SK-BR-3, MDA231, MDA157 and MDA453. A probe for the GAPDH gene was used to normalize expression. Panel B: Densitometry analysis of the Northern blot was performed to quantitate the mRNA expression. The data indicates that the GIPC1 gene is upregulated in breast cancer cell lines.<p><b>Copyright information:</b></p><p>Taken from "A human monoclonal autoantibody to breast cancer identifies the PDZ domain containing protein GIPC1 as a novel breast cancer-associated antigen"</p><p>http://www.biomedcentral.com/1471-2407/8/248</p><p>BMC Cancer 2008;8():248-248.</p><p>Published online 24 Aug 2008</p><p>PMCID:PMC2529336.</p><p></p

    A human monoclonal autoantibody to breast cancer identifies the PDZ domain containing protein GIPC1 as a novel breast cancer-associated antigen-4

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    S analyzed by confocal microscopy and indicates that the target antigen is present in the membrane and cytoplasm. Staining of human breast cancer tissue was analyzed by standard fluorescent microscopy.<p><b>Copyright information:</b></p><p>Taken from "A human monoclonal autoantibody to breast cancer identifies the PDZ domain containing protein GIPC1 as a novel breast cancer-associated antigen"</p><p>http://www.biomedcentral.com/1471-2407/8/248</p><p>BMC Cancer 2008;8():248-248.</p><p>Published online 24 Aug 2008</p><p>PMCID:PMC2529336.</p><p></p
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