33 research outputs found
Social ecological framework for African migrant patients’ trust of Chinese physicians.
<p>Social ecological framework for African migrant patients’ trust of Chinese physicians.</p
Distribution of delayed HIV and HCV testing rates at methadone clinics in Guangdong, China.
<p>Distribution of delayed HIV and HCV testing rates at methadone clinics in Guangdong, China.</p
Multivariate analysis of factors associated with delayed HIV testing at methadone clinics (N = 10,046).
*<p>103 individuals who had delayed HIV testing did not undergo HCV testing.</p>**<p>Total number of clients is the only clinic-level variable associated with delayed HIV testing in the multivariate analysis. Other non-significant clinic-level variables are not presented in the table. The complete results of the univariate analysis of clinic-level variables are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066787#pone.0066787.s002" target="_blank">Table S1</a>.</p
Individual-level characteristics of individuals at methadone clinics in Guangdong Province (N = 13,270).
<p>Individual-level characteristics of individuals at methadone clinics in Guangdong Province (N = 13,270).</p
Multivariate analysis of factors associated with delayed HCV testing at methadone clinics (N = 10,404).
*<p>196 individuals who had delayed HCV testing did not undergo HIV testing.</p><p>Note: Only individual-level variables are included in this table. None of the clinical-level variables were associated with delayed HCV testing in the final multilevel model. The complete results of the univariate analysis of clinic-level variables are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066787#pone.0066787.s002" target="_blank">Table S1</a>.</p
Anti-amyloid β (Aβ) antibody, GSK933776, effectively blocks Aβ’s ability to inhibit CFI bioactivity.
<p>Increasing doses of the antibody were preincubated with Aβ (30 μM) for 10 min at room temperature. CFI (1 μg/ml was added and incubated for 20 min at 37°C. CFH and C3b (80 μg/ml) were added and the mixture was incubated for an additional 30 min. Aliquots of the reaction mixture were analyzed for iC3b using ELISA. The curve in magenta shows the global fit of the two curves. The right dark red and dark blue bars show the effect of CFI + IgG1 (non-specific antibody control) on production of iC3b. The left 2 bars in lighter colors show the effect of CFI and IgG1 in presence of Aβ, i.e., reduction in CFI bioactivity. GSK933776 reduced Aβ’s ability to inhibit CFI in a dose-dependent manner (EC<sub>50</sub> ~ 20 μg/ml). Data are presented as means ± SEM of triplicate determinations for two experiments conducted over 2 separate weeks. A non-linear mixed effects model was used to estimate the EC<sub>50</sub> of the dose response curves using a reparametrized 4 parameter logistic equation [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#pone.0195751.ref025" target="_blank">25</a>]. Numbers in parentheses indicate 95% confidence intervals for the estimated EC<sub>50</sub>.</p
Schematic representation of phase I clinical study of Alzheimer’s disease (AD).
<p>Please refer to (BA106006) NCT00459550 and to Andreasen et al. (2011)[<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#pone.0195751.ref023" target="_blank">23</a>]) for more details of complete study. AD patients received either anti-amyloid β monoclonal antibody, GSK933776 6 mg/kg or placebo. The schematic shows the samples that were tested in the CFI bioactivity assays described in the text. Only samples from days 29–31 (1<sup>st</sup> and 2<sup>nd</sup> dose periods), and days 57–59 (2<sup>nd</sup> and 3<sup>rd</sup> dose periods) from subjects receiving GSK933776 or placebo were analyzed. A total of 5 subjects per group were assayed. Only 3 samples were available at certain time points. Red arrows indicate samples measured. Reprinted from Andreasen et al. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#pone.0195751.ref023" target="_blank">23</a>] under a CC BY license, with permission from PLOS ONE, original copyright 2015.</p
Postulated mechanism of amyloid β (Aβ)-mediated modulation of the alternative complement cascade [19, 20].
<p>Schematic shows the alternative complement pathway. <b>Magenta text and cross</b>- interaction of Aβ with complement factor I (CFI) causes reduction of its enzymatic activity and a reduction of the conversion of C3bH to iC3b. <b>Light Blue text</b>- Degradation pathway of C3b to C3d via C3bH, modulated by complement factor H (CFH) and CFI. <b>Black text</b>- conversion of C3b to C3 convertase. <b>Orange</b>-Amplification loop C3 to C3a + C3b. <b>Red</b>-Termination phase resulting in conversion of C5 to C5b78(9)n (membrane attack complex [MAC]). Aβ directly and indirectly produces a local inflammatory environment in retinal pigment epithelial (RPE) cells by modulating release of MCP-1, which leads to recruitment of macrophages and microglia locally, and production of TNF-α and IL1β. The action of these factors on the RPE leads to the release of complement factor B (CFB, green), which in turn is the second mechanism leading to activation of the alternative complement cascade [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#pone.0195751.ref020" target="_blank">20</a>].</p
CFI bioactivity in plasma samples of Alzheimer’s disease (AD).
<p>Plasma was collected from the phase I study of AD receiving anti-amyloid β antibody GSK933776 at 6 mg/Kg. CFI bioactivity was determined by measuring the conversion of C3b to iC3b using ELISA for iC3b. Plasma dilutions (0.01–25 nl) were exposed to CFI and CFH (80 μg/ml each) and incubated for 2 hours at 37°C. Samples from same individuals were run in singlets within the same assay. Each assay included a control sample. Data were fitted using a non-linear mixed model that used a reparametrized[<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#pone.0195751.ref025" target="_blank">25</a>] 4-parameter logistic equation and EC<sub>50</sub>s were estimated. The values were converted to bioactivity of CFI-Units/μg of CFI (1mU = 1/EC<sub>50</sub> in pg). The logarithm of CFI bioactivity for study and control samples were analyzed by a non-linear mixed effects model using the control sample as a covariate to correct for inter-run variability. Data are presented as the geometric means ± SE estimated using the Taylor series expansion (n = 3–5 per group). Percentages shown in the graph were calculated from the integrated areas under the curve for each dosing period using the trapezoidal rule on the geometric means.</p
Age distribution of subjects staged for AMD<sup>§</sup>.
<p>Age distribution of subjects staged for AMD<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195751#t001fn001" target="_blank"><sup>§</sup></a>.</p