Rabbit multi-state, dead recovery models

Multi-state, dead-recovery models for 18 years of data from Turretfield rabbit population, South Australia. Code by Louise K. Barnett, November 2017 Before running the script you will need to install program MARK from http://www.phidot.org/software/mark/downloads/ Mac and Linux users might find this post helpful: http://www.phidot.org/forum/viewtopic.php?f=21&t=3233&p=10967&hilit=install+RMark#p1096

Rabbit capture histories

Individual capture histories by immunity state. "0" = not captured. "N" = captured with no immunity. "M" = captured with myxoma virus immunity, "R" = captured with rabbit haemorrhagic disease virus immunity, "B" = captured with immunity to both rabbit haemorrhagic disease virus and myxoma virus. Data collected by Biosecurity, South Australia, Department of Primary Industries and Region

Change in CD25 expression on B and CD4+ T cells negatively correlates with viral load.

<p>PBMCs were cultured overnight with or without anti-CD3 stimulation. Change in CD25 or CD86 expression was determined by subtracting the frequency of expression before stimulation from the frequency of expression after stimulation. (<b>A</b>) Representative plots of CD25 expression on CD4+ T cells and B cells with (bottom) and without (top) anti-CD3 stimulation. CD4+ T cell population shown is CD3+CD4+CD19- and B cell population shown is CD3-CD4-CD19+. (<b>B</b>-<b>D</b>) Change in expression of CD25 on CD4+ T cells (r= -.53; p= .056) (B), CD25 on B cells (r= -.63; p= .018) (C), and CD86 on B cells (r= -.44; p= .11) (D) correlates negatively with viral load. </p

CD86+ B cells are more frequent in HIV+ than HIV- subjects and correlate with viremia.

<p>PBMCs from HIV- (open circles) or HIV+ (closed circles) subjects were incubated overnight without stimulation and evaluated for surface level CD86 expression on B cells. HIV+ subjects had a higher frequency of CD86+ B cells compared to HIV- subjects (unpaired t-test not shown on graph, p=0.03). The frequency of CD19+CD86+ B cells in HIV+ individuals correlates with the level of viremia (r=.63; p=.003). Correlation statistics shown are derived from HIV+ subject data only and do not include data from HIV- subjects. </p

Frequency of PD-1 surface expression on lymphocytes is elevated during HIV infection.

<p>Expression of PD-1 on B cells, CD4+ T cells, and CD8+ cells was measured directly <i>ex </i><i>vivo</i>. (<b>A</b>) In HIV-infected individuals, PD-1 expression on CD4+ is not correlated with viral load (r=.33; p=.17). (B) In HIV-infected individuals PD-1 expression on CD8+ T cells correlated positively with viral load (r= .56; p=.01). (<b>C</b>) PD-1 expression is higher on B cells from HIV+ (closed circles) compared to HIV- (open circles) subjects (p=.04). (<b>D</b>) The frequency of PD-1 surface expression is significantly lower on B cells compared to CD4 (p< .0001) and CD8 T cells (p<.0001) in HIV infection.</p

Magnitude of B cell responses to inactivated HIV-1 inversely correlates with viral load.

<p>(<b>A</b>) Expression of CD86 on B cells after stimulation of PBMC with HIV-1 MN control (left column) or HIV-1 MN (right column). Shown are representative plots from one individual (subject 10071).. (<b>B</b>) PBMCs from 21 HIV-infected individuals (closed circles) and 7 HIV-negative control subjects (open circles) were incubated with inactivated HIV-1 MN, and changes in CD86 expression on B cells were measured. Change was calculated by subtracting the frequency of CD86 expression from stimulation with the HIV-1 MN control (containing no HIV proteins) from stimulation with HIV-1 MN. CD86 expression on B cells in response to HIV-antigen in HIV infected individuals is negatively correlated with viral load (r= -.6; p= .006). Correlation statistics are only applied to HIV-infected individuals and do not include data from uninfected subjects. </p

PD-1 blockade improves B cell responses to stimulation with inactivated HIV-1.

<p>PBMCs were cultured overnight with or without anti-PD-1 and stimulated with inactivated HIV-1 MN protein. Change in response to MN stimulation was calculated by subtracting stimulation with MN control protein from stimulation with HIV-1 MN protein (p= .003).</p

Purified B cell responses to p24 are enhanced by addition of autologous CD4+ T cells.

<p>Change in the frequency of CD86+ B cells in response to SEB (A) or HIV p24 antigen (B) was evaluated in total PBMC culture, purified B cell culture, or purified B cells co-cultured with autologous purified CD4+ T cells. </p

Neither vaginal nor buccal administration of 800 μg misoprostol alters mucosal and systemic immune activation or the cervicovaginal microbiome: a pilot study

<p><b>Objectives:</b> The aim of the study was to assess the extent to which misoprostol alters mucosal or systemic immune responses following either buccal or vaginal administration.</p> <p><b>Methods:</b> This was a prospective, crossover pilot study of 15 healthy, reproductive-age women. Women first received 800 μg misoprostol either via buccal or vaginal administration and were crossed over 1 month later to receive the drug via the other route. Cervicovaginal lavage samples, cervical Cytobrush samples, cervicovaginal swabs, urine and blood were obtained immediately prior to drug administration and the following day. Parameters assessed included urine and cervicovaginal misoprostol levels, whole blood cytokine responses (by ELISA) to immune stimulation with lipopolysaccharide, peripheral blood and cervical lymphocyte phenotyping by flow cytometry, cervicovaginal antimicrobial peptide measurement by ELISA and vaginal microbial ecology assessment by 16S rRNA sequencing.</p> <p><b>Results:</b> Neither buccal nor vaginal misoprostol significantly altered local or systemic immune and microbiological parameters.</p> <p><b>Conclusion:</b> In this pilot study, we did not observe significant alteration of mucosal or systemic immunology or vaginal microbial ecology 1 day after drug administration following either the buccal or vaginal route.</p