Presence 5 for Racial Justice Workshop: Fostering Dialogue Across Medical Education to Disrupt Anti-Black Racism in Clinical Encounters

Introduction: Anti-Black racism has strong roots in American health care and medical education. While curricula on social determinants of health are increasingly common in medical training, curricula directly addressing anti-Black racism are limited. Existing frameworks like the Presence 5 framework for humanism in medicine can be adapted to develop a novel workshop that promotes anti-racism communication. Methods: We performed a literature review of anti-racism collections and categorized anti-racism communication practices using the Presence 5 framework to develop the Presence 5 for Racial Justice Workshop. Implementation included an introductory didactic, a small-group discussion, and a large-group debrief. Participants evaluated the workshop via an online survey, and we analyzed the resulting qualitative feedback. Results: A total of 17 participants took part in two workshops, with nine of the participants responding to the evaluation survey. Themes that emerged from survey responses included strengths of and improvements for the workshop structure (protected time for anti-racism discussion, dialogue between learners and faculty) and content (specific phrases and language, practicing self-reflection). Discussion: The workshop provides participants with a semistructured discussion around the five anti-racism communication practices. Barriers to implementation include incorporating the workshop into existing curricula and ensuring diverse learners. Barriers to evaluating the workshop include the low survey response rate. Recommendations to improve the workshop include using case-based discussion and varying the workshop structure according to institutional needs. Next steps include an implementation study to evaluate the acceptability, feasibility, and effectiveness of the workshop

Investigation of Musanga cecropioides heartwood as a thermal insulator for refrigerators, coolers and food flask

No Abstract Available Ghana J. Sci, Vol.42 2002: 71-7

WGP alters the suppressive capacity of regulatory T cells in spleens.

<p>Groups of mice (n = 6) bearing established Lewis lung carcinoma were treated as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046936#s4" target="_blank">Materials and Methods</a></i>. (A, B, C) Single cell suspensions from spleens (A), draining lymph nodes (B) and tumor tissues (C) were stained with fluorochrome labeled mAbs to evaluate the proportions of CD4⁺CD25⁺Foxp3⁺ Tregs. Cells were gated on CD4⁺ T cells. RNAs from tumor specimens were extracted and Foxp3 mRNA expression was analyzed by qRT-PCR. (D) Splenic CD4⁺CD25⁺ Tregs isolated from tumor-bearing mice treated with or without WGP were co-cultured with CD4⁺CD25⁻ Teffs from wild type C57BL/6 mice in the presence of anti-CD3 mAb and anti-CD28 mAb for 72 h. Wells were pulsed with 1 µCi/well [³H]-thymidine and analyzed as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046936#s4" target="_blank">Materials and Methods</a></i>. **P<0.01, *P<0.05, N.S. represents no significance between columns.</p

Increased GITRL expression on BMDCs by WGP impairs Treg-mediated suppressive effect and enhances Teff proliferation.

<p>Murine CD4⁺CD25⁻ Teff and CD4⁺CD25⁺ Treg cells were purified from C57BL/6 mice splenocytes as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046936#s4" target="_blank">Materials and Methods</a></i>. BMDCs were stimulated with WGP (100 µg/ml) or not for 24 h. Cells were harvested, treated with mitomycin C and then co-cultured at a 1∶5 ratio with CD4⁺CD25⁻ Teff and CD4⁺CD25⁺ Treg cells (A) or Teff cells (B) in the presence of anti-CD3 mAb with or without anti-GITRL blocking antibody or control Igs for 72 h, Treg and Teff cells were added at 1∶1 ratio. Wells were pulsed with 1 µCi/well [³H]-thymidine for the last 16 h. Data are expressed as means ± SD. ***P<0.001, **P<0.01, *P<0.05. N.S. represents no significance between columns.</p

WGP induces enhanced CTL priming <i>in vivo</i>.

<p>Groups of mice (n = 6) bearing established Lewis lung carcinoma were treated as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046936#s4" target="_blank">Materials and Methods</a></i>. (A, B) Single cell suspensions prepared from spleens (A) and draining lymph nodes (B) were stimulated with PMA plus ionomycin and stained intracellular IFN-γ. Cells were gated on CD3⁺CD8⁺ T cells. Culture supernatants from splenocytes and lymphoid cells were collected and assayed for IFN-γ using ELISA. (C) Tumor specimens from each group were prepared for single cell suspensions. Cells were stained with mAbs against CD3, CD8 and were assessed by flow cytometry. Cells were gated on CD3⁺ T cells. RNAs from tumor specimens were extracted and qRT-PCR was performed for IFN-γ. Results are expressed as mean ± SD. **P<0.01, *P<0.05, N.S. represents no significance between columns.</p

WGP treatment up-regulates GITRL expression on DCs in tumor-bearing C57BL/6 mice.

<p>(A) Groups of mice (n = 6) bearing established Lewis lung carcinoma were treated as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046936#s4" target="_blank">Materials and Methods</a></i>. Tumors were measured with a caliper at indicated time. (B) The proportions of CD11c⁺ DCs in spleens, draining lymph nodes (dLN) and tumor tissues from WGP-treated or untreated mice were analyzed using flow cytometry. (C) Expression of GITRL on CD11c⁺ cells in spleens, draining lymph nodes and tumor sites treated with or without WGP were assessed by flow cytometry. Histograms are gated on CD11c⁺ cells (isotype: solid gray). RNAs extracted from spleens, draining lymph nodes and tumors were subjected to qRT-PCR for GITRL expression. Numbers indicate percentages of events in gate (dot plot) or geometric mean fluorescence intensity (GeoMFI; histograms). Results are expressed as mean ± SD. ***P<0.001, **P<0.01, *P<0.05, ^###P<0.001, N.S. represents no significance between columns.</p

Up-regulation of GITRL on BMDCs via dectin-1 upon WGP stimulation.

<p>(A) Expression of dectin-1 on BMDCs. BMDCs were stained for dectin-1 with anti-dectin-1 antibody (thick line) or rat IgG2b (solid gray) and then analyzed using flow cytometry. (B) Analysis of the activation of SYK by immunoblot of lysates of BMDCs stimulated with WGP (time, above lanes), assessed with anti-phospho-SYK antibody (upper band). β-actin levels were measured as protein loading controls (lower band). (C) Flow cytometry for surface expression of GITRL on BMDCs after no stimulation or stimulation with WGP for 24 h, 48 h and 72 h. (D) BMDCs were pretreated with anti-dectin-1 mAb or rat IgG (5 µg/ml) for 1 h at 37°C and then treated with 100 µg/ml WGP, after 48 h stimulation, cells were subjected to analyze the GITRL expression. The values shown in the flow cytometry profiles are geometric mean fluorescent intensity. Data are representative of three independent experiments.</p