Considering a participatory approach to social work – Service user research

Service-user involvement in social work research is much vaunted and considered desirable. Yet, it is not common. This is despite the fact that research-funding bodies are increasingly mandating inclusion of service users in the research process. It would seem timely for the profession to look again at participatory research as an approach to working collaboratively with service users in the co-production of research. This article reviews the arguments for service-user collaboration in social work research; it considers the evolution of service-user engagement and its current status in practice. Building on the foundations of social work research methodologies, the article considers the practicalities of participatory research and the potential barriers. The article draws on vignettes of published participatory research to illustrate this type of research in social work

Specific compounds enhance autophagy or inflammatory cytokine release.

<p>(A) J774 murine macrophages were infected with H37Rv, then treated with the indicated compounds. Cells were harvested for Western-blot analysis of LC3 conversion from LC3-I to LC3-II as an indicator of autophagy. Data represents one of three independent experiments. Densitometry for LC3-II to LC3-I ratio for the shown Western blot was performed using ImageJ image analysis software. (B) Cells were infected with H37Rv, then treated with compound after a 4 hour phagocytosis. Supernatants were collected at 24 hours after infection and TNF-α concentration was determined by ELISA. Points represent average for 2 wells +/− standard deviation. Data represents one of two independent experiments.</p

AKT and ABL are important for mycobacterial infection of macrophages.

<p>(A) J774 cells were infected with H37Rv at an MOI of 1 or an MOI of 10. Cells were harvested two hours after infection, and lysates were probed for AKT activation using an antibody to phospho-serine at position 473. (B) J774 cells were infected with H37Rv at an MOI of 1 for 4 hours, then washed and treated with compound. Cells were harvested at 3 hours after treatment and lysates were probed for AKT activation using an antibody to phospho-serine at position 473. (C) <i>akt1</i> and <i>akt2</i> or <i>akt1</i>, <i>akt2</i>, and <i>akt3</i> were silenced with siRNA in J774 cells. Cells were then infected with H37Rv at an MOI and 1, and infection was allowed to progress for 3 days. Cells were then lysed and plated for CFU. (D) <i>abl1</i> was silenced in J774 macrophages using siRNA. Cells were then infected with H37Rv. After 4 hours of phagocytosis, wells were lysed and plated for CFU to determine uptake (day 0). Infection was allowed to progress in the remaining wells; day 3 after infection, cells were lysed and plated for CFU. Each experiment was repeated a minimum of three times, and a representative experiment is shown. Error bars are standard deviation, *p = 0.0195 by Mann Whitney U for (C) and (D).</p

Selected screen hits have dose-dependent activity in J774 cells and bone-marrow derived macrophages.

<p>Selected hit compounds were retested at varying doses in (A) J774 murine macrophages and (B) mouse bone marrow-derived macrophages (BMDM). Cells were infected with <i>M. tuberculosis</i> strain H37Rv at an MOI of 1∶1 and treated with each compound at the indicated doses (µM) after a 4 h phagocytosis period. At day 3 (J774) or day 5 (BMDM) after infection, cells were washed, lysed, and plated for CFU. Each column represents the mean and standard deviation of four biological replicates. Each experiment was repeated three times and a representative experiment is shown. With the exception of fluoxetine at 6.25 µM, all p-values were <0.05 for the comparison of each compound treatment condition with DMSO. p-values were calculated using the Mann Whitney U test.</p

Inhibitors of protein kinases impair mycobacterial growth in macrophages.

<p>(A) J774 cells or (B) BMDM were infected with <i>M. tuberculosis</i> strain H37Rv at an MOI of 1∶1, and treated with each kinase inhibitor at the indicated concentrations (µM) after a 4 h phagocytosis period. At day 3 (J774) or day 5 (BMDM) after infection, cells were washed, lysed, and plated for CFU. Each column represents the mean and standard deviation of four biological replicates and each graph represents one of three independent experiments. For (A) all p<0.001 with the exception of GNF-2 at 2.5 µM, imatinib at 5 µM and gefitinib at 5 µM. For (B) inhibitors were used at the following concentrations: AKTi1/2 5 µM (p<0.03), H-89 5 µM (p<0.03), GNF-2 10 uM (not significant), imatinib 5 µM (p<0.03), gefitinib 5 µM (p<0.03), lapatinib 5 µM (p = <0.06). All p values were calculated using the Mann Whitney U test.</p

Small molecules discovered in a pathway screen target the Rho pathway in cytokinesis

We report the discovery of small molecules that target the Rho pathway, which is a central regulator of cytokinesis—the final step in cell division. We have developed a way of targeting a small molecule screen toward a specific pathway, which should be widely applicable to the investigation of any signaling pathway. In a chemical genetic variant of a classical modifier screen, we used RNA interference (RNAi) to sensitize cells and identified small molecules that suppressed or enhanced the RNAi phenotype. We discovered promising candidate molecules, which we named Rhodblock 1–8, and we identified the target of Rhodblock 6 as Rho kinase. Several Rhodblocks inhibited one function of the Rho pathway in cells: the correct localization of phosphorylated myosin light chain during cytokinesis. Rhodblocks differentially perturb Rho pathway proteins in cells and can be used to dissect the mechanism of the Rho pathway during cytokinesis. © 2010 Nature America, Inc. All rights reserved. Rho GTPases are key regulators of cell division and control other processes that involve the cytoskeleton, such as cell migration, contraction and adhesion1. With Rho GTPases at the center of complicated signaling cascades that are only partially understood, different branches of these pathways cooperate to coordinate these processes. Small GTPases regulate their downstrea

Identification of Regulators of Polyploidization Presents Therapeutic Targets for Treatment of AMKL

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