Researching peers and disaster vulnerable communities: an insider perspective

Conducting research among peers and communities that a researcher also serves may be both daunting and rewarding. Researching peers may make the researcher feel uncomfortable raising certain questions that are sensitive or that could be construed to be testing their competencies. This paper is inclined more towards showing that it is advantageous to be an insider, whose position can facilitate collection of information that could not have been accessed, or revealed to an outsider. The paper reports on fieldwork conducted in a low-income country in Sub-Sahara Africa as part of a doctoral study with communities affected by disasters and those that work with such communities. The paper demonstrates the complexities of conducting such research and provides some insights that may be useful to insiders, outsiders or “in-betweeners” embarking on fieldwork in low-income countries and among vulnerable population struggling with manifold stresses and shocks

Additional file 2: Figure S2. of GSK-3 directly regulates phospho-4EBP1 in renal cell carcinoma cell-line: an intrinsic subcellular mechanism for resistance to mTORC1 inhibition

Different effects of GSK-3 inhibition on Akt and 4EBP1 phosphorylation. (A) ACHN cells were treated with AR-A014418 (25 μM) or rapamycin (100 nM) for the indicated times. Cells were lysed and analyzed for pAkt by immunoblotting. (B) Caki1 and A498 cells were treated with AR-A014418 at 25 μM or 50 μM for 24 h or 48 h, respectively. Immunoblotting was performed after cell lysis. In (A) and (B), Data are representative of at least three separate immunoblot analyses. (PPTX 107 kb

Additional file 1: Figure S1. of GSK-3 directly regulates phospho-4EBP1 in renal cell carcinoma cell-line: an intrinsic subcellular mechanism for resistance to mTORC1 inhibition

Differences in suppressive effects of mTORC1 and GSK-3 inhibitors on cell proliferation. Relative cell viability was measured by an MTS assay in ACHN, Caki1 and A498 cells treated with rapamycin (A), and AR-A014418 (B) at the indicated concentrations at 72 h. A498 cells, highly insensitive to rapamycin, did not reach maximal inhibitory effect even at 10 μM rapamycin, with IC50 not assessable (NA). Data are the mean ± SE from six replicates of each cell line. In (A) and (B), significant interaction between cell lines and drug concentrations was statistically detected with two-way ANOVA (p < 0.05). As for the simple main effect, the difference in cell lines (ACHN, Caki1 or A498) was statistically significant for rapamycin (one-way ANOVA; p < 0.05, Bonferroni test; p < 0.05 for ACHN vs. Caki1 and A498) and not significant for AR-A014418 (one-way ANOVA; p = 0.47). (PPTX 60 kb

Additional file 1: Figure S1. of A diagnostic marker for superficial urothelial bladder carcinoma: lack of nuclear ATBF1 (ZFHX3) by immunohistochemistry suggests malignant progression

Specificity and sensitivity of the seven anti-ATBF1 antibodies. Western blot analysis of ATBF1 in HEK293T cells using the seven anti-ATBF1 antibodies (Fig. 5a MB33, MB34, MB39, D1-120, MB44, MB47 and MB49). Lanes 1, 3, 5, 7, 9, 11, and 13 represent HEK293T cells with an HA-tag expression vector (pCI-HA). Lanes 2, 4, 6, 8, 10, 12, and 14 represent HEK293T cells containing an HA-tagged ATBF1 expression vector (pCI-HA-ATBF1). HEK293T cells were grown in DMEM supplemented with 10 % fetal bovine serum at 37 °C and 5 % CO2. HEK293T cells were transfected with the HA-tagged expression vector or the HA-tagged ATBF1 expression vector (HA-ATBF1) using transIT-293 reagent. (PPTX 215 kb