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

Ženy v top managemente: Prípadová štúdia spoločnosti EY

The thesis analyses the course and tempo of women´s careers in comparison with those of men, based on an analysis of my own research conducted at the company EY. The results of the research demonstrates, whether it is more challenging for women or men to achieve a managerial position. The thesis identifies and analyse the different factors that may influence the career of women, based on the theoretical findings and on a qualitative interview

Additional file 8: Figure S2. of Corepressive function of nuclear receptor coactivator 2 in androgen receptor of prostate cancer cells treated with antiandrogen

Full membranes of Western blotting (corresponding to Fig. 7). The membrane in the left panel showed NCOA2 staining part, and the right showed actin beta staining part. Starting from the left lane, NCOA2 expressions in LNCaP with bicalutamide and without bicalutamide, and positive control were shown. Twenty-seven ug of Jurkat cell lysate (Catalog #611451, BD Biosciences, Franklin Lakes, NJ, USA) was used as positive control. Densitometry data of Western blotting were attached below them. (DOC 1266 kb

Additional file 1: Figure S1. of Corepressive function of nuclear receptor coactivator 2 in androgen receptor of prostate cancer cells treated with antiandrogen

Screening of the siRNA efficacy on target mRNA expression levels. Catalog numbers were s20580, s20581, and s20582 (Neon Transfection System; Life Technologies, Carlsbad, CA, USA) for siRNA NCOA2 #1 (siNCOA2 #1), #2 (siNCOA2 #2), and #3 (siNCOA2 #3), respectively. Based on this result, siRNA NCOA2 #2 was selected, and the relevant data were indicated in Fig. 5. (DOC 54 kb

Additional file 5: Table S4. of Corepressive function of nuclear receptor coactivator 2 in androgen receptor of prostate cancer cells treated with antiandrogen

Ct values of quantitative PCR in LNCaP cells cultured with dihydrotestosterone-added media. (DOC 31 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 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

Association Study of a Functional Variant on <i>ABCG2</i> Gene with Sunitinib-Induced Severe Adverse Drug Reaction

<div><p>Sunitinib is a tyrosine kinase inhibitor and used as the first-line treatment for advanced renal cell carcinoma (RCC). Nevertheless, inter-individual variability of drug’s toxicity was often observed among patients who received sunitinib treatment. This study is to investigate the association of a functional germline variant on <i>ABCG2</i> that affects the pharmacokinetics of sunitinib with sunitinib-induced toxicity of RCC patients in the Japanese population. A total of 219 RCC patients were recruited to this pharmacogenetic study. <i>ABCG2</i> 421C>A (Q141K) was genotyped by using PCR-Invader assay. The associations of both clinical and genetic variables were evaluated with logistic regression analysis and subsequently receiver operating characteristic (ROC) curve was plotted. About 43% (92/216) of RCC patients that received sunitinib treatment developed severe grade 3 or grade 4 thrombocytopenia according to the National Cancer Institute-Common Terminology Criteria for Adverse Events version 3.0, the most common sunitinib-induced adverse reaction in this study. In the univariate analysis, both age (<i>P</i> = 7.77x10^-3, odds ratio (OR) = 1.04, 95%CI = 1.01–1.07) and <i>ABCG2</i> 421C>A (<i>P</i> = 1.87x10^-2, OR = 1.71, 95%CI = 1.09–2.68) showed association with sunitinib-induced severe thrombocytopenia. Multivariate analysis indicated that the variant <i>ABCG2</i> 421C>A is suggestively associated with severe thrombocytopenia (<i>P</i> = 8.41x10^-3, OR = 1.86, 95% CI = 1.17–2.94) after adjustment of age as a confounding factor. The area under curve (AUC) of the risk prediction model that utilized age and <i>ABCG2</i> 421C>A was 0.648 with sensitivity of 0.859 and specificity of 0.415. Severe thrombocytopenia is the most common adverse reaction of sunitinib treatment in Japanese RCC patients. <i>ABCG2</i> 421C>A could explain part of the inter-individual variability of sunitinib-induced severe thrombocytopenia.</p></div

ROC curve of the combined effects of <i>ABCG2</i> 421C>A (Q141K) and age with severe thrombocytopenia.

<p>ROC curve of the combined effects of <i>ABCG2</i> 421C>A (Q141K) and age with severe thrombocytopenia.</p

Association of <i>ABCG2</i> 421C>A,Q141K (rs2231142) with various sunitinib-induced adverse events.

<p>Association of <i>ABCG2</i> 421C>A,Q141K (rs2231142) with various sunitinib-induced adverse events.</p