46 research outputs found
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The Democratic Value of Strategic Game Reporting and Uncivil Talk: A Computational Analysis of Facebook Conversations During U.S. Primary Debates
This study explores discourse features on Facebook pages of news organizations during the 2020 U.S. primary debates using a state-of-the-art machine-learning model. Informing the scholarly debate about the implications of strategic game reporting in online spaces, we find that it is not necessarily linked to uncivil discourse, yet it might deter from relevant conversations. Second, addressing fears about the undesired outcomes of uncivil talk, our data suggest that incivility can coexist with rational discourse in user comments, although this relationship is not pervasive. Implications of these results are discussed in the context of the role of hybrid media for political engagement during electoral campaigns
State owned enterprises as bribe payers: the role of institutional environment
Our paper draws attention to a neglected channel of corruption—the bribe payments by state-owned enterprises (SOEs). This is an important phenomenon as bribe payments by SOEs fruitlessly waste national resources, compromising public welfare and national prosperity. Using a large dataset of 30,249 firms from 50 countries, we show that, in general, SOEs are less likely to pay bribes for achieving organizational objectives owing to their political connectivity. However, in deteriorated institutional environments, SOEs may be subjected to potential managerial rent-seeking behaviors, which disproportionately increase SOE bribe propensity relative to privately owned enterprises. Specifically, our findings highlight the importance of fostering democracy and rule of law, reducing prevalence of corruption and shortening power distance in reducing the incidence of SOE bribery
Antisense inhibition of microRNA-21 and -221 in tumor-initiating stem-like cells modulates biological functions of pancreatic cancer including tumorigenesis, metastasis, and chemoresistance
Einsatz muriner mesenchymaler Stammzellen zur Expression spenderspezifischer MHC Klasse I Moleküle zur spenderspezifischen Immunsuppression in der allogenen Organtransplantation
Die Überexpression von IFIT3 fördert Tumorwachstum, Metastasierung, Angiogenese und Chemoresistenz beim humanen Pankreaskarzinom
Sox9-associated overexpression of IFIT3 leads to pancreatic cancer progression by activation of "pseudoinflammatory" pathways
Effect of KRAS exon 2 mutations on antitumor activity of afatinib and gefitinib
The aim of this study was to investigate the impact of different KRAS mutations on the inhibitory potential of afatinib and gefitinib in SW48 colorectal cancer cells. The influence of afatinib/gefitinib on cell viability and cell cycle was evaluated in isogenic SW48 KRAS wild-type/mutant cells. Protein levels of phosphorylated/total EGFR, HER-2, HER-3, ERK, and AKT were compared between treated/untreated samples using western blotting. The activity of both afatinib and gefitinib was the lowest in KRAS G12C/G12S/G12D and the highest in G13D/G12A mutant subtypes. A 50% decrease in cell viability was achieved at concentrations of 3.0–7.7 µmol/l for afatinib and 5.4–19.5 µmol/l for gefitinib. The effect of both drugs on apoptosis appeared to be stronger than their influence on proliferation and was generally less pronounced in mutant cells than in wild-type cells. The average number of apoptotic cells after treatment with afatinib was 2.6 times as high as the corresponding value following treatment with gefitinib (P<0.01). Levels of pEGFR, pHER-2, pERK, and pAKT were reduced more extensively by afatinib than by gefitinib (P<0.001). Some KRAS mutations (G12C/G12S/G12D) appear to weaken the activity of afatinib and gefitinib whereas others seem to increase sensitivity to treatment (G13D/G12A) compared with the parental clone (KRAS wild-type). In SW48 colorectal cancer cells, afatinib seems to be more potent than gefitinib because of its superior efficacy in inhibiting both EGFR and HER-2, suppressing signaling along both MEK/ERK and PI3K/AKT pathways to a greater extent