An Economic Study of the Effect of Android Platform Fragmentation on Security Updates

Vendors in the Android ecosystem typically customize their devices by modifying Android Open Source Project (AOSP) code, adding in-house developed proprietary software, and pre-installing third-party applications. However, research has documented how various security problems are associated with this customization process. We develop a model of the Android ecosystem utilizing the concepts of game theory and product differentiation to capture the competition involving two vendors customizing the AOSP platform. We show how the vendors are incentivized to differentiate their products from AOSP and from each other, and how prices are shaped through this differentiation process. We also consider two types of consumers: security-conscious consumers who understand and care about security, and na\"ive consumers who lack the ability to correctly evaluate security properties of vendor-supplied Android products or simply ignore security. It is evident that vendors shirk on security investments in the latter case. Regulators such as the U.S. Federal Trade Commission have sanctioned Android vendors for underinvestment in security, but the exact effects of these sanctions are difficult to disentangle with empirical data. Here, we model the impact of a regulator-imposed fine that incentivizes vendors to match a minimum security standard. Interestingly, we show how product prices will decrease for the same cost of customization in the presence of a fine, or a higher level of regulator-imposed minimum security.Comment: 22nd International Conference on Financial Cryptography and Data Security (FC 2018

Nutritional status in Turkish cystic fibrosis patients

Digitalitzat per Artypla

Systematic review of allelic exchange experiments aimed at identifying mutations that confer drug resistance in Mycobacterium tuberculosis

First published online: September 20, 2013BACKGROUND: Improving our understanding of the relationship between the genotype and the drug resistance phenotype of Mycobacterium tuberculosis will aid the development of more accurate molecular diagnostics for drug-resistant tuberculosis. Studies that use direct genetic manipulation to identify the mutations that cause M. tuberculosis drug resistance are superior to associational studies in elucidating an individual mutation's contribution to the drug resistance phenotype. METHODS: We systematically reviewed the literature for publications reporting allelic exchange experiments in any of the resistance-associated M. tuberculosis genes. We included studies that introduced single point mutations using specialized linkage transduction or site-directed/in vitro mutagenesis and documented a change in the resistance phenotype. RESULTS: We summarize evidence supporting the causal relationship of 54 different mutations in eight genes (katG, inhA, kasA, embB, embC, rpoB, gyrA and gyrB) and one intergenic region (furA-katG) with resistance to isoniazid, the rifamycins, ethambutol and fluoroquinolones. We observed a significant role for the strain genomic background in modulating the resistance phenotype of 21 of these mutations and found examples of where the same drug resistance mutations caused varying levels of resistance to different members of the same drug class. CONCLUSIONS: This systematic review highlights those mutations that have been shown to causally change phenotypic resistance in M. tuberculosis and brings attention to a notable lack of allelic exchange data for several of the genes known to be associated with drug resistance.This work was supported by the Portuguese Foundation for Science and Technology (FCT) (SFRH/BD/33902/2009 to H. N.-G.), the National Institutes of Health/Fogarty International Center (1K01 TW009213 to K.R.J.), departmental funds of the pulmonary division of Massachusetts General Hospital to M. R. F. and the National Institutes of Health/NIAID (U19 A1076217 to M.B.M.)

Potantial clinical application of potassium binders in patients with chronic heart failure in real life clinical practice: results from TREAT HF study

European-Society-of-Cardiology (ESC) Congress -- AUG 29-SEP 01, 2020 -- ELECTR NETWORK[Anstract Not Available]European Soc Cardio

Hyperkalemia in heart failure patients with renal dysfunction in real life clinical practice: Results from TREAT HF Study

[Anstract Not Available

Prevalence of hyperkalemia in patients with chronic heart failure in real life clinical practice: Results from TREAT HF Study

[Anstract Not Available

Preoperative Red Cell Distribution Width and 30-day mortality in older patients undergoing non-cardiac surgery: a retrospective cohort observational study

Increased red cell distribution width (RDW) is associated with poorer outcomes in various patient populations. We investigated the association between preoperative RDW and anaemia on 30-day postoperative mortality among elderly patients undergoing non-cardiac surgery. Medical records of 24,579 patients aged 65 and older who underwent surgery under anaesthesia between 1 January 2012 and 31 October 2016 were retrospectively analysed. Patients who died within 30 days had higher median RDW (15.0%) than those who were alive (13.4%). Based on multivariate logistic regression, in our cohort of elderly patients undergoing non-cardiac surgery, moderate/severe preoperative anaemia (aOR 1.61, p = 0.04) and high preoperative RDW levels in the 3rd quartile (>13.4% and ≤14.3%) and 4th quartile (>14.3%) were significantly associated with increased odds of 30-day mortality - (aOR 2.12, p = 0.02) and (aOR 2.85, p = 0.001) respectively, after adjusting for the effects of transfusion, surgical severity, priority of surgery, and comorbidities. Patients with high RDW, defined as >15.7% (90th centile), and preoperative anaemia have higher odds of 30-day mortality compared to patients with anaemia and normal RDW. Thus, preoperative RDW independently increases risk of 30-day postoperative mortality, and future risk stratification strategies should include RDW as a factor