10 resultados para anti-terrorism security
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In this paper we analyze the effects of social security policies in an unfunded, earnings-related social security system on the incentives to education investment and voluntary retirement, on growth and on income inequality. Growth is endogenously driven by human capital investment, individuals differ in their innate (learning) ability at birth, and the pension scheme includes a minimum pension. More skilled individuals spend more on education, minimum pensions reduce low skill individuals' incentives to invest in human capital, there is no monotonic relationship between per capita growth and income inequality.
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Revised: 2006-11.-- Published as an article in: Journal of Public Economics 90(12), December, 2006, pp. 2323-2349.
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Published as an article in: European Economic Review, 2008, vol. 52, issue 1, pages 1-27.
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13 p.
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Ponencia leída en el Foro de Comunicaciones IkasArt II (BEC Barakaldo, 2010.06.17)
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This paper investigates the role that INTERPOL surveillance – the Mobile INTERPOL Network Database (MIND) and the Fixed INTERPOL Network Database (FIND) – played in the War on Terror since its inception in 2005. MIND/FIND surveillance allows countries to screen people and documents systematically at border crossings against INTERPOL databases on terrorists, fugitives, and stolen and lost travel documents. Such documents have been used in the past by terrorists to transit borders. By applying methods developed in the treatment-effects literature, this paper establishes that countries adopting MIND/FIND experienced fewer transnational terrorist attacks than had they not adopted MIND/FIND. Our estimates indicate that, on average, during 2008–2011, adopting and using MIND/FIND results in 1.23 fewer transnational terrorist incidents each year per 100 million people. Thus, a country like France with a population just above 64 million people in 2008 would have 0.79 fewer transnational terrorist incidents per year owing to its use of INTERPOL surveillance. For most treatment countries, this amounts to a sizeable proportional reduction of about 60 per cent.
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4 p.
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Resveratrol is a non-flavonoid polyphenol which belongs to the stilbenes group and is produced naturally in several plants in response to injury or fungal attack. Resveratrol has been recently reported as preventing obesity. The present review aims to compile the evidence concerning the potential mechanisms of action which underlie the anti-obesity effects of resveratrol, obtained either in cultured cells lines and animal models. Published studies demonstrate that resveratrol has an anti-adipogenic effect. A good consensus concerning the involvement of a down-regulation of C/EBPa and PPAR. in this effect has been reached. Also, in vitro studies have demonstrated that resveratrol can increase apoptosis in mature adipocytes. Furthermore, different metabolic pathways involved in triacylglycerol metabolism in white adipose tissue have been shown to be targets for resveratrol. Both the inhibition of de novo lipogenesis and adipose tissue fatty acid uptake mediated by lipoprotein lipase play a role in explaining the reduction in body fat which resveratrol induces. As far as lipolysis is concerned, although this compound per se seems to be unable to induce lipolysis, it increases lipid mobilization stimulated by beta-adrenergic agents. The increase in brown adipose tissue thermogenesis, and consequently the associated energy dissipation, can contribute to explaining the body-fat lowering effect of resveratrol. In addition to its effects on adipose tissue, resveratrol can also acts on other organs and tissues. Thus, it increases mitochondriogenesis and consequently fatty acid oxidation in skeletal muscle and liver. This effect can also contribute to the body-fat lowering effect of this molecule.
Current Approaches for Predicting a Lack of Response to Anti-EGFR Therapy in KRAS Wild-Type Patients
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Targeting epidermal growth factor receptor (EGFR) has been one of the most effective colorectal cancer strategies. Anti-EGFR antibodies function by binding to the extracellular domain of EGFR, preventing its activation, and ultimately providing clinical benefit. KRAS mutations in codons 12 and 13 are recognized prognostic and predictive biomarkers that should be analyzed at the clinic prior to the administration of anti-EGFR therapy. However, still an important fraction of KRAS wild-type patients do not respond to the treatment. The identification of additional genetic determinants of primary or secondary resistance to EGFR targeted therapy for further improving the selection of patients is urgent. Herein, we review the latest published literature highlighting the most important genes that may predict resistance to anti-EGFR monoclonal antibodies in colorectal cancer patients. According to the available findings, the evaluation of BRAF, NRAS, PIK3CA, and PTEN status could be the right strategy to select patients who are likely to respond to anti-EGFR therapies. In the future, the combination of those biomarkers will help establish consensus that can be introduced into clinical practice.
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VIH-ren fusioa inhibitzeko gai diren antigorputzen adierazpena eta purifikazioa bakterietan. Funtzionaltasunaren analisia (ITC eta pseudobirusak erabiliz egindako neutralizazio saioak) eta optimizazioa.