Análisis de los efectos generados por la decisión 391 sobre el régimen común de acceso a los recursos genéticos de la CAN, en el fenómeno de la biopiratería (1996-2010)

Después que muchos Estados se enriquecieran tanto intelectual como económicamente de la explotación o apropiación ilegal de la biodiversidad andina de la cual los miembros de la CAN eran país de origen, surge la necesidad de proteger la riqueza de la región, razón por la cual nace la Decisión 391 en 1996 sobre un Régimen Común de Acceso a Recursos genéticos. De esta manera los países miembros de la CAN se convirtieron en los primeros con un mecanismo de control para el acceso a los recursos genéticos y partición equitativa de los beneficios; buscando con ello sentar bases para la creación de conocimientos sobre el tema, el desarrollo de capacidades científicas y tecnológicas, y la promoción del uso sostenible de los recursos. Sin embargo por razones de carácter nacional la implementación del mismo no ha progresado, generando que los casos de biopiratería aumenten e incluso sean difíciles de prevenir. Siendo este un tema de gran relevancia para Bolivia, Colombia, Ecuador, Perú y Venezuela, esta monografía examinará en las siguientes páginas la reglamentación nacional para comprender a mayor profundidad los defectos y/o cualidades de las decisiones tomadas por los Estados para la aplicación de la Decisión 391, y así mismo evidenciará las razones por las cuales la implementación de la Decisión no ha tenido éxito total sobre el control de la biopiratería, entre ellas la falta de reglamentación, la especificación de roles, la concientización ciudadana e incluso información al público en general.

The NAFTA investment dispute settlement mechanism and the admissibility of amicus curiae briefs by NGOs

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Molecular mechanism involved in the mutagenicity induced by Aflatoxin B1

The aflatoxin B1 (AFB1) is a mycotoxin that has been identified as the most potent hepatocarcinogen. The metabolite resulting from detoxification process of AFB1 in liver, has the ability to react with the genomic DNA, generating AFB1-DNA adducts; during DNA replication process, this adduct induced the G:C→T:A transversion. Polymorphism in genes encoding for enzymes involved in the activation and detoxification of AFB1 and DNA repair enzymes has been associated with the risk of hepatocellular carcinoma (HCC) development. Additionally, in populations of high exposure to aflatoxin and high prevalence of hepatitis B virus (HBV) infection, has been demonstrated a synergism between these two risk factors for the development of HCC.

The use of insect cells to identify potent and selective inhibitors of the replication of the Dengue and Chikungunya viruses and unravel their molecular mechanism of action

Dengue and Chikungunya viruses cause the most important arthropod-borne viral infections for humans. These viruses are predominant in tropical and subtropical regions. In addition, these viruses are predominant in tropical and subtropical regions. Dengue mortality rate is around 1.2 to 3.5% and deaths due to chikungunya fever are around 1 in 1000; however, half of chikungunya-infected patients evolve into a chronic state that can persist for months up to years. There are no antiviral drugs available for DENV and CHIKV treatment and prevention. Moreover, vector control strategies have failed so far. Thus, the development of potent inhibitors for a broad spectrum of RNA viruses is urgently needed. We established and characterized a new embryonic insect cell line from Culex quinquefasciatus mosquito. Also we established the flaviviruses and alphavirus replication, both in C6/36 and Lulo insect cell lines, as well as in Vero cell line. In addition we carried out a reference compound library and reference panel of assays and data for DENV, which provides a benchmark for further studies. During this study, a panel of 9 antiviral molecules, with proven in vitro anti-dengue virus activity and that act at different stages of the DENV life cycle, was selected. Finally, Favipiravir or T-705, was identified as inhibitor in vitro and in vivo of alphaviruses and the mutation K291R in nsP4, which is responsible of the polymerase activity, was found as the mode of action in CHIKV. Interestingly, lysine in motif F1 is also highly conserved in positive-stranded RNA viruses and this might explain the broad spectrum of T-705 antiviral activity.