Security Analysis of Parlay/OSA Framework

This paper analyzes the security of the Trust and Security Management (TSM) protocol, an authentication protocol which is part of the Parlay/OSA Application Program Interfaces (APIs). Architectures based on Parlay/OSA APIs allow third party service providers to develop new services that can access, in a controlled and secure way, to those network capabilities offered by the network operator. Role of the TSM protocol, run by network gateways, is to authenticate the client applications trying to access and use the network capabilities features offered. For this reason potential security flaws in its authentication strategy can bring to unauthorized use of network with evident damages to the operator and to the quality of the services. This paper shows how a rigorous formal analysis of TSM underlines serious weaknesses in the model describing its authentication procedure. This usually means that also the original system (i.e., the TSM protocol itself) hides the same flaws. The paper relates about the design activity of the formal model, the tool-aided verification performed and the security flaws discovered. This will allow us to discuss about how the security of the TSM protocol can be generally improve

Nivel de sospecha de enfermedad de Fabry en profesionales de la salud en el primer nivel de atención : Buenos Aires, mayo 2015

La enfermedad de Fabry es una enfermedad genética, hereditaria autosómica recesiva, de depósito lisosomal. Pertenece a los errores innatos del metabolismo. La incidencia varía de 1/40.000 a 1/117.000 nacidos vivos. Causa deficiencia total o parcial de la enzima alfa-galactosidasa A. Esta deficiencia interfiere en la degradación de globotriaosilceramida (Gb3), presente en muchos tipos de células, particularmente en las membranas de los eritrocitos. Los signos y síntomas sugestivos de E. de Fabry son: dolor intenso en manos y pies, dolor abdominal, angioqueratomas, opacidad corneal, facie tosca, proteinuria, entre otras. El compromiso vascular aumenta 12 veces el riego de ACV a partir de los 30 años, además de causar distintas afecciones cardíacas. La progresión del daño en el rinón evoluciona a insuficiencia renal crónica con necesidad de diálisis en la tercera década de la vida. Por todo lo expuesto es muy importante la detección temprana de esta enfermedad para instaurar un tratamiento adecuado con el objetivo de detener el deterioro de los órganos antes mencionados y reducir de esta forma la morbimortalidad de la Enfermedad de Fabry.Facultad de Ciencias Médica

Nivel de sospecha de enfermedad de Fabry en profesionales de la salud en el primer nivel de atención : Buenos Aires, mayo 2015

La enfermedad de Fabry es una enfermedad genética, hereditaria autosómica recesiva, de depósito lisosomal. Pertenece a los errores innatos del metabolismo. La incidencia varía de 1/40.000 a 1/117.000 nacidos vivos. Causa deficiencia total o parcial de la enzima alfa-galactosidasa A. Esta deficiencia interfiere en la degradación de globotriaosilceramida (Gb3), presente en muchos tipos de células, particularmente en las membranas de los eritrocitos. Los signos y síntomas sugestivos de E. de Fabry son: dolor intenso en manos y pies, dolor abdominal, angioqueratomas, opacidad corneal, facie tosca, proteinuria, entre otras. El compromiso vascular aumenta 12 veces el riego de ACV a partir de los 30 años, además de causar distintas afecciones cardíacas. La progresión del daño en el rinón evoluciona a insuficiencia renal crónica con necesidad de diálisis en la tercera década de la vida. Por todo lo expuesto es muy importante la detección temprana de esta enfermedad para instaurar un tratamiento adecuado con el objetivo de detener el deterioro de los órganos antes mencionados y reducir de esta forma la morbimortalidad de la Enfermedad de Fabry.Facultad de Ciencias Médica

Nivel de sospecha de enfermedad de Fabry en profesionales de la salud en el primer nivel de atención : Buenos Aires, mayo 2015

La enfermedad de Fabry es una enfermedad genética, hereditaria autosómica recesiva, de depósito lisosomal. Pertenece a los errores innatos del metabolismo. La incidencia varía de 1/40.000 a 1/117.000 nacidos vivos. Causa deficiencia total o parcial de la enzima alfa-galactosidasa A. Esta deficiencia interfiere en la degradación de globotriaosilceramida (Gb3), presente en muchos tipos de células, particularmente en las membranas de los eritrocitos. Los signos y síntomas sugestivos de E. de Fabry son: dolor intenso en manos y pies, dolor abdominal, angioqueratomas, opacidad corneal, facie tosca, proteinuria, entre otras. El compromiso vascular aumenta 12 veces el riego de ACV a partir de los 30 años, además de causar distintas afecciones cardíacas. La progresión del daño en el rinón evoluciona a insuficiencia renal crónica con necesidad de diálisis en la tercera década de la vida. Por todo lo expuesto es muy importante la detección temprana de esta enfermedad para instaurar un tratamiento adecuado con el objetivo de detener el deterioro de los órganos antes mencionados y reducir de esta forma la morbimortalidad de la Enfermedad de Fabry.Facultad de Ciencias Médica

Nampt over-expression recapitulates the braf inhibitor resistant phenotype plasticity in melanoma

Serine–threonine protein kinase B-RAF (BRAF)-mutated metastatic melanoma (MM) is a highly aggressive type of skin cancer. Treatment of MM patients using BRAF/MEK inhibitors (BRAFi/MEKi) eventually leads to drug resistance, limiting any clinical benefit. Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development. Using stable and inducible NAMPT over-expression systems, we showed that forced NAMPT expression in MM BRAF-mutated cell lines led to increased energy production, MAPK activation, colony-formation capacity, and enhance tumorigenicity in vivo. Moreover, NAMPT over-expressing cells switched toward an invasive/mesenchymal phenotype, up-regulating expression of ZEB1 and TWIST, two transcription factors driving the epithelial to mesenchymal transition (EMT) process. Consistently, within the NAMPT-overexpressing cell line variants, we observed an increased percentage of a rare, drug-effluxing stem cell-like side population (SP) of cells, paralleled by up-regulation of ABCC1/MRP1 expression and CD133-positive cells. The direct correlation between NAMPT expression and gene set enrichments involving metastasis, invasiveness and mesenchymal/stemness properties were verified also in melanoma patients by analyzing The Cancer Genome Atlas (TCGA) datasets. On the other hand, CRISPR/Cas9 full knock-out NAMPT BRAFi-resistant MM cells are not viable, while inducible partial silencing drastically reduces tumor growth and aggressiveness. Overall, this work revealed that NAMPT over-expression is both necessary and sufficient to recapitulate the BRAFi-resistant phenotype plasticity

A Formal Security Analysis of an OSA/Parlay Authentication Interface

Abstract. We report on an experience in analyzing the security of the Trust and Security Management (TSM) protocol, an authentication procedure within the OSA/Parlay Application Program Interfaces (APIs) of the Open Service Access and Parlay Group. The experience has been conducted jointly by research institutes experienced in security and industry experts in telecommunication networking. OSA/Parlay APIs are designed to enable the creation of telecommunication applications outside the traditional network space and business model. Network operators consider the OSA/Parlay a promising architecture to stimulate the development of web service applications by third party providers, which may not necessarily be experts in telecommunication and security. The TSM protocol is executed by the gateways to OSA/Parlay networks; its role is to authenticate client applications trying to access the interfaces of some object representing an offered network capability. For this reason, potential security flaws in the TSM authentication strategy can cause the unauthorized use of the network, with evident damages to the operator and the quality of services. We report a rigorous formal analysis of the TSM specification, which is originally given in UML. Furthermore, we illustrate our design choices to obtain the formal model, describe the tool-aided verification and finally expose the security flaws discovered

Nampt over-expression recapitulates the braf inhibitor resistant phenotype plasticity in melanoma

Serine–threonine protein kinase B-RAF (BRAF)-mutated metastatic melanoma (MM) is a highly aggressive type of skin cancer. Treatment of MM patients using BRAF/MEK inhibitors (BRAFi/MEKi) eventually leads to drug resistance, limiting any clinical benefit. Herein, we demonstrated that the nicotinamide adenine dinucleotide (NAD)-biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) is a driving factor in BRAFi resistance development. Using stable and inducible NAMPT over-expression systems, we showed that forced NAMPT expression in MM BRAF-mutated cell lines led to increased energy production, MAPK activation, colony-formation capacity, and enhance tumorigenicity in vivo. Moreover, NAMPT over-expressing cells switched toward an invasive/mesenchymal phenotype, up-regulating expression of ZEB1 and TWIST, two transcription factors driving the epithelial to mesenchymal transition (EMT) process. Consistently, within the NAMPT-overexpressing cell line variants, we observed an increased percentage of a rare, drug-effluxing stem cell-like side population (SP) of cells, paralleled by up-regulation of ABCC1/MRP1 expression and CD133-positive cells. The direct correlation between NAMPT expression and gene set enrichments involving metastasis, invasiveness and mesenchymal/stemness properties were verified also in melanoma patients by analyzing The Cancer Genome Atlas (TCGA) datasets. On the other hand, CRISPR/Cas9 full knock-out NAMPT BRAFi-resistant MM cells are not viable, while inducible partial silencing drastically reduces tumor growth and aggressiveness. Overall, this work revealed that NAMPT over-expression is both necessary and sufficient to recapitulate the BRAFi-resistant phenotype plasticity

Standing in the Breach: Conflict Transformation and the Practice of Preaching

In an era of social and political polarization, the question of how to preach amid divided communities looms large. The field of conflict transformation, which emerged as a corrective to earlier conflict resolution and management models, offers new insight into how conflict might serve as a constructive catalyst for change. Conflict transformation provides perspectives and orientations to conflict that are useful to homiletics—but which also challenge assumptions about conflict that are present in the church and in the larger society. This essay introduces secular and Christian approaches to conflict transformation and analyzes some of their implications for preaching, including the claims that conflict is not sinful and could be a way in which God is acting in the world, that conflict transformation requires broad participation and not top-down solutions, and that restoration of right relationships can be more important to conflict transformation than coming to agreement

Leah D. Schade, Preaching in the Purple Zone: Ministry in the Red-Blue Divide

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Donyelle C. McCray, The Censored Pulpit: Julian of Norwich as Preacher

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