Power Amidst Renewal: Foundation Support for Sustaining Advocacy After Disasters

Follows up a 2007 report on the effectiveness of foundations and nonprofits in advocating for systemic changes in the Gulf Coast and lessons learned. Calls for collaboration, regionalizing agendas, and integrating advocacy into missions and grant periods

Patient needs and point-of-care requirements for HIV load testing in resource-limited settings

Medecins Sans Frontieres (MSF) is an international, independent medical nongovernmental organization. One way in which MSF acts to improve patient care is to assist in the identification and development of adapted and appropriate tools for use in resource-limited settings. One strategy to achieve this goal is through active collaborations with scientists and developers, to make some of the field needs known and to help define the medical strategy behind the implementation of new diagnostic tests. Tests used in the field need to be effective in often extreme conditions and must also deliver high-quality, reliable results that can be used in the local context. In this article, we discuss some patient and health care provider needs for human immunodeficiency virus (HIV) load measurement in resource-limited settings. This is just one of the areas in which effective, quality tools are desperately needed, not only by MSF and other international nongovernmental organizations, but also by many other health service providers. We hope that, by clearly defining the needs of patients in MSF clinics-as well as we can assess this-and by explaining why these tools are needed, how they should perform, and how their results can be integrated into a program, we will encourage the development of such tools and hasten their implementation in areas where they are so urgently needed

Life Detection Subsystem Progress Report No. 1

Radioisotopic biochemical probe for extraterrestrial life detection based on cell uptake of phosphate and sulfu

A study toward development of an automated microbial metabolism laboratory Monthly progress report

Life detection systems based on phosphate and sulfur uptake for automated microbial metabolism laborator

The treatment of fractures of the femur by Perkins' traction

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Towards an agonistic account of democracy, conflict, and institutions

In this paper, I offer a move back from a trend in political theory that posits strong divergence—even a contradiction—between two meanings of democracy. On the one hand, a liberal account of democracy conceives it as the set of institutions that shape a political regime and allow government; on the other, a radical tradition identifies democracy with a critical principle for transforming social order. By discussing these trends through the opposition between institution and conflict, I make the case for an agonistic approach of democratic institutions and conflict that relocates democracy both beyond liberalism and the radical tradition. I will do so by critically examining the works of Claude Lefort and Miguel Abensour, principally, where a Machiavellian ontology of social conflict inhibits this agonistic approach. I then draw on the analysis of Hannah Arendt and Jacques Rancière in order to argue for a political theory of democracy that accounts for this link.peer-reviewe

Power Amidst Chaos: Foundation Support for Advocacy Related to Disasters

Lays out principles for funding effective disaster-related advocacy: build robust civic sectors before disasters hit, support local groups that give voice to vulnerable populations, and establish strong organizations that can advocate for the long term

ATR protects the genome against CGG·CCG-repeat expansion in Fragile X premutation mice

Fragile X mental retardation syndrome is a repeat expansion disease caused by expansion of a CGG·CCG-repeat tract in the 5′ UTR of the FMR1 gene. In humans, small expansions occur more frequently on paternal transmission while large expansions are exclusively maternal in origin. It has been suggested that expansion is the result of aberrant DNA replication, repair or recombination. To distinguish amongst these possibilities we crossed mice containing 120 CGG·CCG-repeats in the 5′ UTR of the mouse Fmr1 gene to mice with mutations in ATR, a protein important in the cellular response to stalled replication forks and bulky DNA lesions. We show here that ATR heterozygosity results in increased expansion rates of maternally, but not paternally, transmitted alleles. In addition, age-related somatic expansions occurred in mice of both genders that were not seen in ATR wild-type animals. Some ATR-sensitive expansion occurs in postmitotic cells including haploid gametes suggesting that aberrant DNA repair is responsible. Our data suggest that two mechanisms of repeat expansion exist that may explain the small and large expansions seen in humans. In addition, our data provide an explanation for the maternal bias of large expansions in humans and the lower incidence of these expansions in mice

Is Friedreich ataxia an epigenetic disorder?

Friedreich ataxia (FRDA) is a debilitating and frequently fatal neurological disorder that is recessively inherited. It belongs to the group of genetic disorders known as the Repeat Expansion Diseases, in which pathology arises from the deleterious consequences of the inheritance of a tandem repeat array whose repeat number exceeds a critical threshold. In the case of FRDA, the repeat unit is the triplet GAA•TTC and the tandem array is located in the first intron of the frataxin (FXN) gene. Pathology arises because expanded alleles make lower than normal levels of mature FXN mRNA and thus reduced levels of frataxin, the FXN gene product. The repeats form a variety of unusual DNA structures that have the potential to affect gene expression in a number of ways. For example, triplex formation in vitro and in bacteria leads to the formation of persistent RNA:DNA hybrids that block transcription. In addition, these repeats have been shown to affect splicing in model systems. More recently, it has been shown that the region flanking the repeats in the FXN gene is enriched for epigenetic marks characteristic of transcriptionally repressed regions of the genome. However, exactly how repeats in an intron cause the FXN mRNA deficit in FRDA has been the subject of much debate. Identifying the mechanism or mechanisms responsible for the FXN mRNA deficit in FRDA is important for the development of treatments for this currently incurable disorder. This review discusses evidence for and against different models for the repeat-mediated mRNA deficit