Pitt Political Review: GSPIA Edition (Spring 2011, Volume 3)

This volume of the Pitt Political Review: GSPIA Edition includes "Legal and Societal Injustice: Gender Inequality and Land Rights in Tanzania" and "The Transformation of Philanthropy in Sub-Saharan Africa: from Traditional Practices to the Establishment of Grantmaking Foundations." The aim of "Legal and Societal Injustice: Gender Inequality and Land Rights in Tanzania" is to increase awareness of the problems surrounding land rights and gender inequality in Tanzania's Karagwe District. "The Transformation of Philanthropy in Sub-Saharan Africa: from Traditional Practices to the Establishment of Grantmaking Foundations" discusses the effectiveness of African foundations in development over the long-term

A detector for CLIC: main parameters and performance

Together with the recent CLIC detector model CLICdet a new software suite was introduced for the simulation and reconstruction of events in this detector. This note gives a brief introduction to CLICdet and describes the CLIC experimental conditions at 380 GeV and 3 TeV, including beam-induced backgrounds. The simulation and reconstruction tools are introduced, and the physics performance obtained is described in terms of single particles, particles in jets, jet energy resolution and flavour tagging. The performance of the very forward electromagnetic calorimeters is also discussed

Individuals with mutations in XPNPEP3, which encodes a mitochondrial protein, develop a nephronophthisis-like nephropathy

The autosomal recessive kidney disease nephronophthisis (NPHP) constitutes the most frequent genetic cause of terminal renal failure in the first 3 decades of life. Ten causative genes (NPHP1–NPHP9 and NPHP11), whose products localize to the primary cilia-centrosome complex, support the unifying concept that cystic kidney diseases are “ciliopathies”. Using genome-wide homozygosity mapping, we report here what we believe to be a new locus (NPHP-like 1 [NPHPL1]) for an NPHP-like nephropathy. In 2 families with an NPHP-like phenotype, we detected homozygous frameshift and splice-site mutations, respectively, in the X-prolyl aminopeptidase 3 (XPNPEP3) gene. In contrast to all known NPHP proteins, XPNPEP3 localizes to mitochondria of renal cells. However, in vivo analyses also revealed a likely cilia-related function; suppression of zebrafish xpnpep3 phenocopied the developmental phenotypes of ciliopathy morphants, and this effect was rescued by human XPNPEP3 that was devoid of a mitochondrial localization signal. Consistent with a role for XPNPEP3 in ciliary function, several ciliary cystogenic proteins were found to be XPNPEP3 substrates, for which resistance to N-terminal proline cleavage resulted in attenuated protein function in vivo in zebrafish. Our data highlight an emerging link between mitochondria and ciliary dysfunction, and suggest that further understanding the enzymatic activity and substrates of XPNPEP3 will illuminate novel cystogenic pathways