Rethinking Sudan Studies: A Post-2011 Manifesto

Abstract This essay appraises “Sudan Studies” following the 2011 secession of South Sudan. It asks two questions. First, what has Sudan Studies been as a colonial and postcolonial field of academic inquiry and how should or must it change? Second, should we continue to write about a single arena of Sudan Studies now that Sudan has split apart? The authors advance a “manifesto” for Sudan Studies by urging scholars to map out more intellectual terrain by attending to non-elite actors and women; grass-roots and local history; the environment and the arts; oral sources; and interdisciplinary studies of culture, politics, and society. They propose that scholars can transcend the changing boundaries of the nation-state, and recognize connections forged through past and present migrations and contacts, by studying the Sudan as a zone rather than a fixed country. Finally, in their introduction to this bilingual special issue, they highlight the increasing relevance of French scholarship to the endeavor of rethinking Sudan Studies. Résumé Cet essai évalue la situation des « études soudanaises » après la sécession du Soudan du Sud. Il pose deux questions. La première : En quoi ont consisté les études soudanaises en tant que domaine colonial et postcolonial de recherche universitaire et dans quelle mesure doivent-elles changer, si tant est qu\u27elles doivent changer ? La seconde : Devrions-nous continuer à baser nos écrits sur un domaine unique d\u27études soudanaises maintenant que le Soudan est divisé ? Les auteurs proposent un « manifeste » pour les études soudanaises en exhortant les experts à cartographier un terrain intellectuel élargi en s\u27intéressant aux acteurs ne faisant pas partie des élites et des femmes ; à l\u27histoire de la base populaire et locale ; à l\u27environnement et à l\u27art ; aux sources orales ; et aux études interdisciplinaires portant sur la culture, la politique et la société. Ils avancent que les chercheurs peuvent aller au-delà des frontières en mutation de l\u27État-nation et reconnaitre les connexions établies grâce aux migrations et aux contacts passés et présents en étudiant le Soudan comme zone plutôt que comme un pays fixe. Enfin, dans leur introduction à ce numéro bilingue spécial, ils mettent en relief la pertinence croissance des travaux universitaires français dans le cadre de l\u27initiative visant à repenser les études soudanaises

Polymorphisms in the Hsp70 gene locus are genetically associated with systemic lupus erythematosus

Background Heat shock proteins (Hsps) play a role in the delivery and presentation of antigenic peptides and are thought to be involved in the pathogenesis of multifactorial diseases. Objective To investigate genes encoding cytosolic Hsp70 proteins for associations of allelic variants with systemic lupus erythematosus (SLE). Methods Case-control studies of two independent Caucasian SLE cohorts were performed. In a haplotype-tagging single-nucleotide polymorphism approach, common variants of HspA1L, HspA1A and HspA1B were genotyped and principal component analyses were performed for the cohort from the Oklahoma Medical Research Foundation (OMRF). Relative quantification of mRNA was carried out for each Hsp70 gene in healthy controls. Conditional regression analysis was performed to determine if allelic variants in Hsp70 act independently of HLA-DR3. Results On analysis of common genetic variants of HspA1L, HspA1A and HspA1B, a haplotype significantly associated with SLE in the Erlangen-SLE cohort was identified, which was confirmed in the OMRF cohort. Depending on the cohorts, OR ranging from 1.43 to 1.88 and 2.64 to 3.16 was observed for individuals heterozygous and homozygous for the associated haplotype, respectively. Patients carrying the risk haplotype or the risk allele more often displayed autoantibodies to Ro and La in both cohorts. In healthy controls bearing this haplotype, the amount of HspA1A mRNA was significantly increased, whereas total Hsp70 protein concentration was not altered. Conclusions Allelic variants of the Hsp70 genes are significantly associated with SLE in Caucasians, independently of HLA-DR3, and correlate with the presence of autoantibodies to Ro and La. Hence, the Hsp70 gene locus appears to be involved in SLE pathogenesis

Ultra-Low-Noise W-Band MMIC Detector Modules

A monolithic microwave integrated circuit (MMIC) receiver can be used as a building block for next-generation radio astronomy instruments that are scalable to hundreds or thousands of pixels. W-band (75-110 GHz) low-noise receivers are needed for radio astronomy interferometers and spectrometers, and can be used in missile radar and security imagers. These receivers need to be designed to be mass-producible to increase the sensitivity of the instrument. This innovation is a prototyped single-sideband MMIC receiver that has all the receiver front-end functionality in one small and planar module. The planar module is easy to assemble in volume and does not require tuning of individual receivers. This makes this design low-cost in large volumes

Dating the detachment fault system of the Ruby Mountains, Nevada: Significance for the kinematics of low‐angle normal faults

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94601/1/tect2138.pd

Induction of Eosinophil Apoptosis by the Cyclin-Dependent Kinase Inhibitor AT7519 Promotes the Resolution of Eosinophil-Dominant Allergic Inflammation

Eosinophils not only defend the body against parasitic infection but are also involved in pathological inflammatory allergic diseases such as asthma, allergic rhinitis and contact dermatitis. Clearance of apoptotic eosinophils by macrophages is a key process responsible for driving the resolution of eosinophilic inflammation and can be defective in allergic diseases. However, enhanced resolution of eosinophilic inflammation by deliberate induction of eosinophil apoptosis using pharmacological agents has not been previously demonstrated. Here we investigated the effect of a novel cyclin-dependent kinase inhibitor drug, AT7519, on human and mouse eosinophil apoptosis and examined whether it could enhance the resolution of a murine model of eosinophil-dominant inflammation in vivo.Eosinophils from blood of healthy donors were treated with AT7519 and apoptosis assessed morphologically and by flow-cytometric detection of annexin-V/propidium iodide staining. AT7519 induced eosinophil apoptosis in a concentration dependent manner. Therapeutic administration of AT7519 in eosinophil-dominant allergic inflammation was investigated using an established ovalbumin-sensitised mouse model of allergic pleurisy. Following ovalbumin challenge AT7519 was administered systemically at the peak of pleural inflammation and inflammatory cell infiltrate, apoptosis and evidence of macrophage phagocytosis of apoptotic eosinophils assessed at appropriate time points. Administration of AT7519 dramatically enhanced the resolution of allergic pleurisy via direct induction of eosinophil apoptosis without detriment to macrophage clearance of these cells. This enhanced resolution of inflammation was shown to be caspase-dependent as the effects of AT7519 were reduced by treatment with a broad spectrum caspase inhibitor (z-vad-fmk).Our data show that AT7519 induces human eosinophil apoptosis and enhances the resolution of a murine model of allergic pleurisy by inducing caspase-dependent eosinophil apoptosis and enhancing macrophage ingestion of apoptotic eosinophils. These findings demonstrate the utility of cyclin-dependent kinase inhibitors such as AT7519 as potential therapeutic agents for the treatment of eosinophil dominant allergic disorders

Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana

Sulphur (S) is an essential element for all living organisms. The uptake, assimilation and metabolism of S in plants are well studied. However, the regulation of S homeostasis remains largely unknown. Here, we report on the identification and characterisation of the more sulphur accumulation1 (msa1-1) mutant. The MSA1 protein is localized to the nucleus and is required for both S adenosylmethionine (SAM) production and DNA methylation. Loss of function of the nuclear localised MSA1 leads to a reduction in SAM in roots and a strong S-deficiency response even at ample S supply, causing an over- accumulation of sulphate, sulphite, cysteine and glutathione. Supplementation with SAM suppresses this high S phenotype. Furthermore, mutation of MSA1 affects genome-wide DNA methylation, including the methylation of S-deficiency responsive genes. Elevated S accumulation in msa1-1 requires the increased expression of the sulphate transporter genes SULTR1;1 and SULTR1;2 which are also differentially methylated in msa1-1. Our results suggest a novel function for MSA1 in the nucleus in regulating SAM biosynthesis and maintaining S homeostasis epigenetically via DNA methylation