Janus’ Voice: Religious Leaders, Framing, and Riots in Kano

This article analyses the role of religious leaders in collective violence in Kano, the major urban centre in northern Nigeria. It compares two episodes of collective action in the city—the violent ‘Plateau riots’ in 2004 and the non-violent ‘cartoon protests’ in 2006—to explore the role of religious leaders in the variation in violence between the two events. The core argument is that the ways in which Islamic and Christian preachers framed the triggering events for these cases facilitated different forms of mobilisation and enemy identification in response. In 2004, the interpretation of violence in Plateau State through the ‘Christians-versus-Muslims’ frame allowed for mobilisation within Kano’s Christian and Muslim communities as well as for the identification of local Christians as enemies. In 2006, in contrast, the infamous Danish cartoons were actively framed as part of the global struggle between faithful Nigerians and nonreligious Westerners, facilitating non-violent mobilisation across Christian-Muslim boundaries. Thus, the divergent discursive strategies employed by religious leaders are likely to have contributed to violent escalation in 2004 and to peaceful mobilisation in 2006. At the same time, however, the article emphasises the interaction of discursive framing with other factors, such as the role of security forces and the inextricable connections between religious and political authorities in Kano. The article is based on mixed-methods data collected in Kano between 2006 and 2012, including perceptions survey data, semi-structured interviews, and newspaper articles.Global Challenges (FGGA

Genome-wide scan for commons SNPs affecting bovine leukemia virus infection level in dairy cattle

Abstract Background Bovine leukemia virus (BLV) infection is omnipresent in dairy herds causing direct economic losses due to trade restrictions and lymphosarcoma-related deaths. Milk production drops and increase in the culling rate are also relevant and usually neglected. The BLV provirus persists throughout a lifetime and an inter-individual variation is observed in the level of infection (LI) in vivo. High LI is strongly correlated with disease progression and BLV transmission among herd mates. In a context of high prevalence, classical control strategies are economically prohibitive. Alternatively, host genomics studies aiming to dissect loci associated with LI are potentially useful tools for genetic selection programs tending to abrogate the viral spreading. The LI was measured through the proviral load (PVL) set–point and white blood cells (WBC) counts. The goals of this work were to gain insight into the contribution of SNPs (bovine 50KSNP panel) on LI variability and to identify genomics regions underlying this trait. Results We quantified anti–p24 response and total leukocytes count in peripheral blood from 1800 cows and used these to select 800 individuals with extreme phenotypes in WBCs and PVL. Two case-control genomic association studies using linear mixed models (LMMs) considering population stratification were performed. The proportion of the variance captured by all QC-passed SNPs represented 0.63 (SE ± 0.14) of the phenotypic variance for PVL and 0.56 (SE ± 0.15) for WBCs. Overall, significant associations (Bonferroni’s corrected -log10p > 5.94) were shared for both phenotypes by 24 SNPs within the Bovine MHC. Founder haplotypes were used to measure the linkage disequilibrium (LD) extent (r2 = 0.22 ± 0.27 at inter-SNP distance of 25−50 kb). The SNPs and LD blocks indicated genes potentially associated with LI in infected cows: i.e. relevant immune response related genes (DQA1, DRB3, BOLA-A, LTA, LTB, TNF, IER3, GRP111, CRISP1), several genes involved in cell cytoskeletal reorganization (CD2AP, PKHD1, FLOT1, TUBB5) and modelling of the extracellular matrix (TRAM2, TNXB). Host transcription factors (TFs) were also highlighted (TFAP2D; ABT1, GCM1, PRRC2A). Conclusions Data obtained represent a step forward to understand the biology of BLV–bovine interaction, and provide genetic information potentially applicable to selective breeding programs

Metabolic syndrome and risk factors for non-alcoholic fatty liver disease

CONTEXT: Non-alcoholic fatty liver disease (NAFLD), hepatic manifestation of metabolic syndrome, has been considered the most common liver disease nowadays, which is also the most frequent cause of elevated transaminases and cryptogenic cirrhosis. The greatest input of fatty acids into the liver and consequent increased beta-oxidation contribute to the formation of free radicals, release of inflammatory cytokines and varying degrees of hepatocytic aggression, whose histological expression may vary from steatosis (HS) to non-alcoholic steatohepatitis (NASH). The differentiation of these forms is required by the potential risk of progression to cirrhosis and development of hepatocellular carcinoma. OBJECTIVE: To review the literature about the major risk factors for NAFLD in the context of metabolic syndrome, focusing on underlying mechanisms and prevention. METHOD: PubMed, MEDLINE and SciELO data basis analysis was performed to identify studies describing the link between risk factors for metabolic syndrome and NAFLD. A combination of descriptors was used, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, metabolic syndrome and risk factors. At the end, 96 clinical and experimental studies, cohorts, meta-analysis and systematic reviews of great impact and scientific relevance to the topic, were selected. RESULTS: The final analysis of all these data, pointed out the central obesity, type 2 diabetes, dyslipidemia and hypertension as the best risk factors related to NAFLD. However, other factors were highlighted, such as gender differences, ethnicity, genetic factors and the role of innate immunity system. How these additional factors may be involved in the installation, progression and disease prognosis is discussed. CONCLUSION: Risk factors for NAFLD in the context of metabolic syndrome expands the prospects to 1) recognize patients with metabolic syndrome at high risk for NAFLD, 2) elucidate pathways common to other co-morbidities, 3) determine risk factors associated with a worse prognosis, 4) develop therapeutic strategies with goal of reducing risk factors, 5) apply acquired knowledge in public health policies focusing on preventive strategies