INFLUENCE OF DIFFERENT SOURCES AND LEVELS OF NITROGEN AND ROCK PHOSPHATE ADDITION ON MAIZE PRODUCTIVITY AND SOIL FERTILITY

n/

Epidemiology and Diagnosis of Feline Intestinal Lymphosarcomas in Egypt

Feline intestinal lymphosarcomas are mostly caused by Feline Leukemia Virus (FeLV). Unfortunately, there is no available vaccine for FeLV in Egypt. The diagnosis of feline intestinal lymphosarcomas depends upon abdominal palpation, x-rays examination, ultrasonography, direct ELISA and histopathology of masses excised during laparotomy. The recorded clinical signs in intestinal lymphosarcoma affected cats were variable including vomiting, fever, anorexia, ascites, anemia, dyspnea, constipation and emaciation. The affected lymph nodes were mesenteric, mediastinal and retropharyngeal. The prevalence of intestinal lymphosarcomas in the examined cats was 4.03 % (11 out of 273 cats). The prevalence was higher in queens than toms (2.93 % and 0.73 % respectively). The Siamese cats had higher prevalence than the Sherazy ones (2.56 % and 1.47 % respectively). X-ray films and ultrasonographic images performed on the eleven cats suffered from intestinal lymphosarcomas revealed ascities and abdominal masses. The comparison of ELISA and histopathology (of excised masses) results showed that 9 out of 11 intestinal lymphosarcoma affected cats were infected with FeLV that proved not all cases of intestinal lymphosarcoma were caused by FeLV. The sensitivity, specificity and accuracy of ELISA to diagnose intestinal lymphosarcoma in cats were 81.81 %, 100 % and 92 % respectively. Gross autopsy of the collected lymph nodes, livers, kidneys revealed that gross lymphadenopathy involving one or more nodes, hepatomegaly and kidney enlargement. Microscopically, the examined tissues specimens showed that the normal architecture of the examined lymph nodes, livers, and kidneys has been replaced by a diffuse infiltrate of both lymphocytes and lymphoblasts. The vast majority of the cells are small lymphocyte-type cells with round basophilic nuclei and a sparse rim of cytoplasm. The eleven intestinal lymphosarcoma affected cats exposed to abdominal exploratory surgery (laparotomy) died at one to three months post-surgery. It is concluded that the vaccination of kittens and cats against FeLV in Egypt is very important to prevent the highly fatal intestinal lymphosarcomas

Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances

We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1, ATXN2/BRAP, FURIN/FES, ZW10, PSORS1C3, and 13q21.31, and identify and replicate novel findings near ABO, ZC3HC1, and IGF2R. We also validate previous findings near 5q33.3/EBF1 and FOXO3, whilst finding contradictory evidence at other loci. Gene set and cell-specific analyses show that expression in foetal brain cells and adult dorsolateral prefrontal cortex is enriched for lifespan variation, as are gene pathways involving lipid proteins and homeostasis, vesicle-mediated transport, and synaptic function. Individual genetic variants that increase dementia, cardiovascular disease, and lung cancer - but not other cancers - explain the most variance. Resulting polygenic scores show a mean lifespan difference of around five years of life across the deciles.Peer reviewe

Genome-wide association analyses identify 143 risk variants and putative regulatory mechanisms for type 2 diabetes

Type 2 diabetes (T2D) is a very common disease in humans. Here we conduct a meta-analysis of genome-wide association studies (GWAS) with ~16 million genetic variants in 62,892 T2D cases and 596,424 controls of European ancestry. We identify 139 common and 4 rare variants associated with T2D, 42 of which (39 common and 3 rare variants) are independent of the known variants. Integration of the gene expression data from blood (n = 14,115 and 2765) with the GWAS results identifies 33 putative functional genes for T2D, 3 of which were targeted by approved drugs. A further integration of DNA methylation (n = 1980) and epigenomic annotation data highlight 3 genes (CAMK1D, TP53INP1, and ATP5G1) with plausible regulatory mechanisms, whereby a genetic variant exerts an effect on T2D through epigenetic regulation of gene expression. Our study uncovers additional loci, proposes putative genetic regulatory mechanisms for T2D, and provides evidence of purifying selection for T2D-associated variants

Integrating sequence and array data to create an improved 1000 Genomes Project haplotype reference panel

A major use of the 1000 Genomes Project (1000GP) data is genotype imputation in genome-wide association studies (GWAS). Here we develop a method to estimate haplotypes from low-coverage sequencing data that can take advantage of single-nucleotide polymorphism (SNP) microarray genotypes on the same samples. First the SNP array data are phased to build a backbone (or 'scaffold') of haplotypes across each chromosome. We then phase the sequence data 'onto' this haplotype scaffold. This approach can take advantage of relatedness between sequenced and non-sequenced samples to improve accuracy. We use this method to create a new 1000GP haplotype reference set for use by the human genetic community. Using a set of validation genotypes at SNP and bi-allelic indels we show that these haplotypes have lower genotype discordance and improved imputation performance into downstream GWAS samples, especially at low-frequency variants. © 2014 Macmillan Publishers Limited. All rights reserved

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden