Megabacteriose em emas (Rhea americana) no Estado do Rio Grande do Sul, Brasil Megabacteriosis in Rhea americana in the State of Rio Grande do Sul, Brazil

Com o objetivo de avaliar as causas de mortalidade de filhotes de ema de uma propriedade, pesquisou-se megabactéria em esfregaços de moelas de oito emas, corados pelo método de Gram, associado a exame histopatológico. Os exames foram positivos para megabactéria em quatro emas. A confirmação de megabacteriose em emas no Rio Grande do Sul é de grande importância, pois a enfermidade pode gerar grandes perdas econômicas. Salienta-se a necessidade de maiores investigações nos diferentes criatórios, tendo em vista a elevada mortalidade inicial dos filhotes relatada pelos criadores, podendo ser a megabacteriose uma das causas.<br>To evaluate the causes of high mortality in great rhea chicks, we performed a study searching for megabacteria in Gram stained smear of eight great rhea gizzards, also examined by histopathology. The results were positive in four great rhea. The confirmation of megabacteriosis in great rhea in Rio Grande do Sul State, Brazil, has great importance, because the disease could be causing severe economic losses. We emphasize the need of further studies in the different great rhea farms to investigate the possible role of megabacteriosis in the high mortality of great rhea chicks

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes

OBJECTIVE - Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired b-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS - We have conducted a meta-analysis of genome-wide association tests of ;2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS - Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10-8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/ C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 3 10-4), improved b-cell function (P = 1.1 × 10-5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10-6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS - We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis