Desempenho produtivo e qualidade da carne de frangos alimentados com ração contendo óleo de linhaça

O objetivo deste trabalho foi avaliar o efeito da utilização de óleo de linhaça, em substituição ao óleo de soja, sobre a produtividade e a qualidade da carne de frangos de corte de ambos os sexos. Foram utilizadas 320 aves, em um arranjo fatorial 4x2 - quatro combinações dos períodos de fornecimento de óleo de soja e óleo de linhaça e dois sexos - e quatro repetições. O desempenho produtivo foi avaliado por pesagens da ração e das aves com 1, 21, 42 dias e no momento do abate, aos 49 dias de idade. Após o abate, foi avaliado o rendimento de carcaça e sua composição: cortes, vísceras e gordura abdominal. Foram determinados os teores de lipídeos totais, umidade e colesterol da carne. A dieta contendo óleo de linhaça melhorou a qualidade nutricional da fração lipídica da carne de frango, mas prejudicou o desempenho produtivo das aves

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease