The effect of analytical temperature on thromboelastography tracings in dogs.

Viscoelastic testing methods such as thromboelastography (TEG) are becoming increasingly available to veterinarians in a clinical setting. TEG is useful in determining therapeutic transfusion needs and assessing global abnormalities of hemostasis of patients, given that it provides a more comprehensive assessment of coagulation than traditional tests. TEG is standardly performed at 37°C, which is considered a normal body temperature for human patients; however, 37°C is lower than normal body temperature for most canine patients. In an in vitro study, we investigated the potential effect that this difference in body temperature and test temperature might have on TEG results. Citrated blood samples were collected from clinically normal, as well as sick, dogs with various body temperatures. Samples were analyzed concurrently at the patient's body temperature and at 37°C. There was very high correlation between TEG performed at body temperature and at 37°C for R (min) and MA (mm), high correlation for K (min) and alpha angle (deg), and moderate correlation for LY30 (%) and LY60 (%). For canine patients with normal to mildly abnormal body temperatures, performance of TEG at the standard 37°C is acceptable.

DDX6 Represses Aberrant Activation of Interferon-Stimulated Genes.

The innate immune system tightly regulates activation of interferon-stimulated genes (ISGs) to avoid inappropriate expression. Pathological ISG activation resulting from aberrant nucleic acid metabolism has been implicated in autoimmune disease; however, the mechanisms governing ISG suppression are unknown. Through a genome-wide genetic screen, we identified DEAD-box helicase 6 (DDX6) as a suppressor of ISGs. Genetic ablation of DDX6 induced global upregulation of ISGs and other immune genes. ISG upregulation proved cell intrinsic, imposing an antiviral state and making cells refractory to divergent families of RNA viruses. Epistatic analysis revealed that ISG activation could not be overcome by deletion of canonical RNA sensors. However, DDX6 deficiency was suppressed by disrupting LSM1, a core component of mRNA degradation machinery, suggesting that dysregulation of RNA processing underlies ISG activation in the DDX6 mutant. DDX6 is distinct among DExD/H helicases that regulate the antiviral response in its singular ability to negatively regulate immunity.