The companion dog as a model for human aging and mortality

Around the world, human populations have experienced large increases in average lifespan over the last 150 years, and while individuals are living longer, they are spending more years of life with multiple chronic morbidities. Researchers have used numerous laboratory animal models to understand the biological and environmental factors that influence aging, morbidity, and longevity. However, the most commonly studied animal species, laboratory mice and rats, do not experience environmental conditions similar to those to which humans are exposed, nor do we often diagnose them with many of the naturally occurring pathologies seen in humans. Recently, the companion dog has been proposed as a powerful model to better understand the genetic and environmental determinants of morbidity and mortality in humans. However, it is not known to what extent the age-related dynamics of morbidity, comorbidity, and mortality are shared between humans and dogs. Here, we present the first large-scale comparison of human and canine patterns of age-specific morbidity and mortality. We find that many chronic conditions that commonly occur in human populations (obesity, arthritis, hypothyroidism, and diabetes), and which are associated with comorbidities, are also associated with similarly high levels of comorbidity in companion dogs. We also find significant similarities in the effect of age on disease risk in humans and dogs, with neoplastic, congenital, and metabolic causes of death showing similar age trajectories between the two species. Overall, our study suggests that the companion dog may be an ideal translational model to study the many complex facets of human morbidity and mortality

Note on Seiberg Duality in Matrix Model

In this note, we give a method to derive the Seiberg duality by the matrix model. The key fact we used is that the effective actions given by matrix model method should be identical for both electric and magnetic theories. We demonstrate our method for SQCD with U(N), SO(N) and Sp(N) gauge groups.Comment: 10 page

Glucagon-stimulated respiration and intracellular Ca2+

AbstractThe effects of extra- and intracellular Ca2+ on glucagon-stimulated respiration were examined in perfused rat liver. Glucagon increased the uptake of O2 to a significantly greater extent in Ca2+ -containing perfusate than in Ca2+-free perfusate. If, however, the livers were perfused first with Ca2+-containing perfusate for 60 min in order to load the hormone-sensitive Ca2+ pool(s) and subsequently with Ca2+-free perfusate, glucagon was able to stimulate O2 uptake to the same extent in Ca2+ -free, as in Ca2+-containing perfusate. These experiments support previous observations of a connection between Ca2+ and the hormonal stimulation of respiration, but indicate a role for intracellular, rather than extracellular, Ca2+ in the process