Our results show that, before reaching the new equilibrium, and especially at the early stages of the adaptive process, there is no simple relationship between the momentary degree of adaptation and the new error rate at which a population evolves. There is also a strong influence of the mutation rate at which populations evolved towards the previous stationary state in their ability to adapt to new selective pressures. Our results are of relevance to understand the adaptive process in changing environments when variations of the mutation rate are allowed. Some actual examples of this situation are the in vitro evolution of structural or catalytic RNA molecules and proteins -where the experimenter can manipulate the extension of the genetic diversity generated- the selection of mutator variants of pathogenic bacteria in response to antibiotics, hampering the treatment of many diseases, and also RNA viruses in which even very mild mutator or antimutator phenotypes can have important consequences in shaping not only virus evolution, but also pathogenesis, transmission, and emergence. Strong Wnt/b-catenin signaling inhibits chondrocyte cell fate determination and maintenance whereas weaker Wnt/b-catenin signaling promotes chondrocyte hypertrophy by reducing PTHrP signaling activities. Acute cortical thinning is commonly caused by increased corticosteroids induced by various stressors, including infection, disease, chemotherapy, irradiation, and malnutrition, or by treatment with dexamethasone or 2,3,7,8-tetrachlorodibenzo-p-dioxin. A key goal for further studies will be to establish if neutrophil motility is a more reliable diagnostic or prognostic indicator of infection among burn patients than the nonspecific parameters of white blood cell count and fever. Despite the profound role that sepsis plays in the morbidity and mortality of burn patients, standard clinical and laboratory markers of infection are unreliable in the setting of severe burn injury. For most clinical conditions, fever, leukocytosis, tachycardia, increased respiratory rate, and hypotension signal the onset of sepsis. In the burn population, however, the GDC-0199 distributor massive inflammatory cascade that follows thermal injury, coupled with insensible volume losses, trigger these findings even in the absence of infection. The dilemma is so profound that in 2007, the American Burn Association published a consensus statement that condemned the peripheral white blood cell count as an appropriate diagnostic criterion for sepsis in burn patients. Our preliminary results suggest that preservation of neutrophil chemotaxis in burn patients may correspond with bacteremia, and may signal the need for antibiotic therapy in the absence of culture data. All but one patient demonstrated depressed neutrophil motility compared with controls, with maximal depression at 3-5 days post-injury.