Ex vivo innate immune cytokine signature of enhanced risk of relapsing brucellosis.

Background: Brucellosis, a zoonotic infection caused by one of the Gram-negative intracellular bacteria of the Brucella genus, is an ongoing public health problem in Perú. While most patients who receive standard antibiotic treatment recover, 5-40% suffer a brucellosis relapse. In this study, we examined the ex vivo immune cytokine profiles of recovered patients with a history of acute and relapsing brucellosis.

Characterizing the relationship between steady state and response using analytical expressions for the steady states of mass action models.

The steady states of cells affect their response to perturbation. Indeed, diagnostic markers for predicting the response to therapeutic perturbation are often based on steady state measurements. In spite of this, no method exists to systematically characterize the relationship between steady state and response.

A protein turnover signaling motif controls the stimulus-sensitivity of stress response pathways.

Stimulus-induced perturbations from the steady state are a hallmark of signal transduction. In some signaling modules, the steady state is characterized by rapid synthesis and degradation of signaling proteins. Conspicuous among these are the p53 tumor suppressor, its negative regulator Mdm2, and the negative feedback regulator of NFκB, IκBα.

A framework for modeling the relationship between cellular steady-state and stimulus-responsiveness.

In cell signaling systems, the abundances of signaling molecules are generally thought to determine the response to stimulation. However, the kinetics of molecular processes, for example receptor trafficking and protein turnover, may also play an important role. Few studies have systematically examined this relationship between the resting state and stimulus-responsiveness.