RESUMEN
The Wells-Riley model has been widely used to estimate airborne infection risk, typically from a deterministic point of view (i.e., focusing on the average number of infections) or in terms of a per capita probability of infection. Some of its main limitations relate to considering well-mixed air, steady-state concentration of pathogen in the air, a particular amount of time for the indoor interaction, and that all individuals are homogeneous and behave equally. Here, we revisit the Wells-Riley model, providing a mathematical formalism for its stochastic version, where the number of infected individuals follows a Binomial distribution. Then, we extend the Wells-Riley methodology to consider transient behaviours, randomness, and population heterogeneity. In particular, we provide analytical solutions for the number of infections and the per capita probability of infection when: (i) susceptible individuals remain in the room after the infector leaves, (ii) the duration of the indoor interaction is random/unknown, and (iii) infectors have heterogeneous quanta production rates (or the quanta production rate of the infector is random/unknown). We illustrate the applicability of our new formulations through two case studies: infection risk due to an infectious healthcare worker (HCW) visiting a patient, and exposure during lunch for uncertain meal times in different dining settings. Our results highlight that infection risk to a susceptible who remains in the space after the infector leaves can be nonnegligible, and highlight the importance of incorporating uncertainty in the duration of the indoor interaction and the infectivity of the infector when estimating risk.
RESUMEN
IBDs (inflammatory bowel diseases) are lifelong manifestations that significantly impair the quality of life of those who suffer from them. Although many therapies are now available, including immunomodulatory drugs such as Infliximab which have efficacy in IBD, not all patients respond and some patients generate autoantibodies against these drugs. Hence the search for novel treatments is ongoing. HDACs (histone deacetylases) are responsible for condensation of chromatin in the nucleus of cells and inhibition of gene transcription and are often dysregulated during cancer. HDAC inhibitors allow normal gene transcription to be restored and provide attractive therapeutic options, as they have been shown to be anti-inflammatory and anti-proliferative in cancer. Indeed, two HDAC inhibitors have been recently approved for the treatment of cutaneous T-cell lymphoma in the U.S.A. Recent research using animal models has shown that HDAC inhibitors may have a beneficial effect in colitis by boosting levels of Foxp3+ (forkhead box P3+) T-regulatory cells that dampen inflammation. In the present paper, we outline the background to IBD, HDACs and their inhibitors as well as discussing their current use in models of IBD.