Lattice Boltzmann Simulation of the Kinetics Process of Methane Diffusion with the Adsorption-Desorption Hysteresis Effect in Coal.

The occurrence of coalbed methane adsorption-desorption hysteresis has been widely observed, but a unified understanding of its mechanism is lacking, and the factors affecting its degree are unclear. This study introduces a microscale LB model for gas diffusion-adsorption-desorption in porous media that also accounts for the adsorption-desorption hysteresis effect. The accuracy of the model has been validated using previous experimental data, and the primary controlling factors of adsorption-desorption hysteresis were analyzed. The findings are as follows: (1) In the process of methane diffusion-adsorption-desorption, Knudsen diffusion dominates in micro- and mesopores, while viscous flow prevails in macropores; our model can adaptively adjust gas transport regimes across a broad range of pore sizes and pressures. (2) The desorption amount and rate are close relative to the correction factors α and ß. A higher α value corresponds to greater initial adsorption as well as longer desorption time, whereas a lower ß value implies weaker desorption capacity and a slower desorption rate. (3) Pore size can affect gas diffusion-adsorption-desorption kinetics, where larger pore size corresponds to efficient gas diffusivity; when r < 10 nm, the desorption process is mainly controlled by the desorption rate. Overall, this study has offered new insights into the mechanism behind methane adsorption-desorption hysteresis at the microscale, identified primary controlling factors of methane diffusion-adsorption-desorption process, and provided a foundation for numerical simulations and experiments related to the adsorption-desorption hysteresis.

Th17: a new participant in gut dysfunction in mice infected with Trichinella spiralis.

Trichinella spiralis infection in rodents is a well-known model of intestinal inflammation associated with hypermotility. Our aim was to elucidate if Th17 cells were involved in the development of gastrointestinal hypermotility in this experimental model. Intestinal inflammation was observed by hematoxylin-eosin (HE) staining. Jejunal smooth muscle contractility was investigated in response to acetylcholine (Ach). The effects of IL-17 on jejunum smooth muscle contractility were explored. Flow cytometry was used to analyze the proportion of Th17 cells in jejunum. The levels of IL-17, IL-23, and TGF-beta1 in jejunum were measured by Western blot. Our results showed that the inflammation in jejunum was severe at 2 weeks postinfection (PI), which was not discernible at 8 weeks PI. Jejunal smooth muscle contractility was increased at 2 weeks PI and kept higher at 12 weeks PI. The proportion of Th17 cells and the expression of IL-17 were upregulated in jejunum at 2 weeks PI and normalized at 8 weeks PI. When jejunual smooth muscle strips were cultured with IL-17, contractions elicited by Ach were enhanced in a concentration-dependent manner. Our data suggest that Th17 cells are increased during acute infection with Trichinella spiralis and IL-17 may contribute to jejunal muscle contractility in mice.