Improving acoustic wave propagation models in highly attenuating porous materials

This article presents an improved and extended modeling approach for acoustic wave propagation in rigid porous materials, focusing on examples such as plastic foams used for noise reduction in automotive applications. We demonstrate that the classical model (Johnson-Champoux-Allard) in the asymptotic high frequency limit, widely employed in the literature, fail to accurately reconstruct the transmitted acoustic signal through high absorbant porous materials characterized by significant wave attenuation. The study focuses on the airborne ultrasonic frequency range (30-200 kHz). To address this limitation, we introduce new non-acoustic parameters Σ and V , and Σ0 and V for thermal effects, with surface and volumetric dimensions, respectively, allowing for the reconstruction of the transmitted signal and accurate modeling of the pronounced acoustic attenuation within the material. These parameters are incorporated into the expansion on skin depths of the dynamic tortuosity α(ω) and thermal tortuosity α'(ω) response functions, which describe the inertial-viscous and thermal interactions between the fluid and the solid, respectively. This novel modeling approach enables a more comprehensive study of high attenuating porous media, which are crucial for effective noise reduction. Additionally, it opens up new possibilities for characterization beyond the capabilities of current models

Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling

International audiencePancreatic ductal adenocarcinoma (PDAC) is one of the solid tumors with the poorest prognosis. The stroma of this tumor is abundant and composed of extracellular matrix and stromal cells (including cancer-associated fibroblasts and immune cells). Nerve fibers invading this stroma represent a hallmark of PDAC, involved in neural remodeling, which participates in neuropathic pain, cancer cell dissemination and tumor relapse after surgery. Pancreatic cancer-associated neural remodeling is regulated through functional interplays mediated by physical and molecular interactions between cancer cells, nerve cells and surrounding Schwann cells, and other stromal cells. In the present study, we show that Schwann cells (glial cells supporting peripheral neurons) can enhance aggressiveness (migration, invasion, tumorigenicity) of pancreatic cancer cells in a transforming growth factor beta (TGFβ)-dependent manner. Indeed, we reveal that conditioned medium from Schwann cells contains high amounts of TGFβ able to activate the TGFβ-SMAD signaling pathway in cancer cells. We also observed in human PDAC samples that high levels of TGFβ signaling activation were positively correlated with perineural invasion. Secretome analyses by mass spectrometry of Schwann cells and pancreatic cancer cells cultured alone or in combination highlighted the central role of TGFβ in neuro-epithelial interactions, as illustrated by proteomic signatures related to cell adhesion and motility. Altogether, these results demonstrate that Schwann cells are a meaningful source of TGFβ in PDAC, which plays a crucial role in the acquisition of aggressive properties by pancreatic cancer cells