Pseudo-shock waves and their interactions in high-speed intakes

In an air-breathing engine the flow deceleration from supersonic to subsonic conditions takes places inside the isolator through a gradual compression consisting of a series of shock waves. The wave system, referred to as a pseudo-shock wave or shock train, establishes the combustion chamber entrance conditions, and therefore influences the performance of the entire propulsion system. The characteristics of the pseudo-shock depend on a number of variables which make this flow phenomenon particularly challenging to be analysed. Difficulties in experimentally obtaining accurate flow quantities at high speeds and discrepancies of numerical approaches with measured data have been readily reported. Understanding the flow physics in the presence of the interaction of numerous shock waves with the boundary layer in internal flows is essential to developing methods and control strategies. To counteract the negative effects of shock wave/boundary layer interactions, which are responsible for the engine unstart process, multiple flow control methodologies have been proposed. Improved analytical models, advanced experimental methodologies and numerical simulations have allowed a more in-depth analysis of the flow physics. The present paper aims to bring together the main results, on the shock train structure and its associated phenomena inside isolators, studied using the aforementioned tools. Several promising flow control techniques that have more recently been applied to manipulate the shock wave/boundary layer interaction are also examined in this review

Focal adhesion kinase: Insight into molecular roles and functions in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Due to the high incidence of post-operative recurrence after current treatments, the identification of new and more effective drugs is required. In previous years, new targetable genes/pathways involved in HCC pathogenesis have been discovered through the help of high-throughput sequencing technologies. Mutations in TP53 and β-catenin genes are the most frequent aberrations in HCC. However, approaches able to reverse the effect of these mutations might be unpredictable. In fact, if the reactivation of proteins, such as p53 in tumours, holds great promise as anticancer therapy, there are studies arguing that chronic activation of these types of molecules may be deleterious. Thus, recently the efforts on potential targets have focused on actionable mutations, such as those occurring in the gene encoding for focal adhesion kinase (FAK). This tyrosine kinase, localized to cellular focal contacts, is over-expressed in a variety of human tumours, including HCC. Moreover, several lines of evidence demonstrated that FAK depletion or inhibition impair in vitro and in vivo HCC growth and metastasis. Here, we provide an overview of FAK expression and activity in the context of tumour biology, discussing the current evidence of its connection with HCC development and progression