Alterations in nasal airflow and air conditioning after endoscopic nasopharyngectomy for recurrent nasopharyngeal carcinoma: a pilot computational fluid dynamics study.

Endoscopic nasopharyngectomy represents a significant intervention for recurrent nasopharyngeal carcinoma (NPC). Various surgical techniques, including transnasal and transoral approaches, are employed. However, the impact of these procedures on nasal airflow dynamics is not well understood. This computational fluid dynamics (CFD) study aimed to investigate alterations in nasal airflow and air conditioning following endoscopic nasopharyngectomy. A 55-year-old male patient with recurrent NPC was selected, whose CT data were utilized for image reconstruction. A preoperative model and two postoperative models, including the transnasal and transoral approach models, were established. The airflow patterns and various CFD parameters were analyzed. In the postoperative models, the high-speed airflow went along the soft palate and into the nasopharyngeal outlet, and there was the low-speed turbulence in the expanded nasopharyngeal cavity. Compared to the preoperative model, the postoperative models exhibited reductions in surface-to-volume ratio, nasal resistance, airflow velocity and proportion of high wall shear stress regions in nasopharynx. The changing trends of nasopharyngeal air temperature and humidity in the preoperative and transoral models were consistent. The heating and humidification efficiency decreased in the transnasal model compared to the transoral model. The endoscopic nasopharyngectomy for recurrent NPC affects the nasal airflow and warming and humidification function. The transoral approach has less influence on aerodynamics of the upper airway compared to the transnasal approach. From a CFD perspective, the endoscopic nasopharyngectomy does not increase the risk of postoperative complications, including the empty nose syndrome and the carotid blowout syndrome.

The role of E2F2 in cancer progression and its value as a therapeutic target.

The E2F family of transcription factors plays a crucial role in the regulation of cell cycle progression and cell proliferation. Accumulative evidence indicates that aberrant expression or activation of E2F2 is a common phenomenon in malignances. E2F2 has emerged as a key player in the development and progression of various types of tumors. A wealth of research has substantiated that E2F2 could contribute to the enhancement of tumor cell proliferation, angiogenesis, and invasiveness. Moreover, E2F2 exerts its influence on a myriad of cellular processes by engaging with a spectrum of auxiliary factors and downstream targets, including apoptosis and DNA repair. The dysregulation of E2F2 in the context of carcinogenesis may be attributable to a multitude of mechanisms, which encompass modifications in upstream regulatory elements or epigenetic alterations. This review explores the function of E2F2 in cancer progression and both established and emerging therapeutic strategies aiming at targeting this oncogenic pathway, while also providing a strong basis for further research on the biological function and clinical applications of E2F2.