Hemoptysis as the Initial Presentation of a Ruptured Aortic Aneurysm: A Case Report and Literature Review.

Hemoptysis has a broad differential diagnosis, with common causes including bronchiectasis, bronchitis, pulmonary tuberculosis, and lung neoplasms. While often benign, it can sometimes indicate more severe, life-threatening conditions. Herein we report the case of an 86-year-old woman who presented to the emergency department with a 30-day history of hemoptysis ultimately leading to hemodynamic instability. She was initially admitted to the emergency department for resuscitation and diagnostic workup. During the hospitalization, we identified a large, ruptured aneurysm of the descending and diaphragmatic aorta contained by a hematoma communicating the tracheobronchial tree. This case highlights the importance of considering a broad differential diagnosis in patients presenting with hemoptysis as it can signal severe underlying conditions such as a ruptured aortic aneurysm. Early recognition and appropriate management of these cases are crucial to improving patient outcomes.

Incorporation of paclitaxel in mesenchymal stem cells using nanoengineering upregulates antioxidant response, CXCR4 expression and enhances tumor homing.

Engineered mesenchymal stem cells (MSCs) have been investigated extensively for gene delivery and, more recently, for targeted small molecule delivery. While preclinical studies demonstrate the potential of MSCs for targeted delivery, clinical studies suggest that tumor homing of native MSCs may be inefficient. We report here a surprising finding that loading MSCs with the anticancer drug paclitaxel (PTX) by nanoengineering results in significantly improved tumor homing compared to naïve MSCs. Loading PTX in MSCs results in increased levels of mitochondrial reactive oxygen species (ROS). In response to this oxidative stress, MSCs upregulate two important set of proteins. First were critical antioxidant proteins, most importantly nuclear factor erythroid 2-like 2 (Nrf2), the master regulator of antioxidant responses; upregulation of antioxidant proteins may explain how MSCs protect themselves from drug-induced oxidative stress. The second was CXCR4, a direct target of Nrf2 and a key mediator of tumor homing; upregulation of CXCR4 suggested a mechanism that may underlie the improved tumor homing of nanoengineered MSCs. In addition to demonstrating the potential mechanism of improved tumor targeting of nanoengineered MSCs, our studies reveal that MSCs utilize a novel mechanism of resistance against drug-induced oxidative stress and cell death, explaining how MSCs can deliver therapeutic concentrations of cytotoxic payload while maintaining their viability.