A new tubular bioabsorbable stent made of poly-L -lactic acid is biocompatible in normal rabbit airways, indicating that poly-L -lactic acid is a promising material for airway stents for clinical use.
Interventional pulmonology, otherwise known as "airway stenting," has developed in the field of pulmonary medicine focused on using advanced bronchoscopic techniques to treat airway disorders. Tracheobronchial disorders can be caused by malignant or benign tumors, extrinsic compression, postintubation tracheal injuries, tracheobronchomalacia, or sequelae after tracheostomy. Tracheobronchial prostheses, known as airway stents, are used to palliate the effects of large airway obstruction. Specially designed stents are being used increasingly, not only in the airways, but also in the biliary tree, esophagus, urinary tract, and vascular system. There are two main types of airway stents currently available; tube stents made of silicone, and expandable metallic stents. Silicone stents are usually placed with the aid of a rigid bronchoscope while the patient is under general anesthesia. Unlike silicone stents, metal stents can be placed with a flexible bronchoscope. We examine the advantages and disadvantages of currently available stents and present our thoughts on the future development of airway stenting.
Bcl-2 family proteins play a crucial role in the cytoprotective action of insulin-like growth factor-I (IGF-I) by regulating cell death signaling at the mitochondrial level. The present study examined the effect of IGF-I on the expression of Bcl-2 family proteins in the rat heart mitochondria in relation to myocardial protection against ischemia-reperfusion injury. Systemic IGF-I (1 mg) treatment in the rat increased Bcl-xL and attenuated Bax 12-24 h later in the heart mitochondria fraction. Permeability transition and cytochrome c release occurred in a Ca(2+) concentration-dependent manner in the vehicle-treated mitochondria. This was significantly inhibited by the IGF-I-pretreatment. Moreover, ATP synthesis was significantly greater in the IGF-I-pretreated mitochondria. IGF-I pretreatment 24 h before 25 min of global ischemia in the isolated rat heart model significantly improved recovery of isovolumic left ventricular function and inhibited creatine kinase release during reperfusion. This was associated with a significantly less number of terminal transferase labeling-positive myocytes and nonmyocytes 2 h after reperfusion. These results suggest that IGF-1 differentially regulates Bcl-xL and Bax in heart mitochondria, which may be causally related to myocardial protection against ischemia-reperfusion injury.
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