Results: Cellular internalization of HA was regulated by CD44 receptors. In mouse xenografts, HA conjugation significantly enhanced tumor cell uptake compared to unconjugated drugs. Discussion: The results suggested that the main mechanism of HA-based conjugate uptake may be active transport via CD44 in conjunction with a clathrin-dependent endocytic

selleck chemical pathway. Other HA receptors, hyaluronan-mediated motility receptor (RHAMM) and lymphatic vessel endothelial hyaluronan receptor (LYVE-1), did not play a significant role in conjugate uptake. Conclusions: HA conjugation significantly increased CD44-mediated drug uptake and extended the residence time of drugs in tumor cells.”
“Previous studies describing the no-reflow phenomenon in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) were largely confined to single-center studies or small registries. To better characterize the incidence, predictors, and outcomes of

the no-reflow phenomenon in a large contemporary population, we analyzed patients with AMI who were undergoing PCI of native coronary artery check details stenoses in the CathPCI Registry from January 1, 2004 through September 5, 2008 (n = 291,380). The angiographic no-reflow phenomenon was site reported using a standardized definition. No-reflow developed in 2.3% of the patients with AMI (n = 6,553) during PCI. Older age, ST-segment elevation AMI, prolonged interval from symptom onset to admission, and cardiogenic shock were clinical variables independently associated with the development of no-reflow (p <0.001). The angiographic factors independently associated with no-reflow included longer lesion length, higher risk class C lesions, bifurcation lesions, and impaired preprocedure Thrombolysis In Myocardial Infarction flow (p <0.001). No-reflow was associated with greater in-hospital mortality (12.6% vs 3.8%, adjusted odds ratio 2.20, 95% confidence interval 1.97 to 2.47, p <0.001) and unsuccessful lesion outcome (29.7% vs 6.6%, adjusted odds ratio

4.70, 95% confidence interval 4.28 Galardin order to 5.17, p <0.001) compared to patients without no-reflow. In conclusion, the development of no-reflow, although relatively uncommon during PCI for AMI, is associated with adverse clinical outcomes. Upfront strategies to reduce the incidence of no-reflow could be considered for high-risk patients to improve outcomes. (C) 2013 Elsevier Inc. All rights reserved. (Am J Cardiol 2013;111:178-184)”
“Autophagy is a catabolic cellular process involving dynamic membrane rearrangement. Here, we review the understanding of autophagy, focusing on the late stages of the process, from the closing of the autophagosome to fusion with the lysosome. We propose the Reverse fusion model, for the closing autophagosome. In this model, autophagosome closure proceeds in a topologically similar but reverse order to membrane fusion during the escape of influenza virus from the endosome.