Integrity testing of a smooth surface resin sealant around orthodontic brackets using a new Fluorescence-aided Identification Technique (FIT)

Objective:To investigate the integrity of a fluorescing resin-based sealant placed around orthodontic brackets using the Fluorescence-aided Identification Technique (FIT).Materials and Methods:Standard brackets were bonded to the buccal surfaces of 17 extracted sound permanent premolar crowns sealed with ProSeal^®. Specimens were thermocycled (20,000 cycles, 5–55°C), and toothbrushing was simulated using an electric toothbrush and artificial aqueous toothpaste slurry. Changes in the sealed area were measured after one, two, three, and four alternating thermocycling-brushing cycles simulating 2 years of wear. Digital images were captured applying FIT (405 nm) using a digital camera–equipped stereomicroscope. ImageJ was used to measure sealant integrity and loss.Results:There was a time-dependent decrease in sealed areas by between 21% and 100% (mean 54%). The sealant lost its integrity immediately after the first cycle, and unfilled areas were observed in all samples.Conclusions:The analyzed sealant lost its integrity over time. Using the proposed FIT, sealed surfaces were easily verified and quantified.     

Circulating Fibronectin Controls Tumor Growth

Fibronectin is ubiquitously expressed in the extracellular matrix, and experimental evidence has shown that it modulates blood vessel formation. The relative contribution of local and circulating fibronectin to blood vessel formation in vivo remains unknown despite evidence for unexpected roles of circulating fibronectin in various diseases. Using transgenic mouse models, we established that circulating fibronectin facilitates the growth of bone metastases by enhancing blood vessel formation and maturation. This effect is more relevant than that of fibronectin produced by endothelial cells and pericytes, which only exert a small additive effect on vessel maturation. Circulating fibronectin enhances its local production in tumors through a positive feedback loop and increases the amount of vascular endothelial growth factor (VEGF) retained in the matrix. Both fibronectin and VEGF then cooperate to stimulate blood vessel formation. Fibronectin content in the tumor correlates with the number of blood vessels and tumor growth in the mouse models. Consistent with these results, examination of three separate arrays from patients with breast and prostate cancers revealed that a high staining intensity for fibronectin in tumors is associated with increased mortality. These results establish that circulating fibronectin modulates blood vessel formation and tumor growth by modifying the amount of and the response to VEGF. Furthermore, determination of the fibronectin content can serve as a prognostic biomarker for breast and prostate cancers and possibly other cancers.     

Akuter Mesenterialarterienverschluss

Notfall + Rettungsmedizin - Die Mortalität der akuten mesenterialen Ischämie ist nach wie vor sehr hoch. Auch bei einem standardisierten viszeral- und gefäßchirurgischen...     

F(ab')2 fragments of anti-Mo1 (904) monoclonal antibodies do not prevent myocardial stunning

To determine if inhibition of leukocyte adhesion and aggregation could improve postischemic ventricular dysfunction ("stunning"), a monoclonal antibody (904) that binds to the adhesion-promoting Mo1 glycoprotein on the cell surface of leukocytes was administered intravenously (0.5 mg/kg) to open-chest dogs before a 15-minute coronary occlusion. Ultrasonic crystals placed in ischemic and control myocardium were used to measure systolic wall thickening during a 15-minute occlusion of the left anterior descending artery and for 3 hours after reperfusion. Myocardial blood flow was measured with tracer-labeled microspheres before occlusion, after 10 minutes of occlusion, 3 minutes of reperfusion, and at 1 and 3 hours after reperfusion. Six animals receiving anti-Mo1 antibody had antibody excess demonstrated with immunofluorescence techniques at 5 minutes and 3 hours of reperfusion; this finding indicated saturation of binding sites. Five animals served as controls and received an antibody (murine immunoglobulin G) that does not influence neutrophils. The two groups did not differ hemodynamically during ischemia and reperfusion. Risk areas and myocardial blood flow were also not significantly different between the two groups. The main parameter used to define regional myocardial stunning, percentage systolic wall thickening in the ischemic/reperfused area, did not differ significantly between the two groups. Specimens from nonischemic myocardium were compared with ischemic specimens for myeloperoxidase content. There were no significant differences within or between groups. These data indicate that the anti-Mo1 monoclonal antibody (904) is not effective in improving the profound myocardial dysfunction that persists for 3 hours of reperfusion after 15 minutes of ischemia.