J. Aguilar, W. Bilnik, L. Bogacz, T. Bulik, A. Christov, D. della Volpe, M. Dyrda, A. Frankowski, M. Grudzińska, J. Grygorczuk, M. Heller, B. Idźkowski, M. Janiak, M. Jamrozy, M. Karczewski, J. Kasperek, E. Lyard, A. Marszalek, J. Michalowski, M. Rameez, R. Moderski, T. Montaruli, A. Neronov, J. Nicolau-Kukliński, J. Niemiec, M. Ostrowski, P. Paśko, Ł. Płatos, E. Prandini, J. Rafalski, P. Rajda, M. Rataj, M. Rupiński, K. Rutkowskai, K. Seweryn, M. Sidz, Ł. Stawarz, M. Stodulska, M. Stodulski, M. Tokarz, S. Toscano, I. Troyano Pujadas, R. Walter, P. Wawer, R. Wawrzaszek, L. Wiśniewski, K. Winiarski, K. Ziętara, P. Ziółkowski, P. Źychowski
The Cherenkov Telescope Array (CTA), the next generation very high energy gamma-ray observatory, will consist of three types of telescopes: large (LST), medium (MST) and small (SST) size telescopes. The small size telescopes are dedicated to the observation of gamma-rays with energy between a few TeV and few hundreds of TeV. The single-mirror small size telescope (SST-1M) is one of several SST designs. It will be equipped with a 4 m-diameter segmented mirror dish and a fully digital camera based on Geiger-mode avalanche photodiodes. Currently, the first prototype of the mechanical structure is under assembly in Poland. In 2014 it will be equipped with 18 mirror facets and a prototype of the camera.
Development of AD is associated with cerebrovascular deposition of amyloid beta (Aβ) as well as a progressive increase in vasular collagen content. Both AΒ and collagen are naturally fluorescent compounds when exposed to UV light. We analyzed autofluorescence emitted from brain tissue samples and isolated brain resistance vessels harvested postmortem from patients with Alzheimer's disease (AD) and age-matched controls. Fluorescence emission, excited at 355 nm with an Nd:YAG laser, was measured using a fiber-optic based fluorescence spectroscopic system for tissue analysis. Significantly higher values of fluorescence emission intensity (P<0.001) in the spectral region from 465 to 490 nm were detected in brain resistance vessel samples from AD patients compared to the normal individuals. Results from western blot analysis showed elevated levels of type I and type III collagen, and reduced levels of type IV collagen in resistance vessels from AD patients, compared to control samples. In addition, using direct scanning of the cortical suface for fluoresxcence emission by the laser-induced fluorescence spectroscopy system we detected a significantly (P<0.05) higher level of apoptosis in AD brain tissue compared to age-matched controls. Fluorescence emission analysis (FEA) appears to be a sensitive technique for detecting structural changes in AD brain tissue.
KEYWORDS: Blood, Luminescence, In vitro testing, Collagen, Fluorescence spectroscopy, Spectroscopy, Control systems, Injuries, In vivo imaging, Arteries
Whether inflammatory responses are always initiated in the vessel wall, followed by secondary blood cell activation, or are initiated by activated circulating cells that trigger secondary changes in arterial structure remains unproved. In a rabbit angioplasty injury model we studied changes in aortic atherosclerotic plaque after autologous re-infusion of blood cells pre-activated in vitro with thrombin. Fluorescence spectroscopic analysis (FSA) was used to measure membrane fluidity of circulating platelets, as well as quantitative changes in collagen and elastin at the arterial inner surface. The results were correlated with atherosclerotic plaque structural characteristics. Injection of activated circulating blood cells caused a significant increase in fluorescence emission intensity from the abdominal aorta at 450 and 500 nm 3 days later. In blood samples treated with thrombin, membrane fluidity was significantly increased compared to controls. In conclusion, our results indicate that activated circulating blood cells can trigger arterial responses, acting not only as a secondary response to arterial inflammation, but also as a primary activation mechanism.
In order to assess the capacity for in vivo fluorescence spectroscopi8c analysis of arterial collagen and elastin, fluorescence emission intensity was recorded form rabbit aorta after angioplasty and stent implant, and correlated with extracted elastin and collagen content. FEI from saline treated rabbits after stent implant was higher between 485 and 500 nm than after anti-inflammatory treatment. FEI was significantly decreased after implantation of shorter stents at 476-500 nm. Multiple regression analysis demonstrated an excellent correlation between FEI and elastin and HPLC- measured collagen content at 486-500 nm and 476-480 nm respectively. Conclusions: FEI recorded in vivo form arterial intimal surface, can be successfully used for quantitative assessment of compositional changes in connective tissue. Stent implant can induce changes in intimal arterial structure at discrete sites distant from the stent implant site.
KEYWORDS: In vivo imaging, In vitro testing, Fluorescence spectroscopy, Spectroscopy, Luminescence, Blood, Control systems, Injuries, Laser induced fluorescence, Laser spectroscopy
Many approaches to imaging of unstable plaque have been applied to detect vascular thrombosis and occlusion with only moderate success. LFS detected significant and specific changes in thrombogenic plaque in a rabbit model. Fluorescence emission intensity analysis of structural characteristics may provide an optical diagnostic technique for early recognition of unstable coronary syndromes.
Alexander Christov, William Kostuk, George Jablonsky, Paulette Desjardins, Ruth Courtis, Bernice Jardine, Anne Bailey, June Odlum-Blair, Janice Motiejunas, Sheila McConnell, Alexandra Lucas
A method for simultaneous fluorescence spectroscopic measurement of surface membrane fluidity, platelet aggregation, and intracellular calcium concentration was developed. The capacity of the system to assess platelet activation associated with coronary artery angioplasty and anti-platelet treatment was confirmed. This approach offers a new analytical technique for circulating platelet activation.
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