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Surgical intervention of second degree burns is often delayed because of the difficulty in visual diagnosis, which increases the risk of scarring and infection. Non-invasive metrics have shown promise in accurately assessing burn depth. Here, we examine the use of spatial frequency domain imaging (SFDI) and laser speckle imaging (LSI) for predicting burn depth. Contact burn wounds of increasing severity were created on the dorsum of a Yorkshire pig, and wounds were imaged with SFDI/LSI starting immediately after-burn and then daily for the next 4 days. In addition, on each day the burn wounds were biopsied for histological analysis of burn depth, defined by collagen coagulation, apoptosis, and adnexal/vascular necrosis. Histological results show that collagen coagulation progressed from day 0 to day 1, and then stabilized. Results of burn wound imaging using non-invasive techniques were able to produce metrics that correlate to different predictors of burn depth. Collagen coagulation and apoptosis correlated with SFDI scattering coefficient parameter [Formula: see text] and adnexal/vascular necrosis on the day of burn correlated with blood flow determined by LSI. Therefore, incorporation of SFDI scattering coefficient and blood flow determined by LSI may provide an algorithm for accurate assessment of the severity of burn wounds in real time., (Published by Elsevier Ltd.)

Telomeres, the short repeated sequences at the ends of chromosomes, are maintained by the telomerase DNA replication complex. In telomerase-deficient cells, telomere shortening occurs until cell proliferation halts, a process called senescence. The precise cause of senescence is unknown, but several models have been proposed. For example, cells may form lethal chromosome rearrangements, the shortened chromosomes may lose essential genes from the ends, or programmed cell death (apoptosis) may be initiated. Alternatively, cells may simply arrest growth in the cell cycle, but remain viable for an extended period of time. Telomerase-deficient cells of the model eukaryote Saccharomyces cerevisiae undergo telomere shortening and senescence in culture. This study has used the advanced molecular genetics available in this organism to investigate the mechanism by which senescing cells halt division. Unique strains of S. cerevisiae have been developed in the lab that allows precise regulation of expression of the polymerase subunit of telomerase Est2. With these strains it is possible to reactivate telomerase expression at any stage of the senescence process, potentially enabling dying cells to lengthen their telomeres and resume growth. Recent experiments suggest that in vitro cell aging is reversible in most cells, even in late senescence. These results and their implications for previously suggested models will be discussed. [ABSTRACT FROM AUTHOR]