Light transmission through and its complete stoppage in an ultra slow wave optical medium

Light Wave transmission -- its compression, amplification, and the optical energy storage -- in an Ultra Slow Wave Medium (USWM) is studied analytically. Our phenomenological treatment is based entirely on the continuity equation for the optical energy flux, and the well known distribution-product property of Dirac delta-function. The results so obtained provide a clear understanding of some recent experiments on light transmission and its complete stoppage in an USWM. Keywords : Ultra slow light, stopped light, slow wave medium, EIT.Comment: (single-column 5pages PDF). Simple class-room phenomenological model of stopped light. Comments most welcom

Metamorphic Detection Using Singular Value Decomposition

Metamorphic malware changes its internal structure with each infection, while maintaining its original functionality. Such malware can be difficult to detect using static techniques, since there may be no common signature across infections. In this research we apply a score based on Singular Value Decomposition (SVD) to the problem of metamorphic detection. SVD is a linear algebraic technique which is applicable to a wide range of problems, including facial recognition. Previous research has shown that a similar facial recognition technique yields good results when applied to metamorphic malware detection. We present experimental results and we analyze the effectiveness and efficiency of this SVD-based approach

FUS/TLS in Stress Response - Implications for Amyotrophic Lateral Sclerosis: A Dissertation

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease is a fatal neurodegenerative disease. ALS is typically adult onset and is characterized by rapidly progressive loss of both upper and lower motor neurons that leads to death usually within 3-5 years. About 90% of all the cases are sporadic with no family history while the remaining 10% are familial cases with mutations in several genes including SOD1, FUS/TLS, TDP43 and C9ORF72. FUS/TLS (Fused in Sarcoma/Translocated in Liposarcoma or FUS) is an RNA/DNA binding protein that is involved in multiple cellular functions including DNA damage repair, transcription, mRNA splicing, RNA transport and stress response. More than 40 mutations have now been identified in FUS that account for about 5% of all the familial cases of ALS. However, the exact mechanism by which FUS causes ALS is unknown. While significant progress has been made in understanding the disease mechanism and identifying therapeutic strategies, several questions still remain largely unknown. The work presented here aims at understanding the normal functions of FUS as well as the pathogenic mechanisms by which it leads to disease. Several studies showed the association of mutant-FUS with structures made up of RNA and proteins, called stress granules that form under various stress conditions. However, little is known about the role of endogenous FUS under stress conditions. I have shown that under hyperosmolar conditions, the predominantly nuclear FUS translocates into the cytoplasm and incorporates into stress granules. The response is specific to hyperosmolar stress because FUS remains nuclear under other stress conditions tested, such as oxidative stress, ER stress and heat shock. The response of FUS is rapid, and cells with reduced FUS levels are susceptible to the hyperosmolar stress, indicating a pro-survival role for FUS. In addition to investigating the functions of endogenous wild-type (WT) FUS, the work presented also focuses on identifying the pathogenic mechanism(s) of FUS variants. Using various biochemical techniques, I have shown that ALS-causing FUS variants are misfolded compared to the WT protein. Furthermore, in a squid axoplasm based vesicle motility assay, the FUS variants inhibit fast axonal transport (FAT) in a p38 MAPK dependent manner, indicating a role for the kinase in mutant-FUS mediated disease pathogenesis. Analysis of human ALS patient samples indicates higher levels of total and phospho p38, supporting the notion that aberrant regulation of p38 MAPK is involved in ALS. The results presented in this dissertation 1) support a novel prosurvival role for FUS under hyperosmolar stress conditions and, 2) demonstrate that protein misfolding and aberrant kinase activation contribute to ALS pathogenesis by FUS variants