Simulating Large-Scale Microscopic Traffic Data

Traffic situations are continuous, uncertain, highly dynamic and partially observable, and they affect the day-to-day lives of people in a society. A worthwhile endeavor is to develop algorithms that can predict abnormal traffic situations by exploiting data from the myriad of sensors on the streets, in vehicles and in smartphones, leading to smoother flow of traffic. Unfortunately, the large volumes of microscopic (i.e. individual vehicle-level) data required for developing statistical/machine learning algorithms cannot be collected from the field by the public. The data collected by transportation agencies is either macroscopic or not widely available. In this thesis, a framework is developed for simulating large-scale traffic data using a microscopic simulation model and limited real-world data. Five kinds of sensors are simulated: inductor loop detector, lane area detector, multi-entry multi-exit detector, Bluetooth, and edgebased traffic measure. Data is simulated using this framework from multiple sensors over an area covering Montgomery County and Prince George County in Washington DC for 720 hours (30 days). The synthesized data is validated with respect to real-world data for volume and speed. Widely-used classifiers are used to recognize eight traffic events, namely Collision, Disabled Vehicle, Emergency Roadwork, Injuries Involved, Obstructions, Road Maintenance Operations, Traffic Signal Not Working and with no events in the synthesized dataset with high accuracy. Given limited real-world microscopic traffic data from a particular area, this framework is the first of its kind that can simulate data from multiple kinds of sensors over a very long duration with high-fidelity to the given data

Pro-invasive role of MMP-9 and c-Met in faslodex-resistant breast cancer

The pure anti-oestrogen faslodex presents a valuable therapeutic option for post-menopausal women with endocrine-sensitive advanced breast cancer. However, emergence of resistance following long-term treatment constitutes a major clinical problem as faslodex-refractory disease is associated with poor prognosis. Consequently, elucidation of the mechanisms underlying resistance is imperative. An in vitro MCF-7 cell model of acquired resistance to faslodex (FAS-R) has been developed in our laboratory. Previous studies using this model revealed endocrine insensitivity to be accompanied by development of an invasive phenotype. Since proteolytic degradation of extracellular matrix components by matrix metalloproteinases (MMPs) is a prerequisite for tumour invasion and metastasis, the objective of this project was to explore the role of these proteases and tissue inhibitors of matrix metalloproteinases (TIMPs) hi the aggressive behaviour of faslodex-resistant breast cancer cells. Additional studies were performed to identify the dominant growth factor signalling pathway regulating these pro-invasive events. MMP and TIMP mRNA expression in FAS-R cells was variable. MMP-2 mRNA was increased in FAS-R cells compared with WTMCF-7 cells. Significantly, treatment with a broad-spectrum MMP inhibitor significantly reduced the invasive behaviour of FAS-R cells suggesting a central role for. MMPs in FAS-R invasion. Importantly, FAS-R cells were found to overexpress c-Met receptor tyrosine kinase which, when activated by HGF/SF, induced latent MMP-9 protein expression and considerably augmented the motile, migratory and invasive capacities of these cells. Both ERK1/2 and PI3K/AKT pathways were activated by HGF/SF, and signalling through both resulted in increased secretion of latent MMP-9 protein. However, HGF/SF-enhanced FAS-R cell invasion was only suppressed by inhibition of the PI3K/AKT pathway or following treatment with the MMP inhibitor. Collectively, these data suggest that in FAS-R cells HGF/SF/c-Met signalling enhances aggressive behaviour via PI3K-mediated MMP-9 secretion. c-Met may therefore present a therapeutic target in faslodex resistance

Translation of Organic Compound to 2D Graphical Representation using SDT

IUPAC (The International Union of Pure and Applied Chemistry) customary is employed to explain structure and characteristic of chemical compound. This paper describes translation of IUPAC (International Union of Pure and Applied Chemistry) name into Two-dimensional structure of substance that consists of graphical entities. OpenGL graphical language is wont to generate graphical structure of IUPAC name. Chemical names square measure a typical manner of act chemical structure data. Basic graphical entities square measure wont to generate 2nd graphical structure of IUPAC name from Intermediate Graphical Language. computer file is generated on analyzing IUPAC name. computer file is OpenGL graphical functions to show graphical entities. This translation is achieved victimisation Syntax – Directed Translation theme by associating linguistics action. This offers internet 2nd graphical illustration of IUPAC name. This paper proposes a strategy for achieving this translation. DOI: 10.17762/ijritcc2321-8169.150512

Measurement of (n,γ) reaction cross section of 186W-isotope at neutron energy of 20.02±0.58 MeV

The cross-section of 186W(n,γ)187W reaction has been measured at an average neutron energy of 20.02±0.58 MeV by using activation technique. The 27Al(n,α)24Na and 115In(n,n´)115mIn reactions have been used for absolute neutron flux measurement. Theoretically the reaction cross-sections have been calculated by using the TALYS-1.9 code. The results from the present work and the EXFOR based literature data have been compared with the evaluated data and calculated data from TALYS-1.9 code

Measurement of (n,) reaction cross section of W-186-isotope at neutron energy of 20.02±0.58 MeV

The cross-section of 186W(n,)187W reaction has been measured at an average neutron energy of 20.02±0.58 MeV by using activation technique. The 27Al(n,)24Na and 115In(n,n´)115mIn reactions have been used for absolute neutron flux measurement. Theoretically the reaction cross-sections have been calculated by using the TALYS-1.9 code. The results from the present work and the EXFOR based literature data have been compared with the evaluated data and calculated data from TALYS-1.9 code

Measurement of (n,γ) reaction cross section of 186W-isotope at neutron energy of 20.02±0.58 MeV

392-396The cross-section of 186W(n,γ)187W reaction has been measured at an average neutron energy of 20.02±0.58 MeV by using activation technique. The 27Al(n,α)24Na and 115In(n,n´)115mIn reactions have been used for absolute neutron flux measurement. Theoretically the reaction cross-sections have been calculated by using the TALYS-1.9 code. The results from the present work and the EXFOR based literature data have been compared with the evaluated data and calculated data from TALYS-1.9 code

TNF-α mediated keratinocyte expression and release of matrix metalloproteinase 9: putative mechanism of pathogenesis in Stevens-Johnson syndrome/ toxic epidermal necrolysis.

Stevens Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) are severe cutaneous adverse drug reactions (ADRs) characterised by widespread keratinocyte cell-death and epidermal detachment. At present, there is little understanding of how the detachment occurs or how it is abrogated by the TNF-α inhibitor etanercept, an effective SJS/TEN treatment. RNA-sequencing was used to identify upregulated transcripts in formalin-fixed paraffin-embedded SJS/TEN skin biopsies. Epidermal matrix metalloproteinase 9 (MMP9) expression was assessed by immunohistochemistry in skin biopsies and cultured human skin explants exposed to serum from cutaneous ADRs patients. TNF-α-induced MMP9 expression and activity, and its abrogation by etanercept was determined using the HaCaT immortalised keratinocyte cell-line. Epidermal MMP9 expression was significantly higher in SJS/TEN skin (70.6%) vs. healthy control skin (0%, p=0.0098) and non-bullous skin reactions (10.7%, p=0.0002). SJS/TEN serum induced significant MMP9 expression and collagenase activity in healthy skin explants, which was reduced by etanercept. Etanercept was also able negate the TNF-α induced MMP9 expression in the HaCaT cell line. Data suggest that elevated epidermal MMP9 expression and collagenase activity is a putative pathogenic mechanism in SJS/TEN, which is limited by etanercept. Modulation of MMP9 expression and activity represents to our knowledge a previously unreported therapeutic target for the treatment of SJS/TEN

Defense against network attacks using game theory

As Internet has become ubiquitous, the risk posed by network attacks has greatly increased. Network attacks have been used to achieve a wide gamut of objectives ranging from overloading a website to accessing classified data. Effective defense against such attacks is a critical research area. In this thesis, we demonstrate how game theory can be used to devise effective defense systems. We utilize game theory for defense systems in two scenarios in this thesis. The first scenario is that of the attacker carrying out a Distributed Denial of Service (DDoS) attack. The second scenario involves the attacker possessing the ability to carry out a number of different attacks such as Denial of Service (DoS), Dictionary attacks and Portscans. An important restriction imposed in repeated complete-information games is that each player has complete knowledge of the adversary???s payoffs. This assumption is unrealistic when the adversaries are the defense system and the attacker. We employ a Fictitious-Play approach in order to remove this restriction