A study in the financial valuation of a topping oil refinery

Oil refineries underpin modern day economics, finance and engineering – without their refined products the world would stand still, as vehicles would not have petrol, planes grounded without kerosene and homes not heated, without heating oil. In this thesis I study the refinery as a financial asset; it is not too dissimilar to a chemical plant, in this respect. There are a number of reasons for this research; over recent years there have been legal disputes based on a refiner's value, investors and entrepreneurs are interested in purchasing refineries, and finally the research in this arena is sparse. In this thesis I utilise knowledge and techniques within finance, optimisation, stochastic mathematics and commodities to build programs that obtain a financial value for an oil refinery. In chapter one I introduce the background of crude oil and the significance of the refinery in the oil value chain. In chapter two I construct a traditional discounted cash flow valuation often applied within practical finance. In chapter three I program an extensive piecewise non linear optimisation solution on the entire state space, leveraging off a simulation of the refined products using a set of single factor Schwartz (1997) stochastic equations often applied to commodities. In chapter four I program an optimisation using an approximation on crack spread option data with the aim of lowering the duration of solution found in chapter three; this is achieved by utilising a two-factor Hull & White sub-trinomial tree based numerical scheme; see Hull & White (1994) articles I & II for a thorough description. I obtain realistic and accurate numbers for a topping oil refinery using financial market contracts and other real data for the Vadinar refinery based in Gujurat India

A study in the financial valuation of a topping oil refinery

Oil refineries underpin modern day economics, finance and engineering – without their refined products the world would stand still, as vehicles would not have petrol, planes grounded without kerosene and homes not heated, without heating oil. In this thesis I study the refinery as a financial asset; it is not too dissimilar to a chemical plant, in this respect. There are a number of reasons for this research; over recent years there have been legal disputes based on a refiner's value, investors and entrepreneurs are interested in purchasing refineries, and finally the research in this arena is sparse. In this thesis I utilise knowledge and techniques within finance, optimisation, stochastic mathematics and commodities to build programs that obtain a financial value for an oil refinery. In chapter one I introduce the background of crude oil and the significance of the refinery in the oil value chain. In chapter two I construct a traditional discounted cash flow valuation often applied within practical finance. In chapter three I program an extensive piecewise non linear optimisation solution on the entire state space, leveraging off a simulation of the refined products using a set of single factor Schwartz (1997) stochastic equations often applied to commodities. In chapter four I program an optimisation using an approximation on crack spread option data with the aim of lowering the duration of solution found in chapter three; this is achieved by utilising a two-factor Hull & White sub-trinomial tree based numerical scheme; see Hull & White (1994) articles I & II for a thorough description. I obtain realistic and accurate numbers for a topping oil refinery using financial market contracts and other real data for the Vadinar refinery based in Gujurat India

Femtosecond pulse generation in passively mode locked InAs quantum dot lasers

Optical pulse durations of an InAs two-section passively mode-locked quantum dot laser with a proton bombarded absorber section reduce from 8.4 ps at 250K to 290 fs at 20 K, a factor of 29, with a corresponding increase in optical bandwidth. Rate equation analysis of gain and emission spectra using rate equations suggests this is due to the very low emission rate of carriers to the wetting layer in the low temperature, random population regime which enables dots across the whole inhomogeneous distribution to act as independent oscillators. (C) 2013 AIP Publishing LLC

Investigation of the molecular profile of basal cell carcinoma using whole genome microarrays

BACKGROUND: Skin cancer accounts for 1/3 of all newly diagnosed cancer. Although seldom fatal, basal cell carcinoma (BCC) is associated with severe disfigurement and morbidity. BCC has a unique interest for researchers, as although it is often locally invasive, it rarely metastasises. This paper, reporting the first whole genome expression microarray analysis of skin cancer, aimed to investigate the molecular profile of BCC in comparison to non-cancerous skin biopsies. RNA from BCC and normal skin specimens was analysed using Affymetrix whole genome microarrays. A Welch t-test was applied to data normalised using dCHIP to identify significant differentially-expressed genes between BCC and normal specimens. Principal component analysis and support vector machine analysis were performed on resulting genelists, Genmapp was used to identify pathways affected, and GOstat aided identification of areas of gene ontology more highly represented on these lists than would be expected by chance. RESULTS: Following normalisation, specimens clustered into groups of BCC specimens and of normal skin specimens. Of the 54,675 gene transcripts/variants analysed, 3,921 were differentially expressed between BCC and normal skin specimens. Of these, 2,108 were significantly up-regulated and 1,813 were statistically significantly down-regulated in BCCs. CONCLUSION: Functional gene sets differentially expressed include those involved in transcription, proliferation, cell motility, apoptosis and metabolism. As expected, members of the Wnt and hedgehog pathways were found to be significantly different between BCC and normal specimens, as were many previously undescribed changes in gene expression between normal and BCC specimens, including basonuclin2 and mrp9. Quantitative-PCR analysis confirmed our microarray results, identifying novel potential biomarkers for BCC

Improving the optical bandwidth of passively mode-locked InAs quantum dot lasers

We examine in detail the relation between the optical gain spectra, mode-locked optical emission spectra, and temporal optical pulse widths as a function of temperature between 80 and 300 K in passively mode-locked InAs quantum dot lasers. By increasing the length of the active region, we can decrease the threshold gain requirement for mode locking. At 300 K, where the dot states and wetting layer are close to thermal equilibrium, the bandwidth of the optical emission spectra and temporal optical pulse width remain largely unaffected when the threshold gain requirement is reduced. At 80 K, where the dots are randomly populated, there is a near doubling of the optical bandwidth for the same reduction of the threshold gain requirement and a corresponding decrease in the temporal optical pulse width. Rate equations, which take explicit account of the photon density in the cavity, are used to qualitatively highlight the key parameters, which are responsible for increasing the optical bandwidth in the random population regime

The Surgical Infection Society revised guidelines on the management of intra-abdominal infection

Background: Previous evidence-based guidelines on the management of intra-abdominal infection (IAI) were published by the Surgical Infection Society (SIS) in 1992, 2002, and 2010. At the time the most recent guideline was released, the plan was to update the guideline every five years to ensure the timeliness and appropriateness of the recommendations. Methods: Based on the previous guidelines, the task force outlined a number of topics related to the treatment of patients with IAI and then developed key questions on these various topics. All questions were approached using general and specific literature searches, focusing on articles and other information published since 2008. These publications and additional materials published before 2008 were reviewed by the task force as a whole or by individual subgroups as to relevance to individual questions. Recommendations were developed by a process of iterative consensus, with all task force members voting to accept or reject each recommendation. Grading was based on the GRADE (Grades of Recommendation Assessment, Development, and Evaluation) system; the quality of the evidence was graded as high, moderate, or weak, and the strength of the recommendation was graded as strong or weak. Review of the document was performed by members of the SIS who were not on the task force. After responses were made to all critiques, the document was approved as an official guideline of the SIS by the Executive Council. Results: This guideline summarizes the current recommendations developed by the task force on the treatment of patients who have IAI. Evidence-based recommendations have been made regarding risk assessment in individual patients; source control; the timing, selection, and duration of antimicrobial therapy; and suggested approaches to patients who fail initial therapy. Additional recommendations related to the treatment of pediatric patients with IAI have been included. Summary: The current recommendations of the SIS regarding the treatment of patients with IAI are provided in this guideline

Ku counteracts mobilization of PARP1 and MRN in chromatin damaged with DNA double-strand breaks

In mammalian cells, the main pathway for DNA double-strand breaks (DSBs) repair is classical non-homologous end joining (C-NHEJ). An alternative or back-up NHEJ (B-NHEJ) pathway has emerged which operates preferentially under C-NHEJ defective conditions. Although B-NHEJ appears particularly relevant to genomic instability associated with cancer, its components and regulation are still largely unknown. To get insights into this pathway, we have knocked-down Ku, the main contributor to C-NHEJ. Thus, models of human cell lines have been engineered in which the expression of Ku70/80 heterodimer can be significantly lowered by the conditional induction of a shRNA against Ku70. On Ku reduction in cells, resulting NHEJ competent protein extracts showed a shift from C- to B-NHEJ that could be reversed by addition of purified Ku protein. Using a cellular fractionation protocol after treatment with a strong DSBs inducer followed by western blotting or immunostaining, we established that, among C-NHEJ factors, Ku is the main counteracting factor against mobilization of PARP1 and the MRN complex to damaged chromatin. In addition, Ku limits PAR synthesis and single-stranded DNA production in response to DSBs. These data support the involvement of PARP1 and the MRN proteins in the B-NHEJ route for the repair of DNA DSBs

Homozygous DBF4 mutation as a cause for severe congenital neutropenia

Background Severe congenital neutropenia presents with recurrent infections early in life due to arrested granulopoiesis. Multiple genetic defects are known to block granulocyte differentiation, however a genetic cause remains unknown in approximately 40% of cases. Objective We aimed to characterize a patient with severe congenital neutropenia and syndromic features without a genetic diagnosis. METHODS: Whole exome sequencing results were validated using flow cytometry, Western blotting, co-immunoprecipitation, quantitative PCR, cell cycle and proliferation analysis of lymphocytes and fibroblasts and granulocytic differentiation of primary CD34+ and HL-60 cells. Results We identified a homozygous missense mutation in DBF4 in a patient with mild extra-uterine growth retardation, facial dysmorphism and severe congenital neutropenia. DBF4 is the regulatory subunit of the CDC7 kinase, together known as DBF4-dependent kinase (DDK), the complex essential for DNA replication initiation. The variant allele demonstrated impaired ability to bind CDC7, resulting in decreased DDK-mediated phosphorylation, defective S phase entry and progression and impaired differentiation of granulocytes associated with activation of the p53-p21 pathway. The introduction of WT DBF4 into patient CD34+ cells rescued the promyelocyte differentiation arrest. Conclusion Hypomorphic DBF4 mutation causes autosomal recessive severe congenital neutropenia with syndromic features

Mutations in KEOPS-Complex Genes Cause Nephrotic Syndrome with Primary Microcephaly

Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue. Furthermore, knockdown of these genes impaired protein translation, caused endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced apoptosis. Knockdown of OSGEP or TP53RK induced defects in the actin cytoskeleton and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS. We thus identified four new monogenic causes of GAMOS, describe a link between KEOPS function and human disease, and delineate potential pathogenic mechanisms