Исследование парогазовой установки, работающей на генераторном газе

Выпускная квалификационная работа 116 страниц, 25 рисунков, 25 таблиц, 35 источников, 2 приложения. Ключевые слова: газификация угля, парогазовая установка, газотурбинная установка, генераторный газ, анализ, котел-утилизатор, показатели эффективности. Объектом исследования является ПГУ, работающая на генераторном газе. Цель работы – анализ работоспособности такой ПГУ с ГТУ, работающей на генераторном газе. В процессе исследования проводилось изучение различных способов газификации угля; производился выбор расчетной схемы ПГУ с газификацией; проводился расчет состава и характеристик генераторного газа и определение основных показателей тепловой эффективности ПГУ. В результате исследования был сделан анализ эффективности работы парогазовой установки.Final qualifying work of 116 pages, 25 figures, 25 tables, 35 sources, 2 annexes. Keywords: coal gasification combined cycle plant, a gas turbine plant, the product gas analysis, waste heat boiler, performance indicators. The object of this study is to CCGT running on syngas. The purpose of work - performance analysis of a CCGT with a gas turbine, operating on syngas. The study was carried out to study different methods of coal gasification; selects the estimated PSU circuit with gasification; conducted calculation and composition of the product gas characteristics and the definition of the main indicators of the thermal efficiency of the CCGT. The survey was made the analysis of the efficiency of the combined-cycle plant

The eyes know it: FakeET -- An Eye-tracking Database to Understand Deepfake Perception

We present \textbf{FakeET}-- an eye-tracking database to understand human visual perception of \emph{deepfake} videos. Given that the principal purpose of deepfakes is to deceive human observers, FakeET is designed to understand and evaluate the ease with which viewers can detect synthetic video artifacts. FakeET contains viewing patterns compiled from 40 users via the \emph{Tobii} desktop eye-tracker for 811 videos from the \textit{Google Deepfake} dataset, with a minimum of two viewings per video. Additionally, EEG responses acquired via the \emph{Emotiv} sensor are also available. The compiled data confirms (a) distinct eye movement characteristics for \emph{real} vs \emph{fake} videos; (b) utility of the eye-track saliency maps for spatial forgery localization and detection, and (c) Error Related Negativity (ERN) triggers in the EEG responses, and the ability of the \emph{raw} EEG signal to distinguish between \emph{real} and \emph{fake} videos.Comment: 8 page

UGT1A1 sequence variants and bilirubin levels in early postnatal life: a quantitative approach

<p>Abstract</p> <p>Background</p> <p>Fundamental to definitively identifying neonates at risk of developing significant hyperbilirubinemia is a better understanding of the genetic factors associated with early bilirubin rise. Previous genetic studies have focused on the UGT1A1 gene, associating common variation in the coding or promoter regions with qualitative assessments of bilirubin (i.e. significantly elevated or not). These studies have had conflicting results and limited success. We chose to approach the problem by focusing on the quantitative (absolute) change in bilirubin levels early in post-natal life. We apply this approach to the UGT1A1 gene - exploring the contribution of both rare and common variants to early bilirubin changes.</p> <p>Methods</p> <p>We sequenced the exons, PBREM, 5'-, and 3'- regions of the UGT1A1 gene in 80 otherwise healthy term neonates who had repeat bilirubin levels measured within the first five days of life.</p> <p>Results</p> <p>Three novel coding variants were observed, but there was no clear relationship between rare coding variants and bilirubin rise. Adjusted linear regression models fit to evaluate the relationship between changing bilirubin levels and common UGT1A1variants found that among 39 neonates whose bilirubin was resampled within 33 hours, individuals homozygous for the mutant allele of a 3'UTR SNP had significantly smaller changes in bilirubin (P = 0.003) than individuals carrying the wild-type allele.</p> <p>Conclusions</p> <p>Collectively, rare UGT1A1 coding variants do not appear to play a prominent role in determining early bilirubin levels; however common variants in the 3' UTR of UGT1A1 may modulate the early bilirubin rise. A quantitative approach to evaluating early bilirubin kinetics provides a more robust framework in which to better understand the genetics of neonatal hyperbilirubinemia.</p

GIS and spatial data analysis: Converging perspectives

We take as our starting point the state of geographic information systems (GIS) and spatial data analysis 50 years ago when regional science emerged as a new field of enquiry. In the late 1950s and 1960s advances in computing technology were making possible forms of automated cartography that in due course would lead to th

FIP1/RCP Binding to Golgin-97 Regulates Retrograde Transport from Recycling Endosomes to the trans-Golgi Network

This study shows that Rab11 and its binding protein FIP1 are required for retrograde delivery of TGN38 and Shiga toxin from early/recycling endosomes to the TGN. We also demonstrate that Golgin-97 as a FIP1-binding protein and that this binding regulates the targeting of retrograde transport vesicles to the TGN

Mucopolysaccharidosis VI

Mucopolysaccharidosis VI (MPS VI) is a lysosomal storage disease with progressive multisystem involvement, associated with a deficiency of arylsulfatase B leading to the accumulation of dermatan sulfate. Birth prevalence is between 1 in 43,261 and 1 in 1,505,160 live births. The disorder shows a wide spectrum of symptoms from slowly to rapidly progressing forms. The characteristic skeletal dysplasia includes short stature, dysostosis multiplex and degenerative joint disease. Rapidly progressing forms may have onset from birth, elevated urinary glycosaminoglycans (generally >100 μg/mg creatinine), severe dysostosis multiplex, short stature, and death before the 2nd or 3rd decades. A more slowly progressing form has been described as having later onset, mildly elevated glycosaminoglycans (generally <100 μg/mg creatinine), mild dysostosis multiplex, with death in the 4th or 5th decades. Other clinical findings may include cardiac valve disease, reduced pulmonary function, hepatosplenomegaly, sinusitis, otitis media, hearing loss, sleep apnea, corneal clouding, carpal tunnel disease, and inguinal or umbilical hernia. Although intellectual deficit is generally absent in MPS VI, central nervous system findings may include cervical cord compression caused by cervical spinal instability, meningeal thickening and/or bony stenosis, communicating hydrocephalus, optic nerve atrophy and blindness. The disorder is transmitted in an autosomal recessive manner and is caused by mutations in the ARSB gene, located in chromosome 5 (5q13-5q14). Over 130 ARSB mutations have been reported, causing absent or reduced arylsulfatase B (N-acetylgalactosamine 4-sulfatase) activity and interrupted dermatan sulfate and chondroitin sulfate degradation. Diagnosis generally requires evidence of clinical phenotype, arylsulfatase B enzyme activity <10% of the lower limit of normal in cultured fibroblasts or isolated leukocytes, and demonstration of a normal activity of a different sulfatase enzyme (to exclude multiple sulfatase deficiency). The finding of elevated urinary dermatan sulfate with the absence of heparan sulfate is supportive. In addition to multiple sulfatase deficiency, the differential diagnosis should also include other forms of MPS (MPS I, II IVA, VII), sialidosis and mucolipidosis. Before enzyme replacement therapy (ERT) with galsulfase (Naglazyme®), clinical management was limited to supportive care and hematopoietic stem cell transplantation. Galsulfase is now widely available and is a specific therapy providing improved endurance with an acceptable safety profile. Prognosis is variable depending on the age of onset, rate of disease progression, age at initiation of ERT and on the quality of the medical care provided

Assembly, organization, and function of the COPII coat

A full mechanistic understanding of how secretory cargo proteins are exported from the endoplasmic reticulum for passage through the early secretory pathway is essential for us to comprehend how cells are organized, maintain compartment identity, as well as how they selectively secrete proteins and other macromolecules to the extracellular space. This process depends on the function of a multi-subunit complex, the COPII coat. Here we describe progress towards a full mechanistic understanding of COPII coat function, including the latest findings in this area. Much of our understanding of how COPII functions and is regulated comes from studies of yeast genetics, biochemical reconstitution and single cell microscopy. New developments arising from clinical cases and model organism biology and genetics enable us to gain far greater insight in to the role of membrane traffic in the context of a whole organism as well as during embryogenesis and development. A significant outcome of such a full understanding is to reveal how the machinery and processes of membrane trafficking through the early secretory pathway fail in disease states