Predicting Service Life of 347 Stainless Steel Pipes by Carburization Rate Measurement

Chevron Corporation and other refiners face challenges predicting the service life of piping in coker furnaces. This is largely due to a build up coke on a single surface of the piping. This coke build up results in carbon penetration into the surface of the 347 stainless steel used for the pipes. Carbon penetration can lead to degradation of the surface and ultimately, the failure of the pipe. Current modeling software has difficulty predicting the influence of sulfur on the carbon penetration rate. This study aims to provide a baseline for further study into the subject. The carbon penetration rate of 347 stainless steel was investigated at four temperatures ranging from 900°F to 1400°F on a bed of activated charcoal over a period of 100 to 200 hours. It is expected that higher temperatures and longer times will allow for greater diffusion of carbon into austenite, although some chromium carbide may form at the surface. Apart from chromium carbide formation, the carbon absorption into the austenitic matrix should remain a single phase process. Carburization rate was characterized by EDS, metallographic analysis, and microhardness measurements. Results will lead to determination of the non-steady state diffusion coefficient for carbon into 347 stainless steel

Stochastic modelling of intermittent scrape-off layer plasma fluctuations

Single-point measurements of fluctuations in the scrape-off layer of magnetized plasmas are generally found to be dominated by large-amplitude bursts which are associated with radial motion of blob-like structures. A stochastic model for these fluctuations is presented, with the plasma density given by a random sequence of bursts with a fixed wave form. Under very general conditions, this model predicts a parabolic relation between the skewness and kurtosis moments of the plasma fluctuations. In the case of exponentially distributed burst amplitudes and waiting times, the probability density function for the fluctuation amplitudes is shown to be a Gamma distribution with the scale parameter given by the average burst amplitude and the shape parameter given by the ratio of the burst duration and waiting times.Comment: 11 pages, 1 figur

Staphylococcal infections among leukemic patients

Staphylococcus are cause hospital community acquired infection and they are an important cause of health –care associated infection.The Coagulase positive Staphylococcus are Staphylococcus aureus which can implicated in toxic shock syndrome. Methicillin and Vancomycin Staphylococcus aureus resistant (MRSA, VRSA) become major cause of hospital- acquired infection and community acquired infection.Coagulase negative staphylococcus emerged as major cause of infection in immunocompromised patients.The main objective of this study was to evaluate the distribution of Staphylococci among leukemic patients since it is well known that leukemic patients are prone to be infected easily due to their immunosuppressed status.This study was undertaken between oct. 2009 and Jun 2010 at Iraqi center of hematology and medical genetics. 140 clinical specimen(aspirated wound,superficial wound,urine, blood) have deen collected carefully from leukemic patients and subjected to well known established microbiological methods for diagnosis and identification of the isolates .All isolates were tested for their susceptibility to antimicrobials according to Kirby –Bauer technique.Out of 140 clinical specimen collected from leukemic patients, it was possible to obtain( 63) bacterial isolates form which(43) of Coagulase negative staphylococci (CONS) and (20) of Coagulase positive staphylococci. Out of 43(CONS) isolates has been found that S.epidermidis constitutes (28)the highest of all isolates. Antimicrobial susceptibility reveald that S.aureus is highly sensitive to Gentamycin (85%), Erythromycin (80%), while it is resistant to the drugs Cefotaxim (45%), Choramphenicol(40%),and Tetracycline(20%). S.epidermidis show highly sensitive to Erythromycin(100%),Vancomycin (100%), and Cefotaxim(70%) and highly resistant to the drugs Chloromphenicol(45%), Augmentin(45%),Gentamycin (10%), and Tetracycline(10%).It is concluded that S.epidemidis rankes the first( 28)among the isolates and S.aureus ranke the 2nd .All isolates were highly resistant to Chloramphenicol and highly sensitive to Erythromycine

Turkish D-light : accentuating heritage values with daylight

Historic buildings have their own cultural identity, which is often related to their aesthetic qualities such as period characteristics (geometry, size, colour, form and shape), materials and construction. Daylight is one of the primary elements contributing to the distinctiveness of the visual environment of many historic buildings, but is rarely considered as one of the components that shape the character of a building when adaptive preservation schemes of historical buildings are planned. Many historic buildings were originally designed to accommodate activities different to their new use and preserving the quality of daylight that originally contributed to their visual identity is a challenging task. Maintaining the ‘day-lit appearance’ of a building can be particularly problematic if the building is to be used as a museum or a gallery owing to the artefacts’ conservation requirements. This work investigated the opportunities of maintaining the original ambient conditions of renovated historical buildings while meeting the required daylight levels of the proposed new use. The study utilised an annual daylight simulation method and hourly weather data to preserve daylight conditions in renovated historic buildings. The model was piloted in a Turkish bathhouse situated in Bursa, Turkey, that is currently under renovation. The simulation model produces 4483 hourly values of daylight illuminance for a period of a whole year using the computer program Radiance. It is concluded that daylight characteristics should be taken into account when developing a renovation scheme. With increasing pressure on valuing historic buildings in many parts of the world, the work reported here should be beneficial to those concerned with the conservation and adaptive reuse of historic buildings. The study findings could also be useful to those interested in predicting potential energy savings by combining daylighting and electric lighting in historic buildings

De Novo Transcriptome Assembly and Comparative Analysis Elucidate Complicated Mechanism Regulating Astragalus chrysochlorus Response to Selenium Stimuli

Astragalus species are medicinal plants that are used in the world for years. Some Astragalus species are known for selenium accumulation and tolerance and one of them is Astragalus chrysochlorus, a secondary selenium accumulator. In this study, we employed Illumina deep sequencing technology for the first time to de novo assemble A. chrysochlorus transcriptome and identify the differentially expressed genes after selenate treatment. Totally, 59,656 unigenes were annotated with different databases and 53,960 unigenes were detected in NR database. Transcriptome in A. chrysochlorus is closer to Glycine max than other plant species with 43,1 percentage of similarity. Annotated unigenes were also used for gene ontology enrichment and pathway enrichment analysis. The most significant genes and pathways were ABC transporters, plant pathogen interaction, biosynthesis of secondary metabolites and carbohydrate metabolism. Our results will help to enlighten the selenium accumulation and tolerance mechanisms, respectively in plants

Teratology Primer-2nd Edition (7/9/2010)

Foreword: What is Teratology? “What a piece of work is an embryo!” as Hamlet might have said. “In form and moving how express and admirable! In complexity how infinite!” It starts as a single cell, which by repeated divisions gives rise to many genetically identical cells. These cells receive signals from their surroundings and from one another as to where they are in this ball of cells —front or back, right or left, headwards or tailwards, and what they are destined to become. Each cell commits itself to being one of many types; the cells migrate, combine into tissues, or get out of the way by dying at predetermined times and places. The tissues signal one another to take their own pathways; they bend, twist, and form organs. An organism emerges. This wondrous transformation from single celled simplicity to myriad-celled complexity is programmed by genes that, in the greatest mystery of all, are turned on and off at specified times and places to coordinate the process. It is a wonder that this marvelously emergent operation, where there are so many opportunities for mistakes, ever produces a well-formed and functional organism. And sometimes it doesn’t. Mistakes occur. Defective genes may disturb development in ways that lead to death or to malformations. Extrinsic factors may do the same. “Teratogenic” refers to factors that cause malformations, whether they be genes or environmental agents. The word comes from the Greek “teras,” for “monster,” a term applied in ancient times to babies with severe malformations, which were considered portents or, in the Latin, “monstra.” Malformations can happen in many ways. For example, when the neural plate rolls up to form the neural tube, it may not close completely, resulting in a neural tube defect—anencephaly if the opening is in the head region, or spina bifida if it is lower down. The embryonic processes that form the face may fail to fuse, resulting in a cleft lip. Later, the shelves that will form the palate may fail to move from the vertical to the horizontal, where they should meet in the midline and fuse, resulting in a cleft palate. Or they may meet, but fail to fuse, with the same result. The forebrain may fail to induce the overlying tissue to form the eye, so there is no eye (anophthalmia). The tissues between the toes may fail to break down as they should, and the toes remain webbed. Experimental teratology flourished in the 19th century, and embryologists knew well that the development of bird and frog embryos could be deranged by environmental “insults,” such as lack of oxygen (hypoxia). But the mammalian uterus was thought to be an impregnable barrier that would protect the embryo from such threats. By exclusion, mammalian malformations must be genetic, it was thought. In the early 1940s, several events changed this view. In Australia an astute ophthalmologist, Norman Gregg, established a connection between maternal rubella (German measles) and the triad of cataracts, heart malformations, and deafness. In Cincinnati Josef Warkany, an Austrian pediatrician showed that depriving female rats of vitamin B (riboflavin) could cause malformations in their offspring— one of the early experimental demonstrations of a teratogen. Warkany was trying to produce congenital cretinism by putting the rats on an iodine deficient diet. The diet did indeed cause malformations, but not because of the iodine deficiency; depleting the diet of iodine had also depleted it of riboflavin! Several other teratogens were found in experimental animals, including nitrogen mustard (an anti cancer drug), trypan blue (a dye), and hypoxia (lack of oxygen). The pendulum was swinging back; it seemed that malformations were not genetically, but environmentally caused. In Montreal, in the early 1950s, Clarke Fraser’s group wanted to bring genetics back into the picture. They had found that treating pregnant mice with cortisone caused cleft palate in the offspring, and showed that the frequency was high in some strains and low in others. The only difference was in the genes. So began “teratogenetics,” the study of how genes influence the embryo’s susceptibility to teratogens. The McGill group went on to develop the idea that an embryo’s genetically determined, normal, pattern of development could influence its susceptibility to a teratogen— the multifactorial threshold concept. For instance, an embryo must move its palate shelves from vertical to horizontal before a certain critical point or they will not meet and fuse. A teratogen that causes cleft palate by delaying shelf movement beyond this point is more likely to do so in an embryo whose genes normally move its shelves late. As studies of the basis for abnormal development progressed, patterns began to appear, and the principles of teratology were developed. These stated, in summary, that the probability of a malformation being produced by a teratogen depends on the dose of the agent, the stage at which the embryo is exposed, and the genotype of the embryo and mother. The number of mammalian teratogens grew, and those who worked with them began to meet from time to time, to talk about what they were finding, leading, in 1960, to the formation of the Teratology Society. There were, of course, concerns about whether these experimental teratogens would be a threat to human embryos, but it was thought, by me at least, that they were all “sledgehammer blows,” that would be teratogenic in people only at doses far above those to which human embryos would be exposed. So not to worry, or so we thought. Then came thalidomide, a totally unexpected catastrophe. The discovery that ordinary doses of this supposedly “harmless” sleeping pill and anti-nauseant could cause severe malformations in human babies galvanized this new field of teratology. Scientists who had been quietly working in their laboratories suddenly found themselves spending much of their time in conferences and workshops, sitting on advisory committees, acting as consultants for pharmaceutical companies, regulatory agencies, and lawyers, as well as redesigning their research plans. The field of teratology and developmental toxicology expanded rapidly. The following pages will show how far we have come, and how many important questions still remain to be answered. A lot of effort has gone into developing ways to predict how much of a hazard a particular experimental teratogen would be to the human embryo (chapters 9–19). It was recognized that animal studies might not prove a drug was “safe” for the human embryo (in spite of great pressure from legislators and the public to do so), since species can vary in their responses to teratogenic exposures. A number of human teratogens have been identified, and some, suspected of teratogenicity, have been exonerated—at least of a detectable risk (chapters 21–32). Regulations for testing drugs before market release have greatly improved (chapter 14). Other chapters deal with how much such things as population studies (chapter 11), post-marketing surveillance (chapter 13), and systems biology (chapter 16) add to our understanding. And, in a major advance, the maternal role of folate in preventing neural tube defects and other birth defects is being exploited (chapter 32). Encouraging women to take folic acid supplements and adding folate to flour have produced dramatic falls in the frequency of neural tube defects in many parts of the world. Progress has been made not only in the use of animal studies to predict human risks, but also to illumine how, and under what circumstances, teratogens act to produce malformations (chapters 2–8). These studies have contributed greatly to our knowledge of abnormal and also normal development. Now we are beginning to see exactly when and where the genes turn on and off in the embryo, to appreciate how they guide development and to gain exciting new insights into how genes and teratogens interact. The prospects for progress in the war on birth defects were never brighter. F. Clarke Fraser McGill University (Emeritus) Montreal, Quebec, Canad

Calmodulin is responsible for Ca2+-dependent regulation of TRPA1 channels

TRPA1 is a Ca2+-permeable ion channel involved in many sensory disorders such as pain, itch and neuropathy. Notably, the function of TRPA1 depends on Ca2+, with low Ca2+ potentiating and high Ca2+ inactivating TRPA1. However, it remains unknown how Ca2+ exerts such contrasting effects. Here, we show that Ca2+ regulates TRPA1 through calmodulin, which binds to TRPA1 in a Ca2+-dependent manner. Calmodulin binding enhanced TRPA1 sensitivity and Ca2+-evoked potentiation of TRPA1 at low Ca2+, but inhibited TRPA1 sensitivity and promoted TRPA1 desensitization at high Ca2+. Ca2+-dependent potentiation and inactivation of TRPA1 were selectively prevented by disrupting the interaction of the carboxy-lobe of calmodulin with a calmodulin-binding domain in the C-terminus of TRPA1. Calmodulin is thus a critical Ca2+ sensor enabling TRPA1 to respond to diverse Ca2+ signals distinctly

Exploring scale-up, spread, and sustainability: an instrumental case study tracing an innovation to enhance dysphagia care

Background Adoption, adaptation, scale-up, spread, and sustainability are ill-defined, undertheorised, and little-researched implementation science concepts. An instrumental case study will track the adoption and adaptation, or not, of a locally developed innovation about dysphagia as a patient safety issue. The case study will examine a conceptual framework with a continuum of spread comprising hierarchical control or ‘making it happen’, participatory adaptation or ‘help it happen’, and facilitated evolution or ‘let it happen’. Methods This case study is a prospective, longitudinal design using mixed methods. The fifteen-month (October 2012 to December 2013) instrumental case study is set in large, healthcare organisation in England. The innovation refers to introducing a nationally recognised, inter-disciplinary dysphagia competency framework to guide workforce development about fundamental aspects of care. Adoption and adaptation will be examined at an organisational level and along two, contrasting care pathways: stroke and fractured neck of femur. A number of educational interventions will be deployed, including training a cadre of trainers to cascade the essentials of dysphagia management and developing a Dysphagia Toolkit as a learning resource. Mixed methods will be used to investigate scale-up, spread, and sustainability in acute and community settings. A purposive sample of senior managers and clinical leaders will be interviewed to identify path dependency or the context specific particularities of implementation. A pre- and post-evaluation, using mealtime observations and a survey, will investigate the learning effect on staff adherence to patient specific dysphagia recommendations and attitudes towards dysphagia, respectively. Official documents and an ethnographic field journal allow critical junctures, temporal aspects and confounding factors to be explored. Discussion Researching spread and sustainability presents methodological and practical challenges. These include fidelity, adaptation latitude, time, and organisational changes. An instrumental case study will allow these confounding factors to be tracked over time and in place. The case study is underpinned by, and will test a conceptual framework about spread, to explore theoretical generalizability

Клинико-экономическое исследование целесообразности применения препарата Симбикорт Турбухалер для лечения бронхиальной астмы средней степени тяжести

This prospective randomized trial involved 150 outpatients receiving Symbicort Turbuhaler and 150 patients who continued treatment administered before they entered the trial (the typical practice group). The administration of Symbicort was more beneficial according to 4 criteria of clinical efficacy (physical activity limitation, rate of daytime and nighttime symptoms, need in short-acting β2-agonists which were assessed with 5-point scales) and to FEV1. Therapy with Symbicort was slightly more expensive but its cost-effectiveness ratio was more beneficial compared with that of typical therapy with cromones or inhaled steroids alone or when combined with long-acting β2 -agonists.Проспективное рандомизированное исследование включало 150 амбулаторных больных, получающих Симбикорт Турбухалер, и 150 пациентов, продолжающих назначенное ранее лечение (группа "Типичная практика"). Применение Симбикорта Турбухалер показало лучшие результаты по 4 критериям клинической эффективности (степень ограничения физической активности, частота дневных и ночных симптомов, потребность в β2-агонистах короткого действия), оцениваемым по 5-балльным шкалам, и динамике ОФВ1. Лечение Симбикортом Турбухалер было незначительно дороже, но соотношение "затраты / эффективность" было более благоприятным по сравнению с "типичной практикой" противовоспалительной терапии кромонами или ингаляционными глюкокортикостероидами в качестве монотерапии или комбинации с β2-агонистами длительного действия