Characterization of Si/Si_(1-y)C_y superlattices grown by surfactant assisted molecular beam epitaxy

Si/Si_(0.97)C_(0.03) superlattices grown on Si(001) substrates by Sb surfactant assisted molecular beam epitaxy are characterized by in situ reflection high energy electron diffraction (RHEED), atomic force microscopy, transmission electron microscopy (TEM), and high resolution x‐ray diffraction. The RHEED shows that, in the absence of Sb, the growth front roughens during Si_(0.97)C_(0.03) growth and smooths during subsequent Si growth. In contrast, when Sb is present, the growth front remains smooth throughout the growth. This observation is confirmed by cross‐sectional TEM, which reveals that for samples grown without the use of Sb, the Si/Si_(0.97)C_(0.03) interfaces (Si_(0.97)C_(0.03) on Si) are much more abrupt than the Si_(0.97)C_(0.03)/Si interfaces. In the case of Sb assisted growth, there is no observable difference in abruptness between the two types of interfaces. Atomic force microscopy micrographs of the Si_(0.97)C_(0.03) surface reveal features that could be the source of the roughness observed by RHEED and TEM

Studies on novel interactors in human adipose tissue

Obesity is associated with a mild inflammation and altered protein secretion in adipose tissue. These changes have been suggested to contribute to the development of obesity-associated disorders including, insulin resistance, dyslipidemia, type 2 diabetes and cardiovascular disease. The aim of this thesis was to identify novel factors expressed in the adipose tissue that could be important in the development of obesity and obesity-associated disorders. In paper I we studied the transcriptional control of the human CIDEA gene and the effects of TNFα. CIDEA has previously been shown to be differentially expressed in lean and obese subjects and repressed by tumor necrosis factor α (TNFα), however the human CIDEA promoter has not been investigated. Reporter assays demonstrated that the minimal transcriptional activity of the human CIDEA promoter was confined to a region 97 bp upstream of the transcriptional start site (TSS). TNFα attenuated the transcriptional activity of CIDEA and this regulation was confined to a region between 244 and 123 bp upstream of the TSS. Electrophoretic mobility shift assays and mutational analysis suggested that the regulation by TNFα is mediated by a nuclear factor (NF)-κB binding site. In paper II and III we investigated the function of the twist1 gene in human white adipocytes and its relationship with obesity. Twist1 is involved in various processes, such as bone development, cancer progression, inflammation and brown adipose tissue function, but the role in white adipose tissue is not known. In paper II we assessed the expression of twist1 in human white adipose tissue, liver, skeletal muscle and pancreas as well as in different cell types in adipose tissue. Twist1 mRNA expression was significantly higher in adipose tissue compared to the other organs and within adipose tissue; the expression was highest in the adipocyte fraction. In vitro silencing of twist1 by RNA interference was used to investigate the role of twist1 in lipid turnover and inflammation in human adipocytes. In contrast to mice where twist1 reduces fatty acid oxidation, reduction of twist1 expression in human in vitro differentiated adipocytes lead to a reduction in fatty acid oxidation. Furthermore, expression of the rate-limiting enzyme for fatty acid oxidation, carnitine palmitoyl transferase 1, was also reduced when twist1 was silenced, suggesting that twist1 is required for fatty acid oxidation in human white adipocytes. We were also able to demonstrate that twist1 regulates the expression of inflammatory proteins, including interleukin (IL) -6 and monocyte chemoattractant protein 1. Chromatin immunoprecipitation demonstrated direct binding to sequences in the promoter regions of these genes. In paper III, we further explored the expression of twist1 in non-obese and obese subjects and correlated the expression with different clinical parameters of insulin resistance. Interestingly and in contrast to studies in mice, low twist1 expression associated with a higher BMI and a more adverse clinical profile, characterized by higher HOMA-IR values, large adipocytes and an increased secretion of pro-inflammatory factors. We also assessed the effect of twist1 silencing on TNFα-induced cytokine and chemokine expression and secretion in human adipocytes. Twist1 knockdown accentuated the pro-inflammatory effects of TNFα- suggesting that twist1 may have a protective role in adipose inflammation. In conclusion, we have defined the minimal promoter needed for transcription of human CIDEA and a region in the promoter regulated by TNFα. We have also demonstrated that twist1 is expressed in white adipocytes and that low expression of twist1 associates with high BMI, markers of insulin resistance and an increased secretion of pro-inflammatory factors. Additionally, silencing of twist1 in human in vitro differentiated adipocytes demonstrates a role for this transcription factor in fatty acid oxidation and inflammation. We hypothesize that low twist1 expression in obesity renders the adipose tissue more vulnerable to the pro-inflammatory effects of TNFα, which could be of importance in the development of obesity-associated insulin resistance and type 2 diabetes

Sb-surfactant-mediated growth of Si/Si1–yCy superlattices by molecular-beam epitaxy

Si/Si0.97C0.03 superlattices were grown on Si(001) substrates by molecular beam epitaxy (MBE) to study the use of Sb as a surfactant during Si1–yCy growth. In situ reflection high energy electron diffraction (RHEED) shows that while carbon easily disrupts the two-dimensional growth of homoepitaxial Si, such disruption is suppressed for layers grown on Sb-terminated Si(001) surfaces. Cross-sectional transmission electron microscopy (TEM) reveals that for samples grown without the use of Sb, the Si/Si0.97C0.03 interfaces (Si0.97C0.03 on Si) were much more abrupt than Si0.97C0.03/Si interfaces. In the case of Sb-mediated growth, differences in abruptness between the two types of interfaces were not readily observable

Current AATS guidelines on surgical treatment of infective endocarditis

© Annals of Cardiothoracic Surgery. The 2016 American Association for Thoracic Surgery (AATS) guidelines for surgical treatment of infective endocarditis (IE) are question based and address questions of specific relevance to cardiac surgeons. Clinical scenarios in IE are often complex, requiring prompt diagnosis, early institution of antibiotics, and decision-making related to complications, including risk of embolism and timing of surgery when indicated. The importance of an early, multispecialty team approach to patients with IE is emphasized. Management issues are divided into groups of questions related to indications for and timing of surgery, pre-surgical work-up, preoperative antibiotic treatment, surgical risk assessment, intraoperative management, surgical management, surveillance, and follow up. Standard indications for surgery are severe heart failure, severe valve dysfunction, prosthetic valve infection, invasion beyond the valve leaflets, recurrent systemic embolization, large mobile vegetations, or persistent sepsis despite adequate antibiotic therapy for more than 5-7 days. The guidelines emphasize that once an indication for surgery is established, the operation should be performed as soon as possible. Timing of surgery in patients with strokes and neurologic deficits require close collaboration with neurological services. In surgery infected and necrotic tissue and foreign material is radically debrided and removed. Valve repair is performed whenever possible, particularly for the mitral and tricuspid valves. When simple valve replacement is required, choice of valve-mechanical or tissue prosthesis-should be based on normal criteria for valve replacement. For patients with invasive disease and destruction, reconstruction should depend on the involved valve, severity of destruction, and available options for cardiac reconstruction. For the aortic valve, use of allograft is still favored

A Method to Measure the Permeability of Dry Fiber Mats

Close to the finalization of the medium density fiberboard process, a fairly thick bed of loosely entangled fibers is compressed in a belt-press to often less than a tenth of its original unstressed thickness. This single unit operation is very important to consider when the manufacturing process of the boards is to be optimized. Despite this, there is a lack of knowledge of the interaction between the fiber mat strength and how the fluid flows through it, i.e. de-aeration. Thus, it is of greatest importance to find reliable methods for studying this stage of the manufacturing process. Following this quest, a method is developed with which the gas permeability of fiber mats can be measured. The method offers the potential to measure the permeability at different flow rates and thus at arbitrary pressure gradients through the material. The method is successfully validated with a porous reference material consisting of polymer spheres, and it is shown that the flow follows Darcy's law at the flow rates of interest. Finally, the method is demonstrated by a presentation of permeability measurements on fiber mats consisting of spruce fibers

First ice core records of NO3− stable isotopes from Lomonosovfonna, Svalbard

Samples from two ice cores drilled at Lomonosovfonna, Svalbard, covering the period 1957–2009, and 1650–1995, respectively, were analyzed for NO3− concentrations, and NO3− stable isotopes (δ15N and δ18O). Post-1950 δ15N has an average of (−6.9 ± 1.9) ‰, which is lower than the isotopic signal known for Summit, Greenland, but agrees with values observed in recent Svalbard snow and aerosol. Pre-1900 δ15N has an average of (4.2 ± 1.6) ‰ suggesting that natural sources, enriched in the 15 N-isotope, dominated before industrialization. The post-1950 δ18O average of (75.1 ± 4.1) ‰ agrees with data from low and polar latitudes, suggesting similar atmospheric NOy (NOy = NO + NO2 + HNO3) processing pathways. The combination of anthropogenic source δ15N and transport isotope effect was estimated as −29.1 ‰ for the last 60 years. This value is below the usual range of NOx (NOx = NO + NO2) anthropogenic sources which is likely the result of a transport isotope effect of –32 ‰. We suggest that the δ15N recorded at Lomonosovfonna is influenced mainly by fossil fuel combustion, soil emissions and forest fires; the first and second being responsible for the marked decrease in δ15N observed in the post-1950s record with soil emissions being associated to the decreasing trend in δ15N observed up to present time, and the third being responsible for the sharp increase of δ15N around 2000

Structural Kinetic Modeling of Metabolic Networks

To develop and investigate detailed mathematical models of cellular metabolic processes is one of the primary challenges in systems biology. However, despite considerable advance in the topological analysis of metabolic networks, explicit kinetic modeling based on differential equations is still often severely hampered by inadequate knowledge of the enzyme-kinetic rate laws and their associated parameter values. Here we propose a method that aims to give a detailed and quantitative account of the dynamical capabilities of metabolic systems, without requiring any explicit information about the particular functional form of the rate equations. Our approach is based on constructing a local linear model at each point in parameter space, such that each element of the model is either directly experimentally accessible, or amenable to a straightforward biochemical interpretation. This ensemble of local linear models, encompassing all possible explicit kinetic models, then allows for a systematic statistical exploration of the comprehensive parameter space. The method is applied to two paradigmatic examples: The glycolytic pathway of yeast and a realistic-scale representation of the photosynthetic Calvin cycle.Comment: 14 pages, 8 figures (color

Dealing with change and uncertainty within the regulatory frameworks for flood defense infrastructure in selected European countries

Whereas existing literature on the interactions between law, adaptive governance and resilience in the water sector often focuses on quality or supply issues, this paper addresses adaptation in national water laws in relation to increasing flood risks. In particular, this paper analyzes the extent to which legal rules governing flood defense infrastructure in a selection of European countries (Sweden, France, England and the Netherlands) allow for response and adaptation to change and uncertainty. While there is evidence that the legal rules on the development of new infrastructure require that changing conditions be considered, the adaptation of existing infrastructure is a more complicated matter. Liability rules fail to adequately address damages resulting from causes external to the action or inaction of owners and managers, in particular extreme events. A trend towards clearer, and in some cases, increased public powers to ensure the safety of flood defense infrastructure is observed. The paper concludes that legal rules should ensure not only that decisions to build flood defenses are based on holistic and future-oriented assessments, but also that this is reflected in the implementation and operation of these structures