Miracle-dz/UniFAR-FTUs huggingface dataset:
Robust Wide Area Fault Location Considering Network Parameters Error

Network parameters error may seriously affect the accuracy of fault location results, even making them unacceptable in extreme cases. This paper proposes a new method that incorporates these errors in wide area fault location problem using phasor measurement units to estimate inaccurate network parameters employing robust state estimation. Our proposed method is composed of two stages. The first stage or the primary stage provides an initial point for the second stage, which is the main contribution of this paper. Additionally, the set of measurements contaminated with bad data could be obtained from the first stage, and its intersection with leverage measurements are then eliminated from the measurement set before feeding it into the second stage. Finally, fault point and faulted line parameters are estimated by the main (second) stage of the method. The proposed method has been applied to two test systems, namely Institute of Electrical and Electronics Engineers (IEEE) 14-bus and IEEE 57-bus systems, to evaluate its accuracy. Simulation results indicate high accuracy and consistency of the proposed method.
A Survey on Virtual Machine Migration with Compression

— Cloud computing is evolving as a key computing platform for sharing resources that include hardware infrastructures, software, applications and business. Cloud services help individuals and organization to use data that are hosted and managed by third party at remote location. Though when planning to move a legacy style application to the cloud computing various challenges arise. The potential size and complexity of such a project might especially discourage small or medium. In cloud computing, Virtual Machine Migration is a useful tool for migrating Operating System instances across multiple physical machines. VM migration methodology shifts current-hosted workload from one server to another by either employing live or non-live migration pattern. In comparison to non-live migration, live migration does not suspend application services prior to VM migration process. VM migration enables the cloud operator to achieve various resource management goals such as green computing, load balancing, fault management and real time server maintenance. In this paper, we have thoroughly surveyed VM migration methods and briefly discussed VM migration application.
Re-evaluating the role of FOXOs in cancer

FOXO transcription factors are negatively regulated by the PI3K-PKB/AKT signaling pathway and have been mainly considered to be tumor suppressors due to their inhibitory effect on cancer cell growth and survival. However, FOXOs can also support tumor development and progression by maintaining cellular homeostasis, facilitating metastasis and inducing therapy resistance. In agreement with these opposing views on the role of FOXOs in cancer, studies using FOXO levels or activity as prognostic markers for cancer patient disease progression and survival came to contradicting results. While it is clear that FOXOs are involved in various aspects of cancer, it is debatable whether FOXOs function as tumor suppressors or supporters, or may be both depending on the context. In this review, we describe the role of FOXOs in signaling pathways and processes relevant to cancer and evaluate recent advances in understanding the role of FOXOs in cancer. Based on recent insights it becomes clear that FOXOs may not be classical tumor suppressors and that targeting FOXO activity might hold promise in cancer therapy.
Influence of Acute Alterations

To study the effects of acute alterations in heart rate and systemic arterial pressure on the mean velocity of left ventricular circumferential fiber shortening (Vcf) and on mean posterior wall velocity (Vpw), we performed ultrasound studies in 25 normal human subjects between the ages of 21 and 29 years. When heart rate was augmented by the administration of intravenous atropine from 64 + 2.2 (SEM) to 98 ± 2.7 beats/min, mean normalized Vcf increased from 1.22 i 0.05 to 1.38 ± 0.06 circumferences (circ)/sec (P < 0.001). Mean normalized Vpw increased from 0.76 + 0.03 to 0.89 ± 0.04 sec1 (P < 0.001). Mean Vcf and mean Vpw uncorrected for end-diastolic diameter increased in a similar fashion (P < 0.01). After atropine administration, systemic arterial pressure was augmented by means of a phenylephrine infusion in 23 subjects by an average of 39 mm Hg (range 20-50 mm Hg). During the phenylephrine infusion, average heart rate decreased from 96 ± 2.6 to 91 ± 3.1 beats/min (NS), while mean normalized Vcf declined from 1.38 ± 0.06 to 1.09 ± 0.05 circ/sec (P < 0.001) and normalized Vpw from 0.89 ± 0.04 to 0.65 ± 0.04 sec`1 (P < 0.001). Nonnormalized velocities exhibited similar alterations (P < 0.01). We conclude that in the normal human subject mean Vcf and mean Vpw are sensitive to acute alterations in heart rate and systemic arterial pressure. Thus, when ultrasound measures are used for serial assessment of left ventricular performance, the level of heart rate and systemic arterial pressure at which studies are obtained must be considered. Further, the sequential use of atropine and phenylephrine, as described in this study, provides an experimental model for the evaluation of the effects of drug treatment and other interventions on left ventricular performance in man.
Sequence Variation In the Promoter of the Ica1 gene, which encodes a protein implicated in type 1 diabetes, causes the Transcription Factor AIRE to Increase Its Binding and downregulate Expression

The Islet Cell Autoantigen 69 kDa (ICA69) is a protein implicated in type 1 diabetes (T1D) in both the non-obese diabetic (NOD) mouse model and humans. ICA69 is encoded by the Ica1 gene on mouse chromosome 6 A1-A2. We previously reported reduced ICA69 expression in the thymus of NOD mice compared to thymus of several non-diabetic mouse strains. We propose that reduced thymic ICA69 expression could result from variations in transcriptional regulation of the gene and that polymorphisms within the Ica1 core promoter may partially determine this transcriptional variability. We characterized the functional promoter of Ica1 in NOD mice and compared it to the corresponding portions of Ica1 in nondiabetic C57BL/6 mice. Luciferase reporter constructs demonstrated that the NOD Ica1 promoter region exhibited markedly reduced luciferase expression in transiently transfected medullary thymus epithelial (mTec + ) and B-cell (M12) derived cell lines. However, in a non-diabetic strain, C57BL/6, the Ica1 promoter region was transcriptionally active when transiently transfected into the same cell lines. We concomitantly identified five single nucleotide polymorphisms (SNPs) within the NOD Ica1 promoter. One of these SNPs increases the binding affinity for the transcription factor Autoimmune Regulator (AIRE), which is highly expressed in thymic epithelial cells where it is known to play a key role regulating self-antigen expression. We conclude that polymorphisms within the NOD Ica1 core promoter may determine AIRE-mediated down-regulation of ICA69 expression in medullary thymic epithelial cells, thus providing a novel mechanistic explanation for the loss of immunologic tolerance to this self-antigen in autoimmunity. Introduction Accumulating evidence indicates that organ-specific molecules are naturally expressed in the thymus and peripheral lymphoid organs (1,2). Tolerance to tissuerestricted self-molecules is believed to begin at the level of the thymus with negative selection where the deletion of thymocytes with T-cell receptors (TCR) exhibiting strong affinity towards self-molecules are expressed during maturation of the immune system (3-5). The insulin gene is one of the most widely studied genes in both humans and mice exhibiting thymic expression as well as a beta-cell expression-dependent association with T1D susceptibility (2,6-9). For instance, in humans the IDDM2 susceptibility locus of the insulin gene (INS) is a region associated with T1D and has been finely mapped to reveal Variable Number of Tandem Repeat (VNTR) polymorphisms upstream of the INS promoter. The length of these repeats has been directly implicated in the control of the expression levels of insulin mRNA in the thymus (9-11). In addition to insulin, islet cell autoantigen 69 kDa (ICA69), a neuroendocrine protein targeted by autoimmmune responses in human T1D and by gest on July 0, 2020 hp://w w w . jb.org/ D ow nladed from
A Machine Vision Based Surveillance System for California Roads

In this report we address the problem of automation of heavy-duty vehicles. After a brief description of the dynamic model used in our design and simulations, we develop nonlinear controllers with adaptation, rst for speed control and then for vehicle follower longitudinal control. We consider both autonomous operation as well as intervehicle communication, and evaluate the performance of our controllers in several di erent scenarios through simulation.
Optimal Design and Experimental Assessment of a Wireless Power Transfer System for Home-Cage Monitoring

Techniques of long-term in vivo electrophysiological recording play important roles in brain research and neural rehabilitation. To avoid interruption of experiment and risk of infection, use of wireless power transfer (WPT) technique has been suggested to eliminate cumbersome wires and batteries attached to the animals in rodent electrophysiological applications. This paper presents a holistic assessment of the relationships among the physical sizes of the transmitting and receiving coils, power transfer characteristics, and specific absorption rate (SAR) in animals of a simple WPT system using two rectangular coaxial transmitting coils. With given space for the animal and size of the receiving coil, a procedure for designing the minimum driving current, and the transmitting coil dimensions and separation to deliver sufficient power to the receiver, and interactions between the transmitting and receiving coils is derived. A π-capacitor network that can match the impedances of the receiving coil and the load to operate the receiver at the maximum power transfer condition is proposed. It is also optimized for the overall volume. A 100-mW prototype with an operating zone of 400 × 240 × 40 mm3 and a receiving coil with a diameter of 11.45 mm is built and studied. The SAR in the animal is evaluated and compared with the recommended restriction level.
On groups generated by three-dimensional special unitary groups I

This paper is the result of our attempt to carry over the method of our characterization of the linear groups PSL(n, q) (Phan (1972)) to that of the unitary groups PSU (n, q). It appears desirable to have available a result on the generation of the unitary groups more closely related to the splitting of the underlying hermitian spaces of these groups into orthogonal direct sum of anisotropic lines. Another motivation comes also from our work on the unitary groups in which we obtained a fusion pattern different from that of the unitary group when the dimension of the underlying space is eight. This fusion pattern produces a group whose structure is not immediately apparent. In order to identify this group, the result of this paper appears to be a necessary step.
New Era for Molecular Diagnosis of Retinitis Pigmentosa: From Research to Therapy

Retinitis pigmentosa (RP) is a clinical entity composed of a group of genetically heterogeneous retinal dystrophies. It has been known for a long time that RP consists of at least 3 different hereditary forms, i.e., autosomal dominant (AD), autosomal recessive (AR), and X-linked recessive (XL) traits; therefore, it has been thought that the putative causative genes for RP might also be heterogeneous. Due to the inability to completely analyze human genes up until the late 20th century, previous research has been unable to determine any of the disease mechanisms for RP, even though various combinations of biochemical, morphological, physiological and/or pharmacological studies have been undertaken. During the 1980’s, however, evolutionally developed techniques and knowledge of molecular biology finally achieved a level that made it possible for researchers to use polymerase chain reaction (PCR) combined with nucleotide sequencing to relatively easily identify mutations in patients’ genomic DNA. A landmark was finally reached in 1990 when Dryja reported for the first time a point mutation in the rhodopsin (RHO) gene in patients with one form of ADRP [1]. The discovery that mutations in the RHO gene caused RP opened up new research pathways that led many other researchers to try and find mutations in different retina-specific genes that might possibly be candidates responsible for causing RP. Currently, over 80 different causative genes have been reported to be responsible for RP [2,3] (also summarized in the RetNet: http//sph.uth.edu/retnet), which is far more than what was originally expected during the 1980’s. Interestingly, although most of the causative genes for RP are specifically expressed in the photoreceptor or retinal pigment epithelial cells, some, such as the PRPF31 gene, are ubiquitously expressed in numerous tissues other than the retina. The protein product of the PRPF31 gene, i.e., PRPF31, is a component of the spliceosome [4] that is involved in the process of protein biosynthesis. Although previous molecular genetic studies have yet to reveal the entire causative genes for RP, we now know RP is caused by mutations in the genes that are responsible for encoding proteins specifically expressed in the photoreceptor cells or retinal pigment epithelium, or that are important in protein biosynthesis. These results have led to various hypotheses being proposed on the nature of the pathogenesis of the photoreceptor degeneration in RP. Editorial
Graded Brauer Groups.

This paper arose out of the observation that the definitiori of a Clifford algebra äs an invariant of a quadratic form is made awkward by the fact that the algebra eorresponding to the orthogonal direct sum of two quadratic forms is not simply the tensor product of their separate Clifford algebras. In fact, äs is well known, the Clifford algebra admits a grading modulo 2, and we must consider the graded tensor product.
Insulin Causes [Ca ]i-Dependent and [Ca ]i-Independent Positive Inotropic Effects in Failing Human Myocardium

Background—Insulin has been shown to exert positive inotropic effects in several in vitro and in vivo models, but signal transduction and substrate dependency remain unclear. We examined inotropic responses and signal transduction mechanisms of insulin in human myocardium. Methods and Results—Experiments were performed in isolated trabeculae from end-stage failing hearts of 58 nondiabetic and 3 diabetic patients undergoing heart transplantation. The effect of insulin (0.3 and 3 IU/L) on isometric twitch force (37°C, 1 Hz) was tested in the presence of glucose or pyruvate as energetic substrate. Furthermore, intracellular Ca transients (aequorin method), sarcoplasmic reticulum (SR) Ca content (rapid cooling contractures), and myofilament Ca sensitivity (semiskinned fibers) were assessed. In addition, potential signaling pathways were tested by blocking glycolysis, PI-3-kinase, protein kinase C, diacylglycerol kinase, insulin-like growth factor-1 receptors, or transsarcolemmal Ca entry via the Na /Ca exchanger. Insulin exerted concentration-dependent and partially substrate-dependent positive inotropic effects. The phosphatidylinositol-3-kinase inhibitor wortmannin and the Na /Ca exchanger reverse-mode inhibitor KB-R7943 completely or partially prevented the functional effects of insulin. In contrast, insulin-like growth factor-1 receptor blockade, protein kinase C inhibition, and diacylglycerol kinase blockade were without effect. The inotropic response was associated with increases in intracellular Ca transients, SR Ca content, and increased myofilament Ca sensitivity. Conclusions—Insulin exerts Ca -dependent and -independent positive inotropic effects through a phosphatidylinositol-3-kinase– dependent pathway in failing human myocardium. The increased [Ca ]i originates at least in part from enhanced reverse-mode Na /Ca exchange and consequently increased SR-Ca load. These nongenomic functional effects of insulin may be of clinical relevance, eg, during insulin-glucose-potassium infusions. (Circulation. 2005;111:2588-2595.)
Hypothesis for a Serine Proteinase-like D o m a i n at the C O O H Terminus of Slowpoke Calcium-activated Potassium Channels

A B S T RA C T Bovine pancreatic trypsin inhibitor (BPTI) is a 58-residue protein with three disulfide bonds that belongs to the Kunitz family of serine proteinase inhibitors. BPTI is an extremely potent inhibitor of trypsin, but it also specifically binds to various active and inactive serine proteinase homologs with KD values that range over eight orders of magnitude. We previously described an interaction of BPTI at an intracellular site that results in the production of discrete subconductance events in large conductance Ca 2+ activated K + channels (Moss, G.W.J., and E. Moczydlowski. 1996. J. Gen. Physiol. 107:47-68). In this paper, we summarize a variety of accumulated evidence which suggests that BPTI binds to a site on the Kca channel protein that structurally resembles a serine proteinase. One line of evidence includes the finding that the complex of BPTI and trypsin, in which the inhibitory loop of BPTI is masked by interaction with trypsin, is completely ineffective in the production of substate events in the gca channel. To further investigate this notion, we performed a sequence analysis of the ~x-subunit of cloned slowpoke I~: a channels from Drosophila and mammals. This analysis suggests that a region of ~250 residues near the COOH terminus of the Kca channel is homologous to members of the serine proteinase family, but is catalytically inactive because of various substitutions of key catalytic residues. The sequence analysis also predicts the location of a Ca2+-binding loop that is found in many serine proteinase enzymes. We hypothesize that this COOH-terminal domain of the slowpoke Kca channel adopts the characteristic double-barrel fold of serine proteinases, is involved in Ca2+-activation of the channel, and may also bind other intracellular components that regulate Kca channel activity.
Business Process Evaluation in Agile Business Process Management Using Quality Models

—Agile business process management is an adaptation of the agile methodology, which is well-known in the area of software development. It supports the tight and efficient collaboration between customer and process analysts when designing processes. However, this methodology requires a governance approach that ensures the high quality of the processes. This article shows the usage of quality models to evaluate business processes in agile business process management environments and its specific challenges. To illustrate the approach, an existing quality model is reused and formalized. Afterwards, a business process in the context of offer management is captured and evaluated by means of this quality model.
Towards a Framework for Educational Robotics

Educational robotics has been considered as a field with a good potential to teach difficult concepts (e.g. friction) in appealing way. As a consequence, the interest in educational robotics has grown in the last decade, which is reflected in increasing number of robotic platforms, kits, and programming interfaces now available. Nevertheless, researches still fail on describe activities that could be used by teachers and other people with no technological fluency, who are scared by the overwhelm amount of information that made them avoid the use of robotics to teach. Moreover, most of the activities developed until now do not consider pedagogical methodologies to inform the design and implementation of them. As a direct consequence of the misinformation about the correct use of pedagogical methodologies and robotics' multidisciplinary, the number of people who master the use of robotics in education is still scant. This paper presents ongoing work on the development of a framework in the European project Educational Robotics for Science, Technology, Engineer, and Mathematics (ER4STEM). The framework aims to make evident the connection between 21 st century skills, robotics and pedagogical methodologies to support the creation of pedagogical activities, which is defined in ER4STEM as an activity that has clear learning outcomes and evidence of learning, use of one or more pedagogic methodologies during the activity, and detail description of the activity. This is achieve through the critical use of tools and examples of activities developed ER4STEM.
Obesity, Diabetes, and Cardiovascular Diseases Compendium Lipid Use and Misuse by the Heart

1736 T he heart uses large amounts of fatty acids (FAs) as energy-providing substrates. More than 70% of all substrates used for ATP generation are derived from FAs, with the remaining sources being glucose, lactate, ketone bodies, and amino acids. The relatively tight coupling between lipid uptake and oxidation prevents accumulation of excess lipids in the cardiomyocyte. Several processes that affect heart function, including ischemia, sepsis, and heart failure, are associated with a reduction in FA oxidation (FAO) with a relative increase in anaerobic glycolysis and, in some cases, accumulation of nonoxidized FA derivatives in the form of lipids. In addition, excess circulating FA levels in type 2 diabetes mellitus and its precursor, the metabolic syndrome, also cause cardiac lipid accumulation. There is increasing evidence that many of these lipids worsen heart function and lead to structural myocardial damage, including cardiac fibrosis, myocyte apoptosis, and reduced contractility, which is often thought to be caused by mitochondrial dysfunction. However, the reversibility of this dysfunction along with several key steps of oxidative and glycolytic metabolism after the correction of cardiac stress and failure suggest that mitochondrial dysfunction is a reversible adaptation and is secondary to the altered metabolic pathways. 1 Several altered metabolic pathways lead to lipid accumulation. Experimental and clinical data provide evidence that lipid accumulation causes or exacerbates heart dysfunction, a process termed cardiac lipotoxicity. In support of this hypothesis, several recent studies have shown that reduction of toxic lipids is associated with improved metabolism and function of the heart. Abstract: The heart utilizes large amounts of fatty acids as energy providing substrates. The physiological balance of lipid uptake and oxidation prevents accumulation of excess lipids. Several processes that affect cardiac function, including ischemia, obesity, diabetes mellitus, sepsis, and most forms of heart failure lead to altered fatty acid oxidation and often also to the accumulation of lipids. There is now mounting evidence associating certain species of these lipids with cardiac lipotoxicity and subsequent myocardial dysfunction. Experimental and clinical data are discussed and paths to reduction of toxic lipids as a means to improve cardiac function are suggested.