Miracle-dz/UniFAR-FTUs huggingface dataset:
A new model based tracking controller for robot manipulators using the trajectory pattern inverse dynamics

An inverse-dynamics-model-based tracking controller is presented. The inverse dynamics models are derived using the trajectory pattern method. The inverse dynamics models are in the form of a summation of a fundamental sinusoidal time function and a number of its harmonics with constant coefficients. The coefficients were computed offline using analytical expressions that are derived for the selected trajectory pattern. The structure of the inverse dynamics models is fixed for all trajectory patterns and robot manipulators. The controller permits ultrahigh-speed generation of the desired trajectory and feedforward signals. The online computations are minimal. The controller structure and simulation results indicating its effectiveness are presented for a spatial 3R manipulator. <<ETX>>
Smooth Muscle Notch1 Mediates Neointimal Formation After Vascular Injury

Background— Notch1 regulates binary cell fate determination and is critical for angiogenesis and cardiovascular development. However, the pathophysiological role of Notch1 in the postnatal period is not known. We hypothesize that Notch1 signaling in vascular smooth muscle cells (SMCs) may contribute to neointimal formation after vascular injury. Methods and Results— We performed carotid artery ligation in wild-type, control (SMC-specific Cre recombinase transgenic [smCre-Tg]), general Notch1 heterozygous deficient (N1+/−), SMC-specific Notch1 heterozygous deficient (smN1+/−), and general Notch3 homozygous deficient (N3−/−) mice. Compared with wild-type or control mice, N1+/− and smN1+/− mice showed a 70% decrease in neointimal formation after carotid artery ligation. However, neointimal formation was similar between wild-type and N3−/− mice. Indeed, SMCs derived from explanted aortas of either N1+/−- or smN1+/− mice showed decreased chemotaxis and proliferation and increased apoptosis compared with control or N3−/− mice. This correlated with decreased staining of proliferating cell nuclear antigen–positive cells and increased staining of cleaved caspase-3 in the intima of N1+/−- or smN1+/− mice. In SMCs derived from CHF1/Hey2−/− mice, activation of Notch signaling did not lead to increased SMC proliferation or migration. Conclusions— These findings indicate that Notch1, rather than Notch3, mediates SMC proliferation and neointimal formation after vascular injury through CHF1/Hey2 and suggest that therapies that target Notch1/CHF1/Hey2 in SMCs may be beneficial in preventing vascular proliferative diseases.
“Making a good time”: The role of friendship in living successfully with aphasia

Abstract Loss of friendship post-onset of aphasia is well documented, with reduced social network size and social isolation commonly reported. Because friendship has strong links to psychological well-being and health, increased knowledge about friendships of individuals with aphasia will have important clinical implications. This study aimed to explore the perspectives of 25 community dwelling individuals with chronic aphasia on the role of friendship in living successfully with aphasia. Thematic analysis of transcripts from semi-structured in-depth interviews revealed three over-arching themes relating to the role of friendship in participants’ experience of life with aphasia: living with changes in friendships, good times together and support from friends, and the importance of stroke and aphasia friends. Overall, findings highlighted the valued role of friendship in living successfully with aphasia, while also providing evidence of how friendships change and evolve in both negative and positive ways following onset of aphasia. Clinicians are challenged to work creatively to address the role of friendship in life post-stroke in partnership with individuals with aphasia, their families, and friends.
Credible Group-Stability in General Multi-Partner Matching Problems ∗

Pairwise-stable matching mechanisms are practically used and perform very well in the real world two-sided matching markets (e.g., the US hospital-intern market, and the British hospital-intern markets: see Roth 1984 and 1991, respectively). It is known, however, that in a twosided many-to-many matching market (the British market), pairwisestability is not logically related with the (weak) core unlike in a oneto-many matching market (the US market) [see Blair (1988) and Roth and Sotomayor (1990)]. In this paper, we use a graph representation of matching problems, and we define strong group-stability, a matchingvariation of a solution concept in the network literature (Jackson and van den Nouweland, 2002). Although strong group-stability is equivalent to pairwise-stability in a one-to-many matching market, unfortunately, the solution concept is too strong for many-to-many matching markets. Therefore, we proceed to define executable coalitional deviations to discuss the credibility of coalitional deviations, and define credibly group-stable matchings. We prove that credible group-stability is equivalent to pairwise-stability in a wide class of matching problems. We also prove the equivalence between the set of pairwise-stable matchings and the set of matchings resulting from coalition-proof Nash equilibria in an appropriately defined strategic form game.
Acquired Resistance to Imatinib in Gastrointestinal Stromal Tumor Occurs Through Secondary Gene Mutation

Most gastrointestinal stromal tumors (GIST) have an activating mutation in either KIT or PDGFRA. Imatinib is a selective tyrosine kinase inhibitor and achieves a partial response or stable disease in about 80% of patients with metastatic GIST. It is now clear that some patients with GIST develop resistance to imatinib during chronic therapy. To identify the mechanism of resistance, we studied 31 patients with GIST who were treated with imatinib and then underwent surgical resection. There were 13 patients who were nonresistant to imatinib, 3 with primary resistance, and 15 with acquired resistance after initial benefit from the drug. There were no secondary mutations in KIT or PDGFRA in the nonresistant or primary resistance groups. In contrast, secondary mutations were found in 7 of 15 (46%) patients with acquired resistance, each of whom had a primary mutation in KIT exon 11. Most secondary mutations were located in KIT exon 17. KIT phosphorylation was heterogeneous and did not correlate with clinical response to imatinib or mutation status. That acquired resistance to imatinib in GIST commonly occurs via secondary gene mutation in the KIT kinase domain has implications for strategies to delay or prevent imatinib resistance and to employ newer targeted therapies.
Errata for "Crowdsourcing Algorithms for Entity Resolution" (PVLDB 7(12): 1071-1082)

We discovered that there was a duplicate figure in our paper. We accidentally put Figure 13(b) for Figure 12(b). We have provided the correct Figure 12(b) above (See Figure 1). Figure 1 plots the recall of various strategies as a function of the number of questions asked for Places dataset. There was no error in the discussion in our paper (See Section 6.2.1 in our paper for more details).
ODCRE : On-Demand Cluster Routing based on Energy Density in Wireless Sensor Networks

The Energy balancing is one of the critical issue in the wireless sensor networks. The residual energy plays an important role in maintaining the balanced energy status in the network. Many research works have suggested numerous solutions related to energy balancing. In this paper, we proposed an efficient algorithm, which is mainly considering the energy density of the clusters to balance the energy and prolong the network lifetime. A unique two-step cluster head method is devised to select the proper cluster head and the shortest path selection from source to sink is performed by using On-demand routing approach. The simulation results of our research work shows greater improvements in packet delivery ratio and network lifetime.
The past, present, and future of software evolution

Change is an essential characteristic of software development, as software systems must respond to evolving requirements, platforms, and other environmental pressures. In this paper, we discuss the concept of software evolution from several perspectives. We examine how it relates to and differs from software maintenance. We discuss insights about software evolution arising from Lehmanpsilas laws of software evolution and the staged lifecycle model of Bennett and Rajlich. We compare software evolution to other kinds of evolution, from science and social sciences, and we examine the forces that shape change. Finally, we discuss the changing nature of software in general as it relates to evolution, and we propose open challenges and future directions for software evolution research.
Occupational exposure to environmental tobacco smoke.

OBJECTIVES To measure occupational exposures to environmental tobacco smoke in diverse settings, including offices and production areas, and to evaluate the effectiveness of policies that restrict or ban smoking in the workplace. DESIGN Survey. The average weekly concentration of environmental tobacco smoke was measured with passive monitors that sample nicotine. Approximately 25 samples were placed in each worksite for 1 week. SETTING Twenty-five Massachusetts worksites, including fire stations, newspaper publishers, textile dyeing plants, and manufacturers of valves, fiberoptics, flight instruments, batteries, adhesives, semiconductor equipment, filters, and tools and dies. Samples were collected in offices and production areas. MAIN OUTCOME MEASURES The distribution of nicotine concentrations in various work settings as a function of company smoking policy. These data were interpreted with three approaches: comparing measured concentrations with a published risk assessment; comparing occupational exposures with home exposures; and evaluating the "cigarette equivalents" to which workers were exposed. RESULTS Worksite smoking policy had a major effect on the nicotine concentrations, which fell from a median of 8.6 micrograms/m3 in the open offices at worksites that allowed smoking to 1.3 micrograms/m3 in sites that restricted smoking, and to 0.3 microgram/m3 in worksites that banned smoking. The nonoffice workspaces were affected similarly, with median concentrations of 2.3, 0.7, and 0.2 microgram/m3 at worksites that allowed, restricted, and banned smoking, respectively. CONCLUSION All three evaluation methods indicated that occupational exposure to environmental tobacco smoke presents a substantial risk to workers in the absence of a policy restricting or banning smoking.
Extracellular signal‐regulated activation of Rap1 fails to interfere in Ras effector signalling

The small GTPase Rap1 has been implicated in both negative and positive control of Ras‐mediated signalling events. We have investigated which extracellular signals can activate Rap1 and whether this activation leads to a modulation of Ras effector signalling, i.e. the activation of ERK and the small GTPase Ral. We found that Rap1 is rapidly activated following stimulation of a large variety of growth factor receptors. These receptors include receptor tyrosine kinases for platelet‐derived growth factor (PDGF) and epithelial growth factor (EGF), and G protein‐coupled receptors for lysophosphatidic acid (LPA), thrombin and endothelin. At least three distinct pathways may transduce a signal towards Rap1 activation: increase in intracellular calcium, release of diacylglycerol and cAMP synthesis. Surprisingly, activation of endogenous Rap1 fails to affect Ras‐dependent ERK activation. In addition, we found that although overexpression of active Rap1 is able to activate the Ral pathway, activation of endogenous Rap1 in fibroblasts does not result in Ral activation. Rap1 also does not negatively influence Ras‐mediated Ral activation. We conclude that activation of Rap1 is a common event upon growth factor treatment and that the physiological function of Rap1 is likely to be different from modulation of Ras effector signalling.
Pathogenesis of Helicobacter pylori infection

Five years after publication of the complete genome sequence of Helicobacter pylori, research interest is shifting from the descriptive association of virulence factors with clinical outcome in infected patients to the molecular mechanisms of virulence factor action. This is particularly noticeable for VacA and CagA, for both of which detailed understanding of the interaction with host signalling pathways has accumulated over the last year. The role of H. pylori Lewis antigens for clinical outcome was further substantiated. Various strategies of H. pylori to fool or evade the human immune system are described, which all lead to the dysfunction of specific compartments of the host cellular immune system. Finally, a number of animal models indicate that inflammation is a key factor for gastric carcinogenesis, which is finally supported by a large prospective study identifying corpus atrophy and intestinal metaplasia as precancerous conditions.
Online Learning with Sample Path Constraints

We study online learning where a decision maker interacts with Nature with the objective of maximizing her long-term average reward subject to some sample path average constraints. We define the reward-in-hindsight as the highest reward the decision maker could have achieved, while satisfying the constraints, had she known Nature's choices in advance. We show that in general the reward-in-hindsight is not attainable. The convex hull of the reward-in-hindsight function is, however, attainable. For the important case of a single constraint, the convex hull turns out to be the highest attainable function. Using a calibrated forecasting rule, we provide an explicit strategy that attains this convex hull. We also measure the performance of heuristic methods based on non-calibrated forecasters in experiments involving a CPU power management problem.
Demonstrating the BigDAWG Polystore System for Ocean Metagenomics Analysis

In most Big Data applications, the data is heterogeneous. As we have been arguing in a series of papers, storage engines should be well suited to the data they hold. Therefore, a system supporting Big Data applications should be able to expose multiple storage engines through a single interface. We call such systems, polystore systems . Our reference implementation of the polystore concept is called BigDAWG (short for the Big Data Analytics Working Group). In this demonstration, we will show the BigDAWG system and a number of polystore applications built to help ocean metage-nomics researchers handle their heterogenous Big Data.
Analysis of Malware behavior: Type classification using machine learning

Malicious software has become a major threat to modern society, not only due to the increased complexity of the malware itself but also due to the exponential increase of new malware each day. This study tackles the problem of analyzing and classifying a high amount of malware in a scalable and automatized manner. We have developed a distributed malware testing environment by extending Cuckoo Sandbox that was used to test an extensive number of malware samples and trace their behavioral data. The extracted data was used for the development of a novel type classification approach based on supervised machine learning. The proposed classification approach employs a novel combination of features that achieves a high classification rate with a weighted average AUC value of 0.98 using Random Forests classifier. The approach has been extensively tested on a total of 42,000 malware samples. Based on the above results it is believed that the developed system can be used to pre-filter novel from known malware in a future malware analysis system.
Identification of Novel AR-Targeted MicroRNAs Mediating Androgen Signalling through Critical Pathways to Regulate Cell Viability in Prostate Cancer

MicroRNAs (miRNAs) have been recognized as significantly involved in prostate cancer (PCa). Since androgen receptor (AR) plays a central role in PCa carcinogenesis and progression, it is imperative to systematically elucidate the causal association between AR and miRNAs, focusing on the molecular mechanisms by which miRNAs mediate AR signalling. In this study, we performed a series of time-course microarrays to observe the dynamic genome-wide expressions of mRNAs and miRNAs in parallel in hormone-sensitive prostate cancer LNCaP cells stimulated by androgen. Accordingly, we introduced Response Score to identify AR target miRNAs, as well as Modulation Score to identify miRNA target mRNAs. Based on theoretical identification and experimental validation, novel mechanisms addressing cell viability in PCa were unravelled for 3 miRNAs newly recognized as AR targets. (1) miR-19a is directly up-regulated by AR, and represses SUZ12, RAB13, SC4MOL, PSAP and ABCA1, respectively. (2) miR-27a is directly up-regulated by AR, and represses ABCA1 and PDS5B. (3) miR-133b is directly up-regulated by AR, and represses CDC2L5, PTPRK, RB1CC1, and CPNE3, respectively. Moreover, we found miR-133b is essential to PCa cell survival. Our study gives certain clues on miRNAs mediated AR signalling to cell viability by influencing critical pathways, especially by breaking through androgen’s growth restriction effect on normal prostate tissue.
Neuromedin U facilitates oxytocin release from the pituitary via &bgr; adrenoceptors

Neuromedin U activates noradrenergic neurones in the medulla oblongata and oxytocin neurones in the hypothalamus. Here we examined roles of noradrenergic transmission in oxytocin release from the pituitary after intracerebroventricular administration of neuromedin U in rats. Neuromedin U administration facilitated noradrenaline release in the supraoptic nucleus. Administration of a &bgr;1 adrenoceptor antagonist, metoprolol, or a &bgr;2 antagonist, ICI 118551 but not an &agr;1 antagonist, benoxathian, reduced increases in plasma oxytocin concentrations observed after administration of neuromedin U, but plasma ACTH concentrations were not significantly changed. All theses data suggest that neuromedin U stimulates oxytocin release from the pituitary, at least in part, via activation of &bgr; adrenoceptors.
Pigment Epithelium–Derived Factor Alleviates Tamoxifen-Induced Endometrial Hyperplasia

Tamoxifen is a cornerstone component of adjuvant endocrine therapy for patients with hormone-receptor–positive breast cancer. Its significant adverse effects include uterine hyperplasia, polyps, and increased risk of endometrial cancer. However, the underlying molecular mechanism remains unclear. Excessive angiogenesis, a hallmark of tumorigenesis, is a result of disrupted balance between pro- and anti-angiogenic factors. VEGF is a pro-angiogenic factor shown to be elevated by tamoxifen in the uterus. Pigment epithelium–derived factor (PEDF) is a potent anti-angiogenic factor that suppresses strong pro-angiogenic factors, such as VEGF. Our aim was to investigate whether angiogenic balance plays a role in tamoxifen-induced uterine pathologies, elucidate the molecular impairment in that network, and explore potential intervention to offset the proposed imbalance elicited by tamoxifen. Using in vivo mouse models, we demonstrated that tamoxifen induced a dose-dependent shift in endogenous uterine angiogenic balance favoring VEGF over PEDF. Treatment with recombinant PEDF (rPEDF) abrogated tamoxifen-induced uterine hyperplasia and VEGF elevation, resulting in reduction of blood vessels density. Exploring the molecular mechanism revealed that tamoxifen promoted survival and malignant transformation pathways, whereas rPEDF treatment prevents these changes. Activation of survival pathways was decreased, demonstrated by reduction in AKT phosphorylation concomitant with elevation in JNK phosphorylation. Estrogen receptor-α and c-Myc oncoprotein levels were reduced. Our findings provide novel insight into the molecular mechanisms tamoxifen induces in the uterus, which may become the precursor events of subsequent endometrial hyperplasia and cancer. We demonstrate that rPEDF may serve as a useful intervention to alleviate the risk of tamoxifen-induced endometrial pathologies. Mol Cancer Ther; 14(12); 2840–9. ©2015 AACR.
Reciprocity: Understanding online social relations

Reciprocity is a key concept for understanding social behaviour. It involves complex interactions of giving and returning. This paper examines the concept of reciprocity to think about, and design for, online social interactions. We argue that reciprocal exchange is symbolic insofar as it produces and enacts many forms of social life by drawing individuals into a relation of recognition. Indeed, reciprocal interactions underlie much online activity, and a fuller understanding of the concept explains important aspects of how social life is conducted with others online. We contrast our understanding of reciprocity with those of more dominant theories of interaction built on the assumption that actions, including those that seek reciprocity, are self–interested or otherwise altruistic. This assumption ignores how social actions that solicit a return–action seek to neither profit nor benefit, but rather express a desire to draw in others into social life and relationships. After analysing three kinds of online activity (web forums, social networking sites, and online games) using our view of this concept, we conclude with implications for designers who seek to support the development of our digitally–mediated social life.
Fusion of Hidden Markov Random Field Models and Its Bayesian Estimation

In this paper, we present a Hidden Markov Random Field (HMRF) data-fusion model. The proposed model is applied to the segmentation of natural images based on the fusion of colors and textons into Julesz ensembles. The corresponding Exploration/Selection/Estimation (ESE) procedure for the estimation of the parameters is presented. This method achieves the estimation of the parameters of the Gaussian kernels, the mixture proportions, the region labels, the number of regions, and the Markov hyper-parameter. Meanwhile, we present a new proof of the asymptotic convergence of the ESE procedure, based on original finite time bounds for the rate of convergence
Meat and fish consumption and risk of pancreatic cancer: Results from the European Prospective Investigation into Cancer and Nutrition

Pancreatic cancer is the fourth most common cause of cancer death worldwide with large geographical variation, which implies the contribution of diet and lifestyle in its etiology. We examined the association of meat and fish consumption with risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 477,202 EPIC participants from 10 European countries recruited between 1992 and 2000 were included in our analysis. Until 2008, 865 nonendocrine pancreatic cancer cases have been observed. Calibrated relative risks (RRs) and 95% confidence intervals (CIs) were computed using multivariable‐adjusted Cox hazard regression models. The consumption of red meat (RR per 50 g increase per day = 1.03, 95% CI = 0.93–1.14) and processed meat (RR per 50 g increase per day = 0.93, 95% CI = 0.71–1.23) were not associated with an increased pancreatic cancer risk. Poultry consumption tended to be associated with an increased pancreatic cancer risk (RR per 50 g increase per day = 1.72, 95% CI = 1.04–2.84); however, there was no association with fish consumption (RR per 50 g increase per day = 1.22, 95% CI = 0.92–1.62). Our results do not support the conclusion of the World Cancer Research Fund that red or processed meat consumption may possibly increase the risk of pancreatic cancer. The positive association of poultry consumption with pancreatic cancer might be a chance finding as it contradicts most previous findings.